ПАРОДОНТОЛОГИЯ

Учебное пособие
для студентов IV курса
стоматологического факультета

Москва
Российский университет дружбы народов
2018
PERIODONTOLOGY

Tutorial guide
for dental students of IV year
of Dental Faculty

Moscow
Peoples' Friendship University of Russia
2018
УДК 616.31(075.8) Утверждено
ББК 56.6 РИС Ученого совета
П18 Российского университета
дружбы народов

Рецензент–
доктор медицинских наук, профессор
РНИМУ им. Н.И. Пирогова И.С. Копецкий

Коллектив авторов:
Ф.Ю. Даурова, М.К. Макеева, З.С. Хабадзе,
И.В. Багдасарова, А.И. Маркова

П18 Пародонтология = Periodontology : учебное пособие для студентов IV курса

стоматологического факультета / Ф. Ю. Даурова, М. К. Макеева, З. С. Хабадзе,
И. В. Багдасарова, А. И. Маркова. – Москва : РУДН, 2018. – 156 с. : ил.

ISBN 978-5-209-08700-7

Учебное пособие предназначено для студентов стоматологических факультетов,

проходящих обучение на английском языке в медицинских ВУЗах России, четвертого года
обучения. Излагаемый материал разделен на главы. В учебнике освещены анатомия и
функции тканей пародонта, этиология и патогенез воспалительных заболеваний пародонта,
классификации пародонтологических заболеваний, основные и дополнительные методы
обследования пародонтологического пациента, микробиология полости рта и способы
удаления зубных отложений, принципы лечения воспалительных заболеваний пародонта.
Данные темы рассмотрены с точки зрения современных данных и в соответствии с
принципами доказательной медицины.
The tutorial guide is intended for students of dental faculties, who are trained in English in
medical universities in Russia, the fourth year of study. The material is divided into chapters. The
textbook covers the anatomy and functions of periodontal tissues, the etiology and pathogenesis of
periodontal inflammatory diseases, the classification of periodontal diseases, basic and additional
methods for examining the periodontal patient, microbiology of the oral cavity and methods for
removing dental deposits, the principles of treatment of inflammatory periodontal diseases. These
topics are considered from the point of view of modern data and in accordance with the principles
of evidence-based medicine.

ISBN 978-5-209-08700-7 УДК 616.31(075.8)

ББК 56.6

© Ф.Ю. Даурова, М.К. Макеева, З.С. Хабадзе,

И.В. Багдасарова, А.И. Маркова, 2018
© Российский университет дружбы народов, 2018

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Content

Study 1. Anatomy and functions of periodontium. Age-related changing in periodontium.

Prevalence of periodontal diseases…………………………………………………………..…5
Study 2. Etiology of inflammatory diseases of periodontal tissues
(local and systemic factors). Pathogenesis of inflammatory diseases of periodontal tissue…..23
Study 3. Examination of patients with periodontal diseases. Basic and additional methods
of diagnosis of periodontal diseases…………………………………………………………...42
Study 4. Colloquium 1………………………………………………………………………..65
Study 5. Basic treatment of inflammatory periodontal diseases – professional oral hygiene
and anti-inflammatory therapy………………………………………………………………...66
Study 6. Classification of periodontal diseases. Catarrhal gingivitis. Histopathology.
Clinical Features. Diagnostics. Treatment. Prevention………………………………………..80
Study 7. Hypertrophic gingivitis. Histopathology. Clinical Features. Diagnostics.
Treatment. Prevention…………………………………………………………………………91
Study 8. Ulcerative gingivitis. Histopathology. Clinical Features. Diagnostics. Treatment.
Prevention……………………………………………………………………………………..96
Study 9. Medical History Presentation 1…………………………………………………..100
Study 10. Colloquium 2……………………………………………………………………..103
Study 11. Chronic Marginal Periodontitis. Clinical features. Diagnostics. Prevention……..104
Study 12. Aggressive periodontitis. Histopathology. Etiology. Clinical Features.
Diagnostics…………………………………………………………………………………...112
Study 13. Treatment Planning of Marginal Periodontitis. Methods of treatment of periodontal
diseases. Splinting. Jankelson's technique for occlusal equilibration………………………...116
Study 14. Periodontal surgery procedures…………………………………………………....121
Study 15. Colloquium 3……………………………………………………………………..127
Study 16. Gingival recessions. Etiology. Classification. Mucogingival surgery…………....128
Study 17. Periodontosis. Clinical features, diagnosis, treatment…………………………....139
Study 18. Periodontomas. Clinical features, diagnosis, treatment…………………………..140
Study 19. Medical History Presentation 2…………………………………………………142
Study 20. Colloquium 4……………………………………………………………………..145

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Study 1. Anatomy and functions of periodontium. Age-related changing in periodontium.
Prevalence of periodontal diseases.
Anatomy and functions of periodontium
The normal periodontium provides the support to maintain teeth in function. It consists of four
components:
• gingiva
• periodontal ligament
• cementum
• alveolar bone
Each of these periodontal components is distinct in its tissue architecture, biochemical and
chemical composition, but all of them function together as a single unit. Pathologic changes that
occur in one periodontal component may have significant ramifications for the maintenance,
repair, or regeneration of other components of the periodontium.

Gingiva
Gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and
surrounds the necks of the teeth. Healthy gingiva may be pink color or may have physiological
pigmentation (Fig. 1).

Figure 1. Physiological pigmentation of gingiva

A gingiva is divided into three part (Fig. 2):
• marginal gingiva (also called “unattached gingiva”, or “free gingiva”)
• attached gingiva
• interdental areas (papillae)

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 Figure 2. Scheme of anatomical features of gingiva

All parts are specifically structured to function appropriately against mechanical and microbial
damage.
Marginal gingiva (free gingiva). The marginal or unattached gingiva is the terminal edge of the
gingiva that surrounds the teeth in collar-like fashion. In about 50% of cases, it is demarcated
from the adjacent attached gingiva by a shallow linear depression called the free gingival groove
(Fig. 3). Free gingival groove is a projection of the bottom of the gingival sulcus on the outer
surface of gingiva. The marginal gingiva is usually about 1-2 mm wide, and it forms the soft-
tissue wall of the gingival sulcus.

A B
Figure 3. In this photo (A) free gingival groove is visible as depression line near lower central
incisors. (A) clinical view; (B) dotted black line shows free gingival groove. Note discoloration
of teeth cause by tetracycline.

Marginal gingiva forms gingival sulcus (Fig. 4). The gingival sulcus is the shallow crevice
around the tooth bounded by the surface of the tooth on one side and the epithelium lining the
free margin of the gingiva on the other side.

6
 Figure 4. Two periodontal probe show the depth of the gingival sulcus.
The clinical determination of the depth of the gingival sulcus is an important diagnostic
parameter. Gingival sulcus has a depth of 0.5 – 3 mm (average 1.8), any depth greater than 3
mm, considered pathological, a sulcus this depth is known as periodontal pocket.
Attached gingiva. The attached gingiva is continuous with the marginal gingiva. It is firm,
resilient, and tightly bound to the tooth in the neck area and to the underlying periosteum of
alveolar bone. Attached gingiva is demarcated with non-keratinized alveolar mucosa by
mucogingival junction. Actually, attached gingiva is distance from free gingival groove to a
mucogingival junction. The width of an attached gingiva differs in different areas of the mouth.
Generally, the widest is in incisors area, the width decreases to the molar area, but the narrowest
width of attached gingiva is in area of premolars and third molars.
Interdental gingiva. The interdental gingival (or interdental papilla) occupies the interproximal
space between neighboring teeth and beneath the contact point. Shape of interdental gingival is
variable. It may be pyramidal, where papilla has one tip is located immediately beneath the
contact point. Or papilla may have two tips on facial and lingual sides; and these tips are
connected by valley like depression conforms to the shape of the interproximal contact. The
shape of the gingiva in a given interdental space depends on the presence or absence of a contact
point between the neighboring teeth, the distance between the contact point and the osseous
crest, and the presence or absence of gingival recession. If tremas or diastema is present, the
gingiva is firmly bound over the interdental bone to form a smooth, rounded surface without
interdental papillae
In gingival anatomy there are three important parameters:
• biological width of gingiva
• width of the attached gingiva.
• width of the keratinized gingival is measured from the mucogingival junction to the free
gingival margin.
The role of biological width of gingiva in maintaining of periodontal health. Biologic width is the
term applied to the dimensional width of epithelial attachment and underlying connective tissue
that attached to the tooth. It is also defined as the dimension of the soft tissue, which is attached
to the portion of the tooth coronal to the crest of the alveolar bone (Fig. 5).

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 Figure 5. Scheme of anatomical features of gingiva: a – gingival sulcus, b – epithelial
attachment; c – connective tissue attachment above alveolar crest; d – biological width of
gingiva; e – periodontal ligament.

Gargiulo et al. reported in 1961 dimensions of some components of biologic width:

• mean depth of the histologic sulcus is 0.69 mm,

• mean junctional epithelium measures 0.97 mm (0.71-1.35 mm),
• mean supraalveolar connective tissue attachment is 1.07 mm (1.06-1.08 mm).

The total of the attachment is therefore 2.04 mm and is called the biologic width. In fact,
biological width is variable.
Biologic width functions as a barrier against the entrance of microorganisms into the internal
medium of the periodontal ligament and into a gingival connective tissue and alveolar bone.
The role of attached gingiva in maintaining of periodontal health. In 1979 Cohen & Goldman in
“tissue barrier concept” postulated that dense collagenous band of attached gingiva retard or
obstruct the spread of inflammation better than does loose fibers arrangement of the alveolar
mucosa. Insufficient width of attached gingiva will facilitate subgingival plaque formation
because of improper sulcus/periodontal pocket closure resulting from movability of marginal
tissue. Some people are born without sufficient width of attached gingiva which result in muscles
of lips and cheeks to pull gingiva down cause recessions and bone resorption because of
increased plaque accumulation and chronic ischemia as a result of pulling.
Significance of attached gingiva for the maintenance of periodontal health:
• to dissipate the pull on the gingival margin created by the muscles of the adjacent
alveolar mucosa during chewing, speaking and other functioning, also in case of external
trauma.
• to retard spreading of inflammation infiltrate from inflamed gingival margin apically
because dense collagen fibers obstruct space inside tissue where infiltrate may move.
Thus dense collagen fibers of attached gingiva make progression of inflammation slower.

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The role of keratinized gingiva in maintaining of periodontal health. The maintenance of
periodontal health is thought to be related to the presence of sufficient width of keratinized
gingiva. Keratinized gingiva is measured from the mucogingival junction to the free gingival
margin. Keratinized gingiva to compare with nonkeratinized alveolar mucosa is more protective
and better withstand mechanical irritation.
Keratinized gingiva functions:
• to protect the periodontium from injury caused by forces encountered during mastication
(because keratinized epithelium is always more resistant to compare with non-
keratinized).
• more resistant to frictional contact that occurs during oral hygiene procedures thus
improve patients’ comfort during brushing. Lack of keratinized gingiva may create an
environment that is less amenable to oral cleansing and more susceptible to irritation and
discomfort during such routine procedures. Adequate keratinized gingiva provide stable
base for maintaining good oral hygiene procedure.
• provides a barrier to inflammatory infiltrate migration inside tissue. When inflammation
is present, it apical migration may occur more rapidly in zones with less keratinized
gingiva compared to those sites with wider zones of keratinized gingiva because of rete
pegs in keratinized gingiva are long, deep and locates close to each other thus provide
obstructions for inflammatory infiltrate spreading.
Lang and Loe in 1972 stated that at least 2 mm of keratinized gingiva, of which 1 mm must be
attached, is required for stability of the periodontium. This conclusion also rationalized the
introduction of numerous surgical procedures to increase the width of keratinized gingiva in
deficient area.
Later studies challenged this concept of the need for a minimal amount of keratinized gingiva,
and have shown that by controlling inflammation with adequate oral hygiene, periodontal
stability can be maintained with almost no keratinized gingiva. An exception to this was in teeth
with subgingival restorations (including crowns and implants). There was a significant
association between subgingival restorations and gingival inflammation in areas of minimal
keratinized gingiva. An increase in plaque and inflammation infiltrate are observed in areas
where subgingival restorations were placed with minimal keratinized gingiva (Greenstein, 2011).
Implants surrounded by less than 2 mm of keratinized gingiva are more susceptible to plaque
accumulation, gingival inflammation, marginal bone loss, and increased gingival recession.
It is necessary to understand that attached gingiva and keratinized gingiva are not separate
structures. Attached gingiva is a part of keratinized gingiva. Actually, they provide periodontal
stability together but here their functions were described separately for better understanding
physiological mechanisms of protection.

Dentogingival junction. The dentogingival junction (Fig. 6) is the junction between the enamel
or cementum of the tooth and the gingival tissue. It consists of gingival epithelium, sulcular
epithelium, junctional epithelium (Table 1) and connective tissue above alveolar crest. The
dentogingival junction is unique feature that function is the attachment of the gingiva to the
tooth.

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Figure 6. Scheme of dentogingival junction: 1 – junctional epithelium, 2 – sulcular epithelium, 3
– gingival epithelium,

Connective tissue above the alveolar crest consists of dentogingival fibers and circular fibers
(Fig. 7)

Figure 7. Connective tissue above alveolar crest.

Table 1. Characteristics of the epithelial components of the dentogingival junction

Gingival Epithelium

• Stratified squamous keratinized epithelium.

• Continuous with the sulcular epithelium at the gingival margin.
• Covers both the free and attached gingival tissues.
Sulcular Epithelium

• Stratified squamous epithelium.

• Non-keratinized.
• Faces the tooth surface but is not attached to it.
• Forms the soft tissue lining of the gingival sulcus or periodontal pocket.

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 Junctional Epithelium

• Forms the epithelial attachment between the gingiva and the tooth.
• Non-keratinized.
• Forms the floor of the sulcus/pocket.
• Wraps around the tooth like a collar, in health following the morphology of the cementoenamel
junction.
• Wider at the floor of the sulcus (15-30 cells thick) and tapers apically to 3-4 cells thick.
• Comprised of layers of flattened squamous cells oriented parallel to the tooth surface.
• Cells attach to the tooth surface via hemidesmosomes.
• The basal lamina is unique because it binds with calcified surface of cementum.

Oral Vestibule
Oral cavity divided in to oral cavity proper and oral vestibule. Depth of oral vestibule along with
width of attached gingiva are important factors of periodontal health. Vestibular depth is defined
as the distance between the coronal border of the attached gingiva (free gingival sulcus) and
greatest concavity of the mucobuccal fold. In 1953, Goldman emphasized that a shallow
vestibule leads to food impaction against the gingival margin and into the interproximal spaces,
which makes it difficult for the patient to clean the area.
The oral vestibule contains frenula of upper and lower lips and buccal frenula.

Frenula of upper and lower lips play an important role in maintaining of health status of
periodontal tissues in that areas. Labial frenula are thin folds of mucous membrane with
enclosed muscle fibers originating from orbicularis oris muscle that attach at the lips to the
alveolar mucosa and underlying periosteum. The labial frenum is located in the middle of the
oral vestibule. Their primary function is to provide stability of the upper and lower lips.
Histological observation of the labial frenum has demonstrated the existence of the epithelium
and muscle fibers. Clinically, an abnormal labial frenum can retract the gingival margin and
cause its ischemia, cause gingival recession and also cause a median diastema.

The upper and lower labial frenula are commonly attached below the upper and lower alveolar
crests, respectively. Depending upon the extension of attachment of fibers, it has been classified
as:

1. Mucosal frenal attachments – when the frenal fibers are attached up to mucogingival
junction (Fig. 8)
2. Gingival frenal attachments – when fibers are inserted within attached gingiva (Fig. 9)
3. Papillary frenal attachments – when fibers are inserted into interdental papilla (Fig. 10)
4. Papillary penetrating frenal attachment – when fibers cross alveolar crest between teeth
and penetrates palatine part of interdental papilla (Fig. 11).

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 Figure 8. Mucosal frenal attachment – fibers of frenum are inserted in the area of
mucogingival junction

Figure 9. Gingival frenal attachment – fibers of frenum are inserted into the attached gingiva
zone

Figure 10. Papillary frenal attachment – fibers of frenum are inserted into the gingival papilla

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 Figure 11. Papillary penetrating frenal attachment – fibers cross alveolar crest between teeth
and penetrates palatine part of interdental papilla

Clinically, papillary frenal attachment and papillary penetrating frenal attachment are considered
as pathological and have been found to be associated with loss of papilla, recession, diastema
(Fig. 9, 10), difficulty in brushing and it may also prejudice the denture fit or retention leading to
psychological disturbances to the individual.

A frenula can become a significant problem if tension from lip movement pulls the gingival
margin away from the tooth, encroach on the marginal gingiva distend the gingival sulcus,
fostering plaque accumulation, increasing the rate of progression of periodontal recession.

Buccal frenum (Fig. 12) is mucous membrane fold that overlies dense fibrous connective tissue
and muscle fibers of mimetic muscles. Their functions is to prevent overstretching of oral
vestibule. Buccal frenula may be located in both upper and lower jaws, most often in area of
canines and premolars but other locations are also possible. Depending on an anatomy, buccal
frenula may cause the same negative effect as labial frenula.

Figure 12. Buccal frenum in area of canine and premolar in upper right maxilla

Histological Features of Gingiva. Histological features differ in different part of gingiva. From
histological point of view two types of mucosa may be found in periodontal tissues: masticatory
mucosa and lining mucosa.
Masticatory mucosa consists of stratified squamous epithelium and lamina propria (loose
connective tissue). No distinct submucosa is noted as overlying mucosa is directly attached to
underlying periosteum of alveolar bone.
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Stratified squamous epithelium may be:
• keratinized – cells of surface layer contain only keratohyaline granules and doesn’t
contain nuclei, cytoplasm and organelles
• parakeratinized – cells of surface layer contain not only keratohyaline granules but also
nuclei and cytoplasm (like differentiation of keratinocytes is not finished).
• non-keratinized – has living cells in the surface layer but they lose their desmosomes
contacts and exfoliate.
External aspect of marginal gingiva and attached gingival in most cases are covered by
keratinized epithelium. In some cases it may contain parakeratinized area and non-keratinized
zones. Internal aspect of marginal gingival (gingival sulcus wall) is covered by non-keratinized
sulcular epithelium. It is a thin, nonkeratinized stratified squamous epithelium without rete pegs,
and it extends from the coronal limit of the junctional epithelium to the crest of the gingival
margin.
Keratinized epithelium better withstands masticatory loads to compare with parakeratinized and
non-keratinized. Cells of epithelium locate on basal membrane. Keratinized epithelium of oral
cavity differ from epithelium of skin by the absence of translucent layer (stratum lucidum).
Comparison of cells layers of keratinized and non-keratinized epithelium of oral cavity is
presented in table 2.
Table 2. Comparison of cells layers of keratinized and non-keratinized epithelium of oral cavity

Epithelial cells with basal membrane invade into underlying lamina propria by rete pegs – an
epithelial extensions. In masticatory mucosa rete pegs are long, deep and locates close to each
other in lamina propria. This fact makes masticatory mucosa dense, firm, not movable and highly
resisted to masticatory loads. In the epithelium of the mouth, the attached gingiva exhibits rete
pegs, while the sulcular and junctional epithelia do not.

Unique histological feature of gingiva is junctional epithelium (or attachment epithelium) which
response for the firm connection of gingiva to the tooth surface. A basal lamina-like material is
secreted by this epithelium and adhere firmly to the tooth structure. The cells then attached to
this substance by hemidesmosomes. The basal lamina and hemidesmosomes are together
responsible for attachment. In young individuals, this attachment is to enamel; in older
individuals, where passive tooth eruption and gingival recession expose the root, the attachment
is to cementum.
Lamina propria consist of loose connective tissue and exhibit two layers – papillary layer (this is
connective tissue locates between epithelial rete pegs) and reticular layer (this is connective
tissue locates beneath rete pegs). Structural elements of lamina propria are ground substance,
fibers and cells typical for connective tissues (Table 3).
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Table 3. Composition of lamina propria of oral cavity

Periodontal Ligament
The periodontal ligament is the fibrous connective tissue structure, with neural and vascular
components, that locates between root surface and alveolar socket wall; and joins the cementum
covering the root to the alveolar bone. The thickness of the periodontal ligament varies from 0.1
to 0.4 mm with a mean of around 0.2 mm. The ligament is thicker in functioning than in non-
functioning teeth. The periodontal ligament plays a key role in protecting the tooth from being
resorbed by the normal remodelling process that affects the adjacent alveolar bone.
Functions of the periodontal ligament:
1) Supportive function. The periodontal ligament serves primarily a supportive function by
attaching the tooth to the surrounding alveolar bone by principal fibers.
2) Force absorption. The periodontal ligament also serves as a shock-absorber by
mechanisms that provide resistance to light as well as heavy forces. Light forces are
cushioned by intravascular fluid that is forced out of the blood vessels. Moderate forces
are also absorbed by extravascular tissue fluid that is forced out of the periodontal
ligament space into the adjacent marrow spaces. The heavier forces are taken up by the
principal fibers.
3) Remodeling function. The periodontal ligament provides remodeling by providing cells
that are able to form as well as resorb all the tissues that make up the attachment
apparatus, i.e. bone, cementum and the periodontal ligament Undifferentiated
ectomesenchymal cells, located around blood vessels, can differentiate into the
specialized cells that form bone (osteoblasts), cementum (cementoblasts), and connective
tissue fibers (fibroblasts). Bone-resorbing cells (osteoclasts) are derived from blood-
borne macrophages.
4) Sensory function. The periodontal ligament is richly supplied with nerve endings that are
primarily receptors for pain and pressure.
5) Nutritive function. The ligament is well-vascularized and provide nutrition for all cells.

Periodontal ligament is a connective tissue in nature, thus consists of fibers, cells and ground
substance. Despite its fibrous nature, the periodontal ligament is a highly cellular structure that is
15
able to perform a number of important functions that are essential for the long-term health of the
masticatory apparatus.
Periodontal fibers. The periodontal fibers of the periodontal ligament are primarily composed of
bundles of type I collagen fibrils. They have been classified into several groups on the basis of
their anatomic location. The following constitute the principal fiber groups of the periodontal
ligament (Fig. 13):
1) Alveolar crest fibers
2) Horizontal fibers
3) Oblique fibers
4) Periapical fibers
5) Interradicular fibers

Figure 13. Principal fibers of periodontal ligament: AC – alveolar crest fibers, H – horizontal
fibers, OBL – oblique fibers, PA – periapical fibers, IR – interradicular fibers

In addition to the collagen fibers, the periodontal ligament also contains oxytalan fibers that are
related to the microfibrillar component of elastic fibers. They generally run parallel to the root
surface, although they can occasionally insert into cementum.
The periodontal ligament is composed of collagen fibers. Fibers start as fibers of different
diameters at the bone or cementum surface (diameter on the bone side is wider than the
cementum side). Here collagen fibers are continuation of mineralized fibers embedded into
mineralized tissue (bone or cementum) – so called Sharpey’s fibers. Thus, the Sharpey's fibers
are the mineralized continuation of the thick fiber bundles of periodontal ligament.
Whether fibers originate from bone or cementum, they starts as thick bundles and then unravel
into smaller fibers, which join up with those of adjacent fibers to produce a meshwork of
interconnected fibers oriented between bone and cementum. Thus, the periodontal fibers do not
stretch cable-like from cementum to bone, but form a meshwork of interconnected fibers.
After they unravel and become intermeshed with adjacent fibers, they form thicker fiber bundles
again and insert into bone or cementum. Alveolar socket wall adjacent to the periodontal
ligament in covered by bundle bone, so named because it contains numerous Sharpey's fibers.
In addition to the collagen fibers, the periodontal ligament also contains oxytalan fibers that are
related to the microfibrillar component of elastic fibers. They generally run parallel to the root
surface, although they can occasionally insert into cementum.
Periodontal ligament cells. The periodontal ligament contains a unique assortment of cells that
are capable of generating and maintaining three distinct tissues, namely the ligament itself as
well as the mineralized tissues on either side of it, i.e. the cementum and the alveolar bone.

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The major cell types of the periodontal ligament include the following:
• Fibroblasts, macrophages and undifferentiated ectomesenchymal cells.
• Cementoblasts and cementoclasts.
• Osteoblasts and osteoclasts.
• Cell rests of Malassez.
These cells are responsible not only for the synthesis of collagen and its assembly into collagen
fibers, but also for the removal of collagen fibers during the continuous remodeling that takes
place in the ligament. Collagen fibrils are removed, in part, through intracellular degradation by
fibroblasts in digestive vacuoles by lysosomal enzymes.
Blood supply. The periodontal ligament has a rich blood supply that originates primarily from
the dental arteries that enter through the apical foramen and from blood vessels in the adjacent
bone marrow spaces. Anastomoses between these vascular supplies are numerous throughout
the ligament. The ligament vessels also communicate with the supraperiosteal vessels, the
adjacent marrow spaces and the gingiva.
Neural elements. The periodontal ligament in the apical region of the alveolar socket is richly
supplied with nerves that enter through the apical foramen and then branch out to supply the pulp
and the periodontal ligament. Most of the branches near the apical end are mixed nerves
consisting of myelinated and non-myelinated axons. As the nerves ascend coronally, they lose
their myelin sheath so that most nerves in the ligament are non-myelinated. They terminate
within the periodontal ligament as free endings that are sensitive to pain, or as endings with
specialized receptors for pressure. Thus, nerve endings in the periodontal ligament register only
pain and pressure.

Cementum
Cementum is the calcified, avascular mesenchymal tissue that forms the outer covering of the
root. The two main types of cementum are acellular cementum and cellular cementum. Both
consist of a calcified interfibrillar matrix and collagen fibrils embedded into matrix.
Acellular cementum is the first cementum formed; it covers cervical third or half of the root, and
it does not contain cells. This cementum is formed before the tooth reaches the occlusal plane.
Sharpey fibers make up most of the structure of acellular cementum, which has an important role
in supporting the tooth.
Cellular cementum, which is formed after the tooth reaches the occlusal plane, is more irregular
and contains cells (cementocytes) in individual spaces (lacunae) that communicate by processes
with each other through a system of anastomosing canaliculi. Cellular cementum is less calcified
than the acellular type Sharpey fibers occupy a smaller portion of cellular cementum.
The two main sources of collagen fibers in cementum are Sharpey fibers (so called extrinsic),
which are the embedded portion of the principal fibers of the periodontal ligament and which are
formed by the fibroblasts, and fibers that belong to the cementum matrix (intrinsic), which are
produced by the cementoblasts.
Morphologically, the cementoblasts do not differ to any extent from the periodontal ligament
fibroblasts. Cementoblasts locates on the cement surface close in proximity of periodontal
ligament. They are identified primarily by their intimate relationship to the cementum surface
and the characteristic cytoplasmic projections that extend toward the cementum. Cementoblasts
also form the non-collagenous components of the interfibrillar ground substance (cementum
matrix), such as proteoglycans, glycoproteins, and phosphoproteins.

17
Unlike bone, which is continuously remodeled, the cementum grows slowly in thickness,
throughout life, by apposition of new cementum at the surface. While cementum can be
resorbed, it is not continuously remodeled like bone.
Alveolar Bone
The alveolar process is the portion of the maxilla and mandible that forms and supports the tooth
sockets. It forms when the tooth erupts to provide the osseous attachment to the forming
periodontal ligament; it disappears gradually after the tooth is lost. Proper development of the
alveolar process is dependent on tooth eruption and its maintenance on tooth retention. When
teeth fail to develop (e.g. anodontia), the alveolar process fails to form. When all teeth are
extracted, most of the alveolar process becomes involuted, leaving basal bone as the major
constituent of the jawbone. The remaining jawbone, therefore, is much reduced in height.
The alveolar process consists of the following:
1. An external plate of cortical bone is formed by haversian bone and compacted bone
lamellae.
2. The inner socket wall of thin, compact bone called the alveolar bone proper is seen as the
lamina dura in radiographs. Histologically, it contains a series of openings (i.e., the
cribriform plate) through which neurovascular bundles link the periodontal ligament with
the central component of the alveolar bone. Where the alveolus contacts the inner and
outer cortical plates, the alveolar bone proper often fuses with the bone of the cortical
plates to form a single layer of compact bone – the coronal rim or crestal cortication. The
coronal rim of the alveolar bone forms the alveolar crest, which generally parallels the
cemento-enamel junction at a distance of 1-2 mm apical to it.
3. The cancellous bone. Outer and inner cortical plate of compact bone that enclose the
spongiosa, a compartment composed of spongy bone (also called trabecular or cancellous
bone). Forces exerted on the tooth also influence the number, density, and alignment of
cancellous trabeculae. The bony trabeculae are aligned in the path of the tensile and
compressive stresses to provide maximal resistance to the occlusal force with a minimum
of bone substance. When forces are increased, the cancellous bony trabeculae increase in
number and thickness.
Where roots are prominent and the overlying bone very thin, the bone may actually resorb
locally, creating a window in the bone through which the root can be seen. This window-like
defect in the bone is referred to as a fenestration.
In some cases, the rim of bone between the fenestration and the alveolar crest may disappear
altogether and produce a defect known as a dehiscence. Awareness of these defects is important
when surgical flaps are reflected, as the exposure of such defects during surgery may aggravate
their severity.
Bone histology. Bone is produced by osteoblasts that are found in the periosteum, endosteum
and periodontal ligament adjacent to bone-forming surfaces. These specialized cells originate
from less differentiated precursor cells close to the bone. These cells are in turn derived from
undifferentiated ectomesenchymal cells found in the periosteum, endosteum and the periodontal
ligament. During bone formation, osteoblasts become incorporated into bone as osteocytes that
are completely surrounded by bone. The chamber in which they are trapped is called a lacuna
(plur. lacunae). Osteocytes remain connected to osteoblasts and other osteocytes by cytoplasmic
processes that run through small canals in the bone, or canaliculi.
The bulk of the compact bone consists of cylindrical units of bone, the osteons or Haversian
systems. Each osteon has a central canal, the Haversian canal that houses a blood
vessel. Haversian canals are linked to one another and the periphery of the cortex by Volkman
canals that course perpendicularly to the Haversian canals. The outer and inner layers of the
18
cortex consist of parallel lamellae of compact bone, called the external and internal
circumferential lamellae. The bone that fills the spaces between adjacent osteons is the
interstitial bone.
The cortical plate undergoes continuous remodeling. The regulation of bone remodeling is a
complex process that involves hormones and local factors acting in an autocrine and a paracrine
manner on the generation and activity of differentiated bone cells. Bone contains 99% of the
body’s calcium ions and therefore is the major source for calcium release when the calcium
blood levels decrease; this is monitored by the parathyroid gland.
Alveolar bone on radiograph (Fig. 14) The radiograph represents a summed image of all the
structures between the x-ray source and the film. Dense structures like teeth and bone appear
light, while non-mineralized tissues are dark. The image that corresponds to the alveolar bone
proper is the thin, white line that parallels the outline of the roots of the teeth. The radiographic
term for this image is the lamina dura. The periodontal ligament space appears as a dark line
between the lamina dura and the root surface. The trabecular pattern of the cancellous bone can
also be readily detected.

Figure 14. Periapical radiograph of lower teeth. Note lamina dura, periodontal ligament space
and cancellous bone
Periodontal Biotypes
The periodontium has been described as having two basic forms are thin and scalloped or thick
and flat. Olsson & Lindhe referred to these as periodontal biotype. He found the thick and flat
periodontal biotype to be more prevalent than the thin and scalloped form (85 to 15 %
respectivly). Each biotype has its own characteristics. Thick biotype is characterized by thick
gingiva, flattened interdental papillae, thick alveolar bone and square shape of teeth (Fig 15 A).
Thin biotype is characterized by thin gingiva, scalloped gingival margin with high thin
interdental papillae, thin bone (relief of roots may be visible), triangular shape of teeth (Fig 15
B). The stability of the osseous crest and position of the free gingival margin are directly
proportional to the thickness of the bone and gingival tissue.

19
 A B
Figure 15. (A) Patient with thick biotype; (B) thin biotype

Age changing of periodontal tissues

Aging affects all the organ systems in the body and oral tissues are no exception to it. Due to
widespread awareness about oral health, there has been an improvement in the oral health status
of the general population worldwide. However, the process of aging is a natural process and
sooner or later it affects various tissues in the body. The moderate loss of periodontal bone
support can be related to the natural aging process; however, severe bone loss of periodontal
tissue is diseases-related breakdown and should not be considered to be related to aging. It has
been demonstrated that aging results in histopathological and clinical alterations in the oral
tissues, however, this alteration should be distinguished from the pathological changes.
Periodontium consists of gingiva, cementum, periodontal ligament and alveolar bone. All these
tissues are subjected to changes associated with aging.
Age-related changes in gingiva
• thinning of epithelium and reduction in the keratinization of the gingival epithelium
• reduction in stippling of the attached gingiva
• cellular turnover rate does slow down for all regions of the oral cavity
• decline in the production of both young cells and fibers in the gingiva
• the number of cellular components of the connective tissue decreases with age.
• the synthesis of collagen decreases.
• imbalance between the synthesis and degradation of collagen, thus affecting the
extracellular matrix homeostasis.
Age-related changes in periodontal ligament
• decrease cellularity has been demonstrated in periodontal ligament (PDL) of older
individuals to compare with younger individuals
• the fibers content of periodontal ligament is reduced
• the structure of PDL becomes more irregular with increasing age, degeneration or hyaline
changes can be observed
• calcified bodies can also be observed in PDL
• the amount of organic matrix decreases with advancing age
• the vascularity of PDL also reduces with age
• Decrease in the acid mucopolysccharide content
• decreasing of soluble collagen with increasing age because of increasing of cross-linking
in collagen which decreases it solubility
• decreasing of mobility and chemotactic ability of PDL cells

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Age-related changes in cementum
• the thickness of cementum increases throughout life.
• areas of cementum resorption followed by new cementum apposition can be observed,
which may result in the irregular surface of cementum.
Age-related changes in alveolar bone
• decline in the rate of bone formation with advancing ages, resulting in reduction of bone
mass
• decrease of cell in osteogenic layer of bone
Effect of advancing age on inflammatory response
In general there is a gradual deterioration of the immune response associated with the natural
process of aging. The inflammatory response has been shown to be altered in advanced age. The
inflammatory response is primary mediated by leucocytes. An immunological alteration in
leukocytes and an altered cytokine production has been observed with advancing age. The total
blood count of T-lymphocytes in the blood is reduced in elderly individuals.
Effect of aging on wound healing
In general, the wound healing is delayed in elderly individuals as compared to young individuals.
In healthy elderly individuals there is no impairment of wound healing in terms of the quality of
healing. The delayed wound healing is due to altered inflammatory response that includes
delayed T-cell infiltration into the wound area with alteration in chemokine production and
reduced macrophage phagocytic capacity. Other factors associated with delayed wound healing
in elderly individuals include increased platelet aggregation, increased secretion of inflammatory
mediators, decreased secretion of growth factors, delayed re-epithelization, delayed
angiogenesis, reduced collagen turnover.

Prevalence of periodontal diseases

Epidemiology is the study of health and disease in populations and how the different social strata
are influenced by hereditary, biological, physical, environmental, and socioeconomic factors, as
well as by individual behavior. Epidemiology has helped to understand the multiple aspects of
the interplay that characterizes periodontal healthy and diseased populations and individuals.
Incidence is defined as the number of new cases in a population over a given time period. In
public health practice, “cases” means people, so that when applied to a tuderculosis, for example,
it will mean the number of new people diagnosed with the condition during a stated time period.
In periodontitis, “incidence” is often taken to mean new sites that meet a definition of
periodontitis, even if these occur in people who already have other diseased sites. The term is
also applied to an increase in CAL or bone loss in a site that has already been recorded as
diseased.
Prevalence is the number of cases of a disease in a designated population at a given point. Due to
WHO study (1990, 53 countries were observed) periodontal diseases prevalence:
• in age 35-44 is 65%-98%
• in age 15-19 is 55%-89%.
Total prevalence of periodontal diseases in Russia is about 92% with maximum in age 35-44
where it is about 81% (Bulkina NV, 2008).
Gingivitis
Gingivitis is the most common form of periodontal disease and is found globally. Its prevalence
and severity are less pronounced in industrialized, developed countries as compared to less
developed regions. Gingivitis is less frequent in children, increases its occurrence in adolescents
21
and young adults and tends to level in adulthood. In fact, gingivitis and periodontitis are
considered a continuum of the same disease. These observations point out for a renewed interest
in the preventive measures for gingivitis. The prevalence of gingivitis among schoolchildren in
the United States has ranged from 40% to 60% in national surveys.
Periodontitis
Periodontitis is present in higher proportions in developing countries and, within the same
country, it affects higher proportions of the lower socioeconomic classes. Destructive forms of
periodontal disease are rather infrequent in childhood, tend to increase during adolescence and
present a steady increase with age.
In the USA, 80% of the adult population present at least one tooth with clinical attachment loss
(CAL) of 2 mm. If CAL of 4 mm is taken as a threshold, then this proportion falls to 50% and it
is further reduced to less than 20% with a CAL of 6 mm. (Brown LJ et al.1989). Baelum (1998)
showed that the prevalence of a CAL of 4 mm was approximately 90% in Kenya. In Brazil, it
was shown that nearly 100% of the population 14-30 years of age had marginal bleeding in
approximately 70% of the teeth present (Valle P, 2002).

Aggressive periodontitis. Gjermo et al. (1984) examined bone loss in radiographs of 304
adolescents from a low socioeconomic area: aggressive periodontitis was diagnosed in 2.6%.
Albandar et al. (1991) also reported a prevalence of 1.3% among a population of 13-year-old
schoolchildren of high socioeconomic status in Brazil.

Chronic periodontitis. Periodontitis, viewed for years as primarily the outcome from infection, is
now seen as resulting from a complex interplay between bacterial infection and host response,
often modified by behavioral factors. The prevalence of it varied from 40% to 80% in the overall
population of Brazil. In the United Kingdom, 42% of those with 35-44 years of age and 70% of
those with 55-64 years of age are reported as showing a CAL ≥ 4 mm (Morris AJ, 2001). What
epidemiology has demonstrated is that the majority of adult population has chronic periodontitis
to some degree, but that mild attachment loss, as measured by CAL of 2 mm, is compatible with
good health and function for many years.

22
Study 2. Etiology of inflammatory diseases of periodontium. Pathogenesis of inflammatory
diseases of periodontium
Inflammation of periodontal tissues is the result of an interaction between the microorganisms
found in the dental plaque and inflammatory cells of the host. Thus the primary cause of gingival
inflammation is bacterial plaque. The plaque–host interaction can be altered by the effects of
local factors and systemic factors, all of which can influence the severity and duration of the
response. Local factors are contributory because of their ability to retain plaque microorganisms,
to inhibit the removal of those microorganisms via patient-initiated plaque-control techniques;
and to enhance bacteria aggression on periodontal tissues.
LOCAL FACTORS
The main local factor is bacterial plaque. Other local contributory factors include:
• Calculus
• Aberrant frenal position
• Inadequate width of attached gingiva and keratinized gingiva
• Occlusal trauma
• Iatrogenic factors
• Complications associated with orthodontic therapy
• Self-inflicted injuries
• Mouth breathing
• Smoking (this factor has both local and systemic influencing)

Bacterial Plaque
Bacteria adhere both on hard and soft tissues of oral cavity.
The soft-tissue surfaces are actively involved in the process of bacterial adhesion and
colonization. The high turnover rate of the intraoral epithelial cells, especially of the gingiva,
prevents the permanent accumulation of large masses of microorganisms on these surfaces. In
essence, this is a natural cleansing mechanism.
Bacteria also adhere to hard tissues – teeth. From a microbiological viewpoint, teeth provide
unique hard, nonshedding surface that allows for the development of extensive structured
bacterial deposits. Teeth has unique ectodermal interruption - special seal of epithelium
(junctional epithelium) and connective tissue between the external environment and the internal
parts of the body. There are several types of dental deposits (Table 1):
• Materia alba (also called “soft plaque”) refers to soft accumulations of bacteria, food
matter, and tissue cells that lack the organized structure and that are easily displaced with
a water spray.
• Calculus is a hard deposit that forms via the mineralization of dental plaque and that is
generally covered by a layer of non-mineralized plaque.
• Bacterial plaque (also called “dental plaque”, “dental biofilm”) (Fig. 1,2) is defined
clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to
the intraoral hard surfaces, including removable and fixed restorations. The tough
extracellular matrix makes it impossible to remove plaque by rinsing or with the use of
sprays.
• Pigmented deposits on the tooth surface are called “dental stains” (Fig. 3). Stains are
primarily an aesthetic problem and do not cause inflammation of the gingiva.

23
 Figure 1. Dental plaque locates in cervical area of teeth #33, 43.

Figure 2. Dental plaque stained by plaque-detector solution adheres in cervical area,

interproximal and lingual surfaces.

A B
Figure 3. Pigmented deposits in cervical area of lower incisors (A); on lingual surfaces of lower
incisors, canines and premolars (B).

Table 1. Differences between tooth deposits

Material alba Dental biofilm Calculus Pigmented

deposits

White cheeselike Resilient clear to Hard deposit that It is an esthetic

accumulation. yellow-grayish forms via the problem and do
substance. mineralization of dental not cause gingival
plaque. inflammation.

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 Soft accumulation of Composed of bacteria Generally covered by a
salivary proteins, some in a matrix of salivary layer of unmineralized
bacteria, desquamated glycoproteins and dental plaque.
epithelial cells, and extracellular
disintegrating food polysaccharides.
debris.

Lacks an organized Is well-structured biofilm.

structure and is
therefore not as
complex as dental
plaque.

Easily displaced with a Impossible to remove

water spray. by rinsing or with the
use of sprays.

Dental biofilm is composed of microbial cells encased within a matrix of extracellular

polymeric substances, such as polysaccharides, proteins, and nucleic acids. Biofilm bacteria are
more resistant to antimicrobial agents than planktonic bacteria. In multispecies biofilms bacteria
interact closely with neighboring cells. How fast dental plaque is grown depends on individual
oral hygiene level and on quantity of carbohydrates intake. Biofilm’s features are:
• bacteria in biofilm are surrounded by intercellular matrix.
• system of channels in biofilm
• heterogeneity of bacterial species inside biofilm
Dental biofilm matrix. The matrix forms a specialized environment that distinguishes the
bacteria that exist within the biofilm from those that are free-floating (so-called “planktonic
state” in solutions such as saliva or crevicular fluid). The biofilm matrix functions as a barrier to
protect bacteria form outside environment.
The intercellular matrix consists of organic materials and inorganic materials derived from
saliva, gingival crevicular fluid, and bacterial by-products.
Organic constituents of the matrix include:
• polysaccharides produced by bacteria play a major role in maintaining the integrity of the
biofilm
• proteins, e.g. albumin, which probably originates from crevicular fluid
• glycoproteins from the saliva are an important component of the pellicle that initially
coats a clean tooth surface, but they also become incorporated into the developing plaque
biofilm.
• lipid material, consists of debris from the membranes of disrupted bacterial vesicles, and
possibly food debris.
The inorganic components of plaque are predominantly calcium and phosphorus, with trace
amounts of sodium, potassium, and fluoride. The source of inorganic constituents of
supragingival plaque is primarily saliva, subgingival plaque – cervical fluid.
Dental biofilm channels. Channels run through a biofilm and form a primitive circulatory system
that removes waste products and brings fresh nutrients to the deeper layers. Nutrients make
contact with the bacteria by diffusion from the water channels rather than from the matrix.
Microorganisms of dental biofilm. Dental plaque is composed primarily of microorganisms.
Dental plaque is classified as supragingival or subgingival on the basis of its position on the
tooth surface toward the gingival margin. In general, the subgingival microbiota differs in
25
composition from the supragingival plaque, primarily because of the local availability of blood
products and a low oxygen availability in supragingival area, which characterizes the anaerobic
environment.
• Supragingival plaque is found at or above the gingival margin on hard surfaces of teeth,
implants, restorations, and prostheses; when in direct contact with the gingival margin, it
is referred to as marginal plaque. Supragingival plaque typically demonstrates the
stratified organization of bacterial morphotypes. Gram-positive cocci and short rods
predominate at the tooth surface, whereas gram-negative rods and filaments predominate
in the outer surface of the plaque. This plaque is dominated by gram-positive rods and
cocci, including S. mitis, S. sanguinis, Actinomyces oris.
• Subgingival plaque is found below the gingival margin. Subgingival region is
characterized by the presence of crevicular fluid, the root cementum (or implant surface),
and the pocket/sulcus epithelium. The gingival crevice or pocket is bathed by the flow of
crevicular fluid, which contains many substances that bacteria may use as nutrients. In
subgingival plaque, there is a distinction between the tooth-associated regions and the
soft-tissue–associated regions:
 The tooth-associated cervical plaque that adheres to the root cementum
does not markedly differ from that observed in marginal plaque. In the
deeper parts of the pocket, the filamentous organisms become fewer in
number; in the apical portion, they seem to be absent; this region shows
an increased concentration of gram-negative rods.
 The soft-tissue-associated region has lack a definite matrix and contain
primarily gram-negative rods and cocci as well as large numbers of
filaments, flagellated rods, and spirochetes. The composition of the
subgingival plaque depends on the pocket depth. The apical part is more
dominated by spirochetes, cocci, and rods, whereas in the coronal part
more filaments are observed. Bacteria are also found within the host
tissues, such as in the soft tissues, and within epithelial cells.

The site specificity of plaque is significantly associated with diseases of the periodontium.
Marginal plaque, for example, is of prime importance during the initiation and development of
gingivitis. Supragingival plaque and tooth-associated subgingival plaque are critical in calculus
formation and root caries, whereas subgingival plaque is important in the tissue destruction that
characterizes different forms of periodontitis.
It has been recognized for some time that bacterial species exist in complexes in subgingival
plaque. Universal periodontal pathogen has not been revealed yet. Pathological process in
periodontium is caused by combination of different species of bacteria. Many periodontal
pathogens are strict anaerobes and as such may contribute little to the initiation of disease in
shallow gingival pockets. In deep periodontal pockets, however, they find their preferred habitat.
In 1968 Sigmund Socransky classified the bacterial species found in subgingival plaque samples
involved in the initiation and progression of periodontal disease. He classified several complexes
of bacteria dividing them in groups, labeled by colors. Classification of microbial complexes:
• Red
• Green
• Yellow
• Orange
• Purpur

26
The categories were based upon the pathogenicity of the bacteria and their role in the
development of dental biofilm. The red complex and the individual species in that group were
also strongly associated with bleeding on probing.
The red complex is a group of bacteria that are categorized together based on their association
with severe forms of periodontal disease, bleeding on probing and fast progression of destruction
of periodontal tissues. The three members of the red complex are:

• Porphyromonas gingivalis
• Tannerella forsythia
• Treponema denticola

There are obvious data that bacteria of red complex and also Аctinobacillis
Actinomycetemcomitans, are key periodontal pathogens, because they are strongly associated
with periodontal disease status and progression. The roles and cooperation of microorganisms of
different complexes is summarized in figure 4.

Figure 4. A diagram of the complexes in subgingival species. The complexes to the left are
comprised of species that are thought to colonize the tooth surface and to proliferate at an early
stage. The orange complex becomes numerically dominant later; it is thought to bridge the early
colonizers and the red complex species, which become numerically more dominant during the
later stages of plaque development. (Adapted from Socransky SS et al: J Clin Periodontol
25:134, 1998)

The orange complex is constituted by:

• Fusobacterium nucleatum
• Prevotella intermedia
• Prevotella nigrescens
• Peptostreptococcus micros
• Streptococcus constellatus
• Eubacterium nodatum
• Campylobacter showae
• Campylobacter gracilis
• Campylobacter rectus

27
Similarly to the red complex, all species in the orange complex showed a significant association
with increasing pocket depth. For these bacteria, moderate evidence for etiology has been
reported, at least if their concentration passes a certain threshold level.

Characteristics of key periodontal pathogens

Аctinobacillis Actinomycetemcomitans is small, non-motile Gram-negative rod. AA. initially
colonizes the oral cavity by attachment to the surfaces of the oral epithelium is able to invade
epithelial cells, vascular endothelial cells penetrate the underlying connective tissues. It has next
virulence factors:
• leukotoxin - can destroy PMN leukocytes and monocytes
• endotoxin - direct effect on endothelial cells, adverse effects on pocket epithelia, liberates
cytokines, it is a strong antigen to provoke immune reactions
• bacteriocin - antibacterial substance can depress the multiplication of streptococci
collagenase
• fibroblast inhibitory factor
• bone resorption inducing factor
Porfiromonas gingivalis is Gram-negative, obligatory anaerobic, non-motile short rod can occur
in very limited number in healthy sulcus and gingivitis, significantly increased in periodontitis.
[Link] can invade epithelial cells. Virulence factors are:
• special fimbriae mediate the binding of the bacteria to epithelial cells and also to different
bacterial surface protein
• collagenase and protease
• different factors that adversely affect leucocytes
• invasion is important component of virulence
Prevotella intermedia is Gram-negative, anaerobic short rod. It has been revealed in very high
number in acute ulcerative gingivitis, pregnancy gingivitis and chronic periodontitis.
Fusobacterium nucleatum is Gram-negative, anaerobic spindle shape rod. This bacteria play an
important role in the subgingival ecosystem is its function as “bridging” species, facilitating
coaggregation of different species.
Mechanism of pathogenicity of pathogenic microorganisms:
• adhesion - with adhesion molecules - adhesins, most bacteria can find certain specific
surface receptors on host cells/surfaces to which to adhere;
• coaggregation - most bacteria do not directly attach to host cells, but rather attach to other
bacteria which had already attached;
• overcoming host defensive mechanisms.
However, the mere presence of putative periodontal pathogens in the gingival crevice is not in
itself sufficient to initiate or cause periodontal inflammation. An elevation in the relative
proportion or number of these pathogens to reach a critical mass seems more crucial to mount an
effective tissue-damaging process. Indeed, even in health, periodontal pathogens are or can be
present in the gingival crevice, albeit in low numbers, as members of the normal resident flora.

Calculus
Calculus is mineralized bacterial plaque that forms on the surfaces of natural teeth and dental
prostheses. The soft plaque is hardened by the precipitation of mineral salts, which usually starts
between the first and fourteenth days of plaque formation. There are two types of calculus:
• supragingival
28
 • subgingival
Saliva is the source of mineralization for supragingival calculus, whereas the serum transudate
called gingival crevicular fluid furnishes the minerals for subgingival calculus.
Supragingival calculus locates coronal to the gingival margin and therefore is visible in the oral
cavity. It is usually white or whitish-yellow in color (Fig. 5); hard, with a claylike consistency.

Figure 5. Supragingival calculus on lower central incisors

The color is influenced by contact with such substances as tobacco and food pigments. It may
localize on a single tooth or group of teeth, or it may be generalized throughout the mouth. The
two most common locations of supragingival calculus are the lingual surfaces of the mandibular
frontal teeth (Fig. 6A) an the buccal surfaces of the maxillary molars (Fig. 6B). Saliva from the
parotid gland flows over the buccal surfaces of the upper molars via the parotid duct, whereas the
submandibular ducts and the lingual ducts empty onto the lingual surfaces of the lower incisors
from the submandibular and sublingual glands, respectively. The calcification of supragingival
plaque and in the attached component of subgingival plaque begins along the inner surface
adjacent to the tooth.

A B
Figure 6. A – supragingival calculus and pigmented deposits on lingual surface of lower frontal
teeth; B – supragingival calculus on buccal surface of second upper molar;
Subgingival calculus locates below the gingival margin and therefore is not visible on routine
clinical examination. The location and extent of subgingival calculus may be evaluated by
careful tactile perception with a delicate dental instrument such as an explorer. Subgingival
calculus is typically hard and dense; and it is firmly attached to the tooth surface. Subgingival

29
calculus is typically dark green or dark brown (Fig. 7), which probably reflects the presence of
blood products that are associated with subgingival hemorrhage.

Figure 7. Piece of dental calculus. A border between supragingival (upper yellowish) and
subgingival (lower brown) parts is visible.
Subgingival calculus is likely to be the product rather than the cause of periodontal pockets.
Plaque initiates gingival inflammation, which leads to pocket formation, and the pocket in turn
provides a sheltered area for plaque and bacterial accumulation. The increased flow of gingival
fluid associated with gingival inflammation provides the minerals that mineralize the continually
accumulating plaque that results in the formation of subgingival calculus.
Supragingival calculus and subgingival calculus generally occur together, but one may be
present without the other.
Subgingivalcalculus may be seen on radiograph (Fig. 8).

A B
Figure 8. (A) Fragment of panoramic radiograph: calculus locates on lower frontal teeth. (B) The
same fragment of radiograph; calculus is shown by arrows

Effect of calculus on gingiva. Distinguishing between the effects of calculus and plaque on the
gingiva is difficult, because calculus is always covered with a nonmineralized layer of plaque.
Calculus does not contribute directly to gingival inflammation, but it provides a fixed nidus for
the continued accumulation of plaque and its retention in close proximity to the gingiva (Fig. 9).

30
 Figure 9. Abundant dental stone cover almost all surfaces of lower incisors. Greyish dental
plaque covered cervical area of stones is close proximity to reddish inflamed gingiva

The initiation of periodontal disease in young people is closely related to plaque accumulation,
whereas calculus accumulation is more prevalent in chronic periodontitis found in older adults.
Although the bacterial plaque that coats the teeth is the main etiologic factor in the development
of periodontal disease, the removal of subgingival plaque and calculus constitute the cornerstone
of periodontal therapy. Calculus plays an important role in maintaining and accentuating
periodontal disease by keeping plaque in close contact with the gingival tissue and by creating
areas where plaque removal is impossible.
Aberrant frenal position
Short thick frenula in oral vestibule cause local trauma of soft tissues because of mechanical
pulling gingiva out from teeth and alveolar bone during speaking and chewing. It cause ischemia
of area of frenula attachment and may lead to encroach on the marginal gingiva distend the
gingival sulcus, fostering plaque accumulation, bone resorption, gingival recessions and
diastema. These are actual also for buccal frenula.
Inadequate width of attached and keratinized gingiva
Lack of keratinized and attached gingiva leads to less resistance to frictional contact during
mastication and oral hygiene procedures and faster spreading of inflammatory infiltrant in
gingiva.
Occlusal trauma

Many animal experiments and clinical studies have investigated the role of occlusion in the
pathogenesis of periodontitis. The results suggest that premature contact or excessive occlusal
force could be an etiologic factor in the progression of periodontitis. In the periodontally
compromised tooth, the normal occlusal force could affect the periodontal tissue and cause
further attachment loss. When occlusal forces exceed the adaptive capacity of the tissues, tissue
injury results. Trauma from occlusion refers to an injury to the periodontal tissues caused by
abnormal occlusal force. An occlusion that produces such an injury is called a traumatic
occlusion.

The presence of traumatic occlusion can accentuate the damage of periodontium. Any occlusion
that produces periodontal injury is traumatic. Malocclusion is not necessary to produce trauma;
periodontal injury may occur when the occlusion appears normal. The dentition may be
anatomically and aesthetically acceptable but functionally injurious.

Occlusal trauma may be caused by:

• alterations in occlusal forces

31
 • reduced capacity of the periodontium to withstand normal occlusal forces
• both

Trauma from occlusion is divided into three categories:

• Primary occlusal trauma results from excessive occlusal force with normal periodontal support
that is usually caused by parafunctional forces (“para” – beyond; “function” – normal range)
such as clenching or grinding habits.
• Secondary occlusal trauma is caused by excessive force applied on teeth with a damaged
periodontium.
• Combined occlusal trauma. A combination of both, in which excessive biting forces are applied
to weakened or reduced periodontal structures (teeth that have lost bone due to periodontal
disease).

Trauma from occlusion may be caused by two variants:

• direct occlusal trauma – when the cause of periodontal problems is in the same place as
periodontal destruction. For instance, restorations that do not conform to the occlusal
pattern of the mouth (e.g. too high) result in occlusal disharmonies that may cause injury
to the supporting periodontal tissues.
• indirect occlusal trauma – when the cause of periodontal problems in not in the same
place as periodontal destruction. For instance, the failure to replace missing posterior
teeth may have adverse consequences on the periodontal support for the anterior teeth,
because patient will try to use it for chewing of food and this will cause functional
overloading. If only some posterior teeth are missed, the drifting and tilting of the
remaining posterior teeth with an accompanying alteration of the proximal contacts is
generally a consequence of not replacing posterior teeth that have been extracted.

Periodontal tissue response to excessive occlusal forces. Occlusal forces may cause two main
effects on periodontal tissues: compression and tension. Sever compression produces a
gradation of changes in the periodontal ligament, starting with compression of the fibers,
which produces areas of hyalinization. Subsequent injury to the fibroblasts and other
connective tissue cells leads to necrosis of areas of the ligament. Vascular changes also
occurs. In addition, increased resorption of alveolar bone and resorption of the tooth
surface may occur. Slight tension will cause elongation of periodontal fibers and bone
apposition. Severe tension causes widening of the periodontal ligament, thrombosis,
hemorrhage, tearing of the periodontal ligament, and resorption of alveolar bone.
Excessive occlusal force cause injury of periodontal tissues. The body then attempts to repair the
injury and restore the periodontium. This can occur if the forces are diminished or if the tooth
drifts away from them. If the offending force is chronic, however, the periodontium is remodeled
to cushion its impact; the periodontium is remodeled in an effort to create a structural
relationship in which the forces are no longer injurious to the tissues. The ligament is widened at
the expense of the bone, which results in angular bone defects without loss of attachment and
with no periodontal pockets, and the tooth becomes loose to drift away from the load.
Histopathology of reaction on excessive occlusal forces. The first reaction to increased occlusal
loading is increased vascularity in periodontal ligament space. Normal periodontal ligament with
normal occlusal forces showing dense collagen fibers attached to bone and cementum with
minimal vascularity. This initial increased vascularity results in a more compressible periodontal
ligament and increased clinical mobility. After the initial increasing of vascularity, there is a
32
stimulation of osteoclasts which cause bone loss and a widened periodontal ligament space. This
also causes increased tooth mobility.
Iatrogenic factors
Iatrogenic factors are problems caused by mistakes and complications of treatment procedures.
Some iatrogenic factors which may affect periodontal health are listed below:
o Overcontoured restoration
o Overhanging margin of restoration or crown
o Open contacts
o Rough fillings
Overcontoured crowns and restorations tend to accumulate plaque and handicap oral hygiene
measures in addition to possibly preventing the self-cleaning mechanisms of the adjacent cheek,
lips, and tongue.
Overhanging margins (Fig. 10,11) of dental restorations contribute to the development of
periodontal disease by:
• changing the ecologic balance of the gingival sulcus to an area that favors the growth of
disease-associated organisms (predominantly gram-negative anaerobic species) at the
expense of the health-associated organisms (predominantly gram-positive facultative
species)
• inhibiting the patient’s access to remove accumulated plaque.

A B
Figure 10. A – original radiograph; B – the same radiograph with arrow and tooth number.
Overhanging margin of restoration on distal surface of tooth #26

33
 B
Figure 11. A – original radiograph; B – the same radiograph with arrow and teeth numbers.
Overhanging margins of restoration on tooth #25 (distal surface), tooth #26 (mesial surface),
tooth #35 (distal surface) and associated interproximal bone resorption

Open contact (Fig. 12) is an absence of contact point between neighboring teeth, which may
cause inflammation of gingival papilla and interproximal bone loss because of food compaction,
plaque accumulation and difficulties of plaque control.

A B
Figure 12. (A) Fragment of panoramic radiograph with open contact (black gap between white
restorations) between teeth #17 and #18 and large interproximal bone resorption. (B) The same
radiograph with teeth numbers and resorption landmarks (white line), compare contacts between
teeth #17-18 and #17-16 (arrows).

Roughness of filling in the subgingival area is considered to be a major contributing factor to

plaque buildup and subsequent gingival inflammation.
Iatrogenic trauma to the gingiva can be caused by the induction of orthodontic cement or
preventive or restorative materials under the gingiva.

Complications after orthodontic therapy

Orthodontic therapy may affect the periodontium:
• by favoring plaque retention
• by directly injuring the gingiva as a result of overextended bands
34
 • by creating excessive forces, unfavorable forces, or both on the tooth and its supporting
structures
Orthodontic tooth movement is possible because the periodontal tissues are responsive to
externally applied forces. Alveolar bone is remodeled by osteoclasts that induce bone resorption
in areas of pressure and by osteoblasts that form bone in areas of tension. Although moderate
orthodontic forces ordinarily result in bone remodeling and repair, excessive force may produce
necrosis of the periodontal ligament and the adjacent alveolar bone.
Orthodontic bands should not be forcefully placed beyond the level of gingival attachment,
because this will detach the gingiva from the tooth and result in the apical proliferation of the
junctional epithelium with an increased incidence of gingival recession.

Self-inflicted injuries
Patients may not be aware of their self-inflicted injurious habits that may be important to the
initiation and progression of their periodontal disease. Mechanical forms of trauma can be
because of the improper use of a toothbrush, the wedging of toothpicks between the teeth.
Abrasions of the gingiva as well as alterations in tooth structure may result from aggressive
brushing in a horizontal or rotary fashion. The deleterious effect of excessively forceful brushing
is accentuated when highly abrasive dentifrices are used. The gingival changes that are
attributable to toothbrush trauma may be acute or chronic. The acute changes vary with regard to
their appearance and duration, from scuffing of the epithelial surface (Fig. 13) to denudation of
the underlying connective tissue with the formation of a painful gingival ulcer.

Figure 13. Scratching of gingiva caused by toothstick

Chronic toothbrush trauma results in gingival recession with denudation of the root surface.
Mouth breathing
Mouth breathing has some influence on periodontal health status because of:
• overdrying of oral mucosa thus decreasing of protective properties of saliva.
• affecting of ecological balance of bacteria species in oral cavity promote increasing
growth of dental plaque.
Smoking
Smoking has both local and general effect on human organism. Local effects are listed below:
• Decreases blood circulation through tissues because of spasm of capillaries and
aggregation of thrombocytes (local).
• Decreased bactericidal property of saliva.

35
SYSTEMIC FACTORS
Many systemic diseases, disorders, and conditions have been implicated as risk factors in
periodontal disease. The interrelationships between periodontal infections and host defense are
complex. A number of environmental, physical, and psychosocial factors have the potential to
alter periodontal tissues and the host immune response, thereby resulting in more severe
periodontal disease expression.
Systemic factors that contribute to periodontal diseases may be exacerbated as a result of
alterations in the gingival inflammatory response to plaque. This altered response appears to
result from the effects of systemic conditions on the host’s cellular and immunologic functions.
Next systemic conditions are considered to be risk factors to contribute periodontal diseases:
• Vitamins deficiency
• Hormonal Changes
• Endocrinal disorders
• Hematologic disorders
• Stress
• Using of some medication
Vitamin Deficiency
Nutritional deficiencies are known to affect immune function, and they may alter the host’s
ability to protect himself or herself against bacteria and some of the detrimental effects of
cellular products such as oxygen radicals.
Vitamin С deficiency (or scurvy) cause disorders of collagen and proteoglicans synthesis,
increasing of permeability of ground substance, osteoclasts activation, impaired osteoblasts
differentiation. Clinical manifestation are bright red, swollen, and bleeding gingiva.
Vitamin A deficiency cause disorder of epithelization of gingiva after traumatic injuries and
decreasing of barrier function of gingiva.
Vitamin E deficiency makes reparation process slower, stimulates bone atrophy.
Vitamin D deficiency causes impaired calcium adsorption in gastrointestinal tract, promotes
osteoporosis, causes impaired mineralization of osteoid.
Hormonal Changes
Hormonal fluctuations that are associated with puberty and pregnancy are well-known examples
of systemic conditions that affect the condition of the periodontium. It modify the tissue response
to local factors, and produce anatomic changes in the gingiva that may favor plaque
accumulation and disease progression. During puberty and pregnancy, these changes are
characterized by nonspecific inflammatory reactions with a predominant vascular component,
which leads clinically to a marked hemorrhagic tendency.
Puberty is often accompanied by an exaggerated response of the gingiva to plaque. Pronounced
inflammation, edema, and gingival enlargement result from local factors that might ordinarily
elicit a comparatively mild gingival response. Although the prevalence and severity of gingival
disease are increased during puberty, with good oral hygiene, it can be prevented.
Pregnancy. Increased concentration of estrogen and progesterone in blood causes increasing of
permeability of periodontal blood vessels and capillaries. Accumulation of growth hormone
(somatotropin) in gingiva causes proliferation of gingiva.

36
Endocrinal disorders
Diabetes Mellitus. Numerous oral changes have been described in patients with diabetes,
including cheilosis, mucosal drying and cracking, burning mouth and tongue, diminished
salivary flow, and alterations in the flora of the oral cavity, with greater predominance of
Candida albicans.
Although it is difficult to make definitive conclusions about the specific effects of diabetes on
the periodontium, a variety of changes have been described. The most striking changes in
patients with uncontrolled diabetes are the reductions in the defense mechanisms and the
increased susceptibility to infections, which lead to destructive periodontal disease.
Changes take place in all tissues of patients with uncontrolled diabetes, its affect also
periodontium.
Polymorphonuclear neutrophils deficiencies in:
• chemotaxis
• adhesion
• phagocytosis
As a result, the primary defense mounted by PMNs against periodontal pathogens is diminished,
and bacterial proliferation is more likely.
Altered collagen metabolism:
• decreased collagen synthesis
• increases collagenase activity
Chronic hyperglycemia impairs collagen structure and function, which may directly impact the
integrity of the periodontium. Chronic hyperglycemia adversely affects the synthesis, maturation,
and maintenance of collagen and extracellular matrix. In the hyperglycemic state, numerous
proteins and matrix molecules undergo a non-enzymatic glycosylation, thereby resulting in
accumulated glycation end-products (AGEs). Collagen is crosslinked by AGE formation, which
makes the collagen less soluble and less likely to be normally repaired or replaced. Cellular
migration through cross-linked collagen is impeded.
Altered metabolism:
• glucose is not absorbed by cells
• acidosis
Angiopathy and microangiopathy of periodontal capillaries:
• sclerosis and hyalinosis of capillaries walls cause not only problems with
periodontium but also nephropathy, retinopathy
Another one factor, which influence periodontium in patients with diabetes, is increasing of
glucose concentration in gingival cervical fluid. As far as gingival fluid consist of blood serum
transported through sulcus epithelium, high concentration of glucose in blood cause high
concentration of glucose in serum and provide a good media for growing of pathogenic bacteria.
Clinical manifestation of diabetes mellitus is inflammation of gingiva, bleeding on probing,
periodontal pockets formation, in some cases proliferation of gingiva (Fig. 14). Good individual
oral hygiene and adequate control of glucose level in blood prevent inflammation in periodontal
tissues.

37
 Figure 14. Patient with uncontrolled diabetes mellitus
Hyperparathyroidism. Parathyroid hypersecretion produces generalized demineralization of the
skeleton, increased osteoclasts activity with proliferation of the connective tissue in the enlarged
marrow spaces, and the formation of bone cysts and giant cell tumors.
Hematologic disorders
Thrombocytopenia is a term that is used to describe the condition of a reduced platelet count that
results from either a lack of platelet production or an increased loss of platelets. The gingivae of
such patients are swollen, soft, and friable; petechiae on skin and oral mucosa. Bleeding occurs
spontaneously or with the slightest provocation, and it is difficult to control. Gingival changes
represent an abnormal response to local irritation.
Leukemia. Oral and periodontal manifestations of leukemia may include:
• leukemic infiltration
• bleeding
• oral ulcerations
• infections
The expression of these signs is more common with acute and subacute forms of leukemia than
with chronic forms.
Leukemic cells can infiltrate (excessive infiltration of blood cells) the gingiva and, less
frequently, the alveolar bone. Leukemic gingival infiltration often results in leukemic gingival
enlargement that creates pockets in which bacterial plaque accumulates, thereby initiating a
secondary inflammatory lesion that contributes to the enlargement of the gingiva.
Gingival hemorrhage is a common finding in leukemic patients, even in the absence of clinically
detectable gingivitis. This bleeding tendency can also manifest in the skin and throughout the
oral mucosa, where petechiae are often found, with or without leukemic infiltrates.
In patients with leukemia, the response to bacterial plaque or other local irritation is altered. The
inflamed gingiva in patients with leukemia differs clinically from that found in non-leukemic
individuals. The gingiva is a peculiar bluish red, it is spongelike and friable, and it bleeds
persistently on the slightest provocation or even spontaneously in leukemic patients. This greatly
altered and degenerated tissue is extremely susceptible to bacterial infection. Discrete ulcers that
penetrate deeply into the submucosa and that are covered by a firmly attached white slough can
be found on the oral mucosa. Such lesions that resemble necrotizing ulcerative gingivitis are
more frequent and severe in patients with terminal cases of acute leukemia.
Stress
Habitat changes:
• Increased alcohol consumption, smoking, need for sedative-hypnotic drugs
• Sleep disorders
38
 • Alter food intake (increasing carbohydrates intake)
• Decrease in oral hygiene
In stress, there is a systemic decrease of host defense.
Using of some medications
Using of some medications cause gingiva proliferation (diphenine (anticonvulsant), cyclosporine
(immunosuppressant), corticosteroids, calcium channel blockers) (See chapter 7).

Pathogenesis of inflammatory diseases of periodontium

According to Merriam Webster’s Collegiate Dictionary, the word pathogenesis is defined as “the
origination and development of a disease.” Essentially, this refers to the step-by-step processes
that lead to the development of a disease and that result in a series of changes in the structure and
function of, in this case, the periodontium. In broad terms, the pathogenesis of a disease is the
mechanism by which a causative factor or factors causes the disease.
Although different periodontal diseases are categorized in several subgroups, many of
microbiological and host response features of these diseases are common to several of the forms
of periodontitis. Here only general features of inflammatory periodontal diseases will be
described. Specific features of pathogenesis of different subgroups will be discussed in
corresponding sections.
Inflammatory periodontal diseases results from a complex interplay between the microorganisms
of dental biofilm and the host immune defense mechanisms. As in many other tissues, in
periodontium these defense mechanisms are realized through:
• Neutrophils. Neutrophils form a barrier at the plaque-tissue interface, controlling bacteria
numbers and preventing ingress of bacteria or their products into the tissue surface.
• Antibodies. The local depot of antibodies is gingival cervical fluid (or inflammatory
exudate of periodontal pocket). Among plenty of functions, antibodies in periodontium
may:
o Opsonize bacteria allowed the neutrophil to recognize, ingest and degrade
bacteria.
o Activate complement system.
o Neutralization of bacterial toxins and enzymes
o Disrupt bacterial colonization by preventing adherence to the tooth or epithelial
surface or to other bacteria.
• Cytokines, mainly complement system – antibacterial cascade of naturally occurring
proteins which can:
o Occur additional opsonins on the bacteria surface.
o Release chemical mediators that recruit additional neutrophils.
o Deposit macromolecules complexes onto the bacteria surface that will lyse and
kill certain bacteria.
The interaction between neutrophils, antibody, and complement provides primary protection
against the deleterious effects of periodontal pathogens.
It is widely accepted that the initiation and progression of periodontitis are dependent on the
presence of microorganisms capable of causing diseases. Bacteria need to posses the ability to
survive and propagate in periodontal pockets in the complex ecosystem of the biofilm and they
use different mechanisms for that. Pathogenesis of inflammatory periodontal disease is in part
dependent on:
• Presence of pathogenic microorganisms

39
 • Number of microorganisms. When concentration of pathogens in subgingival plaque
reaches critical level it will cause initiation or progression of tissue destruction.
• Virulence. Microorganisms have virulence factors that are responsible for causing
diseases. At least three virulence factors of periodontal microorganisms have been
identified that can contribute to their ability to act as pathogens:
o Capacity to colonize. Virulent organisms can express appendages such as
fimbriae or molecules such as adhesins which promote association with tissue or
other bacteria.
o Ability to evade antibacterial host defense mechanisms. An important feature of
nearly all pathogenic microorganisms is that ability to evade the host defense
mechanisms that would ordinary control infection and prevent disease. Virulence
can be enhanced via the presence of a capsular polysaccharide (as in P.
gingivalis) which provides resistance to host defense such as antibodies and
complement. Some strains of A. actinomycetemcomitans and Campylobacter
rectus, produce leukotoxins that can kill neutrophils directly, thus disrupting the
primary antibacterial defense mechanism in the gingival sulcus. Some bacteria,
such as [Link], produce proteolytic enzymes that either directly degrade
antibody and complement proteins or prevent accumulation of these molecules on
the bacterial surface. This activity would prevent accumulation of complement-
derived chemotactic factors, which would ordinarily recruit many additional
neutrophils to the site of infection. Some bacteria, such as A.
actinomycetemcomitans produce factors that suppress the immune response to
itself and to other bacteria, thereby diminished the production of protective
antibodies. A. actinomycetemcomitans can pass through epithelial cells into the
underlying connective tissues, while [Link] can invade and persist in
epithelial cells. Fusobacterium nucleatum excretes by-products that may directly
affects the gingival vasculature. The resultant edema and increased production of
gingival cervical fluid may provide the environment and nutrients that allow
pathogens to flourish. P. gingivalis produces metabolic by-products such as H2S
and NH3 and fatty acids that a toxic to surrounding cells.
o Ability to produce substances that can directly destruct tissues. Some
microorganisms are able to invade into or through host tissues, thereby creating a
sequestered environment for their protection. P. gingivalis is known to produce
enzymes (proteases, collagenases, fibrinolysin, phospholipase A) that could
directly degrade surrounding tissue in the superficial layer of the periodontium.
Two major periodontal pathogens A. actinomycetemcomitans and [Link] are
able to invade into the tissue.
Besides direct destruction of tissue, periodontal pathogens may cause pathological changes in
tissues by indirect means. Bacterial products gain access to the cellular constituent of the
gingival tissue and activate cellular processes that are destructive to connective tissue and bone.
Once the major protective elements in the periodontium have been overwhelmed by bacterial
virulence mechanisms, a number of host-mediated destructive processes are initiated:
• Polymorphonuclear leukocytes, which normally provide protection, can themselves
contribute to tissue damage. During the phagocytosis, these cells typically “spill” some of
their enzyme content extracellulary during a process known as degranulation; some of
these enzymes are able to degrade surrounding tissues, namely collagen and basement
membrane, contributing to tissue damage.
• Cytokines, molecules which are released by host, normally have protective functions, its
take part in killing of pathologic bacteria, act as signaling in inflammatory process.
Among the cytokines most consistently found to be associated with periodontitis are
interleukin 1 (IL-1), interleukin 6 (IL-6), Tumor necrosis factor alpha (TMF-α),
40
interleukin 8 (IL-8), prostaglandin E2. Normally cytokines act in specific order to provide
inflammatory reaction and healing, but massive bacteria aggression may alter these
normal sequence and stimulate uncontrolled secretion of cytokines. Thus cytokines are
not able to function normally and take part in catabolic process of tissue damage.
Lipopolysacharides of bacterial cell walls is thought to stimulate production of catabolic
cytokines and inflammatory mediators that in turn promote the release of tissue-derived
enzymes, the matrix metalloproteinases, which are destructive to the extracellular matrix
and bone.

41
Study 3. Examination of patients with periodontal diseases. Basic and additional methods
of diagnosis of periodontal diseases
A thorough periodontal examination is a critically important data-collection activity that is
necessary to arrive at a diagnosis and develop a treatment plan. A decision is then made
regarding the disease category that is most closely associated with the patient's clinical status.
To get this information clinician uses different methods of examination, which conceptually
divided into basic methods of examination and additional methods of examination.
In medically healthy patients with simple and rather straightforward periodontal conditions, the
examination can usually be completed in one visit with basic methods only. For medically
compromised patients with complex periodontal and dental problems, multiple visits with
several additional methods of examination may be needed to complete the data-gathering
process. The examination of all non-periodontal tissues in the oral cavity should be performed.
In the other words, a detailed periodontal evaluation is the last component of a thorough oral
examination. In this chapter all examination methods will be described from periodontal point of
view because general examination of dental patients was described in previous courses.

Basic examination methods

Results of full periodontal examination should be recorded in the patient’s clinical notes. This
information can be used to monitor treatment outcomes, inform your treatment choice, educate
the patient and, from a medico-legal standpoint, show that you have diagnosed and treated the
condition appropriately.
Basic examination of patient with periodontal disease is quite similar with regular dental patient.
Basic methods of examination of patient with periodontal diseases:
1) Questioning
2) Extraoral examination:
• visual examination
• lymph nodes palpation
3) Intraoral examination:
• visual examination
• palpation
• probing of gingival sulcus/periodontal pockets for evaluation of
probing depth and bleeding on probing
• measurement of furcation involvement
• charting of recession
• checking of teeth mobility
• checking of occlusion
Questioning. Prior to conducting the hands-on examination, the information-gathering process
begins with taking medical and dental histories from the patient. Many practitioners prefer to
initiate this process by having the patient fill out a questionnaire. However, a questionnaire are
only a starting point, since a discussion with the patient about past and present medical/dental
problems always provides additional important information about medical history and history of
previous and current periodontal problems. This initial conversation is a start on patient-doctor
relationship that ideally should be a partnership.
A key component of history-taking session is determination of the patient’s chief complaint. The
most widespread chief complaints of patients with periodontal diseases are listed below:
• Gum bleeding on toothbrushing, chewing of hard food, or spontaneous bleeding.
42
 • Teeth mobility. Patients may complain that their teeth feel loose or that they have
difficulty eating certain foods.
• Burning/pain in inflamed gingiva
• Suppuration (or abscesses) of gingiva. In such cases patient also may mention unpleasant
salty taste of pus in oral cavity.
• Pathologic tooth migration (PTM). These teeth displacements may affect patients
aesthetically as well as functionally. PTM is defined as a change in the position of a tooth
that occurs when the balance of forces, which maintains it in its normal position, was
broken. Main reason of migration is massive alveolar bone resorption. When bone does
not surround tooth root and does not keep it inside alveolar socket, occlusal loads
displace tooth.
• Halitosis
Extraoral examination. Prior to conducting a periodontal examination it is customary to routinely
inspect the extraoral tissues of the head and neck. This part is described in previous course.
Intraoral examination. Intraoral periodontal examination is multi-task activity. An overall
inspection is made during which changes in color, shape and texture of the gingival tissues are
assessed. Detailed measurement of probing depth/clinical attachment los/recessions are taken
and recorded. Finally, teeth are inspected for occlusal relationships and restorative needs.
Visual examination
During the examination, notation should be made of any deviations from normal periodontal
anatomy such as:
• alteration in gingiva color
• alteration in gingival contour (enlargement or recession)
• aberrant labial frenula attachments and buccal frenula
• lack of attached gingiva.
Gingiva. Recognition of gingival inflammation is possible if clinician understand how healthy
gingiva looks like. Healthy gingiva (Fig.1) is pinkish color (coral pink or pink with
pigmentation; depends on individual feature and nationality), firm and resilient, tightly encircles
teeth necks, whereas inflamed tissues are altered in color and contour. The surface of normal
gingiva usually exhibits numerous small depressions and elevations that give the tissue an
orange-peel appearance referred as stippling (Fig. 2). Stippling is restricted to the attached
gingiva and predominantly localized to the subpapillary area, but it extends to a variable degree
into the interdental papilla. This pattern and extent vary in different mouth areas, among patients,
and with age.

Figure 1. Healthy gingiva is light pink color, tightly encircles teeth necks, gingival papilla
occupied interdental spaces.

43
 Figure 2. Stippling of gingiva is visible
The most common visual signs of gingival inflammation are redness and swelling. In case of
mild inflammation gingiva is pale red, in acute inflammation – bright red, in chronic
inflammation – magenta, purple or bluish red (Fig. 4). It should be noted that visual color
evaluation is subjective. Gingival redness and swelling are usually seen together (Fig. 3). It can
be seen at the gingival margin and in interproximal area.

Figure 3. Inflamed gingiva is reddish and edematous, picks of interdental papilla are rounded

Figure 4. Chronically inflamed gingiva is bluish-red color and edematous; it is not tightly
encircle teeth necks, gingival papilla do not occupied interdental spaces, picks of papilla are
rounded

Exposure to heavy metals (e.g., lead, bismuth) may cause gingivitis and a dark line at the
gingival margin.

Edematous tissue are enlarged and puffy. To identify edema of gingiva clinician can gently press
the side of periodontal probe to the tissue for a few seconds and then remove it. At edematous
sites, the imprint of the periodontal probe will be seen, whereas at sites without edema no
imprint will be observed.
44
Alteration in gingival contour manifests as: recessions (Fig. 5) or enlargement (Fig. 6). Gingival
enlargement may be presented because of edema and fibrosis. Tissues edema will disappear after
professional oral hygiene, and fibrotic enlargement will not. The best way to know is it fibrotic
or edematous enlargement is to gently press on the gingiva with side of periodontal probe. In
case of edema there will be imprint there, in case of fibrotic enlargement no imprint will occur.

Figure 5. Gingival recessions

Figure 6. Gingival enlargement

Aberrant frenula attachment. Abnormal or aberrant frenula are detected visually, by applying
tension over it to see the movement of papillary tip or blanching produced due to ischemia of the
region of frenum attachment to the alveolar process (Fig. 7).

Figure 7. Short thick frenum of upper lip (left picture) and blanching of the gingiva in the area of
frenum attachment (right picture)

Buccal frenula may be evaluated when stretching cheeks and lips laterally down on lower jaw
and laterally up on upper jaw by index fingers or mirrors (Fig. 8).

45
 Figure 8. Buccal frenula in area of lower premolars
Amount of attached gingiva. The amount of attached gingiva is considered to be insufficient if
stretching of cheek and lips induce movements of free gingival margin (Fig. 9).

Figure 9. Gingival recessions, insufficient amount of attached gingiva and shallow vestibule.
Stretching of lower lip cause gingival margin near central incisors moving out from teeth necks.

Palpation
In examination of periodontal patient palpation may be helpful to reveal:
• consistency of soft tissues
• purulent exudate
Palpation may give some additional information about consistency of gingival enlargement, e.g.
for diagnostics of different types of epulis (fibrous epulis will be dense on palpation and
granulomatous epulis will be soft on palpation).
Purulent exudate is most often detected at sites with chronic periodontitis. The best way to detect
the presence of pus is to apply pressure gently by finger to the gingiva from apical to coronal
direction. If any purulent exudate is inside periodontal pocket, after palpation it will be visible in
area of gingival margin as a yellowish viscous substance.

Probing
In periodontal examination probing is carried out for two goals:
46
 • to evaluate bleeding on probing
• to measure periodontal pocket depth or clinical attachment loss
Bleeding on probing is an objective earliest clinical sign of gingival inflammation that precede
established gingivitis. In general, gingival bleeding on probing indicates an inflammation both in
the epithelium and in the connective tissue that exhibits specific histologic differences as
compared with healthy gingiva. Histopathologic alterations that result in abnormal gingival
bleeding include:
• dilation and engorgement of the capillaries
• fragility of the vessels
• thinning or ulceration of the sulcular epithelium
Because the capillaries are engorged and closer to the surface and because the thinned,
degenerated epithelium is less protective, stimuli that are normally innocuous cause
rupture of the capillaries and gingival bleeding.
Bleeding on probing is easily detected clinically and therefore is of value for the early diagnosis
and prevention of more advanced gingivitis. It has been shown that bleeding on probing appears
earlier than a change in color or other visual signs of inflammation; in addition, the use of
bleeding rather than color changes to diagnose early gingival inflammation is advantageous in
that bleeding is a more objective sign that requires less subjective. Therefore, bleeding on
probing is widely used by clinicians to measure disease prevalence and progression, to measure
outcomes of treatment, and to motivate patients to perform necessary home care.
Several gingival indices that are based on bleeding have been developed for evaluation of
gingiva status. Scoring with indices allows clinician to compare gingiva status between
appointments. Laceration of the gingiva by toothbrush bristles during aggressive toothbrushing
or by sharp pieces of hard food can cause gingival bleeding, even in the absence of gingival
disease. Gingival burns from hot foods or chemicals increase the ease of gingival bleeding.
The periodontal pocket is the cardinal symptom of periodontitis. Periodontal pocket is a
pathologic fissure between tooth and gingival margin.
The number, type, depth, and extension of periodontal pockets constitute a record of disease
history. The correct identification and accurate assessment of periodontal pockets is therefore of
fundamental importance for the diagnosis of periodontitis. In addition, the identification of
changes in periodontal pockets is important for the evaluation of disease severity, disease
progression, and therapeutic efforts.
Pocket depth may not reflect real loss of periodontal attachment as a sign of periodontal disease.
This is because gingival swelling will increase the distance from the gingival margin to the
bottom of the clinical pocket. In such cases, probing depth is a measure of pseudopocketing, and
the extent of periodontal destruction is overestimated. In case of recession pocket depth is less
than real attachment loss. In contrast, in situations of gingival recession or after periodontal
surgery, probing depth can substantially underestimate the true extent of periodontal destruction.

A better reflection of periodontal destruction can be obtained by the measurement of the clinical
attachment loss (CAL), This is the measurement of the position of the soft tissue in relation to the
cemento-enamel junction (CEJ) that is a fixed point that does not change throughout life, albeit
at times it is hard to visualize (e.g. in case of abfraction lesions or chemical root erosions). CAL
is the distance from the bottom of periodontal pocket to the level of CEl. Clinical attachment loss
shows real loss of connective tissue attachment of gingiva to the tooth and of periodontal
ligament to the tooth because of alveolar bone resorption (Fig. 10). Interproximal attachment
loss is generally a consequence of bacteria-induced periodontitis, whereas buccal and lingual
attachment loss is frequently the result of toothbrush abrasion.

47
 Figure 10. 1 – clinical attachment loss, 2 – gingival recession, 3 – periodontal pocket depth
(picture source: By Lesion - Own work, CC BY-SA 3.0,
[Link]

Two measurements are used to calculate the clinical attachment loss: the probing depth (PD) and
the distance from the gingival margin to the CEJ. Where it gets confusing is that the gingival
margin may be in one of three places:
1. The CEJ may be at the same level as the gingival margin. In that case CAL=PD.
2. The gingival margin extends significantly over the CEJ. In that case CAL˂PD (Fig 11 A).
CAL = PD minus distance between gingival margin and CEJ, but accurate measurement
here is quite difficult.
3. The CEJ may be coronal to the gingival margin. This is known as recession and is very
simple to measure. In that case CAL˃PD (Fig 11 B). CAL = PD + distance between
gingival margin and CEJ.

Figure 11. (A) periodontal probe in periodontal pocket shows CAL˂PD; (B) periodontal probe
in periodontal pocket shows CAL˃PD. CAL – clinical attachment loss, PD – periodontal pocket

To date, the periodontal probe is the only instrument that has been found to be reliable and
convenient in pocket examination. In comparison with sharp explorer, periodontal probe is blunt
at the tip.

Pihlstrom (1992) proposed periodontal probes classification:

• 1st generation: conventional, manual probes that do not control for probing force or
pressure and that are not suited for automatic data collection. There are a lot of
modifications of periodontal probes of this category: Marquis probe, Glickman probe,
Williams probe, Probe CPITN (WHO).
48
 • 2nd generation: constant-force or pressure- sensitive probes allowed for improved
standardization of probing.
• 3rd generation: computer-assisted direct data capture was an important step in reducing
examiner bias and also allowed for greater probe precision.

Probes of first generation is the most popular nowadays. These are hand probes consist of three
parts, including handle, shank, and working part (Fig. 12).

Figure 12. Periodontal probe

The working part may differ and is usually calibrated with millimeter or/and dark color markings
(Fig. 13,14). Most periodontal probes are made of stainless steel, but more recently titanium and
plastic have been used as well.

Figure 13. Marquis color-coded periodontal probe. Calibrations are in 3-mm sections

The World Health Organization (WHO) recommended a special periodontal probe (Fig. 14) for
use with the community periodontal index of treatment needs (CPITN; WHO, 1978). It is
different from other probes because of its ball-end of 0.5 mm in diameter, which is attached to a
16-mm-long tapered tip. The tip of the clinical probe has markings at 3 5, 5.5, 8.5, and 11.5 mm.
The ball-end permits the clinician to detect root surface roughness like calculus deposits The
probe has been advocated for use in epidemiology and the routine periodontal screening of
patients in general practice.

49
 Figure 14. Periodontal probe CPITN (WHO)

An example of second generation probe is Click-Probe® (KerrHawe) (Fig. 15). It is a calibrated

plastic periodontal probe with a click-system. This probe permits an operator-independent,
reproducible periodontal pocket measurement thanks to the clearly perceptible click. Click
always occurs at a pressure of 20-25 g (corresponding to 0.2-0.25N).

Figure 15. Plastic periodontal probe Click-Probe®, arrows shows the area where click occurs if
pressure on probe is more than 20-25 gram (picture courtesy by KerrHawe).

An example of third generation probe is Florida Probe (Fig. 16). It is a probing and charting
system consists of probe which attaches by USB port with computer with special software. Probe
introduces in periodontal pocket and probing depth is automatically charted in computer data
base.

Figure 16. Florida Probe System (picture courtesy Florida Probe Corporation)

Technique of probing. The periodontal probe is introduced into the pocket parallel to the root
surface or almost parallel (Fig. 17), with slight force used until further penetration is limited by
50
increased resistance as the probe tip approaches the bottom of the pocket. Waerhaug (1952) had
suggested that pockets should be assessed using "light hand pressure". He had estimated that
probing pressure, as measured at the probe tip, should not exceed 0.2 N/mm2. A light probing
force of about 25 g, equivalent to the force required to blanch a fingernail when press a probe to
it, is used when probing the periodontal tissues. Probing is carried out in six points – three from
vestibular surface and three from oral surface.

A B
Figure 17. Periodontal probing. (A) In tooth 21 depth of cervical gingival sulcus is 2 mm; (B) In
tooth 43 deep periodontal pocket is 8 mm.
Periodontal indices. An index is a numerical value describing the relative status of the population
on a scale with definite upper and lower limits. The use of indices permits comparison between
different populations classified by the same criteria and methods. A large number of gingival and
periodontal indices have been described in the dental literature.
Sulcus Bleeding Index (SBI). In 1958, Muhlemann & Mazor had stressed that bleeding was a
much more sensitive indicator of disease than either edema or color change. They considered
that bleeding occurred before the other signs were present. In 1971, Muhlemann & Son
introduced the SBI. Bleeding is the determining factor in the SBI and is the first sign to appear in
periodontal diseases.
Technique of index measurement. Four gingival units are scored systematically for each tooth:
the labial and lingual marginal gingival (M units) and the mesial and distal papillary gingival (P
units), using a periodontal probe with a 0.5mm diameter tip. Scores (Table 1) for these units are
added and divided by four. Adding the scores of the undivided teeth and dividing them by the
number of teeth, and multiplying by 100 % can determine the sulcus bleeding index.
Number of teeth examined: 16 (the anterior 4 in each quadrant, 2 on maxilla and 2 on mandible).
Each surface of each tooth is examined grossly for color and swelling, then a probe is gently
placed in the sulcus to see if bleeding occurs.
Teeth in each quadrant:
• central incisor
• lateral incisor
• cuspid
• first premolar
Four surfaces on each tooth are probed:
• M labial
• M lingual
• P mesial
• P distal
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Table 1. Observation and scores

Appearance Sulcus Probing Scores

healthy no bleeding 0

apparently healthy with no bleeding on probing 1

change in color and no
swelling

change in color due to bleeding on probing 2

inflammation; no swelling or
macroscopic edema

change in color due to bleeding on probing 3

inflammation; slight
edematous swelling

obvious swelling bleeding on probing 4

spontaneous bleeding; bleeding on probing 5

changes in color; marked
swelling with or without
ulceration

Modified Papillary Bleeding Index (MPBI) Barnett et al. (1980) modified the PBI index
(Muhlemann, 1977) by stipulating that the periodontal probe should be gently placed in the
gingival sulcus at the mesial line angle of the tooth surface to be examined and carefully swept
forward into the mesial papilla. They timed the appearance of bleeding and graded it as follows:
• 0 = no bleeding within 30 s of probing;
• 1 = bleeding between 3 and 30 s of probing;
• 2 = bleeding within 2 s of probing;
• 3 = bleeding immediately upon probe placement.
The mesial papillae of all teeth present from the second molar to the lateral incisor were
assessed. Indices were derived for the maxillary left and mandibular right buccal segments, and
the maxillary right and mandibular left lingual segments, and from these a full-mouth index was
calculated. This distribution of test sites was utilized since each mesial papilla could only be
tested once, i.e. from either the buccal or lingual side.
Measurement of Furcation Involvement
Damage from periodontal disease can lead to furcation involvement of multi-rooted teeth. This is
called furcation defects and measured using a furcation probe and graded depending on the
severity of the furcation involvement (Table 2).
Table 2. Grading of furcation involvement

Grade Description

Grade 1. Initial furcation involvement The furcation opening can be felt on probing but the
involvement is less than one third of the tooth width.
52
 Grade 2. Partial furcation involvement Loss of support exceeds one third of the tooth width
but does not include the total width of the furcation.

Grade 3. Through-and-through The probe can pass through the entire furcation.
involvement

Teeth Mobility
Loss of alveolar bone from periodontitis cause of abnormal tooth mobility. It is assessed both
horizontally and vertically. Horizontal mobility is measured by applying gentle pressure in a
buccal-lingual direction, using two rigid instrument handles, or the index finger and an
instrument handle if preferred, on either side of the tooth, and assessing the level of
displacement. Vertical mobility is measured by applying gentle pressure on the crown of the
tooth with a rigid instrument handle in a vertical direction. Tooth mobility is evaluated in
degrees (Table 3).
Table 3. Grading of tooth mobility

Degree Description

Degree 0 ‘Physiological’ mobility measured at the crown level. The tooth is mobile within
the alveolus to approximately 0.1–0.2 mm in a horizontal direction.

Degree 1 Increased mobility of the crown of the tooth to at the most 1 mm in a horizontal
direction.

Degree 2 Visually increased mobility of the crown of the tooth exceeding 1 mm in a

horizontal direction.

Degree 3 Severe mobility of the crown of the tooth in both horizontal and vertical directions
impinging on the function of the tooth.

Checking of Occlusion
Incorrect occlusion does not cause marginal periodontitis but may be associated with gingival
recessions. In certain situations occlusal trauma may exacerbate marginal periodontitis. For
example, a mobile tooth with attachment loss and bone loss may drift as a result of occlusal
trauma. During examination of patient with periodontal diseases next parameters should be
evaluated:
• Pathological bite types (deep overbite etc.)
• Occlusal interferences of restorations and prosthetic constructions
• Abnormal teeth position (tilting, rotation, crowding etc.) which may interfere adequate
oral hygiene procedures

Additional Methods of Examination

There are many additional tests may help clinician to make decision about diagnostic treatment
and prognosis. Some of these methods are available for using in every day clinical practice and
some are more appropriate for scientific studies.
Additional methods for clinical practice:
53
 - Radiography – the MOST valuable additional methods for diagnosing of periodontal
diseases
- Microbial analysis
- Blood test
- Genetic test
Some additional methods, which are nowadays mostly used for scientific studies because further
development of tests for easy implemented in clinical practice, are required:
- Gingival cervical fluid analysis
- Saliva analysis
- Rheoperiodontography

Radiography
The most important additional method of diagnostics of patient with periodontal diseases is
radiography. Radiographs are valuable for diagnosis of periodontal disease, estimation of
severity, determination of prognosis, and evaluation of treatment outcome. However,
radiographs are an adjunct to the clinical examination, not a substitute for it. Therefore, only a
careful clinical examination, combined with a proper radiographic examination, can provide
adequate data for diagnosing the presence and extent of periodontal disease.
Radiography is a method to evaluate hard tissues. It does not reliably demonstrate soft tissue
contours, and do not record changes in the soft tissues of the periodontium. Next types of
radiographs may be used for diagnosing of periodontal patients:
1) Panoramic radiography – the most popular radiograph type for evaluation of periodontal
tissues.
2) Bitewing radiography – the optimal projections for periodontal diagnosis in the posterior
teeth are bitewing radiographs.
3) Computed tomography – gives three dimensional view of jaw bone, especially helpful in
planning of implant placement.
Radiographs are especially helpful in evaluation of the following points:
• Amount of bone present
• Condition of the alveolar crests
• Bone loss in the furcation areas
• Width of the periodontal ligament space
• Local factors which can intensify periodontal disease
o Overhanging restorations
o Apical inflammatory lesions
• Anatomic issues:
o Root length and morphology
o Missing, supernumerary and impacted teeth
o Maxillary sinus
o Inferior alveolar nerve canal
• Other pathoses (cysts, benign and malignant lesions)

Normal Anatomy of Periodontal Tissues on Radiograph (Fig. 18). To evaluate pathological

changes in periodontal tissues it is first necessary to know how normal anatomy does look like:
- The bone height is within 2 millimeters of the cemento-enamel junction (CEJ)
- The interdental bone normally is outlined by a thin, radiopaque line adjacent to the
periodontal ligament and at the alveolar crest, referred to as the lamina dura in area of
54
 periodontal ligament and as crestal bone in alveolar crest. The crestal bone is a
continuation of the lamina dura of the teeth.
- Between the anterior teeth, the alveolar crest is pointed.
- Between the posterior teeth, the lamina dura and the crestal bone form a box, with sharp
angles. The angulation of the crest of the interdental septum is generally parallel to a line
between the CEJs of the approximating teeth. When there is a difference in the level of
the CEJs, the crest of the interdental bone appears angulated rather than horizontal.
- The periodontal ligament space varies along the length of the roots. It tends to be wider
at the apex and alveolar crest, and narrower in the midroot areas.

В
Figure 18. Normal anatomy of periodontal tissue A – original panoramic radiograph, B – the
same radiograph with schematic lines. White short lines show interdental bone level. Crestal
bone box is especially well visible between teeth # 35,36,37 and between teeth 46 and 47. Note
continuation of lamina dura into crestal cortication in that places.

Bone Changes in Periodontal Diseases.

Evaluation of bone changes in periodontal disease is based mainly on the appearance of the
interdental bone because the relatively dense root structure mask the facial and lingual bony
plates. In periodontal disease the interdental bone undergoes changes that affect the lamina dura,
55
crestal bone, height and contour of the bone. Interdental bone may be partially hidden by
superimposed anatomy, such as a dense mylohyoid ridge.
Generally next changes of periapical tissues may be seen in radiograph:
- Changes in crestal bone
- Vertical bone defect
- Horizontal bone loss
- Furcation involvement
Changes in Crestal Bone. Fuzziness and disruption of crestal cortication continuity is the
earliest radiographic change in periodontitis (Fig. 19). Therefore it can be concluded that the
presence of an intact crestal lamina dura may be an indicator of periodontal health.

A B
Figure 19. A – original periapical radiograph; B – the same radiograph with schematic line.
Crestal cortication between central incisors appears partially eroded
Horizontal Bone Loss. Horizontal bone loss is the most common pattern of bone loss in
periodontal disease. The bone is reduced in height, but the bone margin remains approximately
perpendicular to the root surface of adjacent teeth (Fig. 20)

Figure 20. Panoramic radiograph demonstrates horizontal bone loss (upper picture – original
panoramic radiograph; lower picture – schematic line of bone level)

56
In this pattern of bone destruction the interdental septa and the facial and lingual plates are
affected but not necessarily to an equal degree around the same tooth. In most cases, it can be
assumed that bone losses seen interdentally continue in the facial or the lingual aspect.
Vertical Bone Defects. Vertical bone defects may be detected radiographically on the distal and
mesial surfaces. It is a wedge-shaped or angular radiolucency at the mesial or distal aspect of the
interdental bone. The tip of wedge is oriented apically to the root and continues to the widening
of the periodontal space (Fig. 21, 22).

В
Figure 21. A – original panoramic radiograph, B – the same radiograph with schematic lines.
Note vertical bone defect mesially to tooth# 37

57
 А

В
Figure 22. A – original panoramic radiograph, B – the same radiograph with schematic lines.
Note vertical bone defect distally to tooth# 34
Radiographs do not indicate the internal morphology or depth of vertical defects. Also,
radiographs do not reveal the extent of involvement on the facial and lingual surfaces.
Furcation Involvement (Fig. 23). The term furcation involvement refers to the invasion of the
bifurcation and trifurcation of multirooted teeth by periodontal disease. Initially seen as widening
of the periodontal ligament space at the crest of the furcation. As lesion progresses, the bone loss
progresses apically. Three rooted teeth, incorrect horizontal angulation of the radiograph, and
overlying structures may interfere with radiographic detection of furcation involvement. The
recognition of a large, clearly defined radiolucency in the furcation area is easy to identify.

58
 А

В
Figure 23. A – original panoramic radiograph, B – the same radiograph with schematic lines.
White lines show furcation involvement of upper and lower molars

Limitation of radiography:
- Conventional radiographs provide a two dimensional image of complex, three
dimensional anatomy.
- Due to superimposition, the details of the bony architecture may be lost.
- Radiographs do not demonstrate incipient disease, as a minimum of 55-60%
demineralization must occur before radiographic changes are apparent. Early destructive
changes of bone that do not remove sufficient mineralized tissue cannot be captured on
radiographs. Therefore slight radiographic changes of the periodontal tissues suggest that
the disease has progressed beyond its earliest stages. The earliest signs of periodontal
disease must be detected clinically.
Blood Test
A blood test is often given during a medical check-up to reveal indicators of general health
conditions. It is known that general health status may influence periodontal health. Blood test is
prescribed not for all patients with periodontal diseases, mostly it is used in next clinical
situations:
59
 • Patient with aggressive periodontitis
• Patient with ulcerative gingivatis/periodontitis
• Patient with refractory periodontitis (not adequate response on treatment procedures
(when in spite of all treatment procedures result is worse than expected)
• Patients are going to have surgery
In case of any alterations of blood test patient should be referred to physician!
In case of refractory periodontitis glucose level is important because uncontrolled glucose level
in blood causes increasing of glucose in serum that promotes growth of periodontal pathogens.
In case of ulcerative periodontitis test on HIV may be useful because ulcerative periodontitis
may be on of manifestation of HIV in oral cavity.
In case of patient is going undergo surgery it is recommended to make next tests before:
• Hepatitis and HIV antibodies
• Complete blood count (CBC), in this test the next positions are important:
- Platelet count (low platelet count means high risk of slow blood clot formation and
bleeding)
- White blood cell count and differentiation
Normal values for total WBC and differential in adult males and females are:
• Total WBC: 4,500 - 10,000
• Granulocytes (or polymorphonuclears)
o Neutrophils: 50 - 70% relative value (2500-7000 absolute value) (high
count of this parameter in most cases means acute inflammation)
o Eosinophils: 1 - 3% relative value (100-300 absolute value) (high count of
this parameter in most cases means possible allergy reactions)
o Basophils: 0.4% - 1% relative value (40-100 absolute value)
• Agranulocytes (or mononuclears)
o Lymphocytes: 25 - 35% relative value (1700-3500 absolute value) (high
count of this parameter in most cases means chronic inflammation)
o Moncytes: 4 - 6% relative value (200-600 absolute value)

Microbial Analysis

With the application of contemporary microbiological methods significant improvements have

been made in the field of periodontal diagnostics. The oral microbiota plays a primary role in the
initiation and progression of periodontal disease. Despite individual differences and the complex
interactions between bacteria and the host, an association has been demonstrated between certain
species and various forms of periodontal disease. The connection between periodontal pathogens
and disease activity serves as the basis for application of microbiological tests in periodontology.

In spite of the presence of a large number of microorganisms identified from a periodontal

pocket, the following are considered periodontal pathogens: Actinobacillus
actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium
nucleatum and Treponema denticola. Most tests are based on the detection of these
microorganisms.

Microbial analysis may be carried out after completion of conventional root scaling and planing
(after healing) to help assess the need for additional therapy, such as antibiotic treatment.

Indications: Microbiological monitoring is usually not indicated as a part of the initial approach.
Bacteriological tests may be valuable for:
60
 • aggressive juvenile periodontitis
• refractory forms of periodontal disease. In spite of proper supportive periodontal
treatment and patient compliance, progressive periodontal disease may reappear in some
patients. In such patients additional antimicrobial therapy may be needed. The
composition of periodontopathogenic microbiota determines in part the choice of
antimicrobial agent.
• Monitoring the response to therapy
Sample of subgingival plaque collection: The sites are isolated with cotton rolls; removal of
supra gingival plaque by a sterile curette; plaque samples are obtained by insertion of
standardized #30 sterile paper points at the deepest part of each periodontal pocket and left there
for 15 seconds. The paper points are transferred in a test tube containing transport medium under
anaerobic conditions.
Microbial test types. According to use:
• Chairside diagnostic tests
• Laboratory tests
According to method of bacteria revealing:
• phase-contrast microscopy
• dark-field microscopy
• bacterial culture
• polymerase chain reaction (PCR).
Detection of periodontal pathogens in periodontal health and disease strongly depends on the
techniques used.
Culture methods. Microbial anaerobic culturing presently provides the most comprehensive
assessment of the periodontal microbiota. Total viable cell count, the relative proportions of
putative periodontal pathogens, and the occurrence of unusual subgingival organisms can be
determined. Culturing remains prerequisite for microbial sensitivity testing. Microbial diversity
can be greatly underestimated by cultivation studies because many microorganisms cannot be
cultivated by standard techniques.
Non-culture techniques. Molecular genetic techniques to detect periodontal bacteria include
species-specific DNA probes and real-time polymerase chain reaction (RT-PCR). These
techniques do not require viable cells and can show high sensitivity and specify. Disadvantages
are the limited number of species that can be routinely detected, the difficulty of quantifying
target organisms, and the inability to perform microbial sensitivity testing.
One of the most serious limitations of using microbial tests in clinical practice is lack of easy-to-
use commercially available chairside diagnostic systems. The increasing availability of
diagnostic laboratory services and chairside diagnostic kits for office use will make it easier for
the practitioner to select appropriate antimicrobial treatments and monitor patients undergoing
antimicrobial therapy.
Antibiotics Susceptibility Testing
Periodontitis is a bacterial disease that can be treated with systemic antibiotics. The occurrence
of bacterial strains resistant to different antimicrobials is a growing problem. Therefore,
antimicrobial susceptibility testing can be important if the clinician contemplates using
antibiotics; especially in the management of patients with refractory periodontitis.
Antibiotics susceptibility testing (another terms are “antibiotic sensitivity testing” “culture
sensitivity test”) is necessary to determine efficacy of antimicrobial agents.

61
For making antibiotic sensitivity test, samples of subgingival plaque should be sent in laboratory
where it is cultivated and test different antibiotics. The laboratory then inform the dentist
regarding the bacterial species present in the sample and also the most suitable antibiotic regime.
Genetic Testing
The role of genetic factors in periodontal disease is now well recognized. There is scientific data
that genetic profile of person may influence periodontal health that is why genetic testing makes
sense for getting prognosis of periodontal diseases and treatment outcome. One of the risk factor
of periodontal disease is variations in different genes responsible for host-defense mechanisms.
Nowadays there is a system for genetic testing PerioPredict® Interleukin-1 genetic risk test (Fig.
24).

Figure 24. PerioPredict® Interleukin-1 genetic risk test (picture courtesy Interleukin Genetic
Inc.)

PerioPredict® is genetic test that identifies individuals with an increased risk for severe and
progressive periodontitis, due to a genetic predisposition to over-produce Interleukin-1 (IL-1), a
key mediator of inflammation. The IL-1 gene variation causes overproduction of IL-1. In the
presence of bacterial plaque, this has been shown to create a heightened inflammatory response.
This inflammation is linked to the destruction of soft tissue and bone.

PerioPredict® can be performed during a routine exam or cleaning. The sample is then sent to
Interluekin Genetics, a CLIA-certified genetics laboratory in Waltham, MA for analysis. Test
results are returned to the dentist in about 2 weeks. Results of this test provide important
information to dental professionals for assessing prevention and treatment options for their
patients.

Gingival Cervical Fluid Analysis

In some situations, supplemental qualitative or quantitative assessments of the gingival
crevicular fluid (GCF) are performed using newly developed and clinically practical tests. It
should be emphasized that, at the present time, supplemental information on GCF is not
commonly used by practitioners in arriving at a diagnosis, but mostly it is used for research
work. Technique of gathering of gingival cervical fluid for analysis:
1. insert paper point or special absorbent paper in gingival sulcus/periodontal pocket
2. wait for 1 minute
3. put paper point or paper in a vial with sterile saline (Fig. 25)

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 Figure 25. Sterile adsordent paper in gingival sulcus (right picture); vial with sterile saline (left
picture)

One of the most widespread laboratory test for assessment of gingival cervical fluid is enzyme-
linked immunosorbent assay (ELISA) (Fig. 26). Tis a test that uses antibodies and color change
to identify a substance.

Figure 26. Preparation for 96-well microtitler plate (A) and insertion it in spectrophotometer (B)
An array of enzymes, tissue breakdown products, and inflammatory mediators are released form
host cells and tissues during the development and progression of periodontal infections. Some of
these substances have been suggested as possible markers for the detection of active (i.e.,
progressing) periodontal lesions. A number of studies have been conducted with the general goal
of devising rapid chairside assays for markers of disease activity in gingival crevicular fluid.
Host-derived enzymes that have received the most attention in this regard are:
- aspartate aminotransferase
- collagenase
- elastase
- alkaline phosphatase
Inflammatory mediators in GCF that might be associated with advancing periodontal lesions are:
- prostaglandin E2
- tumor necrosis factor-α
- interleukin-1β.
Further study and development of certain GCF-based diagnostic tests are warranted. It is quite
possible that some of them might eventually have value in the clinical management and detection
of active periodontitis. Such tests could conceivably be used to identify sites within periodontitis
patients that may require additional treatment prior to the maintenance phase of therapy. They
63
also might be of value in establishing recall intervals for previously treated patients. For
example, patients with persistently positive tests may require more frequent recall visits.
Rheoperiodontography
This method of evaluation of functional status of blood vessels of periodontal tissues. Method is
based on graphic registration of electrical resistance of periodontal tissues.

64
Study 4. Colloquium 1
Questions for preparation to colloquium:
1. List components of periodontium.
2. List parts of gingiva and give histological characteristic of each part. Describe a dental
plaque in details.
3. List local factors of inflammatory periodontal diseases. Describe a dental calculus in
details.
4. List local factors of inflammatory periodontal diseases. Describe a self-inflicted trauma in
details.
5. List local factors of inflammatory periodontal diseases. Describe an influence of an
orthodontic treatment in details.
6. Systemic factors of inflammatory periodontal diseases. Describe an influence of a diabetes
mellitus in details.
7. List local factors of inflammatory periodontal diseases. Describe an influence of an occlusal
trauma in details.
8. List local factors of inflammatory periodontal diseases. Describe an influence of an aberrant
frenal position trauma in details.
9. What is a biological role of an attached gingiva?
10. What is a biological width of gingiva and what are it’s functions?
11. What is a biological role of keratinized gingiva?
12. What is a dentogingival junction?
13. What is the localization and what are the components of masticatory mucosa?
14. List functions of periodontal ligament. Describe the force absorptive function in details.
15. List functions of periodontal ligament. Describe the remodelling function in details.
16. List principle groups of periodontal fibers.
17. What is the alveolar bone structure?
18. What are an age-related changing of gingiva?
19. What are age-related changing of periodontal ligament?
20. What is the effect of advancing age on inflammatory response?
21. List local factors of inflammatory periodontal diseases. Describe an influence of iatrogenic
factors in details.
22. List systemic factors of inflammatory periodontal diseases. Describe an influence of
haematologic disorders in details.
23. What is periodontal tissue response to excessive occlusal forces?
24. List systemic factors of inflammatory periodontal diseases. Describe an influence of a stress
in details.
25. List systemic factors of inflammatory periodontal diseases. Describe an influence of
vitamin C deficiency.
26. List systemic factors of inflammatory periodontal diseases. Describe an influence of
vitamin A deficiency.
27. What are the chief complaints of a periodontal patients?
28. Visual examination of gingiva.
29. Describe technique of using a periodontal probe?
30. List additional methods of diagnostics of periodontal diseases. Describe blood test in
details.
31. List additional methods of diagnostics of periodontal diseases. Describe microbial analysis
in details.

65
Study 5. Basic treatment of inflammatory periodontal diseases – professional oral hygiene
and anti-inflammatory therapy
Properly performed, periodontal treatment can eliminate pain, exudate, gingival inflammation,
and bleeding. It can also reduce periodontal pockets, arrest the destruction of bone, and reduce
abnormal tooth mobility.
As far as main reason of inflammatory periodontal diseases is bacterial plaque accumulation on
the tooth surface close to the gingival tissue, the primary goal of periodontal therapy is
elimination of bacterial factor. This includes cleaning of both supragingival and subgingival
plaque and calculus and improving of individual oral hygiene. After these steps, it is necessary
to reveal and eliminate (if possible) other local that favor plaque accumulation and systemic
factors or diminish its influence on periodontal status of patient.
Basic treatment of inflammatory periodontal diseases is:
1. Professional oral hygiene. Generally term “professional oral hygiene” means
cleaning of all SUPRAgingival plaque and calculus. In patients with periodontal
pockets term “root scaling and planing” was used for many years because in such
patient plaque and calculus locate not only on crown part of tooth but also on the root
surface in periodontal pocket. In this term scaling means the process by which plaque
and calculus are removed from both supragingival and subgingival tooth surfaces. No
deliberate attempt is made to remove root cement along with the calculus. Root
planing is the process by which residual embedded calculus and portions of infected
root cementum are removed from the roots to produce a smooth, hard, clean surface.
Scaling and root planing for treatment should not be viewed as separate procedures
but are carried out together. In the last years there is a tendency to abandon the use of
the term "root planing" and to use the term "root debridement" more often.

2. Anti-inflammatory/antimicrobial therapy
- Local
- Systemic (if necessary)

Professional Oral Hygiene

Instruments for professional oral hygiene include:
• Prophylactic rotary brushes, cups and pastes
• Sand-blasting systems (e.g. Air-Flow)
• Hand instruments (sickle scalers, curretes, hoes, chisels, files)
• Power driven instruments (ultrasound scalers)
Polishing rotary brushes, cups and pastes
Cleaning of dental plaque and polishing of tooth surface may be done with:
• rubber prophylaxis cups + prophylaxis pumice powder OR prophylaxis pastes
• prophylaxis rotary brushes + prophylaxis paste
Rubber prophylaxis cups may be:
• Different internal and external relief (ribbed, webbed, etc.) provides cleaning to
maximize surface contact with tooth, allows to keep paste inside a cup and
prevents splatter of paste.

66
 Figure 1. Different internal and external relief of YoungTM Prophy Cups (picture
courtesy Young Dental, USA)

• Different types of fixation in handpiece

• Latex-contain and latex-free
Prophylaxis rotary brushes may differ in:
• bristles material (nylon and natural bristles)
• shape: cup type, flat type, tapered type

Figure 2. Cup type prophylaxis rotary brushes (left- with nylon bristles, right –
with natural bristles)
For cleaning of tooth surface dentist may use:
• Prophylaxis pumice powder
• Prophylaxis paste. Paste may have different composition and abrasiveness. Paste
may be packed in:
1) Plastic jar
2) Tube
3) Unidose (may be fix in special finger holder)
Prophylactic brushes, cups and pastes are used for removing of dental plaque (Fig. 3).

A B
67
 C
Figure 3. Dental plaque on upper and lower teeth (A); after application of dental plaque detector,
dental plaque is pink color (B); after cleaning (C)
Sand-blasting systems
One of the most common sand blasting system is Air-Flow (Fig. 4). Such system is most
effective for removal of pigmented stains. Dark brown or grey stains on the teeth that are clearly
visible but difficult to remove using normal teeth cleaning methods. Sand-blasting system
polishes away any surface staining because of tea, coffee, tobacco, wine and curry.

Figure 4. Air-Flow system (picture courtesy Electro Medical Systems SA)

Air polishing procedures which uses air and water pressure to deliver a controlled stream of
specially processed powders in a slurry through the handpiece nozzle. Fine particles of powder
are propelled by compressed air in a spray and directed onto the surface of teeth. This
pressurized jet of air, water and powder removes surface strains and plaque.
There are two types of powder:
• Classic powders based on sodium bicarbonate for supragingival areas
• Perio powder based on glycine, 25 microns for shallow subgingival areas.
Hand instruments
Hand instruments:
o Sickle scalers:
 curved sickle scaler
 straight sickle scaler
o Curretes:
 area specific curettes
 universal curettes
o Hoes, chisels, files
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Sickle scalers (Fig. 5) is used for removal of moderate to heavy supragingival calculus or
subgingival calculus, located just below gingiva. There two blade designs: curved and straight
(Fig 6,7).

Figure 5. Double-ended sickle scaler (left side – curved sickle scaler, right side – straight sickle
scaler)

A B
Figure 6. Scheme of working part of straight (A) and curved (B) sickle scalers

Figure 7. Working part of sickle scaler: straight (left) and curved (right)

Curved sickle scaler has two cutting edges on a curved blade that end in a sharp point. To
remove calculus adapt the tip 1/3 of the cutting edge against the tooth, under the deposit. Tilt the
facial surface of a blade toward the tooth, apply lateral pressure against the tooth and pull the
scaler firmly upward to dislodge the deposit (Fig. 8). Both cutting edges of scaler may be used
for mesial, distal, or lingual surfaces.

69
 Figure 8. Scheme of removing calculus by sickle scaler
Curettes (Fig. 11) are used for subgingival scaling and gingival curettage (removal of the inner
wall of periodontal pocket, which consists of depitalization and removing of granulomatous
tissue). Each working end has a cutting edge on both sides of the blade and a rounded toe (Fig.
9,10). In cross-section, the blade appears semicircular with a convex base. The lateral border of
the convex base forms a cutting edge with the face of the semicircular blade.

Figure 9. Working part of curette (left) and sickle scaler (right). Note the rounded toe of curette
and sharp tip of scaler

Figure10. Scheme of working part of curette

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 Figure 11. Different types of curettes

Types of curettes:
• Universal Curettes. Universal curettes have cutting edges that may be inserted in most areas
of the dentition by altering and adapting of hand position of the operator. The blade size
and the angle and length of the shank may vary, but the face of the blade of every universal
curette is at a 90-degree angle (perpendicular) to the lower shank when seen in cross-
section from the tip. The blade of the universal curette is curved in one direction from the
head of the blade to the toe.
• Area specific curette (Gracey curette).A set of these curettes comprises 14 instruments
desined for different surfaces of root. The Gracey curettes also differ from the universal
curettes in that the blade is not at a 90-degree angle to the lower shank. The term offset
blade is used to describe Gracey curettes because they are angled approximately 60 to 70
degrees from the lower shank. This unique angulation allows the blade to be inserted in the
precise position necessary for subgingival scaling and root planing, provided that the lower
shank is parallel with the long axis of the tooth surface being scaled. Gracey curettes are
available different length of shank for removing of deep subgingival calculus (Fig. 12).

Figure 12. Curette Gracey with long shank for removing of deep subgingival calculus and
it’s working part (enlarged image).

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Hoes, chisels, files are used to remove tenacious calculus and altered cement. Their use is limited
compared with that of curettes.

Power driven instruments

Power instrumentation has the potential to make scaling less demanding, more time efficient, and
more ergonomically friendly. The scaling tip vibrates in the ultrasonic range of 20-45 kHz (i.e.
20,000 to 45,000 times per second), with an optimum frequency between 18 kHz and 32kHz.
Modified tip designs allow for improved access in many areas, including furcations. Most of the
scaling power is available at the tip, which is cooled with a jet of water.
Water contributes to three physiologic effects that play a role in the efficacy. These are:
• acoustic streaming
• acoustic turbulence
• cavitation
Acoustic steaming is the unidirectional fluid flow caused by ultrasound waves. Acoustic
turbulence is created when the movement of the tip causes the coolant to accelerate, producing
an intensified swirling effect. This turbulence continues until cavitation occurs. Cavitation is the
formation of bubbles in water caused by the high turbulence. The bubbles implode and produce
shock waves in the liquid, creating further shock waves throughout the water.
Ultrasonic technique is different from instrumentation with hand scalers. Light pressure is
needed with a power instrument. Increased pressure on the tip causes decreased clinical efficacy.

Anti-inflammatory/Antimicrobial Therapy
The primary rationale of using chemotherapeutic (anti-inflammatory/anti-microbial) agents is to
eliminate or reduce effect of microorganism in oral cavity. Periodontal pockets are populated by
various periodontal pathogens which are responsible for the periodontal destruction. Sometimes
these pathogenes may not be accessible to mechanical debridement. Also debridement
procedures doesn’t guarantee total elimination of microorganisms from periodontal pocket; the
bacterial biofilm may be difficult to remove from difficult to reach areas, such as furcation areas.
Another important rationale of using chemotherapeutic agents is poor host defense. Patients with
acute necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis are candidates
which may get benefited from antimicrobial therapy. The success of antimicrobial therapy
depends on the susceptibility of bacteria to the antimicrobial agent.
Anti-inflammatory/antimicrobial agents can be administrated systemically or locally (local drug
delivery). Both systemic and local drug delivery has their own advantages.

Local Drug Delivery

Topically applied antimicrobial solutions as mouth rinses have been used for many years as an
adjunct to mechanical plaque control. Since oral rinses and irrigation at the gingival margin do
not reach subgingival areas on a predictable basis, a subgingival drug delivery system was
desirable.
Thus the primary rationale of local drug delivery is to place an antibiotic or antiseptic in direct
contact with the root surface and periodontal pocket wall, so that pathogenic microorganisms
that are not accessible to mechanical removal by hand or power-driven instruments, can be
reduced or eliminated. By using this method of drug delivery, a high concentration (many folds

72
more than the minimum inhibitory concentration) can be attained at a site for a sufficient
duration of time.
Advantages:
1. A high concentration (up to 100 fold higher as compared to systemic therapy) of the
drug can be achieved at a localized site that can be maintained there, long enough for
the desired effect to be accomplished without causing any side effect.
2. The concentration of the drug in periodontal pocket is not affected by the fluctuation
in plasma levels.
3. The technique is suitable for agents which cannot be given systemically, such as
chlorhexidine.
Disadvantages:
1. Most of the presently available antimicrobial agents for local drug delivery can be
applied by dental professionals that is time-consuming and requires special effort.
2. These agents have a limited action on periodontal pathogens residing within adjacent
gingival connective tissues and on extra pocket oral surface (tonque, tonsils, and buccal
mucosa), which increases the risk of later re-infection.
3. The drug may not get complete access to areas such as deeper pocket areas or furcation.
The most widespread solutions for local use are:
• Chlorhexidine is a biguanide compound used as an antiseptic agent with topical
antibacterial activity in form of chlorhexidine gluconate. Molecule of chlorhexidine is
positively charged and reacts with the negatively charged microbial cell surface, thereby
destroying the integrity of the cell membrane. Subsequently, chlorhexidine gluconate
penetrates into the cell and causes leakage of intracellular components leading to cell
death. Chlorhexidine reduces the adherence of Porphyromonas gingivalis to epithelial
cells. It can be bacteriostatic or bactericidal depending on the dose. It acts against a wide
array of bacteria including Gram positive and Gram negative bacteria, dermatophytes and
lipolytic viruses, fungi, yeasts and some viruses including Hepatitis B virus and Human
Immunodeficiency Virus. Chlorhexidine rinses are available in the form of 0.2% and
0.12%. Chorhexidine also available in gel different concentrations are 1%, 0.2%, 0.12%.
• Povidone iodine. Povidone iodine (PVP-Iodine) is a bactericidal anti-septic whose
mechanism of action include oxidation of amino, thiol and hydroxyl moieties of amino
acids and nucleotide. Povidone-iodine is a chemical complex of povidone, hydrogen
iodide, and elemental iodine. Free iodine, slowly liberated from the povidone-iodine
complex in solution, kills eukaryotic or prokaryotic cells through iodination of lipids and
oxidation of cytoplasmic and membrane compounds. This agent exhibits a broad range of
bactericidal activity against bacteria, fungi, protozoa, and viruses.
• Hydrogen peroxide. Hydrogen peroxide is a strong oxidizing agent used as topical
antibacterial agent. It destroys microorganisms, but usually not bacterial spores; it does
not necessarily kill all microorganisms, but reduces its level. It can create foam,
especially when contact with blood. Most widespread concentration of hydrogen
peroxide is 3%. Higher concentrations can cause burns.
There are two main possibilities of local drug delivery: subgingival irrigation and carrier
systems.
Subgingival irrigation. Subgingival irrigation has been used for many years as a means for local
drug delivery in subgingival areas. As already stated, mouth rinses may not provide the complete
access of an antimicrobial agent to the entire depth of periodontal pockets. So, subgingival
irrigation with a needle or a nozzle that is placed inside periodontal pocket is helpful in pushing
the irrigant till the base of the pocket. Various solutions such as chlorhexidine, povidone iodine,
hydrogen peroxide have been used for this purpose.
73
The problem associated with subgingival irrigation is the quick elimination of the therapeutic
agent from gingival sulcus, which is due to the continuous renewal of gingival cervical fluid in
gingival sulcus.
Local drug delivery carrier systems. Presently, there are various drug carrier systems available to
carry the active anti-microbial agent. These include:
• Fibers
• Films
• Injectable systems
• Gels
Fibers. The fiber system consists of thread-like devices which act as a reservoir for the active
drug. These fibers are placed circumferentially into the periodontal pockets with an applicator
and secured with cyanoacrylate adhesives. While secured in place, these fibers release active
drug for an extend period of time. Various materials have been used to make these fibers
including polyurethane, polypropylene, cellulose. The examples of commercially available
systems using fibers include tetracycline fibers (Fig. 13) and chlorhexidine fibers.

Figure 13. Tetracycline fibers for periodontal therapy “Periodontal Plus AB” (picture courtesy
ADVANCED BIOTECH PRODUCTS Ltd.)

Films. Films used as a carrier for active drugs are made up of synthetic biodegradable polymers
such as polylactide-coglycolide or cross-linked fish gelatin. Films are cut into small pieces
suitable for insertion into periodontal pocket and no additional aids for retention are required
because of the adhesive nature of the carrier material. The film are available for chlorhexidine,
metronidazole, tetracycline and minocycline. An example of such a film may be subgingival
biodegradable gelatin chip PerioChip® with chlorhexidine gluconate 2.5 mg. This chip may be
inserted in the periodontal pocket 5 mm depth or more and will release chlorxehidine there
during 7–10 days. Chlorhexidine from a chip reaches an average concentration equivalent to
125µg per ml of gingival crevicular fluid.

Figure 14. Subgingival biodegradable chip PerioChip® (picture courtesy Dexel pharma)

74
Injectable systems. These are comparatively easy systems for delivered without pain. The drug is
pushed into periodontal pocket so that it can reach the deepest portion of the pocket, thus getting
access to the microflora of periodontal pocket.
Gels. Various gel formulations are also available for local drug delivery. The gel carrying active
drug is applied in the periodontal pocket with the help of a blunt syringe. The examples of
presently available gel based local drug delivery systems include metronidazole gel and
doxycycline gel.

Systemic Drug Delivery

One of the route of drug administration is systemic administration. In that case drug reach the
periodontal tissue via serum and act on bacteria in periodontal tissue and pocket.
The first and foremost problem of using systemic antibiotics for periodontal therapy is that
periodontal diseases are multifactorial disease. Although, bacterial etiology is the primary
etiology of the most of periodontal diseases, but many systemic, environmental and genetic
factors are also associated with periodontal diseases progression.
Second problem is that putative periodontal pathogens vary considerably in sensitivity to several
antibiotics making simplistic approaches to antimicrobial therapy problematic.
Systemic administration is associated with side effect. In accordance with the general principles
of prescribing antibiotics it is essential that the drugs are administered only after careful case
selection, and antibiotic therapy should not substitute the routine and time-honored treatment
regimens (root scaling and debridement, home oral hygiene etc.). The administration of systemic
antibiotic therapy should be considered based on its potential benefits and side effect.
Patients with gingivitis or chronic periodontitis usually respond well to mechanical debridement
and topical antiseptics and may not derive clinically significant additional benefit from antibiotic
therapy. Systemic antibiotic therapy for treatment of the periodontal condition in conjunction
with local therapy is indicated:
1) aggressive periodontitis
2) acute ulcerative necrotizing gingivitis and periodontitis, especially if there are signs of
systemic involvement (fever, malaise, lymphoadenopathy).
3) refractory periodontitis. Antibiotic therapy is warranted in cases of periodontal disease,
which, despite through non-surgical management and good plaque control, continue to
show breakdown and loss of attachment. Refractory periodontitis is often related to
persistent subgingival pathogens and perhaps impaired host resistance and can benefit
from a short course of antibiotic therapy.
4) patients with suppuration. Periodontal abscess can spread within tissue planes to cause
marked facial swelling and systemic manifestations (fever, malaise, lymphoadenopathy).
In these cases, broad-spectrum antibiotics should be prescribed to control the infection in
conjunction with incision and drainage.
5) patient schedule for periodontal surgery for preventing harmful effects of bacteremia
6) acute periodontal infection associated with systemic manifestation
7) for prophylaxis in medically compromised patients
In these cases, systemic antibiotics are used to eliminate the bacteria that invade the gingival
tissues and can repopulate the pocket after scaling and root debridement; and also for preventing
systemic complications.

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Physical disruption of biofilm is essential to achieve maximum benefit from antibiotic therapy
because of bacteria in a well-organized biofilm are more resistant to antibiotics as compared to
planktonic bacteria. Thus root scaling and debridement procedures are essential.
Advantages of systemic administration of antibiotics in periodontal therapy:
• Easy administration of the drug to multiple sites of diseases activity
• Possibility to eliminate or reduce pathogens colonizing on oral mucosa and other extra-
dental sites including tongue and tonsillar areas
Disadvantages of systemic administration of antibiotics in periodontal therapy:
• Inability to reach high drug concentration in gingival cervical fluid
• Possible risk of side effects
• Increasing risk of antibiotic resistance of microorganisms.
Indiscriminate antibiotic administration is contrary to sound clinical practice and may cause
overgrowth of intrinsically resistant pathogens, or may unnecessarily increase in vivo resistance
to antibiotics that are valuable in potentially fatal medical infection. Prescription of inappropriate
antimicrobial agents may lead to overgrowth of pathogens and poor clinical response.
Choice of systemic administration of antibacterial agent:
Antibiotics may be prescribed in a single drug therapy or combination drug therapy.
Combination drug therapy may be useful in periodontitis that involves variety of
periodontopathic species with differing antimicrobial susceptibility. One strategy aimed at
combating resistant subgingival bacteria is the use of treatment regimens that incorporate agents
with complementary but different mechanisms of action. Combination therapy should include
drugs that exhibit synergy or additive effects. Some antibiotics, through combination
antagonism, can lead to a reduction rather than increase in antimicrobial activity. Antagonism
occurs, for example, between bacteriostatic tetracyclines and bactericidal β–lactam antibiotics.
Antibiotics may be divided into next groups based on their spectrum activity:
• Broad spectrum (active against both Gram-positive and Gram-negative organisms.
Examples: tetracyclines, phenicols, fluorquinolones, third-generation and fourth-
generation cephalosporins)
• Narrow spectrum (have limited activity and are primarily only useful against particular
species of microorganisms. Example include: Aminoglicosides and sulfonamides, which
are effective only against aerobic organisms and nitroimidazoles which are generally
effective only against anaerobes).
Spectrum of chosen drug should include the targeted organism/organisms. In empirical therapy
usually broad-spectrum antibiotics are given so that all suspected organisms are covered,
whereas. Empirical antibiotics therapy may be employed for periodontal diseases with known
microbial etiologies, such as acute necrotizing ulcerative that is caused by anaerobic
microorganisms and may be cured by metronidazole, and early stages of aggressive periodontitis
that is mostly caused by Actinobacillus actinomycetemcomitans, which may be control or
eradicated by systemic metronidazole-amoxicillin combination therapy.
Ideally, in rational therapy the choice of an antibiotic depends on the microbial analysis and
antibiotic sensitivity testing. Narrow spectrum drug should be given which targets only the
identified organism/organisms.
Most of the times empirical therapy is used based on the clinical findings and most probable
microorganisms involved in a particular periodontal condition.
The most commonly used antibiotics in periodontal treatment include:
• metronidazole
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 • clindamycin
• azithromycin
• ciprofloxacin
• tetracyclines (tetracyclines, doxycyclines, minocycline)
• amoxicillin with or without clavulanic acid

The optimal dose of antibiotics remains unclear since most current antibiotics regimens are
empirically developed rather than through systematic research. The most widespread
recommended doses are presented in Table 1.
Table 1. Common antibiotic therapies are used in periodontal therapy

Name of antibiotic Doses

Metronidazole 500 mg or t.i.d.1 / 8 days

Clindamycin 300 mg b.i.d.2 or t.i.d. / 8 days

Azithromycin 500 mg q.d.3 / 4-7 days

Ciprofloxacin 500 mg b.i.d. / 8 days

Doxycycline or minocycline 100-200 mg q.d. / 21 days

Metronidazole + amoxicillin 250 mg t.i.d. / 8 days of each drug

Metronidazole + ciprofloxacin 500 mg b.i.d. / 8 days of each drug

1
t.i.d. stands for Latin “ter in die” which means three times thrice daily
2
b.i.d. stands for Latin “bis in die” which means twice daily
3
q.d. stands for Latin “quaque die” which means once a day

Metronidazole (nitroimidazole class) specifically targets anaerobic microorganisms but has

essentially no activity against aerobic or microaerophilic bacteria. Metronidazole penetrates
gingival tissue and gingival cervical fluid for most of putative pathogens. Cytotoxic metabolites
of metronidazole directly interact with the bacterial DNA, resulting in cell death. Metronidazole
crosses placental barrier enter fetal circulatory system. It is also secreted in breast milk so
contraindicated in pregnant and lactate women. It may be indicated in aggressive periodontitis,
periodontitis as manifestation of systemic diseases, refractory periodontitis, and necrotizing
ulcerative gingivatis and periodontitis.
Clindamycin (lincomycin derivative class) is bacteriostatic and inhibits bacterial protein
synthesis by binding to the ribosomal subunits. The drug is most effective against gram negative
anaerobes. Eikenella corrodens is resistant to clindamycin. Clindamycin may be used in
penicillin-allergic patients.
Azithromycin (macrolide class) exhibits an excellent ability to penetrate into both normal and
pathological periodontal tissues. It is also highly active against many periodontal pathogens.
Although some enterococcus, staphylococcus, Eikenella corrodens, Fusobacterium nucleatum
and peptosteptococcus strains may exhibit resistance.
Ciprofloxacin (quinolone class) is bactericidal due to its mode of action on bacterial DNA
replication. It is active against enteric rods, pseudomonas, staphylococci, Actinobacillus
actinomycetemcomitans and other periodontal pathogens. Ciprofloxacin is excreted in human
77
breast milk and may cross the placental barrier. Thus, it is contraindicated during lactation and
pregnancy.
Tetracycline (tetracycline, doxycyclines, minocyclines) was the first antibiotics for treatment of
periodontitis that received scientific evaluation. It may be indicated in periodontal infections in
which Actinobacillus actinomycetemcomitans is the prominent pathogen, however in mixed
infection tetracyclines antibiotics may not provide sufficient suppression of subgingival
pathogens to arrest diseases progression. Doxycycline has the highest protein binding capacity,
and minocycline has the best absorption and tissue penetration of tetracyclines. All tetracyclines
have important adverse reaction in teeth and bones, thus they are contraindicated during
pregnancy and for children below 8 years of age.
Amoxicillin (β-lactame class, penicillin subgroup). Pencillins are broad class of antibiotics that
inhibit bacterial cell wall synthesis and directly result in the death of the cell. Amoxicillin is a
semi-synthetic penicillin with an extended anti-infective spectrum that includes gram-positive
and gram-negative bacteria. It demonstrates excellent absorption after oral administration.
Amoxicillin is susceptible to penicillinase, which is a β-lactamase produced by certain bacteria
that breaks the penicillin ring structure and thus renders penicillins ineffective. The combination
of amoxicillin with clavulanic acid (clavulanate potassium) makes this anti-infective agent
resistant to penicillinase enzymes produced by some bacteria. Amoxicillin with clavulanate
potassium has a trade name Augmentin. Indications: aggressive periodontitis, periodontitis as
manifestation of systemic diseases, and refractory periodontitis.
Metronidazole + amoxicillin provides a relatively predictable eradication of Actinobacillus
actinomycetemcomitans and marked suppression of Porphyromonas gingivalis in aggressive
forms of periodontitis and in refractory chronic periodontitis.
Metronidazole + ciprofloxacin may substitute for metronidazole plus amoxicillin in individuals
who are allergic to β-lactame drugs and are at least 18 years of age. Metronidazole +
ciprofloxacin is also valuable drug combination in periodontitis patients having mixed anaerobic-
enteric rod infection.
Antibiotics always should be prescribed in combination with next:
1. Antihistamine drugs – to reduce sensibilization of human organism against
dying bacteria and components of their cells.
2. Probiotics is a food supplement contains multiple strains of residential
bacteria. When taking antibiotics, not only pathological bacteria are affected
but also normal microflora especially in digestive tract. Probiotics can help
replace them and recreate normal microflora.
3. Antifungal also known as an antimycotic medication, is a pharmaceutical
fungicide or fungistatic used to treat and prevent mycoses. In human
organism fungi growth is suppressed by resident microflora. Antibiotics
suppressed normal resident microflora which may cause growth of fungi.
Prescription of antifungal drug in second day of antibiotics course is
prevention of fungi overgrowth and such complication of antibiotics
therapy as candidosis.
Food doesn’t influence the bioavailability of most oral antibiotics, with exception of
tetracyclines, fluoroquinolones and azithromycin. These three groups of antibiotic should be
taken 1 hour before or 2 hours after food intake.
Cost can be a determinant in selecting antimicrobial periodontal therapy. Antibiotics in the lower
cost group include tetracyclines, amoxicillin, and metronidazole. More expensive antibiotics
include azithromycin, clarithromycin, ciprofloxacin, augmentin, and clindamycin.

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Nonsteroidal Anti-Inflammatory Drugs
The host response is responsible for most of the tissue breakdown that occurs, leading to the
clinical signs of periodontitis (i.e., loss of connective tissue attachment and bone).
Host modulation therapy (HMT) is a means of treating the host side of the host-bacteria
interaction. HMTs offer the opportunity for modulating or reducing this destruction by treating
aspects of the chronic inflammatory response. HMTs do not “switch off” normal defense
mechanisms or inflammation; instead, they ameliorate excessive or pathologically elevated
inflammatory processes to enhance the opportunities for wound healing and periodontal stability.
Characteristics of HMT:
1) HMT can be used to reduce excessive levels of enzymes, cytokines, including
prostaglandins.
2) HMTs can modulate osteoclast and osteoblast function but should not impact normal tissue
turnover.
3) HMT might be used to increase the levels of a person’s own protective or anti-inflammatory
mediators.
“Host modulation” is a relatively new term that has been incorporated into dental terminology,
but it has not been well defined. This approach has been introduced relatively recently and is not
a part of basic periodontal therapy yet.
A variety of different drug classes have been evaluated as host modulation agents, including the
non-steroidal anti-inflammatory drugs (NSAIDs), enamel matrix proteins, growth factors, and
bone morphogenetic proteins.
NSAID are heterogeneous group of compounds whose analgesic, antipyretic and anti
inflammatory result from pharmacological mechanisms that are different from these of anti
inflammatory steroids and opioid analgesics. These drugs act by inhibiting the cyclooxygenase
pathway of arachidonic acid metabolism, thereby reducing prostaglandins formation.
Prostaglandins are important in the pathogenesis of periodontal disease.
NSAIDs are divided into two groups:
• Non-selective cyclooxygenase inhibitors used in periodontal research include compounds
such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam.
• Selective cyclooxygenase-2 (COX-2) inhibitors include meloxicam, nimesulide, etodolac
and celecoxib. One of the major advantages of selective COX-2 inhibition is the
reduction of adverse systemic effects.
Evidences of experimental studies were presented that some nonsteroidal anti-inflammatory
drugs (NSAIDs) can reduce the inflammation in periodontal tissues and bone resorption rate.
However, NSAIDs have some serious disadvantages when considered for use as a HMT for
periodontitis. Daily administration for extended periods is necessary for periodontal benefits to
become apparent, and NSAIDs are associated with significant side effects, including
gastrointestinal problems, hemorrhage (from decreased platelet aggregation), and renal and
hepatic impairment. Therefore, the development of topical NSAIDs formulations (e.g. gels,
rinses) with a daily application seems to be of particular interest.
Nowadays NSAIDs are prescribed more often after surgery as painkillers.

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Study 6. Classification of periodontal diseases. Catarrhal gingivitis. Histopathology.
Clinical Features. Diagnostics. Treatment. Prevention

Classifications of periodontal diseases

Classifying is systemic collection of data or knowledge and its arrangement in sequential manner
in order to facilitate its understanding. Used for a variety of applications:
• identification of the etiology and understanding of the pathogenesis
• knowledge-based and decision support system
• statistical analysis of diseases and therapeutic actions
• treatment method selection
• provides the international healthcare community with a way of communicating in a
common language
The ideal way to classify any disease is to use the name of the etiological agent. However,
periodontal diseases cannot be precisely and easy classified according to their etiology because
they are complex diseases that is occurred because of complex, and often unpredictable,
interactions between microbial complexes and the host’s inflammatory/ immune response. Also
our understanding of the causes and pathogenesis of periodontal diseases and conditions is
continually changing with increased scientific knowledge.
That is why there are several classifications of periodontal diseases with different classifying
principles: according to clinical features, according to etiology, according to histopathology etc.
None is ideally full and convenient.
One of the most recent internationally accepted classifications system of periodontal disease was
developed during the International Workshop for a Classification of Periodontal Diseases and
Conditions (IWCP) organized by American Association of Periodontology in 1999. It is
normally referred to as IWCP 1999 classification but also as the AAP (American Association of
Periodontology) 1999 classification. This system includes eight main categories with several
subdivisions.
The main positions of AAP 1999 Classification are listed below and detailed clarification of each
category are in Table 1 and Table 2.
The International Workshop for the Classification of Periodontal Disease and Conditions
(AAP 1999)
1. Gingival Diseases
• Dental plaque-induced gingival diseases
• Non-plaque-induced gingival lesions
2. Chronic Periodontitis (slight: 1-2 mm CAL1; moderate: 3-4 mm CAL; severe: > 5 mm
CAL)
• Localized (˂ 30% of sites are involved)
• Generalized (> 30% of sites are involved)
3. Aggressive Periodontitis (slight: 1-2 mm CAL; moderate: 3-4 mm CAL; severe: > 5 mm
CAL)
• Localized
• Generalized
4. Periodontitis as a Manifestation of Systemic Diseases
• Associated with hematological disorders
• Associated with genetic disorders
• Not otherwise specified
5. Necrotizing Periodontal Diseases
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 • Necrotizing ulcerative gingivitis
• Necrotizing ulcerative periodontitis
6. Abscesses of the Periodontium
• Gingival abscess
• Periodontal abscess
• Pericoronal abscess
7. Periodontitis Associated With Endodontic Lesions
• Combined periodontic-endodontic lesions
8. Developmental or Acquired Deformities and Conditions
• Localized tooth-related factors that modify or predispose to plaque-induced
gingival diseases/periodontitis
• Mucogingival deformities and conditions around teeth
• Mucogingival deformities and conditions on edentulous ridges
• Occlusal trauma

Table 1. Clarification of category “Gingival diseases” of AAP 1999 Classification

Gingival Diseases

Dental plaque-induced gingival diseases Non-plaque-induced gingival lesions

I. Gingivitis associated with dental plaque I. Gingival diseases of specific bacterial
only origin
A. Neisseria gonorrhoeae
A. Without local contributing factors B. Treponema pallidum
B. With local contributing factors C. Streptococcus species
II. Gingival diseases modified by systemic D. Other
factors II. Gingival diseases of viral origin
A. Herpesvirus infections
A. Associated with the endocrine system
1. Primary herpetic gingivostomatitis
1. Puberty-associated gingivitis 2. Recurrent oral herpes
2. Menstrual-cycle–associated gingivitis 3. Varicella zoster
3. Pregnancy-associated conditions B. Other
a) Gingivitis III. Gingival diseases of fungal origin
b) Pyogenic granuloma A. Candida species infections: generalized
4. Diabetes-mellitus–associated gingivitis gingival candidiasis
B. Associated with blood dyscrasias B. Linear gingival erythema
1. Leukemia-associated gingivitis C. Histoplasmosis
2. Other D. Other
IV. Gingival lesions of genetic origin
III. Gingival diseases modified by medications
A. Hereditary gingival fibromatosis
A. Drug-influenced gingival enlargements B. Other
B. Drug-influenced gingivitis V. Gingival manifestations of systemic
a) Oral-contraceptive–associated conditions
gingivitis A. Mucocutaneous lesions
b) Other 1. Lichen planus
IV. Gingival diseases modified by malnutrition 2. Pemphigoid
3. Pemphigus vulgaris
A. Ascorbic-acid–deficiency gingivitis 4. Erythema multiforme
B. Other 5. Lupus erythematosus
6. Drug-induced conditions
7. Other
B. Allergic reactions
1. Dental restorative materials
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 a) Mercury
b) Nickel
c) Acrylic
d) Other
2. Reactions attributable to the
following:
a) Toothpastes or dentifrices
b) Mouth rinses or mouthwashes
c) Chewing-gum additives
d) Foods and additives
3. Other
VI. Traumatic lesions (factitious, iatrogenic,
or accidental)
A. Chemical injury
B. Physical injury
C. Thermal injury
VII. Foreign-body reactions
VIII. Not otherwise specified

Table 2. Clarification of category others than Gingival diseases of AAP 1999 Classification
A. Chronic periodontitis
a. Localized
b. Generalized
B. Aggressive periodontitis
a. Localized
b. Generalized
C. Periodontitis as a manifestation of systemic diseases
a. Associated with haematological disorders
1) Acquired neutropenia
2) Leukaemias
3) Other
b. Associated with genetic disorders
1) Familial and cyclic neutropenia
2) Down’s syndrome
3) Leukocyte adhesion deficiency syndromes
4) Papillon–Lefèvre syndrome
5) Chediak–Higashi syndrome
6) Histiocytosis syndromes
7) Glycogen storage disease
8) Infantile genetic agranulocytosis
9) Cohen syndrome
10) Ehlers–Danlos syndrome (Types IV and VIII)
11) Hypophosphatasia
12) Other
c. Not otherwise specified (NOS)
D. Necrotizing periodontal diseases
a. Necrotizing ulcerative gingivitis (NUG)
b. Necrotizing ulcerative periodontitis (NUP)
E. Abscesses of the periodontium

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 a. Gingival abscess
b. Periodontal abscess
c. Pericoronal abscess
F. Periodontitis associated with endodontic lesions
a. Combined periodontic-endodontic lesions
G. Developmental or acquired deformities and conditions
a. Localized tooth-related factors that modify or predispose to plaque-induced gingival
diseases/periodontitis
1) Tooth anatomic factors
2) Dental restorations/appliances
3) Root fractures
4) Cervical root resorption and cemental tears
b. Mucogingival deformities and conditions around teeth
1. Gingival/soft tissue recession
a. facial or lingual surfaces
b. interproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Aberrant fraenum/muscle position
5. Gingival excess
a. pseudopocket
b. inconsistent gingival margin
c. excessive gingival display
d. gingival enlargement
6. Abnormal color
c. Mucogingival deformities and conditions on edentulous ridges
1. Vertical and/or horizontal ridge deficiency
2. Lack of gingiva/keratinized tissue
3. Gingival/soft tissue enlargement
4. Aberrant fraenum/muscle position
5. Decreased vestibular depth
6. Abnormal color
d. Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma

This is an extremely complex classification with many disease categories listed and, owing to its
complexity, it is sometimes difficult for general practitioners to use.

Another classification is International Classification of Diseases (ICD). ICD-10 is the 10th

revision of the International Classification of Diseases and Related Health Problems (ICD), a
medical classification list by the World Health Organization (WHO). It is a standard diagnostic
tool for epidemiology, health management and clinical purposes. Nowadays ICD-10 is widely
used in the world. The International version of ICD is the base classification for the national
modifications of ICD. The adapted versions in each country may differ in a number of ways. The
ministry of health of Russia ordered in 1997 to transfer all health organizations to ICD-10.
International Classification is revised from time to time and may differ a little form year to year.

83
International Classification of Diseases 10th revision: Version 2016 (below part about
gingival and periodontal diseases only)
Chapter XI Diseases of the digestive system (K00-K93)
Diseases of oral cavity, salivary glands and jaws (K00-K14)
K05 Gingivitis and periodontal diseases
K05.0 Acute gingivitis
Excl.:
acute necrotizing ulcerative gingivitis (A69.1)
herpesviral [herpes simplex] gingivostomatitis (B00.2)
K05.1 Chronic gingivitis
• NOS (non-other specified)
• desquamative
• hyperplastic
• simple marginal
• ulcerative
K05.2 Acute periodontitis
Acute pericoronitis
Parodontal abscess
Periodontal abscess
K05.3 Chronic periodontitis
Chronic pericoronitis
Periodontitis:
• NOS
• complex
• simplex
K05.4 Periodontosis
Juvenile periodontosis
K05.5 Other periodontal diseases
K05.6 Periodontal disease, unspecified
K06 Other disorders of gingiva and edentulous alveolar ridge
K06.0 Gingival recession
Gingival recession (generalized)(localized)(postinfective)(post-operative)
K06.1 Gingival enlargement
Gingival fibromatosis
K06.2 Gingival and edentulous alveolar ridge lesions associated with trauma
Irritative hyperplasia of edentulous ridge [denture hyperplasia]
Use additional external cause code (Chapter XX), if desired, to identify cause.
K06.8 Other specified disorders of gingiva and edentulous alveolar ridge
Fibrous epulis
Flabby ridge
Giant cell epulis
Peripheral giant cell granuloma
Pyogenic granuloma of gingiva
K06.9 Disorder of gingiva and edentulous alveolar ridge, unspecified

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Nowadays in Russia the Classification of periodontal diseases composed by Grudyanov et all
(2001) is widely accepted (Table 4).

Table 4. Classification of periodontal diseases (Grudyanov et al., 2001)

I. Gingivitis — inflammation of gingiva without destruction of dentagingival junction and other

periodontal tissues; and caused by unfavorable influence of local and systemic factors.
Forms: catarrhal, ulcerative, hypertrophic.
Course: acute, chronic, exacerbation of chronic.
Localization: localized, generalized
Degree is actual only for hypertrophic gingivitis:
• Slight degree – enlarged gingival tissue cover 1/3 of tooth crown
• Moderate degree – enlarged gingival tissue cover up to 1/2 of tooth crown,
• Severe degree - enlarged gingival tissue cover more than 1/2 of tooth crown
It has been decided to refuse subdivision of catarrhal and ulcerative gingivitis according to degree
because of absence objective criteria for it.
Hypertrophic gingivitis is also subdivided into two forms: edematous and fibrous.

II. Periodontitis — inflammation of periodontal tissues is characterized by progressive destruction of

periodontal tissues and alveolar bone
Degree:
• slight – periodontal pocket depth is less than 4 mm
• moderate – periodontal pocket depth is 4–6 mm
• severe – periodontal pocket depth is more than 6 mm
Course: chronic, aggression
Phases: exacerbation, abscess, remission.
Localization: localized, generalized

III. Periodontosis — atrophic and dystrophic lesion of all periodontal tissues. It is characterized by
absence of inflammation in marginal gingiva and periodontal pockets.
Degree:
• slight – bone loss is less than 4 mm
• moderate – bone loss is 4–6 mm
• severe – bone loss is more than 6 mm
Course: chronic
Localization: generalized

IV. Syndromes manifestation in periodontal tissues (earlier this category was called “idiopathic
diseases with progressive destruction of periodontal tissues (periodontolisis)”) — Papillon–Lefèvre
syndrome, neutropenia, agammaglobulinemia, non-compensated diabetes mellitus etc.

V. Periodontomas — tumors and tumor-like lesions (epulis, fibromatosis of gingiva, eosinophilic

granuloma, periodontal cyst etc.).
Course: chronic
85
 Localization: localized, generalized
Forms are actual only for epulis according to histopathology.

It should be noted that to combine ideal correspondence among different classifications is

unrealistic because of different approach in classifying. Correspondence of some positions of these
three classifications are in Table 5.

Table 5. Correspondence of some positions of three classifications

AAP 1999 ICD-10 (2016) Grudyanov et al. (2001)
Dental plaque-induced gingivitis K05.0 Acute gingivitis Catarrhal, acute phase
K05.1 Chronic gingivitis
simple marginal Catarrhal, chronic phase
hyperplastic Hypertrophic gingivitis

Dental plaque-induced gingivitis hypertrophic gingivitis (fibrous

→ Gingival diseases modified form)
–
by medications → Drug-
influenced gingival
enlargements
Dental plaque-induced gingivitis K06.8 Other specified disorders
→ Gingival diseases modified of gingiva and edentulous
by systemic factors → alveolar ridge
Associated with the endocrine –
Pyogenic granuloma of
system → Pregnancy-associated
gingiva
conditions → Pyogenic
granuloma

Non-plaque-induced gingival K06.1 Gingival enlargement Periodontomas: fibromatosis of

lesions → Gingival lesions of gingiva
Gingival fibromatosis
genetic origin → Hereditary
gingival fibromatosis
Chronic periodontitis K05.3 Chronic periodontitis Periodontitis, chronic course
Aggressive periodontitis – Periodontitis, aggressive course
Necrotizing ulcerative gingivitis A69.1 acute necrotizing Ulcerative gingivitis
ulcerative gingivitis
Abscesses of the periodontium K05.0 Acute periodontitis Periodontitis, phase exacerbation
K06.0 Gingival recession
Developmental or acquired
deformities and conditions → –
Mucogingival deformities and
conditions around teeth →
gingival recession
K06.8 Other specified disorders Periodontomas:
of gingiva and edentulous
–
alveolar ridge
Fibrous epulis,
Fibrous epulis
Giant cell epulis
Giant cell epulis

86
Catarrhal Gingivitis. Histopathology. Clinical Features. Diagnostic. Prevention
Gingivitis is an inflammation of gingiva caused by unfavorable influence of local and systemic
factors with no destruction of dentagingival junction and no attachment loss.
Gingivitis is divided:
1. According to number of involved teeth:
• Localized is confined to the gingiva of a single tooth or group of teeth (no more than
30% of sites).
• Generalized – more than 30% of sites involves or entire mouth.
2. According to course and duration:
• Acute – can occur with sudden onset and short duration
• Chronic – slow in onset and long in duration. It is long-standing inflammation of gingiva
(gingivitis may exist for years without changes to periodontitis)
3. According to distribution of inflammation:
• Papillary – involved interdental papillae and extends in the gingival margin. Earlies
sings of gingivitis occur in the papillae.
• Marginal – involved gingival margin
• Diffuse – affects marginal, attached gingiva and interdental papillae

Etiology
Etiology of inflammatory periodontal diseases is described in details in Study 2. Generally the
main reason of gingival inflammation is dental plaque accumulation. Plaque-induced gingivitis
is one of the most common periodontal diseases. It is the result of an interaction between the
microorganisms found in the dental plaque and inflammatory cells of the host. The plaque–host
interaction can be altered by the effects of local factors, systemic factors, medications, and
malnutrition, all of which can influence the severity and duration of the response. Local factors
are contributory because of their ability to retain plaque microorganisms and to inhibit the
removal of those microorganisms via patient-initiated plaque-control techniques. Plaque-induced
gingivitis may be precipitated or exacerbated by hormonal changes, systemic disorders, drugs, or
nutritional deficiencies. Hormonal changes that occur at puberty and pregnancy may exacerbate
inflammation. Systemic disorders (e.g., diabetes, vitamin deficiency, leukemia) can affect the
response to infection.
Non-plaque-induced gingivitis occurs in a small percentage of people. Causes include viral, and
fungal infections, allergic reactions, trauma, mucocutaneous disorders (e.g. lichen planus,
pemphigoid) (mucocutaneous disorders are described in corresponding course), and hereditary
disorders. These effects are observed more frequently among lower socioeconomic groups, in
developing countries, and in immunocompromised individuals.

Histopathology
The sequence of events that culminates in clinically apparent gingivitis is categorized as the
initial, early, and established stages of disease.
The initial stage of gingival inflammation is within 2 days–1 week after plaque accumulation.
There are classic features of acute inflammation in the connective tissue beneath the
junctional epithelium:
1. changes in blood vessels: dilated capillaries and increased blood flow
2. adherence of neutrophils to vessel walls (margination). Leukocytes—mainly
polymorphonuclear neutrophils (PMNs)—leave the capillaries by migrating through
87
 the walls via diapedesis and emigration. They can be seen in increased number in
the connective tissue, the junctional epithelium, and the gingival sulcus.
The early stage of gingival inflammation evolves from the initial lesion within about 1 week –
12 days after the beginning of plaque accumulation with no clear-cut dividing line. All of the
changes seen in the initial lesion continue to intensify with the early lesion.
Microscopic changes involved:
1. Progression of changes in blood vessels:
• proliferation of capillaries
• increased formation of capillary loops between rete pegs of epithelium
2. Junctional epithelium is infiltrated by PMNs.
3. Junctional epithelium develops rete pegs which are not typical for it in healthy
conditions.
4. Connective tissue beneath the junctional epithelium is infiltrated by leukocytes, which
consists mainly of lymphocytes but that also includes some migrating neutrophils as
well as macrophages, plasma cells, and mast cells.
5. Collagen destruction is observed.
Two to three weeks after the beginning of plaque accumulation the established lesion evolves, it
corresponds to chronic gingivitis. It is characterized by:
1. Predominance of plasma cells and B lymphocytes. Plasma cells invade the connective
tissue not only immediately below the junctional epithelium but also deep into the
connective tissue, around the blood vessels, and between the bundles of collagen
fibers.
2. Blood vessels become engorged and congested, venous return is impaired, and the blood
flow becomes sluggish. The result is localized gingival anoxemia, which superimposes a
somewhat bluish hue on the reddened gingiva.
3. Junctional epithelium reveals widened intercellular spaces that are filled with
granular cellular debris, including lysosomes derived from disrupted neutrophils,
lymphocytes, and monocytes.
4. Junctional epithelium develops rete pegs that protrude into the connective tissue,
and the basal lamina is destroyed in some areas.
5. Collagen fibers are destroyed around the infiltrate of plasma cells, neutrophils,
lymphocytes, monocytes, and mast cells.

Clinical Features of Acute Catarrhal Gingivitis

Acute catarrhal gingivitis is an inflammation occur with sudden onset and short duration. It
should be noted that such clinical manifestations of acute gingivitis as pain, redness and swelling
are more typical in children and young patients than in adults. In children acute catarrhal
gingivitis is one of the manifestation of viral or bacterial infection such as flu etc. or after local
trauma. In adults, the acute phase is usually symptomless and after 1 week transfer into a chronic
process.
Diagnosis is based on examination.
Complaints:
• Pain, burning in gingiva
• Fever, headache, myalgia (in children if gingivitis is a manifestation of flu or other
respiratory infections)
Extraoral Examination
Nothing abnormal
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Intraoral Examination
In general, clinical features of gingivitis may be characterized by the presence of any of the
following clinical signs:
• redness of gingiva
• swelling that pits on pressure
• marginal and interdental gingiva is smooth and shiny, no stipping is visible.
• bleeding on probing
• presence of supragingival calculus and/or dental plaque
• no attachment loss
Radiography
• no radiographic evidence of crestal bone loss

Clinical Features of Chronic Catarrhal Gingivitis

Diagnosis is based on examination.
Complaints:
• Bleeding on tooth brushing – gums are easily bleed, even with gentle brushing and on
flossing
• Bad breath (halitosis)
• Pain is usually absent
Extraoral Examination
Nothing abnormal
Intraoral Examination
In general, clinical features of gingivitis may be characterized by the presence of any of the
following clinical signs:
• bluish-red (purple) gingiva; isolated bright-red areas of acute response may be seen (Fig.
1).
• chronic inflammation produces changes in the normal firm and resilient consistency of
the gingiva because of swelling. It becomes sponginess and puffiness. Inflamed gingival
tissues pits on pressure.
• changing in contour – normal gingiva has scalloped contours with knife edge margins. In
case of inflammation, scalloping is exaggerated with rounded margins. Peaks of
interdental papillae are also rounded.
• marginal and interdental gingivae are smooth and shiny, no stipping is visible.
• bleeding on probing
• presence of supragingival calculus and/or plaque
• no attachment loss
Radiorgaphy
• no radiographic evidence of crestal bone loss
The inflammation may resolve, remain superficial for years, or occasionally progress to
periodontitis.

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 Figure 1. Localized, intensely red area on the facial surface of teeth #11, 12, 13, 22, 23, 42 and
rounded gingival marginal in the remaining anterior teeth.

Treatment of Catarrhal Gingivitis

The condition is reversible after the establishment of effective plaque removal. Acute and
chronic catarrhal gingivitis is controlled by professional oral hygiene and proper home oral
hygiene with or without an antibacterial mouth rinse. Treatment sequence:

1. Professional oral hygiene (removing of all plaque and calculus with hand or ultrasound
instruments, prophylactic brushes, cups and paste)
2. Instructions about adequate and regular home oral care with selection of appropriate
products corresponding to clinical situation (floss, interdental brushes, waterpick, dental
rinse etc.)
3. Revealing and correction of local factors of plaque accumulation such as poor restorations
with overhanging margins, rough surfaces, open contacts etc.
4. Prescribing of antibacterial mouth rinse is possible but not oblique. The most common
antibacterial mouth rinse is 0.12% chlorhexidine gluconate. In case of chronic gingivitis it
may be prescribed to rinse with 15 ml twice a day morning and at bedtime after
toothbrushing during 7 days.
5. Check-up one week after professional cleaning for checking healing of gingivitis and
evaluation of home oral care.

Prevention of Catarrhal Gingivitis

Daily removal of plaque with dental floss and a toothbrush and routine cleaning by a dentist or
hygienist at 6 months to 1-year intervals can help minimize gingivitis. Patients with systemic
disorders predisposing to gingivitis require more frequent professional cleanings (from every 1
month to every 3 months).

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Study 7. Hypertrophic gingivitis. Histopathology. Clinical features. Diagnostics. Treatment.
Prevention

Terminology
Terms used for increased size of gingiva are hypertrophic (hyperplastic) gingivitis and gingival
hyperplasia. Nowadays some clinicians and scientists consider these terms not fully correct and
prefer to use terms gingival enlargement and gingival overgrowth. In Russia, term hypertrophic
gingivitis is accepted and widely used.

Hypertrophic gingivitis is a form of gingivitis that causes enlargement of gingival margin.

Hypertrophic gingivitis is designated as follows:
1. According to number of involved teeth:
• Localized is confined to the gingiva of a single tooth or group of teeth (no more than
30% of sites).
• Generalized – more than 30% of sites involves or entire mouth.
2. According to form of inflammation:
• Edematous
• Fibrous
3. According to degree:
• Slight degree (grade I) – enlarged gingival tissue cover 1/3 of tooth crown
• Moderate degree (grade II) – enlarged gingival tissue cover up to 1/2 of tooth crown,
• Severe degree (grade III) – enlarged gingival tissue cover more than 1/2 of tooth crown

Histopathology
In hypertrophic gingivitis proliferative stage of inflammation dominated on all other stages.

Etiology
The main etiologic factors of gingival enlargement are as follows:
• Chronic inflammatory enlargement
• Drug-induced enlargement (anticonvulsants (e.g. phenytoin), immunosuppressants (e.g.
cyclosporin), calcium channel blockers (e.g. nifedipin)). Even if it is surgically
removed, it recurs. Spontaneous disappearance occurs within a few months after the
discontinuation of the drug. Clinical and microscopic features of the enlargements caused
by the different drugs are similar. A genetic predisposition is a suspected factor for
determining whether a person treated with these drugs will develop gingival enlargement.
Drug-induced enlargement may occur in mouths with little or no plaque, and it may be
absent in mouths with abundant deposits.
• Enlargements associated with pregnancy (mostly during the 1st trimester, may persist
throughout pregnancy, and may or may not subside after delivery) or puberty

Clinical Features of Hypertrophic Gingivitis

Diagnostics is based on examination data.
Complaints
• Unusual gingival enlargement
91
 • Esthetic, speech and mastication problems associated with enlarge gingiva
• Sometimes bleeding and discomfort on toothbrushing ( in fibrous stage may appear in
case of secondary inflammation presents)
• Pain is usually absent
• Bad breath (halitosis)
Extraoral Examination
Nothing abnormal
Intraoral Examination
As previously noted, hypertrophic gingivitis manifests in two forms edematous (also called
destructive or exudative) and fibrous (also called reparative or fibrotic). Microscopically in
gingival inflammation, destructive and reparative changes coexist, and the consistency of the
gingiva (and the form of gingivitis) is determined by their relative predominance. In patients
with edematous form destructive processes are dominated. In patients with fibrous form
reparative/proliferative changes are dominated.
Clinical features of edematous and fibrous forms of hypertrophic gingivitis differ.
Edematous form is characterized by soft, reddish discrete sessile or pedunculated gingival
growths often arise in the interdental papillae. It may be also on interproximal or on the marginal
or attached gingiva. If press on it with probe the will be an imprint on the surface. They may
undergo a spontaneous reduction in size that is followed by exacerbation and continued
enlargement. Usually this mass is not painful until acute inflammation or trauma occurs. Painful
ulceration sometimes occurs in the fold between the mass and the adjacent gingiva. The
enlargement may be localized or generalized. Edematous form more often occurs in long-term
chronic inflammation (Fig. 1), pregnancy (Fig. 2) and puberty.

B
Figure 1. (A) Edematous, smooth, shiny gingiva partly covers teeth crowns in cervical are. Peaks
of interdental papilla and gingival margin are rounded. Edema is more evident in anterior region
than in posterior. Note yellowish dental plaque on teeth surfaces. (B) Significant bleeding on
probing is demonstrated.

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 Figure 2. Edematous form of hypertrophic gingivitis of 9 weeks (1st trimester) pregnant patient.
Most evident edema is in anterior region. Note enlarged interdental papilla between central
incisors partly cover teeth crowns; and enlarged interdental papillae in area of lower anterior
teeth. Note areas of reddish color of acute inflammation near dental plaque locates in cervical
area of teeth.
Fibrous form starts as a painless enlargement of the interdental papilla that then extends to the
facial and lingual gingival margins. As the condition progresses it may develop into a massive
tissue fold that covers a considerable portion of the tooth crowns. When uncomplicated with
acute inflammation, lesion is nodular, firm, pale pink, and resilient, with a minutely lobulated
surface and no tendency to bleed. If press on it with probe the will be NO an imprint on the
surface. It progresses slowly and painlessly, unless it is complicated by acute infection or trauma.
However, the presence of the enlargement makes plaque control difficult, often resulting in a
secondary inflammatory process that complicates the gingival overgrowth. Secondary
inflammatory changes not only add to the size of the lesion but also produce a red or bluish-red
discoloration, and increase bleeding tendency.
Fibrous form may be seen as manifestation of some systemic conditions, but it is more typical
for drug-induced cases (Fig. 3). Drug-induced fibrous form of hypertrophic gingivitis in most
cases is generalized but it is more severe in the maxillary and mandibular anterior regions.

93
 B C
Figure 3. Nifedipin-induced fibrous form of hypertrophic gingivitis. (A) Note the prominent pale
pink lesions with the firm, nodular surface, with no tendency to bleeding. Note generalized
character of lesion, both anterior and posterior areas are involved: right side (B) and left side (C)

Treatment
Treatment of edematous and fibrous forms of hypertrophic gingivitis has some difference:
Edematous form:

1. Professional oral hygiene (removing of all plaque and calculus with hand or ultrasound
instruments, prophylactic brushes, cups and paste)
2. Instructions about adequate and regular home oral care with selection of appropriate
products corresponding to clinical situation (floss, interdental brushes, waterpick, dental
rinse etc.)
3. Revealing and correction of local factors of plaque accumulation such as poor restorations
with overhanging margins, rough surfaces, open contacts etc.
4. Prescribing of antibacterial mouth rinse is possible but not oblique. The most common
antibacterial mouth rinse is 0.12% chlorhexidine gluconate. In case of chronic gingivitis it
may be prescribed to rinse with 15 ml twice a day morning and at bedtime after
toothbrushing during 7 days.
5. Check-up one week after professional cleaning for checking healing of gingivitis and
evaluation of home oral care.
6. If after check-up there is no significant improvement next may be prescribed:
a. rinsing against edema e.g. solution of sodium chloride, chamomile etc.
b. periopack with steroidal anti-inflammatory drug and heparin
7. Regular check-up and professional oral hygiene should be recommended

Fibrous form:

1. Professional oral hygiene (removing of all plaque and calculus with hand or ultrasound
instruments, prophylactic brushes, cups and paste)
2. Instructions about adequate and regular home oral care with selection of appropriate
products corresponding to clinical situation (floss, interdental brushes, waterpick, dental
rinse etc.)
3. Revealing and correction of local factors of plaque accumulation such as poor restorations
with overhanging margins, rough surfaces, open contacts etc.
4. In most cases, fibrous enlargement will not heal spontaneously after professional oral
hygiene. To normalize gingival contour gingivectomy is necessary. Gingivectomy means

94
 “excision of the gingiva”, (technique will be described further in corresponding study).
Gingivectomy may be done by scalpel, laser or electrosurgery.

One more method of gingivectomy is chemosurgery (or chemocoagulation). It is a

technique to remove the gingiva with the use of chemicals such as 5% paraformaldehyde,
potassium hydroxide, or 30-40% glucose have been described in the past, but they are not
currently used. They are presented here to provide a historical overview. The chemical
gingivectomy has disadvantage – the depth of action cannot be controlled; therefore,
healthy attached tissue underlying the pocket may be injured. The use of chemical
methods therefore is not recommended.

5. In case of drug-causing gingival enlargement, consultation of physician is necessary to

change drug or stopped to use it if possible.
6. Improved home care and regular professional oral hygiene usually reduce the hyperplasia.

Prevention of Hypertrophic Gingivitis

Daily removal of plaque with dental floss and a toothbrush and routine cleaning by a dentist or
hygienist at 6 months to 1-year intervals can help minimize gingivitis. Patients with systemic
disorders predisposing to gingivitis require more frequent professional cleanings (from every 1
month to every 3 months).

95
Study 8. Necrotizing Ulcerative Gingivitis. Histopathology. Clinical features. Diagnostics.
Treatment. Prevention

Necrotizing Ulcerative Gingivitis (NUG) is a microbial disease of the gingiva in the context of an
impaired host response. It is characterized by the necrosis and sloughing of gingival tissue, and it
presents with characteristic signs and symptoms. NUG is usually identified as an acute disease.
However, the term acute in this case is a clinical descriptor and should not be used as a
diagnosis, because there is no chronic form of the disease. Although the acronym Acute
Necrotizing Ulcerative Gingivitis ANUG is frequently used.

Histopathology
Microscopically, the NUG lesion is a nonspecific acute necrotizing inflammation of the
gingival margin that involves both the stratified squamous epithelium and the underlying
connective tissue. The surface epithelium is destroyed and replaced by a meshwork of
fibrin, necrotic epithelial cells, polymorphonuclear leukocytes (neutrophils) (PMNs), and
various types of microorganisms. The underlying connective tissue is markedly hyperemic,
with numerous engorged capillaries and a dense infiltration of PMNs. The epithelium and
connective tissue alterations decrease as the distance from the necrotic gingival margin
increases, blending gradually with the uninvolved gingiva.
NUG can cause tissue destruction that involves the periodontal attachment apparatus, especially
in patients with long-standing disease or severe immunosuppression. When bone loss occurs, the
condition is called necrotizing ulcerative periodontitis (NUP).

Clinical Features
History (anamnesis)
NUG is characterized by its sudden onset, sometimes after an episode of debilitating disease or
acute respiratory tract infection. A change in living habits, protracted work without adequate
rest, poor nutrition, tobacco use, and psychological stress are frequent features of the patient’s
history. NUG can occur in otherwise disease-free mouths, or most often it can be superimposed
on chronic gingivitis. Very often poor dental status (inadequate restorations, calculus and plaque
etc.) is observed in patients with NUG
Complaints
• constant pain that is intensified by eating foods and chewing.
• excessive amount of saliva
• inability to brush adequately because of pain in gingiva
• halitosis. The reason of halitosis is dental plaque and calculus and also necrotic mass of
gingiva and formation of volatile sulfur compounds (such as hydrogen sulfide (H2S),
dimethyl sulfide ((CH3)2S) etc.) produced by anaerobic microflora.
Systemic Signs and Symptoms
Local lymphadenopathy and a slight elevation in temperature are common features of the mild
and moderate stages of the disease.
In severe cases, there may be:
• lymphadenopathy
• high fever up to 38.5º C
96
 • headache
• loss of appetite
• general lassitude
• insomnia
Systemic reactions are more severe in children and depends on severity of pathological changes
in gingiva.
Extraoral Examination
In severe cases patient has pale-greyish face skin color.
Lymph nodes are enlarged, painful on palpation and no cohesion with underlying tissues
Intraoral Examination
• lesions are painful to touch
• characteristic lesions are punched-out, craterlike depressions at the crest of the interdental
papillae that subsequently extend to the marginal gingiva and rarely to the attached
gingiva and oral mucosa.
• surface of the gingival craters is covered by a gray, pseudomembranous slough (Fig. 1)
that is demarcated from the remainder of the gingival mucosa by a pronounced linear
erythema.

Figure 1. Note gray pseudomembranous slough at the peaks of interdental papillae

• when trying to scratch pseudomembrane, thereby exposing the hemorrhagic gingiva. The
characteristic lesions may progressively destroy the gingiva and the underlying
periodontal tissues.
• spontaneous bleeding or pronounced bleeding after the slightest stimulation. Periodontal
probing of NUG lesions is likely to be very painful and may need to be deferred until
after the acute lesions are resolved.
• increased salivation
• halitosis

Diagnosis
Diagnosis is based on clinical findings, which are typical.
Additional methods of diagnostic are not necessary for diagnosing but may be helpful for the
differential diagnosis of NUG from specific infections of the oral cavity (e.g., diphtheria, thrush,
tuberculosis, actinomycosis, streptococcal stomatitis), revealing of systemic conditions like
AIDS or blood diseases.
Radiography is helpful in differentiation of necrotizing ulcerative gingivitis with necrotizing
ulcerative periodontitis. In case of NUG there is no alveolar bone resorption on radiographs.

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Bacterial smear will show fusobacteria and spirochetes in deep layer of necrotic mass, and also
cocci. It is useful for differentiation of NUG from specific infections of the oral cavity. But it
does not differentiate between NUG and other necrotizing conditions of nonspecific origin, such
as those produced by trauma or caustic medications.
Serologic blood analysis for AIDS or syphilis.
Blood test is especially important to reveal hidden blood diseases (leucosis, agranulocytosis etc.)
in young patient.

Treatment
Treatment of NUG should follow an orderly sequence, according to specific steps at three
clinical visits.
First visit. The goals of initial therapy are to reduce the microbial load and remove necrotic
tissue to the degree that repair and regeneration of normal tissue barriers are reestablished.
1. Removing of necrotic tissues may be done by two methods:
a. Involved area should be isolated with cotton rolls. A topical anesthetic is applied (if
effect is insufficient local anesthesia may be administrated), and after 2-3 minutes the
areas are gently swabbed with a moistened cotton pellet to remove the
pseudomembrane and nonattached surface debris. Bleeding may be profuse. Each
cotton pellet is used in a small area, then discarded; sweeping motions over large areas
with a single pellet are not recommended.
b. Application of enzymes such as trypsin or chemotrypsin for dissolution of necrotic
slough is also possible.
2. Removing of supragingival calculus and plaque. After the area is cleansed with warm water,
the superficial calculus is removed. Ultrasonic scalers are very useful for this purpose
because they do not elicit pain, and the water jet and cavitation aid in lavage of the area.
Subgingival scaling and curettage are contraindicated at this time because these procedures
may extend the infection into the deeper tissues and may also cause bacteremia. Unless an
emergency cases, procedures, such as extractions or periodontal surgery, are postponed until
the patient has been symptom free for 4 weeks, to minimize the likelihood of exacerbating
the acute symptoms.
3. Systemic antibiotics prescription. Patients with moderate or severe NUG and local
lymphadenopathy or other systemic signs or symptoms are placed on an antibiotic regimen of
amoxicillin, 500 mg orally every 6 hours for 10 days. For amoxicillin-sensitive patients,
other antibiotics are prescribed, such as erythromycin (500 mg every 6 hours) or
metronidazole (500 mg twice daily for 7 days). Systemic complications should subside in 1
to 3 days. Antibiotics are not recommended in NUG patients who do not have systemic
complications.
4. Instructions for patient. The patient is discharged with the following instructions:
1. Avoid tobacco, alcohol, hot, spicy food
2. Rinse with a glassful of an equal mixture of 3% hydrogen peroxide and warm water
every 2 hours and/or twice daily with 0.12% chlorhexidine solution.
3. Get adequate rest and nutrition. Pursue usual activities, but avoid excessive physical
exertion or prolonged exposure to the sun.
4. Use ultrasoft toothbrush and avoid aggressive brushing; use of dental floss or
interdental brushes will be painful.
5. An analgesic, such as a nonsteroidal antiinflammatory drug (NSAID; e.g., ibuprofen),
is appropriate for pain relief.

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 6. Patients who have systemic complications, and who have been put on an antibiotic
treatment are told that bed rest is necessary, as well as copious fluid consumption and
administration of analgesics for relief of pain.
7. The patient should be advised of the extent of total treatment that the condition requires
and warned that treatment is not complete when pain stops.
8. The patient should be informed of the presence of chronic gingival or periodontal
disease, which must be eliminated to reduce the likelihood of recurrence of the acute
symptoms.
Fatty ointment should be avoided because it blocks oxygen and thus create conditions for
anaerobic microflora growth under it.
Second Visit. At the second visit, 1 or 2 days after the first visit, the patient is evaluated for
amelioration of signs and symptoms. The patient’s condition is usually improved; the pain is
diminished or no longer present. The gingival margins of the involved areas are erythematous
but without a superficial pseudomembrane. Shrinkage of the gingiva may expose previously
covered calculus. Throughout removing of dental plaque and calculus should be done in this
visit. The instructions to the patient are the same as those given previously.
Third Visit At the next visit, approximately 5 days after the second visit, the patient is evaluated
for resolution of symptoms, and a comprehensive plan for the management of the patient’s
periodontal conditions is formulated. The patient should be essentially symptom free. Some
erythema may still be present in the involved areas, and the gingiva may be slightly painful on
tactile stimulation. If 5-7 days after beginning of treatment resolution of symptoms is not as
significant as it was expected, AIDS or blood diseases should be suspected.
The patient is instructed in home oral care procedures, which are essential for the success of the
treatment and the maintenance of periodontal health. The patient is further counseled on
nutrition, smoking cessation, and other conditions or habits associated with a potential
recurrence. The hydrogen peroxide rinses are discontinued, but chlorhexidine rinses can be
maintained for 2 or 3 weeks. Scaling should be repeated if necessary.
Comprehensive treatment of the patient’s dental problems should be scheduled in this visit. The
patient should be re-evaluated at 1 month to determine compliance with oral hygiene and
periodontal status.
If untreated, NUG may lead to a progressive destruction of the periodontium as well as gingival
recession accompanied by an increase in the severity of systemic complications.

Prevention
To prevent NUG it is necessary to maintain adequate home oral hygiene, to treat periodontal
conditions and other dental problems in time, to visit regular dental check-up. Adequate nutrition
and rest are very important, it is useful to avoid stresses as much as possible. Such unhealthy
habit as smoking should be stopped.

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Study 9. Medical History Presentation 1

On medical history presentation class student should have paper version of Medical History
about given to him/her pathology. Title of Medical History should be written as follow:

University of People Friendship

Operative Dentistry Department

Medical History
“Chronic Catarrhal Gingivitis”

4th year student

[NAME, SURNAME]
Supervisor:
[NAME, SURNAME]

[Year]

EXAMPLE of MEDICAL HISTORY “CHRONIC CATARHAL GINGIVITIS”

I. Passport part:
Name: Ivanov I.
Sex: male
Date of birth: 10.09.1986
Age: 30
Address: Moscow, Basmannay street, 12-24.
Occupation: engineer

II. General medical anamnesis:

Patient denies HIV, hepatitis, syphilis.
Patient reported no cardiovascular diseases or other general pathologies, no
pacemaker, no allergies, no hereditary diseases.

III. Dental anamnesis:

Patient has bleeding on toothbrushing for about 6 month. Brush his teeth twice per
day with toothbrush and tooth paste only. Patient has never visited dentist for
professional oral hygiene.
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IV. Extraoral examination:
Face is symmetrical, skin is normal color and turgor, no erosions, ulcers or other
pathological elements are observed. Lips are normal color with no erosions, fissures
or crusts. Submandibular lymph nodes are not palpable.

V. Intraoral examination:
Teeth:
C F/C

8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8
F F/C F C

Teeth 18 and 38 are tilting in buccal direction.

Bite: teeth crowding in frontal lower jaw

Oral mucosa and gingiva status: Oral mucosa of vestibulum and oral cavity is light
pink color, appears normal moist and smooth with no erosions, ulcers, vesicles or
other pathological elements. Frenulum of upper lip fixed in the middle of alveolar
ridge. If pull out a lip and slightly press at the base of frenulum no ischemia of
gingiva in the area of frenulum fixation is observed; same for frenulum of lower lip.
Gingiva of upper and lower jaw is reddish and edematous.

Oral hygiene status: Silness&Loe index is 1.8 score

OHI–S index is 1.7 scores
Oral hygiene status at the first visit is moderate. Instructions how to brush teeth and
selection of appropriate product for cleaning of interdental spaces are required.

Treatment plan:
1. Professional oral hygiene + instructions how to brush teeth + selection of dental
floss.
2. Local anti-inflammatory therapy
3. Consultation of dental surgeon about extraction of teeth 18 and 38.
4. Treatment of teeth:
a. Primary caries: 16, 37.
b. Secondary caries and restoration replacement: 24, 44.
5. Dental check-up annually.

VI. Dairy:
Date: 26.07.2017
Intraoral examination: Gingiva is reddish and edematous. There is a lot of dental
plaque on all teeth and supragingival calculus on lingual surfaces of teeth
31,32,33,41,42,43. Silness&Loe index is 1.8 scores, OHI–S index is 1.7 scores,
bleeding index = 1,5 scores.
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 Panoramic radiograph: there is no alveolar bone resorption.
Diagnosis: chronic catarrhal gingivitis (chronic gingivitis K05.1)
Treatment: Rinsing with chlorhexidine 0.06 % for 1 minute. Professional oral
hygiene: removing of supragingival calculus by ultrasound scaler, cleaning of dental
plaque by prophylactic brushes and paste. Local anti-inflammatory therapy:
application of chlorhexidine gel 2% on gingival margin for 20 minutes, chlorhexidine
0.06 % rinsing.
Recommendations: 1. For 7 days: rinsing with chlorhexidine 0.06 % twice a day after
toothbrushing.
2. Check-up after 7 days of anti-inflammatory therapy
3. Regularly: improve home oral hygiene, use dental floss to clean
interdental spaces, visit dentist twice a year for check-up and
professional oral hygiene.

Signature: Dr. Ivanov I.I.

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Study 10. Colloquium 2
Questions for preparation for colloquium:
1. Give explanation to terms “professional oral hygiene”, “scaling and root planing”.
2. List types of anti-inflammatory therapy. Describe a local anti-inflammatory therapy in
details.
3. List instruments for professional hygiene. Describe prophylactic rotary brushes, cups and
pastes in details.
4. List instruments for professional hygiene. Describe hand instruments in details.
5. What is the technique of calculus removal by using sickle scaler?
6. What types of curettes do you know and what are their differences?
7. List instruments for professional hygiene. Describe sand-blasting system in details.
8. List instruments for professional hygiene. Describe power-driven systems in details.
9. What is primary rationale for anti-inflammatory/ antimicrobial therapy in periodontal
treatment?
10. What are advantages and disadvantages of local drug delivery?
11. List the most widespread solutions for local drug delivery. Give a characteristic for
chlorhexidine.
12. List the most widespread solutions for local drug delivery. Give a characteristic for
povidone iodine.
13. List the most widespread solutions for local drug delivery. Give a characteristic for
hydrogen peroxide.
14. Which local drug delivery systems do you know? Describe its characteristics.
15. What groups of antibiotics according to the spectrum of action do you know?
16. What is empirical antibiotics therapy?
17. What is rationale antibiotics therapy?
18. What are the most common antibiotics for periodontal therapy?
19. Give a characteristic of Clindamycin.
20. Give a characteristic of Metronidazole.
21. Give a characteristic of Ciprofloxacin.
22. What is Host Modulation Therapy?
23. Give a characteristic of NSAID.
24. What are the main positions of The International Workshop for the Classification of
Periodontal Disease and Conditions?
25. Describe Classification of periodontal diseases (Grudyanov et al., 2001).
26. What are the clinical features of an acute catarrhal gingivitis?
27. What are the clinical features of a chronic catarrhal gingivitis?
28. What is the treatment of catarrhal gingivitis?
29. What are the clinical features of a hypertrophic gingivitis (fibrous form)?
30. What are the clinical features of a hypertrophic gingivitis (edematous form)?
31. What is the treatment of hypertrophic gingivitis (fibrous form)?
32. What is the treatment of hypertrophic gingivitis (edematous form)?
33. What are the clinical features of ulcerative necrotizing gingivitis?
34. What is the treatment of ulcerative necrotizing gingivitis (first appointment)?
35. What is the treatment of ulcerative necrotizing gingivitis (second appointment)?
36. What is the prevention of catarrhal gingivitis?
37. What is the prevention of ulcerative necrotizing gingivitis?
38. What is the prevention of hypertrophic gingivitis gingivitis?
39. Describe histopathology of an acute catarrhal gingivitis.
40. Describe histopathology of a chronic catarrhal gingivitis.
41. Describe histopathology of an ulcerative necrotizing gingivitis gingivitis.

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Study 11. Chronic Marginal Periodontitis. Clinical features. Diagnostics. Prevention
Marginal periodontitis is an inflammation of periodontal tissue characterized by destruction of
epithelial attachment of gingiva and progressive destruction of alveolar bone and attachment
loss.
Marginal periodontitis is divided according to next points:
1. According to course of a diseases marginal periodontitis is divided into
• chronic
• aggressive
2. According to degree of marginal periodontitis:
• slight (also called “mild”) (PD1=3,5mm or 1-2 mm CAL2)
• moderate (PD=4-5mm or 3-4 mm CAL)
• severe (PD>5,5 mm or > 5 mm CAL)
1
periodontal pocket depth
2
clinical attachment loss
3. According to extent:
• localized (˂ 7 teeth are involved or ˂30% of sites are involved)
• generalized (˃7 teeth are involved or > 30% of sites are involved)
4. According to phase:
• activity (exacerbation including abscess phase)
• remission
Chronic Marginal Periodontitis
Chronic periodontitis is the most common form of periodontitis. It is most prevalent in adults,
but it can also be observed in children. The attachment loss associated with periodontitis has
been shown to progress either continuously with slow to moderate rate of disease progression or
in episodic bursts of disease activity. Because of its slow rate of progression, however, chronic
periodontitis usually becomes clinically significant when a patient reaches mid-30s or later. With
increasing age, attachment loss and bone loss become more prevalent and more severe as a result
of an accumulation of destruction.
In case of chronic periodontitis the majority of patients do not have a frequent active phase of the
disease (this can be occasional and irregular).
Etiology
Detailed etiological factors see in study 1. Generally chronic periodontitis is associated with the
accumulation of plaque and calculus. Disease progression is caused by the impact of local,
systemic, or environmental factors that may influence the normal host–bacteria interaction.
Periodontal Pocket
Periodontal pocket it is one of the most important clinical feature of periodontal disease.
Periodontal pocket formation may occur because of:
• coronal movement of the gingival margin because of inflammatory edema or
fibrosis enlargement;
• apical displacement of the gingival attachment;
• combination of these two processes.
Periodontal pocket types are next:
1. Gingival pocket (also called “false” pocket) is formed by gingival enlargement without
destruction of the underlying periodontal tissues. The sulcus is deepened because of the
increased bulk of the gingiva.
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2. Periodontal pocket (also called “true” pocket) is caused by destruction of the supporting
periodontal tissues and apical movement of junctional epithelium.
Periodontal pocket is an abnormal apical extension of the gingival sulcus caused by an extension
of the junctional epithelium along the root surface and formation of a pocket epithelium as the
periodontal ligament is detached and destroyed by the disease process (Definition by American
Academy of Periodontology (AAP), 1992).
Two types of true periodontal pockets exist:
a) Suprabony (supracrestal or supraalveolar) occurs when the bottom of the pocket is
coronal to the underlying alveolar bone
b) Intrabony (infrabony, subcrestal, or intraalveolar) occurs when the bottom of the pocket
is apical to the level of the adjacent alveolar bone. In this type, the lateral pocket wall lies
between the tooth surface and the alveolar bone.
Pockets can involve one, two, or more tooth surfaces, and they can be of different depths and
types on different surfaces of the same tooth.
Periodontal Pocket Formation Histopathology. The initial development of periodontitis is the
inflammation of the gingiva in response to a bacterial challenge. Pocket formation starts as an
inflammatory change in the connective tissue wall of the gingival sulcus. The cellular
and fluid inflammatory exudate causes degeneration of the surrounding connective tissue,
including the gingival fibers. Just apical to the junctional epithelium, collagen fibers are
destroyed.
The two mechanisms associated with collagen loss are as follows:
1. collagenases and other enzymes secreted by various cells in inflamed tissue,
such as fibroblasts, PMNs and macrophages, become extracellular and destroy
collagen (these enzymes that degrade collagen and other matrix
macromolecules into small peptides are called matrix metalloproteinases);
2. fibroblasts phagocytize collagen fibers and the fibrils of the cementum matrix.
As a consequence of the loss of collagen, the apical cells of the junctional
epithelium proliferate along the root.
As the pocket deepens, collagen fibers embedded in the cementum are destroyed, and
cementum becomes exposed to the oral environment. Collagenous remnants of Sharpey
fibers in the cementum undergo degeneration, thereby creating an environment favorable
to the penetration of bacteria. Viable bacteria have been found in the roots of 87% of
periodontally diseased non carious teeth. Bacterial penetration into the cementum can be
found as deep as the cemento-dentinal junction, and it may also enter the dentinal
tubules. Penetration and the growth of bacteria leads to fragmentation and breakdown of
the cementum surface and results in areas of necrotic cementum that are separated from
the tooth by masses of bacteria.
Periodontal pocket content. Periodontal pockets contain:
1. microorganisms and their products (enzymes, endotoxins, and other metabolic
products)
2. gingival fluid
3. food remnants
4. salivary mucin
5. desquamated epithelial cells
6. leukocytes.
7. plaque covered calculus usually projects from the tooth surface.

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 8. purulent exudate, if present in the patient, consists of living, degenerated, and
necrotic leukocytes; living and dead bacteria; serum; and a scant amount of
fibrin.
Periodontal Pocket Measurement. The only reliable method of locating periodontal pockets and
determining their extent is careful probing along each tooth surface. On the basis of depth alone,
however, it is sometimes difficult to differentiate between a deep normal sulcus and a shallow
periodontal pocket.
Periodontal Pocket Depth Decreasing. A periodontal pocket reduction procedure has been
recommended because when periodontal pockets are too deep to clean with daily at-home oral
hygiene it becomes a place of pathologic bacteria living and contribute to periodontal diseases
development. Reducing pocket depth and eliminating existing bacteria are important to prevent
damage caused by the progression of periodontal disease. Eliminating bacteria alone may not be
sufficient to prevent disease recurrence because in deep periodontal pocket there is a good
conditions for bacterial growth.
Two ways of periodontal depth decreasing exists but in some cases for effective treatment it
necessary to combine both:
• PD will be decreases after resolution of inflammation because of decreasing of
inflammatory edema. After decreasing of edema some degree of recession may occur and
patient should be informed about it.
• PD may be decreased by different variants of surgical procedures (see further).

Clinical Features of Chronic Marginal Periodontitis

History (anamnesis)
Depends on severity of inflammation and duration of diseases, patient may reported about
bleeding on tooth brushing and/or suppuration from time to time.
Complaints
Chronic periodontitis is commonly a slowly progressive disease that does not cause the affected
individual to feel pain. Therefore, most patients are unaware that they have developed a chronic
disease. For the majority of the patients, gingival bleeding during toothbrushing or eating may be
the first self-reported sign of disease occurrence. As a result of gingival recession, patients may
notice black triangles between the teeth or tooth sensibility in response to temperature changes
(i.e., cold and heat). In patients with advanced attachment and bone loss, tooth mobility, tooth
movement, and, in rare occasions, spontaneous tooth loss may be reported.
Depends of degree of chronic marginal periodontitis patients may have some of the next
complaints or all of them:
• Bleeding on tooth brushing, chewing or spontaneous bleeding
• Halitosis
• Teeth mobility
• Not esthetic teeth displacement
• Gingival recession
• “black triangles” between teeth
• Hypersensitivity of teeth
• Suppuration from time to time
Extraoral Examination
Nothing abnormal

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Intraoral Examination
Characteristic clinical findings in patients with untreated chronic periodontitis depends on degree
and include the following:
• supragingival and subgingival plaque and calculus
• gingival swelling, redness, and loss of gingival stippling
• altered gingival margins (e.g., rolled, flattened, cratered papillae, recessions)
• true periodontal pockets formation
• bleeding on probing
• attachment loss
• alveolar bone loss (angular or horizontally)
• root furcation involvement (exposure)
• increased tooth mobility (not in all cases, depends on severity)
• change in tooth position (pathological teeth migration pathologic tooth migration (PTM).
PTM is defined as a change in the position of a tooth that occurs when the balance of
forces, which maintains it in its normal position, was broken. Main reason of migration is
massive alveolar bone resorption. When bone doesn’t surround tooth root any more and
doesn’t carry it inside alveolar socket, occlusial loads displace tooth).
• tooth loss
• abscesses (pus) (in exacerbation phase)

Diagnosis
Chronic periodontitis can be clinically revealed with periodontal screening and recording, which
results in a periodontal screening index rating. The condition is diagnosed via the assessment of
the clinical attachment level and the detection of inflammatory changes in the marginal gingiva.
Measurements of periodontal pocket depth in combination with the location of the marginal
gingiva allow for conclusions to be drawn regarding the loss of clinical attachment. Dental
radiographs display the extent of bone loss, which is indicated by the distance between the
cementoenamel junction and the alveolar bone crest.
The clinical feature that distinguishes periodontitis from gingivitis is the presence of clinically
detectable attachment loss. This loss is often accompanied by periodontal pocket formation and
changes in the density and height of the subjacent alveolar bone. In some cases, recession of the
marginal gingiva may accompany attachment loss, thereby masking ongoing disease progression
if only probing depth measurements are taken without measurements of clinical attachment
levels.
The distinction between aggressive and chronic periodontitis is sometimes difficult, because the
clinical features may be similar at the time of the first examination. At later time points during
treatment, aggressive and chronic periodontitis may be differentiated by the rate of disease
progression over time, the familial nature of aggressive disease, the disease’s resistance to
periodontal anti-infective therapy, and the presence of local factors.
Severity
Chronic periodontitis does not progress at an equal rate in all affected sites throughout the
mouth. Some involved areas may remain static for long periods, whereas others may progress
more rapidly. More rapidly progressive lesions occur most frequently in interproximal areas, and
they may also be associated with areas of greater plaque accumulation and inaccessibility to
plaque control measures (e.g., furcation areas, overhanging margins of restorations, sites of teeth
crowding, areas of food impaction). Thus in the same mouth it might be seen areas of different
degree of diseases severity. If there are areas of moderate and severe periodontitis in one patient;
it will be called “moderate to severe degree of marginal periodontitis”.
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Despite clinical features may differ in different patient, different degree of severity are described
below.
Chronic Marginal Periodontitis. Slight Degree
Complaints:
• Bleeding on tooth brushing
• Halitosis (may be or not)
Intraoral examination:
• Reddish gingival margin, edema of gingiva
• Soft plaque and calculus (in most cases big amount of supragingival with small
amount of subgingival. Often localization lower frontal teeth lingual surfaces and
interproximal area).
• PD=3,5mm or CAL=1-2 mm
Radiograph:
• Slight loss of bone height (<1/3) (Fig. 1)
• Resorption of cortical plates of interproximal alveolar bone peaks:
o Loss of sharp border with the lamina dura of the adjacent teeth in posterior
o Loss of spiking in the anterior

Figure 1. Chronic marginal periodontitis, slight degree

Chronic Marginal Periodontitis. Moderate Degree
Complaints:
• Bleeding on tooth brushing
• Halitosis (may be or not)
Intraoral examination:
• Reddish gingival margin, edema of gingiva
• Soft plaque and calculus (both subgingival and supragingival) (Fig. 2).
• PD=4-5mm or CAL=3-4 mm
• I degree of tooth mobility may be presented
Radiograph:
• Resorption of interproximal alveolar bone up to ½ of roots length (Fig. 2).
• Generalized form demonstrates horizontal bone loss
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 • Localized defects include vertical bone loss

Figure 2. Clinical view and panoramic radiograph of patient with chronic marginal periodontitis
(moderate to severe degree). Note alveolar bone level is about ½ of roots. In area of teeth #35, 43
bone resorption is more than ½ of root length. In area of teeth# 37, 38 furcation involvement is
visible

Chronic Marginal Periodontitis. Severe Degree

Complaints:
• Bleeding on tooth brushing
• Halitosis (may be or not)
• Pain in gingiva
• Not esthetic teeth displacement
• Suppuration of gingiva from time to time
Intraoral examination:
• Reddish gingival margin, edema of gingiva
• Soft plaque and calculus (both subgingival and supragingival).
• PD>5,5 mm or CAL > 5 mm
• III and II degree of tooth mobility
• Pathological tooth migration
• Periodontal abscess may be seen
• Gingival recessions may be seen
Radiograph:
• Resorption of interproximal alveolar bone more than 1/2 of roots length (Fig. 3).
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 • Patient may have horizontal or vertical bone loss, or a combination of generalized
horizontal bone loss with localized vertical defects
• Initial appearance is widened periodontal ligament space

Figure 3. Panoramic radiograph of patient with chronic marginal periodontitis, sever degree.
Note resorption of alveolar bone more than ½ of roots length
Treatment of marginal periodontitis will be described in correspondence study.
Prevention
Prevention of chronic marginal periodontitis consists of:
• adequate individual home oral care
• treatment of dental pathologies to prevent formation of local factors of plaque
accumulation
• treatment of gingival inflammation if occur
• regular dental check-up

Clinical case
Patient N., 54 years (Fig. 4)
General anamnesis: hemangioma of face for several years.
Dental anamnesis: Patient has never visited dentist for check-up or for professional cleaning. The
reason of visit was acute pain and suppuration of gingiva. Teeth were extracted because of acute
pain and periodontal problems several years ago.
Extraoral examination: wide reddish area on the skin of face, painless on palpation.

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Figure 4. Clinical view and panoramic radiograph of patient with chronic marginal periodontitis
and hemangioma of face
Intraoral examination: Severe deformation of occlusion, teeth #11,16,26,36,45,46,47 are missed.
Dental plaque and calculus of teeth, denudation of roots, gingiva is reddish and edematous,
easily bleed on provocation.
Diagnosis: Generalized chronic marginal periodontitis moderate to severe degree.
Treatment plan:
1. Consultation of physician because of hemangioma of face
2. Instructions of home oral care.
3. Scaling and root debrigement
5. Local anti-inflammatory therapy
6. Re-evaluation of periodontal status one month after treatment
7. Consultation of prosthodontist.

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Study 12. Aggressive periodontitis. Histopathology. Etiology. Clinical Features. Diagnostics
In 1971, Baer defined aggressive periodontitis as a disease of the periodontium occurring in an
otherwise healthy adolescent, which is characterized by a rapid loss of alveolar bone around
more than one tooth of the permanent dentition. As the disease is rapidly progressing and
aggressive in nature, these patients require early diagnosis and treatment to prevent further
progression of the disease and tissue damage.
This form of periodontitis was previously classified as early-onset periodontitis.
Aggressive periodontitis differs from the chronic form. It is distinguished by the:
• age of onset
• rapid rate of destruction
• inconsistency of the low amounts of present etiological factors (i.e., plaque) and the
observed pronounced tissue destruction
• pathogenicity of the subgingival microflora
• alteration in the host immune response,
• familial aggregation of diseased that is suggestive of a genetic trait.
Etiology
As far as aggressive periodontitis occurs in generally healthy individuals, systemic factors in not
actual for them. Local factors may exacerbate disease.
Microbiology
Since long time Actinobacillis actinomicitemcommitans (A.a) has been considered the primary
pathogen for aggressive periodontitis, especially in its localized form. But there are studies
which states there is no association between A.a and the periodontal disease rather prevalence of
levels of Porfiromonas gingivalis, Treponema denticola, and Prevotella intermedia are
significantly associated with aggressive periodontitis. Nowadays it is known that:
• there are geographic and ethnic variations in relation to aggressive periodontitis
associated microorganisms
• in patients with aggressive process subgingival microflora is more pathogenic
Host response
Aggressive periodontitis should be present in a healthy individual. Multiple systemic conditions
may be associated with attachment loss, which needs to be ruled out before giving the diagnosis
as aggressive periodontitis because in some conditions the oral picture resembles aggressive
periodontitis. Immunological differences that do not entail the diagnosis of periodontitis as a
manifestation of systemic disease but alter host defense and play important role in the
progression of diseases are:
a) Hyper-responsive macrophages
b) Abnormalities of neutrophil function.

Role of Genetics
Both genetic and environmental factors play a crucial role in the development of aggressive
periodontitis. Although a number of genetic models have been tested using genetic segregation
analysis, no consistent mode of inheritance for aggressive periodontitis have been observed. A
number of hypotheses have been proposed implicating candidates for genetic risk factors.
Genetic predisposing factors to aggressive periodontitis are:
• Genetic defect of neutrophil chemotactic activity. The observation that many patients
with aggressive periodontitis, particularly localized form, have neutrophil chemotactic
defects.

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 • Genetic hyper-responsiveness of macrophages. Studies have demonstrated hyper-
responsiveness of macrophages from patients with aggressive periodontitis with respect
to their production of PGE2 in response to lipopolysaccharides of bacterial cell. This
hyper-responsive phenotype could lead to increased connective tissue or bone loss due to
inappropriately excessive production of these catabolic factors.
• Polymorphism of genes of some interleukins. Miscellaneous genes associated with
aggressive periodontitis. Here there are few gene polymorphism and their associations
with aggressive periodontitis. A strong association was found between interleukin (IL)-1a
(889) and IL-1a 3954allele 2 polymorphism and aggressive periodontitis. IL-4-590 T/T,
IL-4-34 T/T genotype are associated with aggressive periodontitis.
It should be noted that genetics is predisposing factor to aggressive course of periodontitis but
NOT causative factor of aggressive periodontitis.
Histopathology
Histopathology of aggressive periodontitis is not well-documented as compared to chronic
periodontitis because of less numbers of aggressive periodontitis patients, changing the
definition of disease entity, and variations in the timing of the biopsies.
However, found increase in the numbers of acid phosphatase positive macrophages (phagocytic
macrophages) in aggressive periodontitis patients. In the pretreatment biopsies of localized
aggressive periodontitis, there was predominant plasma cell inflammatory infiltration and the
root surfaces of individuals with aggressive periodontitis were observed to be heavily covered by
neutrophils.
Classification of Aggressive Periodontitis
In Classification American Academy of Periodontology (AAP) in 1989 there was category
“Early-onset Periodontitis”, and it had next subcategories:
1. Early-Onset periodontitits
A. Prepubertal
• Localized
• Generalized
B. Juvenile
• Localized
• Generalized
C. Rapidly progressive
In 1999 “Aggressive periodontitits” was put in place of “Early-Onset Periodontitis”. The
introduction of the term “aggressive periodontitis” is useful as it addresses the clinical behavior
of the disease but avoids the controversial age barrier.
Aggressive periodontitis is defined as disease in patients who were systemically healthy, had
rapid loss of attachment and alveolar bone, and a high incidence of a familial link.
Clearly, older subjects can experience episodes of more rapid attachment loss; whilst this is rare
it is embraced by the new system. However, it is accepted that most patients falling into this
category will be less than 30 years old.
Nowadays aggressive periodontitis is subcategorized into localized and generalized; but the
principle of this subdivision is not the same as in chronic periodontitis. Tissue loss usually starts
at the permanent first molars and incisors, and with increasing patient age the disease may
progress to involve the adjacent teeth.
Localized aggressive periodontitis (LAP) is interproximal attachment loss in area of first
molars/incisors.

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Generalized aggressive periodontitis (GAP) is generalized interproximal attachment loss
affecting at least three permanent teeth other than incisors and first molar.
Clinical Features
Localized Aggressive Periodontitis

Primary clinical features:

• LAP starts at circumpubertal age and may be observed during the second and third
decades of life,
• It involves interproximal attachment loss of first molar, and/or incisors.
• There will be lack of inflammation with presence of deep periodontal pocket and
advanced bone loss.
• Amount of plaque is minimal which is inconsistent with the amount of destruction, and
rarely mineralizes to form calculus, but the plaque is highly pathogenic.
• Raised serum antibody response to pathogens.
Secondary clinical features may also occur:
• distolabial migration of incisors with diastema formation
• mobility of the involved teeth,
• sensitivity of the denuded root,
• deep dull radiating pain to the jaw,
• periodontal abscess
• lymph node enlargement.
Generalized Aggressive Disease
• GAP has generalized interproximal attachment loss affecting at least three permanent
teeth other than incisors and first molar.
• There will be presence of minimal plaque which is inconsistent with destruction.
• Usually affecting people under 30 years of age.
• Pronounced episodic nature of loss of attachment and alveolar bone.
• Poor antibody response to pathogens.
• Two kinds of gingival responses are seen in GAP patients:
o severe acutely inflamed tissue which is ulcerated and red in color with
spontaneous bleeding indicating destructive stage
o pink gingiva free of inflammation, with some degree of stippling and deep
periodontal pockets are present representing quiescence stage.
Diagnostics
Key diagnostic criteria are:
• Early age of onset. Although in some patients the disease may start before puberty, in
most patients the age of onset is during, or somewhat after, the circumpubertal period. A
typical patient shows disease onset at an early age (i.e., before 25 years of age), although
identification of the affected patient usually occurs after disease commencement.
• A relatively high rate of disease progression and the absence of systemic diseases that
compromise the host's response to infection.
• Initially, the periodontal lesions show a distinctive pattern, depicted radiographically as
vertical bone loss at the proximal surfaces of posterior teeth, and the bone loss usually
occurs bilaterally. In advanced cases of aggressive periodontitis the periodontal lesions
may be depicted radiographically as a horizontal loss of bone.

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Specific Features of Treatment
The overall treatment concepts and goals in patients with aggressive periodontitis are not
markedly different from those in patients with chronic periodontitis. Therefore, the phases of
treatment plan are similar for both types of periodontitis. However, the considerable amount of
bone loss relative to the young age of the patient and the high rate of bone loss warrants a well-
thought-through treatment plan and an often more aggressive treatment approach, in order to halt
further periodontal destruction and regains as much periodontal attachment as possible.
Scaling and root debridement in patients with LAP improves the clinical parameters, but with the
limited data present it is unclear to know the predictability and long-term stability of scaling and
root debridement in LAP. Patients with GAP respond well to scaling and root debridement in
short term (6 months), after 6 months, relapse, and disease progression is reported despite
frequent recall visits and oral hygiene reinforcements.

Systemic antibiotics. Treating patients with aggressive periodontitis is challenging. The disease
responds less predictably to conventional mechanical periodontal therapy. In view of the specific
microbial nature of aggressive periodontal disease, the use of systemic antibiotics can play an
important role in the treatment of these diseases. Systemic antibiotics like tetracycline,
metronidazole, combination of metronidazole and amoxicillin, clindamycin, and azithromycin
are also used as adjunct in the treatment of aggressive periodontitis. The studies concluded that
using antibiotics as an adjunct to scaling and root debridement is beneficial when compared to
scaling and root debridement alone in treating aggressive periodontitis. Combination of
amoxicillin and metronidazole with scaling and root debridement is effective in treating GAP.

Local antimicrobials. Agents like 2% chlorhexidine gel, 40% tetracycline gel, tetracycline fibers,
and chlorhexidine chip have been used as local antimicrobials in the treatment of LAP and GAP.
The studies concluded that the adjunct effect of local antimicrobial is not clear and do not seem
to improve on the adjunct effect of systemic antibiotics. Therefore, it seems reasonable that the
decision to use this type of treatment modality should be made on an individual basis rather than
be evidence-based.

Surgery. Modified Widman flap surgery (technique see further) alone or in combination with
tetracycline is effective in reducing the pocket depths and pathological microbial load. Modified
Widman flap with systemic administration of amoxicillin and metronidazole combination is also
beneficial in treating aggressive periodontitis. Access surgery in combination with systemic
antibiotics was effective than access surgery alone.
Implant treatment in patients with aggressive is not contraindicated, provided that adequate
infection control and an individualized maintenance program is assured.

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Study 13. Treatment Planning of Marginal Periodontitis. Methods of treatment of
periodontal diseases. Splinting. Jankelson's technique for occlusal equilibration

General plan of periodontal treatment consists of sequence of procedures:

Phase I therapy or Etiotropic Phase:
• Training about home oral hygiene
• Scaling and root debridement to remove dental plaque and calculus.
• Correction of poorly fitting restorations and/or prosthetic (polishing of all rough,
overhanging margins of restorations, treatment of food impaction areas)
• Excavation of caries and placing restoration (temporary or final, depending on
whether a definitive prognosis for the tooth has been arrived)
• Antimicrobial therapy (local drug delivery or systemic including plaque sampling and
sensitivity testing.)
• Treatment of occlusal abnormalities
• Splinting if required
• Provisional prosthesis (if required)
• Orthodontic tooth movement (if required)
In the end of this phase evaluation of response to etiotropic phase, i.e. pocket depth re-measuring
and bleeding on probing re-evaluation, should be done.
Phase II or Surgical Phase:
• Once the initial phase of therapy is completed, inflammation subsides and
inflammatory gingival edema also subsides, healing of periodontal tissues is initiated.
• The patients is re-evaluated for periodontal pocket depth after completion of initial
therapy and if indicated the surgical therapy is planned.
• Surgical procedures including placement of implants (if required)
• After surgical therapy, junctional epithelium can be expected to take approximately
one week to heal whereas underlying connective tissue can take 4-6 weeks. Therefore
probing should be avoided for at least one month following periodontal surgery.
• Completion of endodontic therapy are done in this phase.
Phase III or Restoration Phase
• Final direct restorations (if required)
• Final fixed and/or removable prosthodontics (if required)
Phase IV therapy or Maintaince Phase or Supportive Periodontal Therapy
Next parameters should be re-evaluated in this phase:
• Plaque and calculus evaluation
• Periodontal status
• Occlusion
• Tooth mobility
Phase I therapy is defined by the evidence-based American Association of Periodontology
practice guidelines as the initiation of a comprehensive daily plaque control regimen,
management of periodontal-systemic interrelationships as needed, thorough removal of supra
and subgingival bacterial plaque biofilm and calculus, chemotherapeutic agents as necessary, and
elimination of local factors such as defective restorations and treatment of carious lesions. These
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procedures are a required part of periodontal therapy, regardless of the extent of disease present.
In many cases, only phase I therapy will required to restore periodontal health, or it will
constitute the preparatory phase for surgical therapy.
Terminology. Phase I therapy is referred to by a number of names, including initial therapy,
nonsurgical periodontal therapy, cause-related therapy. All terms refer to the procedures
performed to treat periodontal infections, up to and including tissue reevaluation.
The first line of treatment is always non-surgical therapy. Phase I therapy is the first in the
chronologic sequence of procedures that constitute periodontal treatment. The objective of phase
I therapy is to eliminate the microbial etiology and factors that contribute to gingival and
periodontal diseases to the greatest extent possible, therefore returning the dentition to a state of
health and comfort.
Based on the knowledge that microbial plaque biofilm is the major etiologic agent in gingival
inflammation, one specific aim of phase I therapy for every patient is effective daily plaque
biofilm removal at home. These home care procedures can be complex, time consuming, and
often require changing long-standing habits. Good oral hygiene is more easily accomplished if
the tooth surfaces are free of calculus deposits and other irregularities so that surfaces are easily
accessible.
Supportive periodontal therapy (SPT). Following completion of treatment and arrest of
inflammation, supportive periodontal therapy (SPT) is employed to reduce the probability of re-
infection and progression of the disease. According to the American Academy of
Periodontology, SPT should include all components of a typical dental recall examination:
• periodontal re-evaluation and risk assessment
• supragingival and subgingival removal of bacterial plaque and calculus
• re-treatment of any sites showing recurrent or persistent disease.

The inclusion of thorough periodontal evaluation, risk assessment and subsequent treatment -
differentiates SPT from routine care.
Risk assessment in SPT. The enumeration of the residual pockets with probing depths greater
than 4 mm represents - to a certain extent - the degree of success of periodontal treatment
rendered. Although this figure per se does not make much sense, when considered as a sole
parameter, the evaluation in conjunction with other parameters such as bleeding on probing
and/or suppuration will reflect existing ecological niches from and in which reinfection might
occur. It is, therefore, conceivable that periodontal stability in a dentition would be reflected in a
minimal number of residual pockets. Presence of high frequencies of deep residual pockets and
deepening of pockets during supportive periodontal care has, in fact, been associated with high
risk for disease progression.
Methods of Periodontal Treatment
The available treatments are divided into two types, namely non-surgical and surgical therapies.
However, when the periodontal condition does not recover with a non-surgical treatment,
surgical treatment is considered to restore periodontal health.
Non-surgical periodontal treatment include:
• Instructions for home oral hygiene
• Scaling and root debridement (see Study 5)
• Anti-inflammatory therapy (local and/or systemic) (see Study 5)
• Splinting (if necessary)
• Jankelson's technique for occlusal equilibration (if necessary)
Surgical treatment is divided in two types of procedures:
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 • Periodontal surgery includes surgical procedures aimed to reduce/eliminate periodontal
pocket and to get better access for root debridement (see Study 14).
• Mucogingival surgery includes non-pocket procedures utilized to resolve problems
involving the interrelationship between gingiva and alveolar mucosa (see Study 16).
Splinting
The principal causes of tooth mobility are:
• loss of alveolar bone
• inflammatory changes in periodontal ligament
• trauma from occlusion
The latter two are correctable, but mobility due to alveolar bone loss is not likely to be corrected.
Clinical prognosis of periodontally compromised teeth many times hinges on the presence of
tooth mobility. Pockets on clinically mobile teeth do not respond as well to periodontal therapy
as pockets on non-mobile teeth exhibiting the same initial disease severity. Therefore, the
treatment to reduce mobility by splinting periodontally involved teeth is an integral part of
periodontal treatment today.
Splinting is binding of mobile teeth together so any biting force is distributed among groups of
teeth rather than individual loosened teeth.
It has been proved that while a splint is in place, there is a reduction in tooth mobility. Splint has
a beneficial effects on anterior teeth exhibiting Grade I to Grade II degrees of mobility.
Periodontally compromised splinted teeth show a high survival-rate and periodontal stability.
Types of splinting:
1. Temporary splinting can be achieved by joining the teeth together with:
a) Extra-coronal splints (“extra” – outside; “coronal” – crown). With this approach,
splinting materials are attached to a group of teeth generally by bonding to the enamel,
thus making them more rigid.
b) Intra-coronal splints (“intra” – inside; “coronal” – crown). These splints involve cutting a
small channel into the teeth, inserting a rigid metal or flexible glass-fiber reinforced
splint and bonding or cementing it in place to stabilize the teeth.
2. Permanent or fixed splinting. This method permanently “fixes” loose teeth together by
crowning the affected teeth and fabricating a splint in which the crowns are joined or fused
together. Removable denture also may have splinting function.
Variants of materials for splinting:
• Glass-fiber reinforcement band + composite resin.
• Stainless steel wire + composite resin

Technique of splinting with glass-reinforced band FiberSplint:

1. Scaling and polishing of the teeth.

2. Application of rubberdam with wedges in all interproximal areas of splinted teeth. This
provides holes for home oral care (Superfloss and/or interdental brushes).
3. Thoroughly rinse, dry teeth.
4. Cut the glass-fiber reinforced band to desired length and impregnate it with adhesive
resin but do not polymerize.
5. Etch, rinse and dry lingual surface of teeth.
6. Apply a resin adhesive to the etched enamel surfaces and polymerized.
7. Apply light-cured flowable composite onto the lingual surface of teeth.
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 8. Place the glass-fiber band into the composite starting at the midlingual surface of either
canine and pushed it into the composite. The glass-fiber band impregnated with bonding
is flexible, it fits to the surface well.
9. Adapt and embed the fibers into the composite resin.
10. Some systems (e.g. FiberSplint) have special fixators for better adaptation of band to
interproximal areas (Fig. 1).
11. The lingual surfaces light-cured for 60 s/tooth.
12. Apply flowable composite to smooth the irregular surface and to provide an even
thickness of composite covering the band and light-cured for an additional 20 s/tooth
(Fig. 2).
13. Polish the splint.
14. The final step was adjustment of the occlusion if any interferences are there. It is
important to make sure that the fixed splint does not interfere with the patient’s ability to
perform oral hygiene so the interproximal spaces could be cleaned.

A B
Figure 1. Splinting of lower frontal periodontally compromised teeth with FiberSplint band. (A)
– clinical view of adaptation of band with special ring fixators. (B) scheme of adaptation of band
with ring fixators (picture courtesy Polidentia, Switzerland)

Figure 2. Mirror view of a splint on lingual surfaces of lower frontal teeth

Jankelson's technique for occlusal equilibration

Looseness of teeth is mostly caused by secondary trauma. The approach to treatment of loose
teeth is both biologic and mechanical. The biological approach involves treatment of the gum
disease that must be addressed first to provide an environment in which the periodontal
attachment can heal.
The mechanical approach involves modifying the amount of biting force generated by the jaw
muscles and received by the teeth during biting. One of the way to achieve it is occlusal
adjustment. The main idea of Jankelson’s technique for occlusal equilibration is that occlusion
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can be adjusted by minor reshaping of the biting surfaces of the teeth so that they receive less
force. This procedure is known as occlusal adjustment by selective grinding and requires
knowledge and skill.

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Study 14. Periodontal Surgery
Several techniques can be used for the treatment of periodontal pockets: gingivectomy and
gingivoplasty, flap surgery etc. The periodontal flap is one of the most frequently employed
procedures, particularly for moderate and deep pockets in posterior areas. Flap surgery
procedures are used for pocket therapy to accomplish the following:
1. Increase accessibility to root deposits for scaling and root dedridement
2. Eliminate or reduce pocket depth via resection of the pocket wall
3. Expose the area for the performance of regenerative methods
To fulfill these purposes, several flap techniques are available and in current use. In this issue,
two techniques are described:
1) the modified Widman flap;
2) the apically displaced flap
Understanding of periodontal surgery procedure requires knowledge about basics incisions and
flaps.
Incisions
There are many variants of incisions in surgical periodontology. Generally, they are classify into
horizontal incisions and vertical incisions.
Horizontal incisions (Fig. 1) serve to detached the soft tissues from the root surface. These
incisions are directed along the margin of the gingiva in a mesial or distal direction. Generally
there are two types (Fig. 2):
1. External (coronaly directed)
2. Internal (apically directed):
a. Internal bevel incision
b. Crevicular

Figure 1. Horizontal incision (scheme)

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 Figure 2. Types of horizontal incisions
Internal bevel incision (or marginal incision, reverse bevel incision) starts at a distance from the
gingival margin, a scalpel is guided at an acute angle to a tooth crown. The deepest point of the
incision should be on the alveolar crest. The internal bevel incision is basic to most periodontal
flap procedures. It is the incision from which the flap is reflected to expose the underlying bone
and root. This incision has also been termed the first incision, because it is the initial incision for
the reflection of a periodontal flap; it has also been called the, because its bevel is in reverse
direction from that of the gingivectomy incision.
That portion of the gingiva left around the tooth contains the epithelium of the pocket lining and
the adjacent granulomatous tissue. Soft tissue collar is discarded after the crevicular (second) and
interdental (third) incisions are performed.
Crevicular incision (or sulcular incision) starts at the bottom of the pocket and which is directed
to the alveolar bone margin. The crevicular incision, which is also called the second incision, is
made from the base of the pocket to the crest of the bone. This incision, together with the initial
reverse bevel incision, forms a V-shaped wedge that ends at or near the crest of bone. This
wedge of tissue contains most of the inflamed and granulomatous areas that constitute the lateral
wall of the pocket as well as the junctional epithelium and the connective tissue fibers.
Vertical incisions (or oblique releasing incisions) (Fig. 3) are being referred to as releasing
incisions. can It be used on one or both ends of the horizontal incision, depending on the design
and purpose of the flap. They offer increasing flap mobility and better observation of operation
area. In ideal cases, the flap base should be slightly wider than flap margin to provide adequate
blood supply. Vertical incisions must extend beyond the mucogingival junction to reach the
alveolar mucosa; this allows for the release of the flap to be displaced.

Figure 3. Two vertical incisions (scheme)

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Flaps
A periodontal flap is a section of gingiva, mucosa, or both that is surgically separated from the
underlying tissues to provide for the visibility of and access to the bone and root surface. The
flap also allows the gingiva to be displaced to a different location.
A full-thickness flap (also called mucoperiosteal flap) includes epithelium, connective tissue and
periosteum, is reflected to expose the underlying bone.
A partial-thickness (also called split-thickness flap) flap includes only the epithelium and a layer
of the underlying connective tissue. The bone remains covered by a layer of connective tissue
that includes the periosteum. The partial-thickness flap is indicated when the flap is to be
positioned apically or when the operator does not want to expose bone.
Curettage
Curettage (also called “gingival curettage”) is one of the oldest procedure in periodontics. The
word “curettage” is of French origin meaning to clean or to scrape.
Curettage procedure:
1. Mouth rinse with chlorhexidine for one minute.
2. Local anesthesia in area of curettage.
3. Insertion of curette into the pocket, pressing in toward the root surface and pull
instrument back, scrapping the root surface – removal of calculus and plaque from root
surface and root surface planing (Fig. 4).
4. Insertion of curette again in pocket, pressing a pocket wall toward curette with finger and
pull curette outward – depithelization of periodontal pocket wall and removal of infected
granulomatous tissue from inner part of pocket wall (Fig. 5).
5. Periodontal pack application
6. Systemic antibiotics prescription

Figure 4. (a) – insertion of the curette in periodontal pocket; (b) – slight rotation of instrument
and pressing it toward root surface; (c) – removing of calculus with scratching motion up

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Figure 5. (a) – curette is inserted in periodontal pocket and slightly pressed toward pocket wall;
(b) – removing of epithelium and granulomatous tissue from pocket wall; (c) – pocket wall after
removing inflamed inner part.

Advise the patient that he/she may experience some discomfort and sensitivity following
treatment and to expect some gingival recession as a result of healing. Carry out a full
periodontal examination (measure probing depth and evaluate bleeding on probing) a minimum
of eight weeks after treatment.

Periodontal pack (also called “periodontal dressing”) is a physical barrier that is placed in the
surgical site to protect the healing tissue, for comfort and close adaptation, for keeping primary
blood clot in place, for control postoperative bleeding. Surgical area is covered with periodontal
dressing for 3-14 days following periodontal surgery whenever necessary.
Types of dressings:
• Zinc-oxide eugenol dressing (hard pack)
• Non-eugenol dressing

Gingivectomy and Gingivoplasty

Gingivectomy means “excision of the gingiva.” By decreasing of periodontal pocket depth,
gingivectomy provides favorable conditions for adequate home oral hygiene. The gingivectomy
technique was widely performed in the past. Improved understanding of healing mechanisms and
the development of flap methods have relegated the gingivectomy to a less role in the current
treatment techniques. However, it remains an effective form of treatment when indicated.
Indications:
1. Reduction/elimination of true periodontal suprabony pockets, regardless of their depth
2. Dissection of hypertrophic gingival enlargement (false pockets)
3. Elimination of suprabony periodontal abscesses
Steps:
1. Base of pocket should be identified with special forceps (pocket marker) by bloody
marks. Each pocket is marked in several areas to outline its course on each surface.
2. Beveled gingivectomy incision made at 45 degrees to the tooth surface, apical to the
marks and it is directed coronally to a point between the base of the pocket and the crest
of the bone. It should be as close as possible to the bone without exposing. It should
recreate the normal festooned pattern of the gingiva.
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 3. Application of periodontal pack for 7 days.
Gingivoplasty is similar to gingivectomy, but its objective is different. Gingivectomy is
performed to eliminate periodontal pockets, and it includes reshaping as part of the technique.
Gingivoplasty is a reshaping of the gingiva to create physiologic gingival contours with the sole
purpose of recontouring the gingiva, creating a scalloped marginal outline, in the absence of
pockets. Gingivoplasty may be accomplished with a periodontal knife, a scalpel, rotary coarse
diamond stones, or electrodes.

Modified Widman flap

The modified Widman flap facilitates root debridement because of horizontal incision. The
surgery allows:
• access the root surface for scaling and root debridement
• elimination of the pocket lining
The modified Widman flap is not intended to eliminate or reduce pocket depth, except for the
reduction that occurs during healing as a result of tissue shrinkage. Scheme of Modified Widman
flap procedure is presented on figure 6.

Figure 7. Scheme of Modified Widman flap

Apically Repositioned Flap
The objectives for the apically displaced flap — the reduction or elimination of the pocket depth.
The apically displaced flap provides accessibility and eliminates the pocket, but it does the latter
by apically positioning the soft soft-tissue wall of the pocket. Therefore, it preserves or increases
the width of the attached gingiva by transforming the previously unattached keratinized pocket
wall into attached tissue. This increase in the width of the attached gingiva is based on the apical
shift of the mucogingival junction, which may include the apical displacement of the muscle
attachments.
Indications:
1. Reduction/elimination of true periodontal pockets
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Steps (Fig. 8,9):
1) inverse bevel incision to alveolar crest,
2) flap moved apically
3) flap sutured just above the alveolar crest

Figure 8. Scheme of apically repositioned flap: (a) 1 – tooth, 2 – gingiva, 3 – periodontal

ligament, 4 – alveolar bone, 5 – periosteum, PP – periodontal pocket; (b) 6 – internal wall of
periodontal pocket, internal bevel incision and removing of inner wall of periodontal pocket; (c)
replacement of flap apically; (d) suturing

Figure 9. Scheme of apical repositioned flap technique (frontal view)

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Study 15. Colloquium 3
Questions for preparation to colloquium:
1. Give definition of marginal periodontitis.
2. What courses of marginal periodontitis do you know?
3. What degrees of marginal periodontitis do you know?
4. What extent of marginal periodontitis do you know?
5. What phases of marginal periodontitis do you know?
6. What types of periodontal pockets do you know?
7. What is gingival pocket?
8. What is periodontal pocket?
9. What is infrabony pocket?
10. Describe histopathology of periodontal pocket formation.
11. What do periodontal pocket contain?
12. What is a history (anamnesis) of patient with marginal periodontitis?
13. What are complaints of periodontal patient?
14. Describe intraoral examination of patient with periodontal disease
15. What is clinical features of chronic marginal periodontitis (slight degree)?
16. What is clinical features of chronic marginal periodontitis (moderate degree)?
17. What is clinical features of chronic marginal periodontitis (severe degree)?
18. What is prevention of chronic marginal periodontitis?
19. Gives definition of aggressive periodontitis
20. What are the differences of aggressive periodontitis and chronic periodontist?
21. Microbiology of aggressive periodontitis
22. Host response in patient with aggressive periodontitis.
23. What is a role of genetic in development of aggressive periodontitis.
24. Classification of aggressive periodontitis according to the extent
25. What are primary clinical features of localized aggressive periodontitis?
26. What are secondary clinical features of localized aggressive periodontitis?
27. What are features of generalized aggressive periodontitis?
28. What are key diagnostic criteria of aggressive periodontitis?
29. Which systemic antibiotics may be prescribed in case of aggressive periodontitis?
30. Which procedures are included in Phase I therapy?
31. Which procedures are included in Phase II therapy?
32. Technique of apically advanced flap.
33. Technique of curettage.
34. Technique of Widman flap.
35. What is frenectomy?
36. List non-surgical periodontal treatment techniques.
37. List surgical periodontal treatment techniques.
38. What is splinting and which type of splinting do you know?
39. Describe technique of splinting.
40. What are tasks of flap surgery?
41. What types of incisions do you know?
42. What types of flaps do you know?
43. What is periodontal pack and what are its functions?

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Study 16. Gingival Recessions

Definition
Gingival recession is defined as the displacement of marginal gingiva apical to the
cementoenamel junction (CEJ); thereby exposing the root surface to the oral environment which
causes poor esthetic appearance and in some cases root [Link] distance between
the CEJ and gingival margin gives the level of recession. It can occur in patients with good
standards of oral hygiene as well as those with poor oral hygiene and periodontal disease.
Recession may also be associated with cervical lesions such as abrasive class V cavities or root
caries. Gingival recession along with the inadequate width of attached gingiva and inadequate
vestibular depth are very common clinical finding in the front region of the lower jaw.
Prevalence of Recessions
The prevalence of gingival recession has been shown to increase with age. According to the US
National Survey, 88% of seniors (age 65 and over) and 50% of adults (18 to 64) present
recession in one or more sites; progressive increase in frequency and extent of recession is
observed with increase in age. In the younger age cohort (30 to 39 years), the prevalence of
recession was 37.8%.
Etiology of Recession

For decades, it was believed that gingival recession was a part of human aging processes;
however, there is not strong evidence supporting such a statement. Aging might increase the
possibility for the causes of gingival recession to act, but that does not mean they are inherent to
aging.

One of the main reason of gingival recession is resorption of underlying alveolar bone. Over
time in lack of support, normal or inflamed gingival soft tissues tend to keep up with cervical
bone levels; therefore, gingival recession is established.

The etiology of recessions is multifactorial. Factors are below; one or more factor may be
presented:
• Aggressive tooth brushing
• Periodontal disease and periodontal treatment
• Occlusal trauma
• Iatrogenic damage
• Aberrant frenal attachments

Aggressive tooth brushing. It is known that inappropriate daily brushing may physically wounds
gingival tissues. Traumatically using the toothbrush as well as other oral hygiene agents over
delicate gingival margins on a daily basis might gradually and slowly lead to gingival recession
over the years. In general, those cases are presented in combination with cervical wear as a result
of abrasion caused by the same agents.

Periodontal disease and periodontal treatment. Tissue destruction resulting from periodontal
disease encompasses gradual bone loss which might lead to apical gingival migration and root
exposure. At first, tissue loss is apparently compensated by gingival swelling. After periodontal
treatment swelling decreases and retraction of gingival tissue volume occurs. Thus, root will
become exposed to the oral environment, which esthetically, might be considered strange by the
patient, even though periodontal tissues are perfectly healthy at this point. Ideally patient should
be informed about this fact before periodontal treatment.
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Occlusal trauma. Due to the increase in functional demand, alveolar bone resorption may occur.
In those cases, vertical bone loss is radiographically noticeable. On buccal surface, depending on
cortical plate thickness, vertical bone loss results in bone dehiscence over the affected root - a V-
shaped cavity in the bone contour, thereby gingival bone support decreases. Gingival contour
will keep up with buccal bone contour, which results in V-shaped or angled gingival recession in
teeth affected by occlusal trauma and bone dehiscence. It should be once again highlighted that
this process is not associated with local dental plaque buildup and consequent chronic
inflammatory periodontal disease.

Iatrogenic damage caused by:

1. Restorative treatment may be a reason of recession. Restorative treatment, which involves

placement of subgingival margins of restorations, can directly impinge on the biologic width.
To re-establish the biologic width there may be some bone loss and apical migration of the
gingival tissues. Subgingival restoration margins increase the plaque accumulation, gingival
inflammation, and alveolar bone loss. Crowns, veneers and Class V restorations should have
enough prominence of vestibular contour to prevent trauma of gingiva by food, such trauma
also may cause recession.
2. Orthodontic treatment. Orthodontic tooth movement should not be considered as the primary
cause of gingival recession. Induced tooth movement does not cause any damage to gingival
tissues; however, during orthodontic treatment, the following might occur in a few patients.
In those cases, before gingival recession occurs, orthodontic movement had induced
dehiscence at the bone crest, as a result of moving a tooth towards an area with extremely
thin bone. Induced tooth movement should be carried out only at the alveolar bone trabeculae
space; however, during certain types of movement, teeth are also displaced at the expenses of
the outer cortical plate. In such cases dehiscence and fenestration may occur. The latter are
defects found in the outer cortical plate and act as "predisposing factors" of gingival
retraction. A potential means to avoid dehiscence and recession during orthodontic treatment
is to apply light, well-balanced forces to sets of teeth rather than to a single tooth. Movement
should be carefully planned
3. Aberrant frenal attachments have been mentioned as a cause of recession due to an apical
pull on the gingival tissues. Also high frenal attachments (close to the gingival margin) may
make oral hygiene difficult therefore leading to a localized periodontal problem and
subsequent recession.

Classification of Recessions

Various classifications have been proposed to classify gingival recession.

1. According to distribution:

• Localized
• Generalized or horizontal form is associated with chronic inflammatory destructive
periodontal disease. Loss of periodontal support in proximal areas results in apical
displacement of gingiva, including interdental papillae.

2. According to shape:

• V–shaped recession is associated with teeth subjected to occlusal trauma, especially in

patients with bruxism and clenching habits. In cases of severe apical migration, V-shaped
recession is known as Stillman's cleft. At the corresponding enamel, it is common to find

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 abfraction; while on the occlusal surface, wear facets caused by attrition are commonly
found, as being part of a lesion caused by occlusal trauma.
• U–shaped recession is generally associated with chronic inflammatory periodontal
disease, inadequate tooth brushing or inadequate frenulum insertion. U-shaped gingival
recession associated with inadequate traumatic brushing is surrounded by healthy gingiva
and is usually associated with abrasion, with a smooth, polished surface. There are cases
of U-shaped recession in which the area of root exposure is surrounded by a peripheral
festoon made up of swollen, inflamed gingival tissue resulting from local dental plaque
buildup. A few classical studies found in Periodontology literature refer to the
aforementioned condition as McCall's festoon.

3. According to loss of attached tissue:

• with loss of dentogingival junction and attached tissue (e.g. in case of periodontal
diseases)
• without loss of dentogingival junction and attached tissue (e.g. in case of occlusal
trauma)
4. One of the most widely followed classification is Miller's classification (proposed in 1985) of
gingival recession. Miller has primarily based his classification on following aspects:
• Extent of gingival recession defects
• Extent of hard and soft tissue loss in interdental areas surrounding the gingival recession
defects.
Miller’s classification is useful in predicting the final amount of root coverage following a
free gingival graft procedure.
Miller’s Classification of Recessions
Class I (Fig. 1): Recession does not extend to the mucogingival junction (MGJ). There is no
periodontal loss (bone or soft tissue) in the interdental area, and 100% root coverage can be
anticipated.

Figure 1. Recession Class I by Miller, MGJ – mucogingival junction

Class II (Fig. 2): Recession extends to or beyond the MGJ. There is no periodontal loss (bone or
soft tissue) in the interdental area, and 100% root coverage can be anticipated.

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 B
Figure 2. (A) Scheme of recessions Class II by Miller; (B) Clinical view of wide multiple
recessions Class II by Miller. MGJ – mucogingival junction
Class III (Fig. 3): Recession extends to or beyond the MGJ. Bone or soft tissue loss in the
interdental area is present or there is a malpositioning of the teeth, which prevents the attempting
of 100% of root coverage. Partial root coverage can be anticipated.

A B
Figure 3. Scheme of recessions Class III by Miller: recession extends beyond the mucogingival
junction (MGJ), bone or soft tissue loss in the interdental area is present (A) or there is a
malpositioning of the teeth (B)
Class IV (Fig. 4): Recession extends to or beyond the MGJ. The bone or soft tissue loss in the
interdental area and/or malpositioning of teeth is so severe that root coverage cannot be
anticipated.

B С
Figure 4. Gingival recessions class IV by Miller (A) scheme, MGJ – mucogingival junction; (B)
intraoral view of vestibular surfaces; (C) view of lingual surfaces of lower frontal teeth
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Complaints
Patients tend to present with three main concerns, which are poor aesthetics, worry about
potential tooth loss and dentine hypersensitivity due to the exposed root surface following
gingival recession.
Clinical Features
The following clinical parameters should be taking to examine a recession at the mid-buccal
aspect of tooth with recession:

• Probing pocket depth (PD) was measured with a standard periodontal probe to the nearest
millimeter from the gingival margin to the bottom of sulcus
• Clinical attachment level (CAL) was measured from the cemento-enamel junction (CEJ)
to the bottom of the sulcus
• Recession depth (RD) measured from CEJ to the gingival margin
• Recession width (RW) measured across the buccal surface at the CEJ level
• The width of keratinized gingiva (WKG).

Gingival recession may be accompanied with cervical caries (Fig. 5), erosions, wedge-shaped
defects.

Figure 5. Recessions and cervical caries in teeth 13,14, before filling (left) and after filling
(right)

Treatment of Gingival Recessions

First aim for treatment of recessions is to reveal and to remove etiological factors to control
progression. Recessions do not require treatment if:
• they are not large and do not progress
• esthetic concerns not a problem for patient
• hypersensetivity of exposed roots is controlled with desensitizers or absent
There are surgical and non-surgical methods for recession treatment.
1. Non-surgical methods:
• Crowns, veneers, restoration. Crowns may be placed to widen the clinical crown which
may camouflage the exposed root surface
• Construction of gingival mask. Patients who have several teeth with recession may have
unaesthetic appearance because of black triangles. In these cases, where surgical procedure
is not appropriate, silicone flexible gingival veneer or mask may be used.
• Application of desensitizers on exposed roots.

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2. Surgical methods. Surgical methods of recession treatment are among of mucogingival
surgery procedures. Aim of surgical methods is to close exposed root surface with either graft or
flap to repair esthetic and decrease root hypersensitivity.

Mucogingival Surgery
Terminology and Definition
The term mucogingival surgery was initially introduced in the literature by Friedman (1957). It is
applied to surgical procedures utilized to resolve problems involving the interrelationship
between gingiva and alveolar mucosa with reference to next problems:
• increasing of width and thickness of attached gingiva
• gingival recessions
• shallow vestibule
• aberrant frenal attachment.
This term is distinguished from periodontal surgery wherein alveolar mucosa is not handle.
With the advancement of periodontal surgical techniques, the scope of non-pocket surgical
procedures has increased, now encompassing a multitude of areas that were not addressed in the
past. Recognizing this, the 1996 World Workshop in Clinical Periodontics renamed
mucogingival surgery as periodontal plastic surgery, a term originally proposed by Miller in
1993. Periodontal plastic surgery is defined as the surgical procedures performed to correct or
eliminate anatomic, developmental, or traumatic deformities of the gingiva or alveolar mucosa.
Several surgical techniques have been developed for the management of shallow vestibule,
gingival recession, the inadequate width of attached gingiva and aberrant frenal attachment
which set out mucogingival problems.

Mucogingival Surgery Procedures

There are many modifications of mucogingival surgical procedures; the basic procedures are:
• Free gingival graft
• Connective tissue graft
• Coronally advanced flap
• Pedicle flap
• Deepen of vestibule
• Frenectomy
• Guided tissue regeneration for root coverage

Preparation of the exposed root surface. Before any surgical technique root surfaces are
mechanically prepared prior to any mucogingival procedure to allow biological attachment of the
grafted tissue to it. The root surface is thoroughly debrided and irrigated with sterile saline. At
the day of surgery the site should presented a healthy periodontium with the gingiva exhibiting
no evidence of bleeding on probing.

If the plan is to obtain root coverage over existing caries or class V restoration, the caries and
restoration must be completely removed (gingiva will not attach to artificial restorative material).
Significant convexity of the root may be reduced with diamond burs on high speed. Historically,
chemical root surface modifiers such as citric acid, tetracycline, or EDTA had been used to
demineralize and decontaminate the root surface to expose the collagen fibers. The theory is this
will facilitate attachment of gingival fibers to the root surface. However, recent evidence
demonstrates that the use of these chemical modifiers provides no benefit of clinical
significance.
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Postoperative care are the same for all types of mucogingival surgical procedures. Immediately
following surgery, use of icepacks was recommended intermittently for three hours. The patient is
advised not to brush the treated site for 2 weeks. After 1 week toothbrushing of treated site should
be carried out gently with ultrasoft toothbrush. 0.12% chlorhexidine mouth rinse is prescribed
twice a day for 2 weeks. Systemic antibiotics were prescribed (Amoxicillin-500 mg, three times
daily for five days) along with analgesics. Sutures should be removed 7-10 days after surgery.
Patient should be examined weekly for the 1st month.
Free Gingival Graft
Free gingival graft is soft tissue graft comprising epithelium and thin layer of underlying
connective tissue that are completely detached from one site (donor site) and transferred to a
remote site (recipient site). Most common donor site for free gingival graft is hard palate. The
palatal masticatory mucosa is widely used as a connective tissue donor site in gingival recession
treatment. However, concern has been raised regarding the potential risk of damaging the greater
palatine artery during harvesting of graft due to anatomical variations in the palatal vault.
This technique allows:
1. To increase the zone of attached gingiva
2. To augment the thickness of attached gingiva
3. To repair gingival recession
Free gingival graft technique:
1. Preparation of the recipient bed. The recipient site should be prepared as split-thickness flap
(periosteum should not be detached from bone) and extend at least 3 mm laterally and apically to
the recession defect, as this will be the only nutrient supply to the graft during the initial healing
phase. Any muscle or frenal insertions should be removed by sharp dissection to ensure that the
graft lies passively with no movement occurring during function.
2. Harvesting of the graft. Graft should be harvested from donor site and the size should be
adapted. Proper thickness 1.0–1.5 mm is an important factor for survival of the graft because
nutrition of graft first time after surgery will be due to diffusion of nutrients from the recipient
site. If graft is too thick, central part will not have enough nutrition and will become necrotic.
Good adaptation of the graft to the recipient site is essential for adequate diffusion, so care must
be taken on preparing the recipient site the graft to the exact same size to ensure a good fit.
3. Transfer and suturing of the graft. Graft is applied on recipient site, sutured into position and
pressed by finger for several minutes for better adaptation.

Connective Tissue Graft

The connective tissue autograft technique was originally described by Edel and is based on the
fact that the connective tissue carries the genetic message for the overlying epithelium to become
[Link] only connective tissue from beneath a keratinized zone can be used as a
graft. The Connective Tissue Graft (CTG) technique is considered as the gold standard in the
management of recession defects. It is also used in combination with coronally advanced flap.
Terminology: connective tissue graft = free connective tissue graft = subepithelial connective
tissue graft.
The free connective tissue graft (CTG) is differ with the free gingival graft is that the donor tissue
is connective tissue only with no epithelium on it. Donor site may be hard palate, tuber of maxilla,
retromolar region.
Advantages:
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 • double blood supply of graft at the recipient site from the underlying connective tissue
base and the overlying recipient flap.
• donor site is a closed wound, which produces less postoperative discomfort
• excellent color blend can be achieved
• Minimal palatal denudation, less invasive, less prone to hemorrhage, more rapid healing.
• The connective tissue graft results in two sutured closed wound sites, while the free
gingival graft results in two open exposed wounds.

Free connective tissue graft technique:

1. Preparation of the recipient bed. The recipient bed is prepared to accommodate the connective
tissue graft. Divergent vertical incisions are made at the line angles of the tooth to be covered. A
split thickness flap is performed where the periosteum remains attached to the underlyingbone.
The split thickness flap is prepared by sharp dissection and the presence of any muscle fibers or
attachment is eliminated. The flap should be mobile so that it can be repositioned to at least 5 mm
apical to the receded area. Suture the apical mucosal border to the periosteum using a gut suture.

2. Harvesting of the graft. The connective tissue graft is harvested from the hard palate. The ideal
location is 5–6 mm apical to the gingival margin of the palatal aspects of the maxillary premolars
and the mesial half of the maxillary first molar. The ideal thickness of the graft should be 1–1.5
mm thick. The donor site is sutured after the graft is removed. During harvesting the connective
tissue, the vital structure that needs to be avoided is the greater palatine artery. Depending on the
depth of the palatal vault, typically, the artery is about 12 mm apical to the gingival margin.

3. Transfer and suturing of the graft. The harvested connective tissue graft is immediately placed
in the recipient site and secure into position with sutures to the periosteum. Good stability of the
graft must be attained with adequate sutures. Optimized healing requires the graft to be in intimate
contact with the recipient bed with the absence of any dead space.

6. Covering of the graft. Cover the grafted site with dry aluminum foil and periodontal dressing.

Coronal Advanced Flap

The coronally advanced flap is commonly used to treat the Miller Classes I and II recession defects.
Various modifications of the coronally advanced flap (CAF) have been proposed with the attempt
of treating gingival recession.

Coronal advanced flap technique:

1. Horizontal and vertical incisions. Make a horizontal internal bevel incision from the gingival
margin to the bottom of the pocket to eliminate the diseased pocket wall. It is made at the recession
and extended with two vertical releasing incision in correspondence to the line angles. Vertical
incisions should go beyond the mucogingival junction.

2. Management of papilla. The interdental papilla is preserved as much as possible. Their facial
portion is deepithelialized to create a connective tissue bed.

3. Flap elevation. Full thickness flap is elevated. Horizontal incision in periosteum is placed at the
base of the flap to ensure tension free coronal displacement of the flap.

4. Flap repositioning. The flap is then coronally positioned to completely cover the defect and
secured using continuous sling suture.
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5. Suturing of vertical incisions. Vertical releasing incisions are secured using interrupted suture
technique.

Pedicle Flap

There are many variations of pedicle flap, one of them laterally displaced pedicle flap. The
laterally positioned flap can be used to cover isolated, denuded root surfaces that have adequate
donor tissue laterally, adjacent to the gingival recession.

Laterally displaced pedicle flap technique

1. Preparation of the recipient site. Epithelium is removed around the denuded root surface. The
exposed connective tissue will be the recipient site for the laterally displaced flap. The root surface
will be thoroughly scaled and root planed.

2. Preparation of the flap. The periodontium of the donor site should have a satisfactory width of
attached gingiva and minimal loss of bone, without dehiscence or fenestration. A partial-thickness
flap is used. Prepare vertical incision from the gingival margin to outline a flap adjacent to the
recipient site. Extend the incision into the oral mucosa to the level of the base of the recipient site.
The flap should be sufficiently wider than the recipient site to cover the root and provide a broad
margin for attachment to the connective tissue border around the root. Separate a flap consisting
of epithelium and a thin layer of connective tissue, leaving the periosteum on the bone. A releasing
incision is sometimes needed to avoid tension on the base of the flap,

3. Transfer the flap. Slide the flap laterally onto the adjacent root, making sure that it lies flat and
firm without excess tension on the base.

4. Suturing of a flap. Fix the flap to the adjacent gingiva and alveolar mucosa with interrupted
sutures.

Deepen the Vestibule

Among mucogingival problems, shallow vestibule and gingival recessions which cause an
esthetic as well as a functional problem are very common finding in lower front teeth. The
presence of adequate vestibular depth is important for both oral hygiene and retention of
prosthetic appliances. Numerous surgical techniques have been proposed to accomplish the
objective of deepening the vestibule. The aim of this vestibular extension procedure is to
increase the depth of vestibule and the width of attached gingival in a single visit.

Predictable deepening of the vestibule can only be accomplished by the use of free autogenous
graft techniques and their variants. The important clinical aspect in deepening the vestibule is the
proper preparation of the recipient site. The recipient site must be covered by immobile periosteal
tissue. The donor tissue may be either free gingival or connective tissue, but it must be placed over
a nonmobile recipient site. Clinical view of procedure is presented on figure 6.

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 А B

C D

Figure 6. Deepen the vestibule. (A) shallow vestibule of oral cavity and recessions; (B) incision
(C) cutting of muscle and connective tissue strands; (D) clinical view after healing

Frenectomy

When the recession is caused by frenal pull in those cases, frenectomy is advised. If appropriate
hygiene aids do not enable the patient to maintain the area plaque free, then frenectomy is advised
to give ease to entrance to the site. Indication to frenectomy: when place a probe to the lowest part
of free gingival grooves of central incisors, frenum attachment should be lower than this line
showing with the probe. If frenum attachment is above probe line – frenectomy is indicated (Fig.
7). This rule is actual for both upper and lower jaw, but in upper jaw normal frenum attachment
should be above probe line.

Figure 7. Frenum attachment is a little bit higher than probe line.

Guided Tissue Regeneration Technique for Root Coverage

Guided tissue regeneration (GTR) should result in reconstruction of the attachment apparatus,
along with coverage of the denuded root surface.
Guided tissue regeneration technique for root coverage:

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1. A full-thickness flap is reflected to the mucogingival junction, continuing as a partial-
thickness flap 8 mm apical to the mucogingival junction.
2. A resorable membrane is placed over the denuded root surface and the adjacent tissue. It is
trimmed and adapted to the root surface and covers at least 2 mm of marginal periosteum.
3. A suture is passed through the portion of the membrane that will cover the bone.
4. The flap is then positioned coronally and sutured.

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Study 17. Periodontosis. Clinical features, diagnosis, treatment

Periodontosis is an obsolete term that was used to describe what was once thought to be certain
type of unique and distinguishable chronic periodontal disease that manifested as degenerative
bony changes without concomitant inflammation. Although utilized for more than 50 years, the
term has since been dropped in favor of a more contemporary disease classification for
periodontal disease.

Periodontosis is defined as degenerative, non-inflammatory destruction of the periodontium.

Prevalence of periodontosis is about 1–8% in clinical practice. Inflammation, periodontal

pockets and teeth mobility is not typical for this disease. Disease is characterized by bone
destruction, pale-pink or pale-bluish color of gingiva, gingival recessions and wedge-shaped
defects, hypersensitivity of dentin, itching in gingiva.

Bone on radiograph is sclerotic (decreasing of bone marrow spaces), horizontal bone atrophy
with no resorption of crestal cortical bone.

In slight degree bone resorption and gingival recessions is up to 1/3 of root length.

In moderate degree bone resorption and gingival recession is up to ½ of root length. In some
cases there is Grade I teeth mobility may be presented.

In severe degree bone resorption and gingival recessions is up more then ½ of root length.

Treatment of periodontosis includes:

1. Improving of individual oral hygiene.
2. Professional oral hygiene.
3. Application of desensitizers.
4. Filling of wedge-shaped defects.
5. Finger- or hydro-massage of gingiva.
6. Physiotherapy

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Study18. Periodontomas. Clinical features, diagnosis, treatment
Types of periodontomas:
1. Epulis
2. Hereditary fibromatosis

Epulis
Epulis is a general term used to describe a number of tumor-like reactive gingival lesions with
vascular, fibroblastic, and granulomatous tissue proliferation, usually asymptomatic with a
variable growth rate.
Etiology. Epulis is considered to be a reactive massive lesion rather than true neoplasia. Epulis
develops in response to chronic and recurring tissue injury caused by calculus, incorrect
dentures, rough overhanging margin of restorations, sharp parts of orthodontic appliances. These
stimulates an exuberant or excessive tissue growth.
General features of epulis histology. Intact lesions consists of bundles of connective tissue
covered with keratinized squamous cell epithelium. Type of connective tissue depends on epulis
type. When traumatized, the lesion contain inflammatory infiltrate and ulcerated area covered
with fibrin and organisms from the oral flora
Classification of Epulis. Although epulis is classically categorized into different subtypes,
current literature summarized three main types:
• fibrous (or fibromatous) epulis
• granulomatous (angiomatous) epulis
• giant cell epulis
Fibrous Epulis
Clinical features. Fibrous epulis is the growth of well-delimited tissue, usually with normal
colored mucosa, sessile or pedunculated base. Usually it appears in anterior maxilla in the
interdental papilla. Lesions are asymptomatic and have a variable growth rate, in most cases
growth is slow. Fibrous epulis is not painful and dense on palpation. No (or small) bleeding in
case of trauma. Histologically lesion is composed from dense connective tissue. The same
prevalence in male and female patients.
Granulomatous Epulis
Another term for granulomatous epulis is angiomatous epulis.
Clinical features. To compare with fibrous form granulomatous epulis bleeds in case of even
very small trauma. It is not painful and soft on palpation. Granulomatous epulis is covered by
reddish mucosa and has more reddish color to compare with surrounding mucosa. Histologically
lesion is composed from granulation tissue with many blood vessels. Lesions are asymptomatic
and have a variable growth rate. More widespread in children in period of teeth changing.
Giant Cell Epulis
Giant cell epulis (Fig. 1) is also called giant cell granuloma.
Clinical Features. It is painful and has soft elastic consistency with tuberous surface on
palpation. Lesion is covered with bluish-red mucosa. It is more widespread among women
before 30 years old.

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 Figure 1. Giant cell epulis of young female patient
Epulis Treatment
Treatment usually includes complete excision of the lesion and thorough curettage of the area
due to its origin from the periosteum and periodontal ligament cells to prevent recurrence. The
extraction of the neighboring teeth is usually not considered necessary unless there is extensive
underlying bony involvement. Histological evaluation of epulis after dissection is important for
differentiation with any type of tumor.
Hereditary gingival fibromatosis
Hereditary gingival fibromatosis (also known as idiopathic gingival hyperplasia), is a rare
condition of gingival overgrowth. It is characterized as a slowly progressive, non-hemorrhagic,
fibrous enlargement of keratinized gingiva in maxilla and mandibula.
Clinical features. It can cover teeth in various degrees, and can lead to aesthetic and functional
problems. Hereditary gingival fibromatosis transmits as an autosomal dominant trait. It develops
as an isolated disorder but can also be one of the features of various syndromes. The hyperplastic
gingiva may be localized or generalized, usually having normal color and firm consistency with
abundant stippling.
The enlargement usually begins at the time of the eruption of the permanent dentition, although
it may also occur during the eruption of deciduous teeth or even at birth. When the gingiva is the
only tissue involved, gingival fibromatosis might be in association with epilepsy.
Histological features of hereditary gingival fibromatosis: Gingival tissue from hereditary
gingival fibromatosis is characterized by a mucosa in which the epithelium shows rete ridges
extending into the underlying connective tissue, which shows an increased density of collagen
fibrils and a decrease in fibroblasts.
Treatment of hereditary gingival fibromatosis is gingivectomy with recreating scalloped contour
of gingiva. Patient should be informed about likelihood of recurrence. Recurrence may occur
within several months after surgery but will reach initial volume of tissue within several years.
Repeated surgical procedures might be necessary during life. Factors provoke recurrence are bad
oral hygiene and orthodontic treatment.

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Study 19. Medical History Presentation 2
On medical history presentation class student should have paper version of Medical History
about given to him/her pathology. Title of Medical History should be written as follow:

University of People Friendship

Operative Dentistry Department

Medical History
“Chronic Marginal Periodontitis
(Moderate Degree) ”

4th year student

[NAME, SURNAME]
Supervisor:
[NAME, SURNAME]

[Year]

EXAMPLE of MEDICAL HISTORY “Chronic Marginal Periodontitis (Moderate Degree)”

VII. Passport part:

Name: Ivanov I.
Sex: male
Date of birth: 10.09.1986
Age: 30
Address: Moscow, Basmannay street, 12-24.
Occupation: engineer

VIII. General medical anamnesis:

Patient denies HIV, hepatitis, syphilis.
Patient reported no cardiovascular diseases or other general pathologies, no
pacemaker, no allergies, no hereditary diseases.

IX. Dental anamnesis:

Patient has bleeding on toothbrushing from time to time for about 5 years. Patient has
never visited dentist for professional oral hygiene.
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X. Extraoral examination:
Face is symmetrical, skin is normal color and turgor, no erosions, ulcers or other
pathological elements are observed. Lips are normal color with no erosions, fissures
or crusts. Submandibular lymph nodes are not palpable.

XI. Intraoral examination:

Teeth:
C F/C

8 7 6 5 4 3 2 1 1 2 3 4 5 6 7 8
F F/C F C

Teeth #31,32,41,42 have mobility degree II.

Bite: orthognatic

Oral mucosa and gingiva status: Oral mucosa of vestibulum and oral cavity is light
pink color, appears normal moist and smooth with no erosions, ulcers, vesicles or
other pathological elements. Frenulum of upper lip fixed in the middle of alveolar
ridge. If pull out a lip and slightly press at the base of frenulum no ischemia of
gingiva in the area of frenulum fixation is observed; same for frenulum of lower lip.
Gingiva of upper and lower jaw is reddish and edematous.

Oral hygiene status: Abundant dental plaque on all teeth, dental calculus in the area
of lower frontal teeth is visible. Silness&Loe index is 2.0 score
OHI–S index is 3.4 scores
Oral hygiene status at the first visit is inadequate. Instructions how to brush teeth and
selection of appropriate product for cleaning of interdental spaces are required.

Treatment plan:
1. Home oral care instructions + selection of appropriate product
2. Scaling and root debridement
3. Local anti-inflammatory therapy
4. Treatment of teeth:
a. Primary caries: 16, 37.
b. Secondary caries and restoration replacement: 24, 44.
5. Temporary splinting
6. Re-evaluating of periodontal and hygiene status.
7. Periodontal surgery procedure (Widman Flap) in the area with
periodontal pocket ≥ 5 mm
8. Dental check-up with reevaluation of periodontal status annually

XII. Dairy:
Date: 26.07.2017
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 Intraoral examination: Gingiva is reddish and edematous. There is a lot of dental
plaque on all teeth; supragingival and subgingival calculus on lingual and vestibular
surfaces of teeth 31,32,33,41,42,43. Silness&Loe index is 2.0 score, OHI–S index is
3.4 scores. There is severe bleeding on probing. There are periodontal pocket up to 5
mm in area of teeth 31,32,33,41,42,43.

Panoramic radiograph: there is alveolar bone resorption in area of teeth 31,32,41,42 is

½ of length of root.
Diagnosis: chronic marginal periodontitis, moderate degree (K05.3)
Treatment: Rinsing with chlorhexidine 0.06 % for 1 minute. Professional oral
hygiene: removing of supragingival calculus by ultrasound scaler, cleaning of dental
plaque by prophylactic brushes and paste. Local anti-inflammatory therapy:
application of chlorhexidine gel 2% on gingival margin for 20 minutes, chlorhexidine
0.06 % rinsing.
Topical anesthesia gel Benzocain 20%, local anesthesia administration Sol. Articaini
4% - 1.7 ml, root debridement using modified Widman flap procedure, suturing.
Recommendations:
1. Avoid toothbrushing at the day of surgery.
2. Using soft toothbrush for a week after surgery
3. Rinsing with chlorhexidine 0.06 % twice a day after toothbrushing for 7 days.
4. Check-up:
• next day after surgery
• after 7 days of anti-inflammatory therapy
[Link]: improve home oral hygiene, use dental floss to clean interdental spaces,
visit dentist twice a year for check-up and professional oral hygiene.

Signature: Dr. Ivanov I.I.

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Study 20. Colloquium 4
1. Give a definition of recession and level of recession.
2. What is etiology of gingival recession? Describe an influence of aggressive toothbrushing
in details.
3. What is the influence of an occlusal trauma to gingival recessions?
4. What is the influence of an aberrant frenal attachment to gingival recessions?
5. What is the influence of a periodontal diseases attachment to gingival recessions?
6. What is the influence of a periodontal treatment attachment to gingival recessions?
7. What is the influence of iatrogenic attachment to gingival recessions?
8. Miller’s classification of recessions
9. What is the classification of recessions according to distribution?
10. What is the classification of recessions according to shape?
11. What is the classification of recessions according to loss of attached tissue?
12. Clinical features of recessions
13. Give a definition of mucogingival surgery
14. Free gingival graft technique
15. What are advantages of connective tissue graft?
16. Coronal advanced flap technique.
17. Laterally displaced pedicle flap
18. What is a definition of periodontosis?
19. What are clinical features of peridontosis?
20. What are principles of treatment of periodontosis?
21. What is a definition of epulis?
22. What is etiology of epulis?
23. What types of epulis do you know?
24. Histology of epulis.
25. What are clinical features of fibrous epulis?
26. What are clinical features of granulomatous epulis?
27. What are clinical features of giant cell epulis?
28. What is treatment of epulis?
29. Give a characteristic of hereditary gingival fibromatosis.
30. What are histological features of hereditary gingival fibromatosis?
31. What is treatment of hereditary gingival fibromatosis?

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Examples of Tests and Clinical Tasks

Tests

Choose ONE correct answer

1. What is the localization of stippling?

a) Attached gingiva
b) Alveolar mucosa
c) Buccal mucosa
d) All variants are correct
2. What type of frenal attachment are considered to be pathological?

a) papillary frenal attachment

b) papillary penetrating frenal attachment
c) mucosal frenal attachment
d) gingival frenal attachment
e) A and B
f) A and D
3. Flattened interdental papillae and square shape of teeth are characteristics of:

a) Thin biotype
b) Thick biotype
c) All variants are correct
d) None is correct
4. What dental deposit causes only esthetic problem and does not cause inflammation?

a) Material alba
b) Dental biofilm
c) Calculus
d) Pigmented deposits
5. What complex is associated with severe forms of periodontal disease and bleeding on
probing?

a) Red
b) Green
c) Yellow
d) Orange
6. What are characteristics of Аctinobacillis actinomycetemcomitans?
a) small, non-motile Gram-negative rod
b) produces leukotoxin
c) produces endotoxin
d) all above are correct
7. Which calculus has dark color?
a) Supragingival
b) Subgingival
c) All above correct
146
 d) No correct variant
8. Which occlusal trauma results from excessive occlusal force with normal periodontal support?
a) Primary occlusal trauma
b) Secondary occlusal trauma
c) All above are correct
d) No correct variants
9. What is a negative effect of smoking on periodontal tissues?
a) Decreases blood circulation
b) Decreased bactericidal property of saliva
c) All above are correct
d) None is correct
10. Periodontal manifestations of leukemia may include:
a) leukemic infiltration
b) bleeding
c) oral ulcerations
d) all above are correct

Clinical task 1
Patient N, 25 years old complaints on severe pain in gingiva during chewing and tooth brushing,
halitosis. He reported fever 38º C and headache for two days. Patient has pale-greyish face skin
color. Lymph nodes are enlarged and painful on palpation. During intraoral examination punch-
out, craterlike lesion at the crest of the interdental papillae are revealed. Surface of the lesions is
is covered by a gray, pseudomembranous slough; when trying to scratch it, thereby exposing the
hemorrhagic gingiva.
Questions:
1. What is diagnosis?
2. What additional method do you need to verify diagnosis?
3. What is a treatment of this periodontal pathology?
4. What systemic diseases may be manifested in oral cavity by this periodontal pathology?

Clinical task 2
Patient N., 30 years old complaints of gingiva overgrowth in frontal area of upper jaw, no pain or
bleeding on toothbrush has been reported. During intraoral examination localized pedunculated
overgrowth of interdental papilla has been revealed. Overgrowth is normal pink color, dense and
painless on palpation. No bleeding on provocation.
Questions:
1. What is diagnosis?
2. What additional method do you need to verify diagnosis?
3. What is an etiology of this periodontal pathology?
4. What is a treatment of this periodontal pathology?

147
Keys and Answers
Keys for test

Test number Correct answer

1 A
2 E
3 B
4 D
5 A
6 D
7 B
8 A
9 C
10 D

Answers for clinical task 1

1. Diagnosis is necrotizing ulcerative gingivitis
2. Additional methods of diagnostic are:
1) radiography for differentiation of necrotizing ulcerative gingivitis with necrotizing
ulcerative periodontitis. In case of NUG there is no alveolar bone resorption on
radiographs.
2) bacterial smear will show fusobacteria and spirochetes in deep layer of necrotic mass,
and also cocci. It is useful for differentiation of NUG from specific infections of the oral
cavity.
3) serologic blood analysis for AIDS or syphilis.
4) blood test is especially important to reveal hidden blood diseases (leucosis,
agranulocytosis etc.) in young patient.
3. Treatment of NUG should follow an orderly sequence, according to specific steps at three
clinical visits. First visit: After topical anesthesia removing of necrotic tissues should be done by
moistened cotton pellet or application of enzymes. Removing of supragingival calculus and
plaque. Systemic antibiotics prescription: amoxicillin 500 mg orally every 6 hours for 10 days.
Instructions for patient:
1) Avoid tobacco, alcohol, hot, spicy food
2) Rinse with a glassful of an equal mixture of 3% hydrogen peroxide and warm water
every 2 hours and twice daily with 0.12% chlorhexidine solution.
3) Get adequate rest and nutrition.
4) Use ultrasoft toothbrush
5) An analgesic, such as a nonsteroidal antiinflammatory drug (NSAID; e.g., ibuprofen),
is appropriate for pain relief.
Second Visit. Throughout removing of dental plaque and calculus should be done in this visit.
The instructions to the patient are the same as those given previously.
Third Visit. The patient is instructed in home oral care procedures and further counseled on
nutrition, smoking cessation, and other conditions or habits associated with a potential
recurrence. The chlorhexidine rinses maintains for 2 weeks. Scaling should be repeated if
necessary. Comprehensive treatment of the patient’s dental problems should be scheduled in this
visit.
148
4. If 5-7 days after beginning of treatment resolution of symptoms is not as significant as it was
expected, AIDS or blood diseases should be suspected.

Answers for clinical task 2

1. Diagnosis is fibrous epulis
2. Additional method is histological investigation after dissection. Histological findings: bundles
of dense connective tissue covered with keratinized squamous cell epithelium.
3. Etiology of epulis is chronic and recurring tissue injury caused by calculus, incorrect dentures,
rough overhanging margin of restorations, sharp parts of orthodontic appliances.
4. Treatment includes complete excision of the lesion and thorough curettage of the area due to
its origin from the periosteum and periodontal ligament cells to prevent recurrence. Histological
evaluation of epulis after dissection is important for differentiation with any type of tumor.

149
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 Учебное издание

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