PERIODONTICS I Lecture and Laboratory

Dr. Katrina Bianca B. Cruz-Natividad

PERIODONTICS LECTURE

Lecture 1

Anatomy and Structure and Function of Periodontium

The diagnostic skills required to identify periodontal diseases,

particularly in the early stages, are based upon a sound knowledge of
the clinical appearance of healthy tissues.

PERIODONTIUM

Provides the support necessary to maintain teeth in function.

Four principal components:

1. Gingiva (don’t belong to attachment apparatus)
2. Periodontal ligament
3. Cementum
GINGIVA
4. Alveolar bone
• Those part of the masticatory mucosa surrounding the
cervical part of teeth and covering the alveolar process.
• Gingiva is composed of connective tissue and epithelium.
• Main function: protection of underlying tissues
• Morphologic division: marginal, attached, and
interdental papilla.
• The gingiva is uniform pink or pigmented, fits snugly
around the tooth, scalloped, knife-edge, dull, firm, and
resilient in texture and extends from the free-gingival
margin to the mucogingival line.
• Normal clinical feature: the color varies among
different person and appears to be correlated with
cutaneous pigmentation.
• What are the factors the influence gingival color?
 Melanin pigmentation in the epithelium
(the higher, the darker)
 Degree of vascularity (the higher, the
darker)
 Degree of keratinization of the
epithelium (the higher, the lighter)
 Fibrous nature of the connective tissue
GINGIVA (the higher, the lighter)

Anatomic Division of Gingiva

1) Marginal Gingiva
I. Free gingival margin
II. Free gingival groove
a) Gingival sulcus
b) Gingival crevicular fluid (GCF)
2) Attached Gingiva
- Mucogingival Junction
3) Interdental Papilla

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• Circular depth of clinically normal gingival

MARGINAL GINGIVA sulcus = sulcular depth = probing depth
• About 1mm wide
• Unattached or free gingiva
• Terminal edge/border of the gingiva that
surrounds the teeth in collar like fashion.
• (50% cases) demarcated from the adjacent
gingiva by a shallow linear depression called
free gingival groove.
• Forms the soft tissue wall of gingival sulcus –
may be separated from the tooth surface with
the use of periodontal probe. : GINGIVAL CREVICULAR FLUID (GCF)
• The most apical point of the marginal scallop is • Also called gingival sulcular fluid
called gingival zenith. • Transudate that emerges from gingival sulcus
• Contains enzyme and cells, desquamating
epithelium and neutrophils
FREE GINGIVAL MARGIN • (Increase) in crevicular flow is the detectable
• 0.5mm coronal to CEJ – surround in scalloped sign of inflammation has occurred, GCF is
outline (above CEJ) referred to as inflammatory exudates.
• 1.2mm coronal to CEJ – healthy (more than • This exudates contains higher level of serum
2mm – hyperplastic) proteins and leukocytes.
• The most coronal portion of the free gingiva. • (BOP) bleeding on probing – sign of
• Surrounds the teeth in a scalloped outline inflammation
located at/or approximately 0.5mm coronal to
the cementoenamel junction.

ATTACHED GINGIVA
• Continuous with marginal gingiva, firm, resilient,
FREE GINGIVAL GROOVE stippled in texture.
• Demarcation of separation from gingiva to • Tightly bound to the underlying periosteum of
attached gingiva. alveolar bone to the cementum by CT fibers and
• Located 1-1.5mm apical to gingival margin at epithelial attachments.
the base of sulcus (at the level of the CEJ) • Demarcated by mucogingival junction.
• May be found at the level of CEJ due to the • May have an orange peel appearance due to the
prominence of dentogingival and dentoperiosteal prominence of rete pegs (epithelial projection
fibers. that extends to gingival connective tissue)
• 30-40% adults, mandibular and premolar o Lingual aspect of mandible – terminates the
regions junction of the lingual alveolar nerve mucosa
o Labial area – widest in the maxillary incisors,
narrowest in premolar
PARTS OF MARGINAL GINGIVA o Lingual area – widest in the mandibular molars,
narrowest at the mandibular incisors
: GINGIVAL SULCUS o Width of attached gingiva:
• V-shaped shallow crevice or space around the GREATEST IN INCISOR REGION
tooth bounded by the surface of the tooth on  3.5mm to 4.5mm in the maxilla
one side and the epithelium lining of the free  3.3mm to 3.9mm in the mandible
margin of the gingiva on the other side. NARROWER IN POSTERIOR SEGMENTS
• Histologic sections have been reported at 1.8mm  1.9mm in the maxillary 1st premolars
with variations from 0.6mm.  1.8mm in the mandibular 1st premolars
• Probing depth of clinically normal gingival
sulcus in humans is 0.5mm-0.3mm

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MUCOGINGIVAL JUNCTION
• Borderline separating alveolar mucosa from
gingival mucosa
• Absent in the maxillary lingual area since the
same type of mucosa covers the hard palate and
maxillary alveolar process

INTERDENTAL GINGIVA PAPILLAE

• Occupies the gingival embrasure with the
HISTOLOGIC DIVISIONS
interproximal space between the area of tooth
Zone/Areas of Gingival Epithelium
contact.
1) Oral epithelium - oral epithelium covering the ree and
• Can be pyramid or “col” shaped-valley like
attached gingiva
depression that connects facial and lingual
2) Sulcular epithelium - sulcular epithelium that lines the
papillae; below the tooth contact
sulcus
• Lateral border and tips of the interdental papilla
3) Junctional epithelium - junctional epithelium at the
are formed by the marginal gingiva
base o the sulcus
• Intervening portion consists of attached gingiva
• If there is no tooth contact = no col

ORAL EPITHELIUM

• Extending from gingival margin to the mucogingival

junction
NORMAL CLINICAL FEATURES OF GINGIVA
• Keratinized stratified squamous epithelium
 TEXTURE • Has rete pegs
• Gingival margin – dull, smooth surface
• Attached – stippled, orange peel surface present on SULCULAR EPITHELIUM
facial surfaces, may not always be present
• Non-keratinized squamous epithelium
 CONSISTENCY
• No rete pegs
• Gingival margin – firm and resilient; resists
displacement
JUNCTIONAL EPITHELIUM
• Attached – firmly bound to underlying alveolar bone
• Joins the inner surface of the gingiva to the tooth
and cementum
• Non-keratinized squamous epithelium
 CONTOUR AND SHAPE
• No rete pegs
• Papillary contour – pointed; papilla fills proximal
• Connected to the tooth by internal basal lamina and
embrasure space to the contact point
hemidesmosomes
• Marginal contour – most coronal edge form a knife-
• JE is more permeable to cells and fluids than is the oral
like edge with a scalloped configuration
epithelium
mesiodistally (follows CEJ)
• Serves as a route for a passage of fluid and cells from the
• Contour varies with the shape and alignment of the
CT into the sulcus and for the passage of bacteria and
teeth and with the sizes and position of contacts
bacteria products from the sulcus into the CT

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• Is easily penetrated by the periodontal probe; penetration free gingival tissue of facial, lingual, and interproximal
is increased in inflamed gingiva spaces.
• Length ranges 0.25 to 1.35 mm
• Hemidesmosomes – tissue to cell DENTOPERIOSTEAL / CEMENTOPERIOSTEAL
• Desmosomes – cell to cell • Embedded in the same portion cementum, run their
course apically over the vestibular and lingual bone crest
CONNECTIVE TISSUE and terminate in the tissue of attached gingiva.
• Helps in holding the marginal gingival tightly against
tooth ALVEOLINGUAL FIBERS
• MAJOR COMPONENTS OF CONNECTIVE TISSUE: • Insert in crest of alveolar process and spread out through
1) Gingival fibers the lamina propria in the free gingiva
2) Circular fibers
3) Dentogingival/Cementogingival fibers
TRANSSEPTAL FIBERS
4) Dentoperiosteal/Cementoperiosteal
• Extend from tooth to tooth, coronal to the alveolar crest
5) Alveolingual fibers
and are embedded in the cementum of adjacent of
6) Transseptal fibers
adjacent teeth.
 Not found on the facial aspect. No attachment
to alveolar crest bone.
 Connect all teeth and maintain the integrity of
the dental arches.
 Sometimes classified with the PDL

EPITHELIAL ATTACHMENT
• Inner layer of cells of the JE that actually provides the
attachment of gingiva to the tooth
• Consists of – lamina lucida and densa,
hemidesmosomes

PERIODONTAL LIGAMENT

GINGIVAL FIBERS

• Type 1 collagen fibers (60%), oytalan, elaunin and elastic

fibers
 Intercellular ground substance or matrix – proteoglycan,
glycoproteins and water
 Cells – fibroblasts, mast cells, macrophages (histiocyte),
inflammatory cells
 Vessels and neurons

CIRCULAR FIBER

• Run their course in free gingival and encircle the tooth in

a cuff or ring like fashion from cementum, across bony
septum and to the other side
 resist rotational forces

DENTOGINGIVAL / CEMENTOGINGIVAL FIBERS

• Embedded in cementum of the supraalveolar in

cementum of the supraalveolar portion of the root and
project from here is fan like configuration out into the

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• Resist lateral movements

• First to be destroyed in pathologic conditions.

HORIZONTAL FIBERS
• More apical than the former and run perpendicular
from tooth to alveolar bone.
• Responsible on why tooth movement is possible.
• Resists lateral forces

PERIODONTAL LIGAMENT
OBLIQUE FIBERS
• Soft, richly vascular and cellular specialized form of
• Largest group; most abundant
connective tissue derived from dental sac that surrounds
• Runs in a coronal direction tooth obliquely to bone
the roots of the teeth and joins the root cementum with
• More resistant to forces along the long axis of the
the alveolar bone proper.
tooth (vertical masticatory forces).
• 0.1mm to 0.2mm wide
• Most likely to be found in the middle third of the root.
 Fibrous matrix is the dominant component of PDL which is
made up primarily of bundles of continuous intermingling
connective tissue fibers arranged in a network running
APICAL FIBERS
from cementum to the alveolar bone; and ground
• Radiate around the apex of the tooth to adjacent of
substance (proteoglycans, glycoproteins and water).
bone
 Makes it possible to distribute and absorb trajectory of
• Offer initial resistance to tooth movement in an
forces during mastication into the alveolar process via
occlusal direction; prevent tipping and dislocation of
alveolar bone proper.
tooth
• Fibers affected during acute apical pulpitis
PRINCIPAL FIBERS OF PERIODONTAL LIGAMENT
1) Alveolar crest fibers
2) Horizontal fibers
INTERRADICULAR FIBERS
3) Oblique fibers
• Fibers that can only be seen in multirooted teeth
4) Apical fibers
(molars, premolars)
5) Interradicular fibers
• From cementum in the furcation area to the bone
within the furcation
• Is to be destroyed in col de sac incidence

SHARPEY’S FIBERS

• Terminal portion of collagen fibers which are embedded

into the cementum and bone

ALVEOLAR CREST
• From cementum of the tooth, running apically to the
crest of the alveolar bone.
• Counterbalance occlusal forces on the more apical
fibers
• Prevents extrusion of tooth

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CEMENTICLE

• It is the calcified body (rests that degenerates) found in BLOOD VESSELS

the periodontal ligament. Vasculature arises from maxillary artery

• From the apposition of cementum.

CELLS IN THE PDL LYMPHATICS

 FIBROBLASTS Drains to the submandibular lymph nodes

- most common cell of the PDL

- fibrous matrix and ground substance
 OSTEOBLASTS AND OSTEOCLASTS ROLES OF PDL

 CEMENTOBLASTS AND CEMENTOCLASTS • Mechanical – attach tooth to bone; provide a cushion

 RESERVE CELLS OR UNDIFFERENTIATED for absorption and transmission.
MESENCHYMAL CELLS • Formative – contains cells that form periodontium.
 MAST CELLS – (histamine and heparin) • Nutritive – contains vascular network providing
macrophages, eosinophils, cementicles nutrients.
 EPITHELIAL REST OF MALLASEZ – remnants of • Homeostatic – maintain balance of function.
epithelial sheath of Hertwig • Sensory – has afferent nerve fibers for pain (free),
pressure (spindle like) and proprioception. (ruffini like
receptor and Meissner’s corpuscle)

CEMENTUM

INTERCELLULAR SUBSTANCE
• GROUND SUBSTANCE
- proteoglycans, glycosaminoglycans, glycoproteins,
water (70%)
• FIBERS
CEMENTUM
- collagen type 1, elastic fibers, oxytalan fibers
• Specialized calcified tissue covering the root surface
• New cementum cannot be formed on root surfaces that

NERVE FIBERS have been denuded of their connective tissue attachment

• Arise from the branches of the trigeminal nerve (CN because cells in the periodontal ligament form it.
• Cementum is thicker in the apical third of the root – limit
V)
of hypercementosis – in apical third only
 Free nerve endings – pain; most
• Differences with bone:
abundant; Merkel cells; root length
 Avascular
 Ruffini corpuscle – pressure;
 No innervations
proprioception; root apex
 Pacinian corpuscle – pressure;  Fewer cells imbedded
 No resorption or remodeling (instead, a new
mechanoreceptors
layer is laid)
 Coiled Meissner’s endings – midroot
 Encapsulated spindle endings – apex • Origin: ectomesenchymal cells of dental sac
• Composition is 65% hydroxyapatite, 32% collagen, 3%
water

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• Helps in holding the marginal gingival tightly against the

tooth. CELLULAR
• Major components of connective tissue: • Rapidly formed after reaches occlusal plane
 Gingival fibers (connective tissue fibers) – • Most commonly found in apical areas of the tooth,
type I collagen fibers (60%), oxytalan, and in furcation areas of multirooted teeth
elaunin, and elastin fibers. • Within are masses of cementocytes, cementoblasts,
 Intercellular ground substance (or matrix) – and cementoclasts
proteoglycan, glycoproteins, and water. • Forms after passive tooth eruption in response to
 Cells – fibroblasts, mast cells, macrophages function
(histiocytes), inflammatory cells • Main function are: adaption (cellular) and repair
 Vessels and nerves (cellular intrinsic)
• Classification of Cementum:
 By formation:
- primary ALVEOLAR BONE
- secondary
 By cellularity:
- acellular
- cellular

ALVEOLAR BONE
• Parts of maxilla and mandible that form and support
the sockets of the teeth
• Main function: to distribute and absorbed forces
generated by mastication
• Alveolar process is lined with alveolar bone proper or
SECONDARY CEMENTUM cribriform plate (with holes where Sharpey’s fibers
• Covers apical cementum enter) – in radiograph appears as lamina dura; and. Is
• May be either acellular or cellular mainly composed spongy or cancellous bone
• Consists of mixed collagen fibers • Shape of alveolar crest is generally parallel to the CEJ;
1.5mm to 2mm apical to CEJ
ACELLULAR • Biologic width: dimension from the crest of the
• Slowly formed before the tooth erupts to reach the alveolar bone to the base of the sulcus
occlusal plane  Connective tissue = 1.07mm
• Devoid of cells  Epithelial attachment = 0.97mm
• Found principally in coronal areas (cervical half) of the ▪ What is the relationship of the biologic width to
roots and is characterized by dense layers of calcified restorative dentistry?
collagen seen in coronal cementum separated by - If a restorative procedures violates this zone, there
growth lines is a higher likelihood that periodontal inflammation
• Contains mainly bundles of Sharpey’s fibers – are will ensue, causing attachment apparatus to move
periodontal ligament extrinsic fibers embedded in apically
cementum • Unit structure:
• Main function is: Anchorage (acellular extrinsic)  Osteon or haversian system:

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- contains the haversian canal for the

blood vessel
- one osteon is connected to another
through canaliculi
• Lamellae of bone:
 Circumferential
 Concentric
 Interstitial
• Coverings of the bones:
 Periosteum – external surface of bone
 Endosteum – inner; surrounds bone
marrow
• Types of bone formation:
 Endochondral – indirect method;
cartilage becomes bone (examples:
condyle, ethmoid bone, inferior conchae,
sphenoid)
 Intramembranous – direct method;
bone cells secrete bone (examples:
maxillary and mandibular bone)
• Supporting alveolar bone – surrounds alveolar
bone proper
 Supporting compact/cortical
bone/cortical plate – bone in the buccal
and lingual outer surfaces of maxilla and
mandible; thicker in the mandibular molar
are
 Supporting cancellous bone – spongy
bone or trabecular bone which fills the
area between the cortical plates. It makes
up majority of alveolar bone.

SOURCES OF BLOOD IN THE PERIODONTIUM

• Socket and Lamina dura – intraseptal artery
• Gingiva – supraperiosteal blood vessels
• Junctional epithelium – dentogingival plexus
LYMPATHETIC SYSTEM OF THE PERIODONTIUM
• Oral epithelium of the free and attached gingival –
• Labial and lingual gingival of the mandibular incisors –
subepithelial plexus
submental lymph node (digastric)
Innervation of periodontium occurs via branches of the trigeminal
• Palatal gingival – deep cervical lymph nodes (neck
nerve (CN V)
area)
- second branch innervates maxilla
• Buccal gingival of the maxilla, and buccal and lingual
- third branch innervates mandible
of the mandibular premolar and molar region –
submandibular lymph nodes (angle of the jaw)
 The trigeminal nerve – is responsible for sensory
• Mandibular incisors – submental
innervation of teeth and motor function when chewing
• Third molars – jugulodigastric
and talking.
 Nerve receptors in periodontium register pain, touch,
and pressure.
 Nerve in ligaments provide information about pressure
to regulate chewing forces and movement

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Know Know the differential diagnosis of the various

Lecture 2 forms of gingivitis

CLASSIFICATION OF DISEASES AND CONDITIONS Provide Provide appropriate therapy

AFFECTING THE PERIODONTIUM List List systemic factors that may modify gingival
disease
Name Name three types of medications that may
cause gingival enlargement
Explain Explain how the use of certain medications
and malnutrition can modify gingival disease
Name and Name and define the three major categories
Define of periodontitis
Recognize and Recognize and describe clinical and
Describe radiographic features of chronic periodontitis
List List systemic factors that may be contributing
factors to periodontitis

Classification by duration

ACUTE

• Sudden onset
• Short duration
• Usually, some pain or tenderness noticed

CHRONIC

• Long duration
• Painless
• May have periods of subacute or acute episodes

Classification by location
I. Localized – confined to a single tooth or specific groups of
teeth
II. Generalized – involves the entire mouth
III. Papillary – involves interdental papillae only
IV. Marginal – involved the gingival margins including the
papillae

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V. Diffuse – involves the gingival margin papilla and • Common symptoms are fetid breath; metallic taste;
attached gingiva halitosis; increased salivation; malaise; lymphadenopathy,
pain, and fever in advanced stages.
ACUTE PERIODONTAL DISEASE • 01. Its occurrence has been related to: emotional and

I. Acute herpetic gingivostomatitis psychological stress; decreased oral hygiene; decreased

II. Acute necrotizing ulcerative gingivitis (ANUG) systemic defense; smoking.

III. Periodontal abscess • 02. Species implicated: treponema vincentii (spirochete);

IV. Pericoronitis bacillus vincentii (fusiform); varrelia vincentii; prevotella

intermedia

Acute Herpetic Gingivostomatitis • 03. Treatment palliative; plaque control; oxygenating

• Etiology: herpes simplex virus, type I = skin and oral mouthrinsing (hydrogen peroxide); antibiotic therapy
(metronidazole 200 mg q8)
mucosa
• Primary infection occurs most frequently in young children
between 2 and 5 years but the disease can affect young
adults
• Transmitted by droplet spread or intimate contact
• Incubation period is about 5 days. Within 1 to 2 days
numerous small vesicles develop in various parts of the
oral cavity (buccal, mucosa, lips, gingiva). The vesicles
ulcerate and become secondarily infected. Gingival gets
red, tender, and painful (inflamed).
• Eruptions may appear on the skin, vermillion, or mucous
membrane.
• Circumpolar crusting lesions on the lips may be seen due
to coagulation of serum which exudes from ruptured Periodontal Abscess

vesicles. • Gum boil or parulis

• Painful gingival swelling with red/yellowish red color

TREATMENT occurring around and infected tooth

Treatment is mainly palliative: bed, rest, soft diet and maintain • Swelling can involve the vestibule or cheek since infection

fluid intake. follows the path of least resistance.

Paracetamol suspension is given for pyrexia and severe disease is • Obstruction of drainage (of the exudate) predisposes
treated with acyclovir 200 mg, as suspension to swallow five abscess formation.
times daily, for 5 days. • Tooth is tender to percussion but is vital.

Chlorhexidine spray two or three times a day. • Discharge of pus relieves acute symptoms. Thus,
Reactivation of the virus leads secondary or recurrent infection treatment is drainage through gingival crevice by
characterized by herpes labialis – clusters of vesicles appearing on debridement. Antibiotic therapy should only be considered
the lips and skin at adjacent area. Intraorally, it is limited to if healing is still delayed despite debridement or if patient

gingival and hard palate. has decreased host response.

Pericoronitis

Acute Necrotizing Ulcerative Gingivitis (ANUG) • Inflammation of the soft tissues around the crown of a
• Vincent’s infection, trench mouth partially erupting tooth, common in mandibular third
• Characterized by generalized gingivitis with molars.
pseudomembranous ulcerations of papilla. Linear • Space between tooth crown and overlying gum flap is an

erythema - a narrow erythematous zone - is also evident ideal for plaque accumulation.
in the gingival area. • Symptoms include pain, tenderness, bad taste (from pus),
• Ages 5 to 30 limitation of mouth opening and swallowing
• Sudden onset commonly affected are people • Treatment incision and drainage if fluctuant area is

• Necrosis of the gingival tissue occurs, beginning at the tip present; debridement of areas; OHI and plaque control;

of the papilla and proceeding circumferentially, giving a operculectomy, if necessary; antibiotics, when necessary.
punched out cratering appearance.

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CHRONIC PERIODONTAL DISEASE  Bleeding upon probing

A. Stable lesions  Stable attachment levels

Gingivitis  Condition reversible with plaque biofilm removal

B. Progressive lesions  Clinical: resulted in rolled gingival margins and

I. Adult periodontitis enlarged papillae

II. Early onset  Radiograph: no bone loss - no changes in alveolar

Juvenile periodontitis bone height or the character of alveolar bone

Pre-pubertal periodontitis
Rapidly progressive periodontitis I. Gingivitis associated with II. Gingival diseases modified

III. Necrotizing periodontitis dental plaque only by systemic factors,

IV. Refractory periodontitis A. without local contributing medications, malnutrition

factors

STABLE LESIONS B. with local contributing

• A balance exists between destruction and repair factors

• Non-progressive
PREDISPOSING FACTORS
• No attachment loss
• Predisposing factors might increase the probability of

GINGIVITIS disease occurrence and usually have a localized

effects.
• Etiology: microbial plaque
• Retains or hinders the removal of dental plaque.
• Form of periodontal disease that resolves completely after
1) Dental calculus
the plaque is removed
2) Overhangs restoration
• Localized protective response elicited by bacterial invasion
3) Subgingival restorations
• No loss of attachment; no bone loss
4) Subgingival restoration margins
• Inflammation: due to dilation of blood vessels
5) Open contact points
• Appears reddish, dark pink, interdental papilla appears
6) Partial dentures
more rounded/blunted
7) Tilted/rotated/crowded teeth
• Due to enlargement/stretching of tissue from edema,
8) Bulbous crowns
there is decreased stippling
9) Grooves on teeth
• Consistency may either be soft or spongy (edematous) or
firm (fibrotic)
• Edematous – due to vascular dilation, stagnation and
SYSTEMIC FACTORS
retention of fluid
Associated with endocrine system:
• Fibrotic – attempt to repair, deposition of collagen fibers
1) Puberty-associated gingivitis
• Pseudopocket – coronal enlargement of marginal gingival
duet to inflammation
• Bleeding on instrumentation (BOP): due to
microulceration of epithelium and enlargement of
capillaries

DENTAL PLAQUE – INDUCED GINGIVAL DISEASES

2) Menstrual cycle-associated gingivitis
3) Pregnancy associated
a) Gingivitis

 Most common form of periodontal diseases

 Plaque biofilm present. At the gingival margin
 Gingival redness; tenderness
 Increase in sulcular. Temperature

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b) Pyogenic granuloma MALNUTRITION

A. Ascorbic acid deficiency gingivitis

4) Diabetes mellitus-associated gingivitis

Associated with blood dyscrasias B. Others:

1) Leukemia-associated gingivitis - Vitamin A – healthy sulcular epithelium
- Vitamin B – healthy mucosal epithelium

Starvation eliminates all nutrients necessary for healthy

periodontium.

NON-PLAQUE INDUCED GINGIVAL LESIONS

• Bacterial origin – N. gonorrhea, T. pallidum
• Viral origin – HSV-1, HIV, HHV-3(VZV), HHV- 4
MEDICATIONS
(Epstein Barr virus-infectious mononucleosis)
1) Drug-influenced gingival enlargement
• Fungal origin
- Anticonvulsant drugs: Phenytoin, Sodium valproate
• Genertic origin
• Manifestations of systemic conditions
• Traumtaic lesions
• Foreign body reactions

- Immunosuppressive drugs: Cyclosporine

- Calcium channel blockers: Nifedipine, Verapamil,

Diltiazem Stage I: Initial inflammatory lesion
2) Drug-influenced gingivitis • Corresponds to clinicallyy healthy gingival tisssue
- Oral contraceptive: associated gingivitis • Develops after 0-4 days of accumulation
• Slightly elevated vascular dilatation and increased
vascular permeability, leading to leakage of fluid from
vessels, and increased GCF flow
• Migration of leukocytes primarily neutrophils out of
vessels into the tissues, through the junctional and
sulcular epithelium, and into the gingival sulcus
• Breakdown of collagen fibers around blood vessels

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Stage II: Early inflammatory lesion BLEEDING ON PROBING

• Corresponds to early gingivitis that is evident clinically • MILD – pinpoint to slightly linear BOP
• Develops after approximately 4-7 days of. Plaque • MODERATE – linear to triangular BOP
accumulation • SEVERE – triangular to pooling BOP
• Increased vascular dilation and increased
permeability, with increased fluid exudation, and
migration of neutrophils into the tissues
• Increased breakdown of collagen subjacent to the
junctional the epithelium
• Large numbers of infiltrating leukocytes:
 Neutrophils
 Lymphocytes – particulary T lymphocytes
 Macrophages
 Mast cells (release histamine) PROGRESSIVE LESIONS
• Cytotoxic changes in fibroblasts (degeneration), • Destruction occurs at a more rapid rate than repair
resulting in a reduced capacity for collagen formation • Irreversible
• Proliferation of the cells of the junctional epithelium • With attachment loss

C. Progressive lesions
Stage III: Established inflammatory lesion V. Adult periodontitis
• Corresponds to established, chronic gingivitis VI. Early onset
• Is apparent after approximately 14-21 days of Juvenile periodontitis
undisturbed plaque growth Pre-pubertal periodontitis
• Further engorgement of blood vessels, leading to Rapidly progressive periodontitis
venous stasis and the superimposition of a dark blue VII. Necrotizing periodontitis
tinge over the erythematous gingiva VIII. Refractory periodontitis
• Migration of plasma cells (secrete IgG) into the
gingival connective tissues to become the CLINICAL FEATURES OF PERIODONTITIS
predominant inflammatory cell type • Color, texture, and volume alterations of the marginal
• Elevated release of MMPs and lysosomal contents gingiva
from neutrophils • Bleeding on probing
• Continued collagen depletion • Reduced resistance of soft marginal tissues to probing
• Continued proliferation of the junctional epithelium, • Loss of probing attachment level
forming epithelial ridges with widened intercellular • Pocket formation and/or gingival recession
spaces. • Loss of alveolar bone
• Root furcation exposure
• Increased tooth mobility
Stage IV: Advanced inflammatory lesion • Tooth drifting
• The inflammatory changes occurring in gingivitis are
confined to the gingiva and do not involve alveolar World workshop in Clinical Periodontitis (1989)
bone or result in apical migration of the junctional • Adult periodontitis
epithelium • Early onset periodontitis (prepubertal, juvenile, rapidly
• Marks the transition from gingivitis to periodontitis progressing)
• When the inflammation extends beyond the gingiva • Periodontitis associated with systemic disease
• Extension beyond the gingival tissues is coincident • Necrotizing ulcerative periodontitis
with the clinical diagnosis of periodontitis • Refractory periodontitis
• Apical migration of junctional epithelium to preserve
intact epithelial barrier 1st European workshop on periodontology (1993)
- continued collagen breakdown resulting in large • Adult periodontitis
areas of collagen depleted connective tissue • Early onset periodontitis
- osteoclastic resorption of alveolar bone • Necrotizing ulcerative periodontitis

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International workshop for the classification of PDs and

Conditions (1999)
• Chronic periodontitis
• Aggressive periodontitis
• Periodontitis as a manifestation of systemic diseases
• Necrotizing periodontal diseases
• Abscesses of the periodontium
• Periodontitis associated with endodontic lesions
• Developmental or acquired deformities and conditions  Highly visible changes in gingiva: visible signs –
changes in the contour of the tissue.
CHRONIC/ ADULT PERIODONTITIS
• Most prevalent in adults
• Slow to moderate rate of progression, but may have
periods of rapid progression
• Associated with a variable microbial pattern
• Subgingival calculus is a frequent finding
• May be modified by systemic diseases, cigarette
smoking and emotional stress
• The amount of destruction of the periodontal tissue is
commensurate with plaque levels, local predisposing
factors, smoking, stress, and systemic factors
 Minimal visible changes gingiva: minimal visible tissue
• Classified according to extent:
changes
 Localized: ≤ 30% of the sites are affected

 Generalized: > 30% of the sites are

affected
• Classified according to severity:
 Slight: 1-2mm CAL
 Moderate: 3-4mm CAL
 Severe: ≥ 5mm CAL

• Clinical characteristics: varying degrees of pocket

depths and mobility; slow in progression; gingival is
erythematous and may either appear edematous or
fibrotic; may be localized or generalized; presence of  Reveal horizontal pattens of alveolar bone loss
significant amount of plaque and calculus is noted
• Radiographic features: horizontal bone loss is more
dominant, but angular bone loss may likewise be
evident; may present radioluscences at furcation
areas.
• Microbiota: dominant are: Porphyromonas gingivalis;
Bacteroides forsythus; Prevotella intermedia
• Treatment: removal of etiologic factor by scaling and
root planning creating a dentogingival environment for
patient maintenance

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LOCALIZED AGGRESSIVE PERIODONTITIS • Greater number of females, than males, are affected
• Circumpubertal onset • Starts with first molars and incisors
• Robust serum antibody response to infecting agents • Rapid bone destruction noted with minimal clinical
• Localized first molar/incisor presentation with signs of inflammation
interproximal attachment loss on at least two • Two types: localized and generalized
permanent teeth, one of which is a first molar, and  Localized: rapid bone loss with infrabony
involving no more than two teeth other than the first pockets in permanent molars and incisors;
molars and incisors labial migration of maxillary incisors is
frequent
 Generalized: associated with Down’s
syndrome, hypophosphatasia, trisomy 21,
papillion le fever, agranulocytosis;
advanced tissue loss, increasing tooth
mobility and pathological migration of
teeth are noted.
• Various changes in leukocyte function including
 There are not any supragingival calculus deposits
decrease neutrophil chemotaxis, has been noted
evident
• Microbiota dominant: Actinobacillus,
Actinomycetemcomitans; Porphyromonas gingivalis
and Prevotella intermedia may also be noted
• Radiographically: arc shaped bone loss is evident from
the distal of the second premolar to the mesial of the
second molar (in localized cases). A distinctive
 Reveal a pattern of bone loss on the first molars that radiographic pattern of alveolar bone loss wherein one
is similar on both sides of the mandibular arch side is the mirror image of the other, is also evident.
• Treatment: debridement and antibiotic therapy
(metronidazole or combination therapy)
AGGRESSIVE/ JUVENILE PERIODONTITIS
• PRIMARY FEATURES:
o Non-contributory medical history PRE-PUBERTAL PERIODONTITIS
o Rapid attachment loss and bone • Resorption of periodontal tissues occur during or
destruction shortly after eruption of primary teeth
o Familial aggregation • Usually affects individuals below the age of puberty
• SECONDARY FEATURES: • A rare condition, associated with people suffering
o Amounts of microbial deposits are from systemic disease like Chediak Higashi Syndrome,
inconsistent with the severity of Cyclic Neutropenia
periodontal tissue destruction • Sometimes in children with blood disorders
o Elevated promotions of aggretibacter • Associated with lots of plaque and calculus
actinomycetemcomitans and • Affects both permanent and primary dentition
porphyromonas gingivalis • Types: localized and generalized
o phagocyte abnormalities  Generalized: is associated with frequent
o hyper-responsive macrophage phenotype abscess formation, URTI, and otitis media
o progression of attachment loss and bone • Treatment: debridement, OHI and antibiotic therapy
loss may be self-arresting
• Affects adolescents and teenagers from 11 years
onwards RAPIDLY PROGRESSIVE PERIODONTITIS
• May also affect older individuals (post juvenile, mid • Occurs in young adults
30’s) • During the active stage, gingival are extremely
• Often with hereditary background inflamed with exudation
• Gingival tissue may appear normal; no involvement of
primary teeth (permanent only)

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• Intensive bone loss is noted over a very short period Lesson 3

of time. Thus, angular bone loss with deep pocketing MODIFYING FACTORS IN PERIODONTAL DISEASE
is a common feature.
• Patients may have neutrophil disorder or other forms ASSOCIATED WITH GENETIC DISORDERS
of decreased host response. 1) Familial and cyclic neutropenia
• Microbiota: Bacteroides forsythus 2) Down syndrome
• Treatment: debridement, OHI, antibiotic therapy 3) Leukocyte adhesion deficiency syndromes
4) Papillon-Lefvre syndrome
5) Chediak-Higashi syndrome
NECROTIZING PERIODONTITIS 6) Histiocytosis syndromes
• Necrotizing gingivitis – appears like ANUG, with 7) Glycogen strorage disease
punched out, cratering interdental papilla 8) Infantile genetic agrunolocytosis
• Necrotizing periodontitis – bone resorption even in 9) Cohen syndrome
teeth not commonly affected; rapid destruction of 10) Ehlers-Danlos syndrome (types IV and VIII)
bone; sloughing of necrotic tissue; other oral 11) Hypophosphatasia
manifestations of HIV infection are evident at this 12) Other
point (ex. Kaposi's sarcoma, denuded area in tongue)
• Necrotizing stomatitis – lesions have reached beyond NEUTROPENIA
the mucogingival junction
• Affects bone marrow, result low level of neutrophils in the
• Treatment: debridement, OHI, palliative blood
• Agranulocytosis
• Chronic idiopathic neutropenia
REFRACTORY PERIODONTITIS
• Familial benign chronic neutropenia:
• Controversial
- rare: systemic symptoms recurrent; URTI, otitis media
• Continuous loss of attachment despite treatment - autosomal dominant
efforts - oral ulceration persistent in life
• P. gingivalis, Bacteroides forsythus, Fusobacterium
- treatment: strict plaque control, regular recall episodes
nucleatum, Peptostreptococcus. Micros, Eikenella  CHRONIC BEIGN NEUTROPENIA
corrodens, Staphylococssus intermedius o Onset: infancy but self-limiting
• Underlying systemic medical problem course of 10-18 months
• Patients require shorter recall programs o Phagocytosis is absent or assumed
• Antibiotic therapy may be necessary by monocytes
o Ulceration, chronic gingivitis,
periodontitis
 CYCLIC NEUTROPENIA
o Autosomal recessive disorder
o Oral defense mechanisms against
dental caries and apical
periodontitis is affected
o Treatment: regular monthly
professional plaque removal, daily
rinsing with chlorhexidine during
neutropenic
DOWN’S SYNDROME

• Error in cell division, trisomy of chromosome 21

• Mental handicap in children
• Develop severe aggressive periodontitis
• Severe on lower anterior region
• Rapid progression
• Reduced amount of mature T-cells
• Functional defects of PMNs, monocytes

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• Treatment options: local therapy unsuccessful: tooth loss HISTIOCYTOSIS X

inevitable; early tooth extraction; antibiotic therapy in • Localized form: eosinophil granuloma
combination with synthetic retinoids; Bi-weekly plaque • Acute disseminated form: Letterer-Siwe disease
control measures; chlorhexidine rinses • Chronic disseminated form: Hand-Schuller-Christian
diseases
• Periodontal features of histiocytosis:
 Punched-out necrotic ulcers with considerable
granulation tissue, tissue necrosis, and
marked bone loss
 Lesions may be clinically resemble necrotizing
ulcerative periodontitis lesions and biopsy of
the associated granulation tissue assists the
diagnosis of this condition
• Treatment options: radiotherapy/chemotherapy,
corticoids or anti-mitotic drugs, surgery, combination
therapy, thorough root planning, loose teeth and
pathological tissue removed, 16% recurrence rate

EHLERS-DANLOS SYNDROME
LEUKOCYTE ADHESION DEFICIENCY SYNDROME
• Disorder of joints and skin
• Defects in the integrin receptors of WBC
• 10 types; type IV with periodontal involvement ; type
• Impaired leukocyte adhesion and chemotaxis
I/III collagen abnormality
• Increased susceptibility for severe infections; impaired
• Disorder of connective tissue; skin fragility; easy bruising
wound healing
• Abnormal scarring
• Treatment options: transfusion of functionally normal
• Early tooth loss
neutrophils; bone marrow transplantation; gene therapy;
• Severe periodontitis
local therapy not successful
• Treatment options: laboratory evaluation: bleeding
history, CBC; death may occur secondary to internal
PAPILLON-LEFEVRE SYNDROME
manifestations of disease: organ and arterial rupture
• Defects in cementum; hyperkeratosis
• Functional imbalance of collagenolytic activity in the
HYPOPHOSPATASIA
periodontal ligament
• Autosomal transmission
• Impaired chemotaxis: decreased phagocytosis
• Deficiency of serum alkaline phosphatase
• Skin disorder: palmoplantar keratosis
• Increased urinary excretion of phoshoethanolamine
• Clinical symptoms may vary: hyperkeratotic skin lesions
• Suppressed monocyte chemotaxis
may be seen or completely missing
• Defective bone and tooth mineralization
• No sex or race preference
• Cementum hypoplasia or aplasia
• Severe periodontopathy
• Premature exfoliation of primary teeth
• Premature loss of deciduous and permanent dentition
• Treatment options: primary dentition; extraction of mobile
teeth; permanent dentition; selected extraction,
CHEDIAK-HIGASHI SYNDROME
scaling/root planning, OHI, periodontal surgery
• Linked with severe periodontitis
• Rare autosomal recessive immunodeficiency disorder
• Large lysosomal granules in granulocytes
• Neutrophils and monocytes are defective in chemotaxis,
bacterial killing and degranulation
• Hyperactive in phagocytic capacity
• Treatment options: tooth extractions; corticosteroid
therapy; high doses of intravenous immunoglobulin;
splenectomy

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Lesson 1 Laboratory ROOT PLANING STROKE

• Long, overlapping strokes for final smoothing of the root

Scaling and Root Planing (SRP) surface, usually in a “pull” motion (less pressure)
• Strokes can be directed: Vertically, Horizontally, and
SCALING AND ROOT PLANING Obliquely (diagonally)
• are the techniques of instrumentation applied to the root • When root planing,vertical strokes should be used first,
surface to divest of it of plaque, calcified deposits, and then oblique, then horizontal strokes.
softened or roughened cementum.
• Weekly update: post-evaluation therapy lasts around 4-6 Effectiveness and Efficiency of SRP Calculus Removal
weeks • Anatomic features of teeth often limit the
• Uses explorer and bitewing X-rays effectiveness and efficiency of SRP calculus removal
• OBJECTIVE: To provide optimally smooth root surfaces 1. Mesial surfaces of maxillary premolars
to reduce the potential for bacterial accumulation, which
is done to achieve soft-tissue reattachment 2. Proximal surfaces of mandibular incisors
3. Trifurcations of maxillary molars
Commonly observed clinical changes one week after SRP:
- reduced pocket depths The BEST CRITERION to evaluate the success of SRP is NO
- reduced gingival inflammation BLEEDING ON PROBING (since bleeding on probing indicates
active inflammatory periodontal disease)
Series of Appointments
1. Scale and root plane a segment or quadrant of INSTRUMENT DESIGN AND CLASSIFICATION
teeth at a time thoroughly and completely.
2. DO NOT do gross debridement (subgingival What are the parts of a Periodontal Instrument?
and supragingival) of the entire mouth. a) Handle
3. Schedule a series of appointments for fine b) Shank
scaling and polishing. c) Working-end

There is potential for abscess formation in a deep pocket

only when a superficial scaling is performed
a) Post-scaling periodontal abscess
b) Post-surgery periodontal abscess
c) Post-antibiotic periodontal abscess

ROOT PLANING INSTRUMENTS

• Calculus deposit location VARIATION IN HANDLE DESIGN AND CLAFFICATION

• Area of the mouth to be instrumented
• Adaptation of gingiva to the tooth Is handle design important?
- Yes, because it prevents musculoskeletal injury during
Characteristics/ Types of Instrumentation Strokes instrumentation.
- Instruments are often given the name of the task being performed
a) Probing Stroke (Walking Stroke) – upward and Lightweight instruments (15g) with larger diameter handles
downward movement within a periodontal pocket (10mm) require the least amount of pinch force.
b) Exploratory Stroke (Assessment Stroke) – used to
assess the smoothness or roughness of the tooth surface Instrument handle selection Criteria:
and the effectiveness of instrumentation. Instrument a) Weight – optimal weight is 15g or less. Lightweight
handle is grasped lightly to increase tactile sensitivity. instruments require less stress on the muscles and less
c) Scaling Stroke – a short, powerful “pull” stroke to pinch force during periodontal instrumentation.
remove calculus (more pressure). The scaling motion is b) Diameter – optimal diameter is 10mm. Small diameter
preferably initiated in the forearm and transmitted from handles (7mm) require more pinch force to hold which
the wrist to the hand with a slight flexing of the fingers. may cause muscle cramping, while large diameter
Wrist rotation is synchronized with movement of the handles (10mm) require the least pinch force
forearm.

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c) Texture – texturing/knurling pattern increases the static the amount of tactile information transmitted to the
friction between the fingers and handle, requiring reduced clinician’s fingers.
pinch force in the grasp. No texturing decreases the  Explorers – used to locate calculus deposits
control of the instrument in the wet environment of the hidden beneath the gingival margin
oral cavity which increases muscle
FUNCTIONAL AND LOWER SHANK
DESIGN CHARACTERISTICS OF THE INSTRUMENT a) Functional Shank – allows the working-end to be
adapted to the tooth surface. It begins below the
The clinician must rely on his or her sense of touch to locate the working-end and extends to the last bend
calculus deposits hidden beneath the gingival margin. in the shank nearest the handle.
 Short functional shanks are used for
• Tactile sensitivity – is the clinician’s ability to feel crowns
vibrations transmitted from the instrument working-end  Long functional shanks are used for
with his or her fingers as they rest on the shank and both crowns and roots
handle.
• Vibrations – are created when the working- end quivers
slightly as it moves over irregularities on the surface of b) Lower Shank – nearest to the working-end. It provides
the tooth. an important visual clue for the clinician in selecting the
correct working-end for the particular tooth surface to be
SIMPLE AND COMPLEX SHANK DESIGN instrumented. It is also known as terminal shank.
a) Simple shank design – also called straight shank; a  General rule: Lower shank
shank that is bent in one plane (front-to-back); has should be parallel to the
straight shank, and is used for anterior teeth. tooth surface
 Maybe standard or extended
in length: An extended lower
shank has a shank length that
is 3mm longer than that of a
standard lower shank. It is
used in deep periodontal
b) Complex shank design – also called angled or curved pockets.
shank; a shank that us bent in two planes (front-to-back
and side- to-side); has angled or curved shank, and is
used for posterior teeth

DESIGN CHARACTERISTICS OF INSTRUMENT WORKING-END

SHANK FLEXIBILITY CLASSIFICATIONS
• Working end(s) – are functional parts of the
instrument. They are adapted to the function of the
• Strength is the most important characteristic of an particular instrument. They can have a variety of
instrument shank. To remove calculus deposits, the functions including: cutting, packing, carving, placing, and
clinician applies pressure against the handle and shank to condensing. They may also be beveled (i.e., the working
press the working- end against the tooth surface. end is cut at an angle)
a) Rigid Shank – can withstand the pressure needed to • An instrument can be single-ended or double-
remove heavy calculus deposits; it removes large calculus ended:
a. Single-ended instruments – has only one
deposits more quickly; requires less effort working end. (ex. Dental mirrors)
b) Flexible Shank – will not withstand the pressure needed
to remove heavy calculus deposits; works well to remove b. Double-ended instruments – has two

small and medium-sized calculus deposits; also enhances working ends. It has two types:

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i. Unpaired working-ends – has dissimilar INTRODUCTION TO INSTRUMENT CLASSIFICATION

working ends (ex. Curette-sickle combination;
Explorer-probe combination) PERIODONTAL PROBE
ii. Paired working-ends – has exact mirror
images (ex. Gracey 11/12 curette) PERIODONTAL PROBE

• Is a slender assessment instrument

Working-end Identification: • blunt, tapered, rod-like instrument calibrated in
Each working-end is identified by the number closest to it. millimeters
• circular or rectangular in cross section
The first number (on the left) identifies the working-end at the top • used to detect periodontal pockets to determine the
end of the handle, and the second number identifies the working-end health of the periodontal tissues
at the lower end of the handle  we insert the probe into the sulcus with a
firm, gentle pressure to the bottom of the
Parts of the Working End pocket.
 The shank should be aligned with the long
axis of the tooth surface to be probed
• Grooves, colored indentations, or colored bands may be
used to indicate the millimeter markings on the working
end of a periodontal probe

The Working-end in Cross Section

Probe Design Types:

Classification of Hand-Activated Periodontal Instruments

a) Marquis color-coded probe – calibrations are in 3mm

Supragingival vs. Subgingival Instrumentation sections; a total of 12mm

• Supragingival instrumentation – the use of an b) University of North Carolina-15 probe – a 15mm

instrument coronal to (ABOVE) the gingival margin. (ex. long probe with millimeter markings at each millimeter

use of an explorer to examine the margins of restoration and color coding at the fifth, tenth, and fifteenth

or dental sealants) millimeters.

• Subgingival instrumentation – the use of an c) University of Michigan “O” probe, with William’s

instrument apical to (BELOW) the gingival margin. (ex. markings – at 1, 2, 3, 5, 7, 8, 9, and 10mm

use of an explorer to detect calculus deposits hidden d) Michigan “O” probe – with markings at 3, 6, and 8mm

beneath the gingival margin) e) World Health Organization (WHO) probe – has a
0.5mm ball at the tip and millimeter markings at 3.5, 5.5,
8.5, and 11.5mm and color coding from 3.5 to 5.5mm

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f) Novatech probe – has mm markings at 3,6,9, and EXPLORERS

12mm; it has a unique shank deisgn with upward and
right-angled bend to facilitate access to the distal surfaces
g) Florida probe – computer-based probe with digital
readouts and computer storage of data; constant probing
pressure of 15g is provided by coil springs inside the
handpiece; can also record missing teeth, recession,
pocket depth, bleeding, suppuration, furcation
involvement, mobility, and plaque assessment
h) Furcation probe
 Curved #2 Nabers probe – used for detection of furcation Explorer Design Types:
area; with color-coded markings at 3,6,9 and 12mm a) Orban-Type #17
b) Shepherd’s Hook #23
Irving Glickman’s Furcation Classification: c) ODU 11/12 Type
d) Curved #3
e) Pigtail #3

Which has a correct angulation and positioning of your ODU

instrument?

i. GRADE I – incipient bone loss. Furcation probe can

The terminal shank should be parallel to the long axis of the tooth
feel the depression of the function opening,
penetrates no more than 1mm
Common Calculus Formations
ii. GRADE II – partial bone loss. Probe tip enters
a) Spicules - an isolated, minute particle or speck of
under the roof of the furcation, penetrates >1mm
calculus. Commonly found under contact areas, at line
but does not pass completely through furcation
angles, and at the midline line of a tooth
iii. GRADE III – total bone loss with through-and-
b) Ledge - a long ridge of calculus running parallel to the
through opening of the furcation. The furcation
gingival margin. Common on all tooth surfaces
entrance is not visible clinically
iv. GRADE IV – a Grade III furcation where the c) Ring - a ridge of calculus running parallel to the gingival
margin that encircles the tooth
furcation entrance is visible clinically
d) Veneer - a thin, smooth coating of calculus with a
“shield-like shape” located on a portion of the root
Plastic Titanium Instruments for Implants
It is important that plastic or titanium instruments be used to avoid surface
scarring and permanent damage to the implants. In our laboratory activities, apply veneer type of calcular deposit in your model. No
less than 4mm application. It can be a thin layer (around 2 layers). It should be
(Plastic probe: Colorvae) uniformly applied.

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Anterior and Posterior Design Instrument

SICKLE SCALERS

Calculus Removal Stroke with Sickle Scaler

• Stabilization – application of pressure with the index

SICKLE SCALERS finger and thumb inward against the instrument handle;
press the tip of the fulcrum finger against the tooth
• Used for removal of medium-to-large sized supragingival
surface (the ring finger is responsible for your finger rest)
calculus
• Adaptation – only the tip-third (3mm) of cutting edge is
• Provides good access to proximal surfaces on anterior
adapted to the tooth surface
crowns and enamel surfaces apical to contact areas of
• Angulation – angulate your sickle scaler to 70°- 80°
posterior teeth
before activation of your instrument stroke; tilt the lower
• Used with a pull stroke
shank of your sickle scaler slightly toward the tooth
• NOT recommended for use on root surfaces
surface
• Lateral pressure for calculus removal – should use
Working end design
moderate to firm pressure, be composed of controlled
• Pointed back
strokes, and short in length. (Light pressure during
• Pointed tip
instrumentation will lead to burnishing a calculus)
• Triangular in cross section
• Two level cutting edges per working end
Stroke Directions
• Face is perpendicular to the lower shank

Nevi Series of Sickle Scalers

The usual sequence of strokes is vertical-horizontal oblique:

A. Stroke number
• Should be limited to areas where calculus is
present
• Use the minimum number of strokes needed
to remove calculus deposits
B. Application to Anterior Surfaces
• Use the prescribed sequence shown in this
illustration to instrument the colored tooth
surfaces of the facial aspect. Begin with the
left canine and end with the right canine.

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• Work on the most posterior surface of the first

quadrant going to the most posterior surface
of the second quadrant

F. Steps for Calculus Removal with Hand Activated

Instrument
1) Me
2) My patient
C. Adaptation Adjacent to Papillary Gingiva
3) My equipment
• Place the cutting edge against the proximal surface
4) My nondominant hand
positioned in between the papillary area
5) My dominant hand
6) My finger rest
7) My adaptation – adapt the leading-third of the working
end
8) My angulation – establish face-to-tooth surface angulation
of 70-80 degrees by tilting the lower shank tooth surfaces
9) My stabilization – press against the tooth with ring finger.
Apply inward pressure against handle with index finger
D. Adaptation to the Tooth Crown and thumb
10) My activation – activate a short stroke away from the
junctional epithelium
11) Rest my muscles – at the end of stroke, pause briefly and
relax ring finger, index finger, and thumb

CURETTE

CURETTE

E. Application of cutting edges to the posterior teeth • Used for the removal of light to moderate sized

• There are two working ends and four cutting edges of a supragingivally and deep subgingivally calculus of crown

posterior sickle scaler and root surfaces

• An instrument of choice for root planing altered
cementum, and removing the soft tissue lining the
periodontal pocket
• Used with a pull stroke
• Two types: Universal curettes and Area-specific curettes

I. UNIVERSAL CURETTES

• Use the prescribed sequence shown in this illustration to • For removal of small to medium-size calculus

the instrument the facial aspect of the entire sextant, deposits

beginning with the posterior-most molar • Semicircular in cross section, allowing it to be

used in both supragingival and subgingival
instrumentation

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• Two level working cutting edges per working- honed at 90 degrees rather than the offset blade of the Gracey
end Curette
• Face is at a 90 degrees i. Langer #5-6 curette – mesial and distal surfaces of
angle to lower shank
anterior teeth
• Rounded back and toe
ii. Langer #1-2 curette (Gracey #11-12 shank) –
• Straight cutting edges
mesial and distal surfaces of mandibular posterior teeth
with rounded toe
iii. Langer #3-4
• Two curettes are paired on a double-ended
curette (Gracey
instrument (mirror images of one another)
#13-14 shank) –
• Universal use – one double ended
mesial and distal
instrument can be used to instrument all tooth
surfaces of maxillary
surface in the dentition
posterior teeth

II. AREA-SPECIFIC CURETTES

• set of instruments designed and angled to
adapt to specific anatomic areas of the
dentition
 Application of the cutting edges to the posterior teeth • Semicircular in cross section
• Debridement instrument with rounded back, a
rounded toe, (ideal for subgingival use) and
one working cutting edge
• Name signifies that each curette can be
applied only to specific surfaces and areas of
the mouth
- use the sequence shown in this illustration to instrument the facial • Used on crown and root surfaces
aspect of the entire sextant, beginning with the posterior-most molar (supragingivally and subgingivally)
• Edge curves upward at the toe
• Curved cutting edges and rounded toe
enhance adaptation to rounded root surfaces
and root concavities
• Working cutting edge is lower than the non-
working edge (offset blade – tilted 60- to-70-
degree angle)
• Complex shank design
• Examples of Area:
 Examples of Universal Curettes

 Langer and Mini Langer Curettes

- are a set of three curettes combining the shank design of the
standard Gracey 5/6, 11/12, and 13/14 curettes with universal blade

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 PERIODONTICS I Lecture and Laboratory
Dr. Katrina Bianca B. Cruz-Natividad

GRACEY CURETTES MINI-BLADED CURETTES

 Double-ended Gracey curettes are paired in the following

manner:
 Gracey #1-2 and 3-4: Anterior teeth
 Gracey #5-6: Anterior teeth and premolars
 Gracey #7-8 and 9-10: Posterior teeth; facial and
lingual
 Gracey #11-12: Posterior teeth; mesial
 Gracey #13-14: Posterior teeth; distal
 Gracey #15-16: Posterior teeth; mesial
 Gracey #17-18: Posterior teeth; distal
Mini Five Curettes
• Are modifications of the after five curettes
• Blades that are half the length of the after five or
standard gracey curettes which allows easier insertion
and adaptation:
• Can be used with vertical strokes, with reduced tissue
distention, and without tissue trauma
• In the past the only solution in most of these area of
difficult access was to use the gracey curettes with a toe-
down horizontal stroke

Micro Mini Five Gracey Curettes

• Have blades that are 20% thinner and smaller than the
mini five curettes
• These are the smallest of all curettes
• Provide exceptional access and adaptation

EXTENDED-SHANK CURETTES

Schwartz Periotrievers

• Are a set of two double-ended, highly magnetized

instruments designed for the retrieval of broken
instrument tips from the periodontal pocket
• They are indispensable when the clinician has broken a
curette tip in a furcation or deep pocket
After Five Curettes

• Are modifications of the standard Gracey curette design

• Terminal shank is 3mm longer
• Thinned blade for smoother subgingival insertion and
reduced tissue distention
• Large diameter
• Tapered shank
• Available in all standard gracey numbers except for the
#9-10

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 PERIODONTICS I Lecture and Laboratory
Dr. Katrina Bianca B. Cruz-Natividad

Plastic and Titanium Instruments for Implants INSERTION

• It is important that plastic or titanium instruments be

used to avoid scarring and permanent damage to the
implants

Principal types of curettes as seen from the toe of the

instrument

A. Universal curette – blade is straight

B. Gracey curette / Area-Specific – blade is curved; only the
convexing cutting edge is used.
Note the offset blade angulation of the Gracey curette. • Ideal Angulation for Subgingival/Supragingival
Calculus - 70 degrees or between 60 and 80.
• Ideal Angulation for Face-to-tooth surface -
between 40 and 90 degrees
• Ideal Angulation for Root Debridement - between
60 and 70 degrees

Scaler Vs. Curette

Subgingival adaptation around the root is better with the curette than
with the sickle; f, facial; l, lingual.

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 PERIODONTICS I Lecture and Laboratory
Dr. Katrina Bianca B. Cruz-Natividad

Lecture 4 PATHWAY OF PATHOGEN KILLING COMPLEX

• classical pathway or alternate pathway (C1-C9)

HOST RESPONSE CELLS • once there is an injury the classical pathway is triggered
• Origin: bone marrow first (C1-C4)
• Stem cells: immature pluripotent cells - responsible for the initial body response
• Differentiate as need arises (capable of becoming almost • Alternative pathway
anything) - A longer process
• Stay in circulation or reside in organs and tissues - C1-C3, C3 is halfed in C3 A and B à membrane attack
complex (MAC) which attack directly on the pathogens
WOUND REPAIR binding with them causing them to get destroyed.

• Hemostasis - This is an automatic cascade that occurs in a normal

Stop the bleeding person

Clotting cascade
• Inflammation FIRST RESPONDER

Source of porthole for infection to come in • Direct lysis via MAC (membrane attack complex)
• Clean up area • Recognition of antigens
• Proliferation  Oxonins
White-ish area  Enables chemotaxis
• Remodelling  Brings and goes
Only occur in clean area, make sure there is clotting • Clean up and excretion

INNATE DEFENSE MECHANISM ADAPTIVE DEFENSIVE EXCRETION

• Natural, non-specific • Acquired immunity

• All over our body • Specificity to antigens
• First 4 hours upon infection or injury that the IDM comes • Multiplied intensity and response time
in • After 96 hours
• Triggers “complement cascade” • Transport to lymphoid tissue via circulation
• B&T cell response

ANTIBODY DEFENSE

ANTIGEN
 any substance that induces the immune system to
produce antibodies against it
 features of the bacteria

TRIGGERED CASCADES
ANTIBODY
• Series of 9 proteins
• Protein that the immune system produces in response to
• Synthesized in the liver
an antigen
• Circulates in blood as inactive precursors
• Enhances antibody and phagocytic clearance
ANTIGENS

• Bacteria, virus
• Can be component of bacterial or viral cell membranes
• Substances they produce
• Periodontic: LPS (gram negative bacteria), endotoxins
• APC’s able to recognize and bind and initiate immune
response
• Each bacteria may have many different
• Antigenic sites - may be elusive

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 PERIODONTICS I Lecture and Laboratory
Dr. Katrina Bianca B. Cruz-Natividad

ANTIBODY RESPONSE IN PERIODONTAL DISEASE T LYMPHOCYTES

• Shown some evidence of higher antibody fibers to • Effector and non-effector functions
periodontal pathogens after periodontal therapy • T cells are the generals that upregulate immune response
completed (non effector t cells) down regulate the response
• May aggregate bacteria, inhibit colonization, enhance • NK T cells are effector cells that actively kills bacteria
phagocytosis, detoxify endo and exotoxins • Periodontitis excessive upregulation of inflammatory
• Diagnostic and possible predictive and prognostic value in response:
clinical therapy  Exaggeration of the actions of the immune
• Vaccine therapy or intervention for susceptible hosts response cells becomes detrimental to the
periodontal tissues
How the COVID vaccines work?  It’s our own immune response that detached

• Mimicking the actual COVID virus properties the periodontal ligament

• Translation within the body and production processed

spiked proteins GINGIVITIS

• Immune cells (antibodies) now able to target particles • Early infiltration of PMNS and Macrophages
• Untested memory capability • Clinically seen as redness of the gingiva
• Look for local factors (clinical)
FRIEND OR FOE? • In a healthy GCF: there are neutrophils

• Tolerance is the ability for the immune system to • Transudate vs. Exudate: increase in proteins -

recognize itself Gingivitis, PMNS are a lot already (neutrophils)

• Immunoregulation is the key to health

• Evidence during periodontal disease progression Generalized Gingivitis

• Still a “stable lesion”

UP regulation of inflammatory response • Adequate T cell regulation

• Primary under the control of T helper cells (TH1 and TH2) • Reversible once healed

• Precise mechanism for controlling the immune system to

obtain a sufficient response to deal with the pathogen B LYMPHOCYTES

• TH2 cells enhance antibody response in Periodontal • Located throughout the lymphoid organs and tissues
disease - Go and stay in the nodes
• Activated B lymphocytes differentiate
IMMUNE SYSTEM • Antibodies produce by each B cell is specific to an antigen

• Starts early • Memory B cells stay on for long immunity

• Mostly similar for all

• Affected by environment, by genetics, by medical events Severe gingivitis

• Combinations of inflammatory and uncontrolled reparative

PMN’s reactions

• Predominant leukocyte in the gingival tissues and sulcus • Check systemic tissues

• Responsible for initial phagocytosis • Young patients, hormonal

• Signals inflammatory process to begin

• More PMN’s are recruited to the area via the circulation TRUE PERIODONTAL DISEASE PROGRESSION

• UP regulation of the immune response

MACROPHAGE • Stimulation of enzyme production to degrade tissues

• Main function is to eat antigenic substances • It is not the bacteria alone that destroys and melts the

• Presents antigens to T cells by releasing cytokines to tissue alone it is the host

signal upregulation • Osteoclastic activity uncontrolled

• Vascular permeability and inflammation initiator • Collagenase secreted to destroys soft tissues
• MMP’s degrade extracellular matrix

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 PERIODONTICS I Lecture and Laboratory
Dr. Katrina Bianca B. Cruz-Natividad

CELLULAR COMMUNICATION

A. Biologically Active Mediators

• Cytokines
 Soluble proteins secreted by cells
 Messenger molecules
 Allow leukocytes to talk to epithelia,
endothelia, and fibroblasts

PROINFLAMMATORY CYTOKINES

• Interleukin (IL-1, IL-6, IL-8)

• Tumor necrosis factor – alpha
 Both stimulate osteoclasts and inhibit
osteoblasts
 IL-8 has powerful chemotactic functions

OTHER EFFECTS OF CYTOKINES

• Promotes vasodilation
• Blood vessels contains macrophages, PMNS, etc.
• Promotes expression of ELAM 1 and ICAM 1 to enables
circulating lymphocytes to move towards the disease area
• Significance of BOP during examination?
 Sulcular epithelium and JE are not keratinized
so the skin is thin, there is an increase of
bood flow and passage of the cells is
enlarged, madami na nag iinfiltrate in the
blood site. The epithelium is permeable
bacteria
 We can assume that the environment is right
for tissue destruction
• Can we beat periodontal disease?
 Current therapy enough?
 We tried to control it, and do our best clinically but the
problem with PD

AFTER APPROPRIATE THERAPY

• Removal of pathogens
• Enable switch down of T helper cells
• Switch up of T suppressor functions
• Activating collagen repair
• Regeneration and/or reattachment

Will everyone get periodontal disease?

 Roughly 25% susceptible - Genetic theory?
 25 million Filipinos
 < 50 periodontists

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