PERIODONTAL POCKET

CONTENTS

 Definition
 Classification
 Clinical signs & symptoms
 Pathogenesis
 Histopathology
 Contents of a pocket
 Periodontal disease activity
 Site specificity
 Detection of periodontal pocket
 Treatment of periodontal pocket
 Conclusion
 DEFINITION

 A pathologically deepened gingival

sulcus
- by coronal movement of the gingival
margin,
- by apical displacement of the gingival
attachment,
- combination of both processes

 One of the most important clinical

 CLASSIFICATION

Based on morphology

GINGIVAL PERIODONTAL

- Pseudopocket
With destruction of the
- Without destruction of supporting periodontal
underlying periodontal tissues
tissues

Formed by gingival Leads to loosening &

enlargement exfoliation of teeth

Combined
 TYPES OF PERIODONTAL POCKETS

Based on relationship to alveolar crest

• Supracrestal /
supraalveolar
Suprabon • Bottom of the
y pocket is coronal
to underlying
alveolar bone

• Subcrestal /
Intraalveolar
• Bottom of the
Infrabony pocket is apical
adjacent alveolar
bone
 SUPRABONY & INFRABONY POCKET

FEATURE SUPRABONY INFRABONY

POCKET POCKET
Base of pocket Coronal to alveolar Apical to crest of
bone alveolar bone
Pattern of bone Horizontal Vertical
destruction
Interproximal fibers Horizontal (from Oblique (from
base to bone) cementum to
cementum above
bone)
Facial & lingual Horizontal / oblique Angular course
fibers course
Lateral wall of Consists of soft Soft tissue & bone
pocket tissue
 …CLASSIFICATION

Based on number of surfaces

involved

Simple

• Involve 1
tooth
surface
 Based on number of surfaces involved

• 2 or more
tooth surfaces
• Base of the
pocket directly
communicates
with gingival
margin along the
involved surface
Based on number of surfaces involved

• Originates on 1
tooth surface
& twists around
the tooth to
involve 1 / more
surfaces
• communicates
with gingival
margin at
surface were
pocket originates
• Common in
furcation areas
 …CLASSIFICATION

Based on disease activity :

- Active pocket - Inactive
pocket
Based on nature of soft tissue wall :
- Edematous - Fibrotic
Based on pocket depth & width :
Type 1 - Shallow narrow
Type 2 - Shallow wide
Type 3 - Deep narrow
Type 4 - Deep wide
 CLINICAL SIGNS

 Bluish red, thickened marginal gingiva & vertical zone from

gingival margin to alveolar mucosa
 Enlarged rolled edge of marginal gingiva separated from
tooth surface
 A break in the faciolingual continuity of interdental gingiva
 Shiny, discolored & puffy gingiva associated with exposed
root surfaces
 Gingival bleeding & suppuration
 Tooth mobility
 Diastema formation
 Extrusion & migration of teeth
 Probing depth – to locate & determine the extent of
periodontal pockets
 SYMPTOMS

 Localized pain or radiating pain “deep in the bone”

 Gnawing pain / feeling of itching in the gingiva
 Sensation of pressure after eating which gradually
diminishes
 A foul taste in localized areas
 Urge to dig with pointed instrument into the gingiva
 A tendency to suck material from interproximal spaces
 Sensitivity to head & cold
 Toothache in the absence of caries
 CLINICAL FEATURES HISTOLOGICAL
FEATURES
Bluish • Circulatory stagnation
discoloration
Flaccidity • Destruction of gingival fibers

Smooth shiny • Atrophy of epithelium &

surface edema
Pitting on • Degeneration & edema
pressure
• Predominant fibrotic changes
Firm & pink
Bleeding on • Increased vascularity
probing • Thinning & degenerated
• epithelium
Ulceration of inner aspect of
Pain pocket wall
• Suppurative inflammation in
Pus inner wall
PATHOGENESIS
 PATHOGENESIS

Inflammatory changes in the connective tissue of

gingival sulcus

Collagenases & Activate fibroblasts phagocytize

MMPs collagen

Gingival collagen fiber destruction

Proliferation of apical cells of

junctional epithelium (JE) along the
root (PMNs >60%)

Detachment of the coronal portion of

JE from the root
Intraepithelial cleft & pocket
progression
Diseased gingiva is associated with increased
number of spirochetes & motile rods - Lindhe &
Listgarten

INFLAMMATON IN CT WALL

DEGENERATION OF SURROUNDING CT AND

GINGIVAL FIBERS

EDEMA & DETACHMENT OF JE & SHIFTS APICALLY

HISTOPATHOLOGY
 SOFT TISSUE WALL

CONNECTIVE TISSUE

 Edematous & densely infiltrated with 80% plasma cells,

lymphocytes & scattered PMNs
 Blood vessels are increased in number, dilated &
engorged
particularly in subepithelial connective tissue layer
 Varying degree of degeneration
 Single or multiple necrotic foci are occasionally present
 Proliferation of endothelial cells
 Newly formed capillaries, fibroblasts & collagen fibers
 …SOFT TISSUE WALL

JUNCTIONAL EPITHELIUM

 Much shorter at the base of the pocket

 Coronoapical length reduced to 50 to 100
μm
 Cells may exhibit slight to marked

degeneration
 …SOFT TISSUE WALL

LATERAL WALL OF POCKET

 Most severe degenerative changes occur here
 Proliferative & degenerative changes in the epithelium
 Epithelial buds or interlacing cords of epithelial
cells project into inflammed connective tissue
 Projections & lateral epithelium are infiltrated with
leukocytes & edema
 Epithelium at gingival crest of a periodontal pocket is
intact, thickened with prominent rete pegs
 Cells rupture to form vesicles
 Ulceration of lateral wall
 Exposure of underlying inflammed connective tissue
 Suppuration
 BACTERIAL INVASION

 “Passive translocation” of plaque bacteria

 Apical & lateral areas of the pocket wall in chronic
periodontitis
 Between deeper epithelial cells & basement lamina
 Some invade subepithelial connective tissue
 Filaments, rods, coccoid with mostly gram ‘-’ve
cell walls - Frank
found in intercellular spaces of epithelium
 [Link] & [Link] in gingiva of AP
cases – Hillmann et al
 A.a in tissues - Christerrson
 MICROTOPOGRAPHY OF GINGIVAL WALL

 SEM – description of many areas in gingival wall of pocket

where different types of activity take place – Saglie et al,
1975
 Adjacent irregularly oval or elongated areas
 50 to 200 μm

1) Areas of relative quiescence

2) Areas of bacterial accumulation
3) Areas of emergence of leukocytes
4) Areas of leukocyte-bacteria interaction
5) Areas of intense epithelial desquamation
6) Areas of ulceration
7) Areas of hemorrhage
MICROTOPOGRAPHY OF GINGIVAL WALL

Areas of relative quiescence

 Flat surface with minor depressions

& mounds
 Occasional shedding of cells

Areas of bacterial accumulation

 Depressions on epithelial surface

 Debris & bacterial clumps

penetrating into enlarged

intercellular spaces
 Cocci, rods, filaments, few

spirochetes
 MICROTOPOGRAPHY OF GINGIVAL WALL

Areas of emergence of leukocytes

Leukocytes appear in pocket wall
through holes in intercellular spaces

Areas of leukocyte-bacteria
interaction
 Numerous leukocytes covered with

bacteria in phagocytosis
 Bacterial plaque – as organized

matrix covered by fibrin-like material

in contact with surface of cells or
 As bacteria penetrating into

intercellular spaces
MICROTOPOGRAPHY OF GINGIVAL WALL

Areas of intense epithelial

desquamation
 Semi-attached & folded epithelial squames

 Sometimes partially covered with bacteria

Areas of ulceration
Exposed connective tissue

Areas of hemorrhage
Numerous erythrocytes

Transition from 1 area to another leads to

epithelial desquamation, ulceration &
hemorrhage.
 ROOT SURFACE WALL

As the pocket deepens, collagen in cementum gets destroyed

Cementum gets exposed to oral environment

Collagenous remnants of Sharpey’s fibers in cementum

degenerate

An environment favourable to penetration of bacteria (87% of

roots)
Bacterial penetration found as deep as CEJ & dentinal tubules

Fragmentation & breakdown of cementum surface

 ROOT SURFACE WALL CHANGES

Structural
 Pathologic granules – area of collagen degradation
 These may be areas of hypermineralization or demineralization
causing root caries

Chemical
 Increased mineral content of cementum
 Exposed cementum absorb Ca, P, F – develop a highly calcified
layer, highly resistant to decay
 This ability to absorb may be harmful if the materials are toxic

Cytotoxic
Endotoxins in cementum limit proliferation & attachment of
fibroblasts to diseased root surfaces
 DECALCIFICATION & REMINERALIZATION OF
CEMENTUM

Areas of increased
mineralization

Areas of demineralization

Areas of cellular resorption of

cementum & dentin
 AREAS OF INCREASED MINERALIZATION

 As a result of exchange of minerals & organic components at

cementum-saliva interface, on exposure to oral cavity – Selvig
 Increased mineral content of exposed cementum
 Hypermineralized zone – increased perfection of crystal structure
 Organic changes – subsurface cuticle

Microradiographic studies – Fusath

 10 to 50 μm thick.
 No decrease in mineralization in deeper areas
 Reduced cross-banding of collagen near cementum
 Subsurface condensation of organic material of exogenous origin
 AREAS OF DEMINERALIZATION

Exposure of cementum to oral environment

Undergoes fragmentation & cavitations

Progresses around tooth

Root caries

Lesions increase with age – Katz RV et al

Microorganisms - Syed, Loesche
Predominantly – [Link]. Others – [Link], [Link],
[Link].
Pocket depth decreases after treatment - ↓ periopathogens & ↑
 AREAS OF CELLULAR RESORPTION OF
CEMENTUM & DENTIN

 Common in roots unexposed by periodontal disease –

Sottosanti, 1977

 No particular significance – symptom free

 If root is exposed by pocket formation before repair

occurs, these areas appear as isolated cavitations
that penetrate into dentin

 Differentiated from caries of cementum by clear-cut

outline & hard surface

 Source of considerable pain requiring restoration

SURFACE MORPHOLOGY OF TOOTH WALL

Zones found in the bottom of a

periodontal pocket
– Brady JM, Saglie FR at al

Zone 3, 4, 5 – “plaque-free
zone”
In extracted teeth
Width – wider in molars ,
narrower in deeper pockets
Unattached plaque – gram
+’ve’ & gram –’ve’ cocci, rods,
filaments, fusiforms, spirochetes
Most apical zone – gram –’ve’
rods & cocci
POCKET CONTENTS
 POCKET CONTENTS

McMillan et al, 1958

 Debris
 Plaque-covered calculus projects from tooth surface
 Microorganisms & their products – Enzymes, endotoxins,
metabolites
 Gingival fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells
 Resident leukocytes
 Purulent exudate (if present) -
 Living, degenerated & necrotic leukocytes
 Living & dead bacteria
 Serum

 PERIODONTAL POCKETS AS HEALING LESIONS

 Periodontal pockets – chronic inflammatory lesions under constant

repair
 The condition results from the interplay of destructive & constructive
tissue changes. Balance determines clinical features of pocket wall.
Persistence of bacterial attack inflammatory response
degeneration of new tissue elements complete healing does not
occur
Inflammatory
fluid & Newly
formed
cellular EDEMATOU
connective
exudate. S POCKET FIBROTIC tissue cells
Pocket wall-
Bluish red, soft, WALL POCKET & fibers.
spongy, friable WALL Pocket wall -
with a smooth Firm and pink
shiny surface

 Fibrotic pocket walls – misleading

 PERIODONTAL DISEASE ACTIVITY

Periods of Periods of
Quiescence exacerbatio
/ Inactivity n / activity

 Reduced
inflammatory
 Bone & C.t
response attachment loss
 Little / no loss of
bone & C.t  Pocket deepens
attachment
 Buildup of
unattached plaque  Followed by a
 Gram –’ve’, motile
period of
anaerobic bacteria
 Bleeding, gingival remission -
exudate proliferation of
 Thin & ulcerated gram +’ve’
pocket epithelium
 Plasma cells, bacteria.
 SITE SPECIFICITY

 Periodontal destruction does not occur in all teeth at the

same time.

 Few teeth at a time / only some sites of teeth affected at

any given time – “site specificity of periodontal
disease”

 Sites of active destruction are found next to sites with

little or no destruction.

 Severity of periodontitis increases with development of

new disease sites & the increased breakdown of existing
sites.
 PULPAL CHANGES

 Spread of infection from periodontal pockets may cause

pathologic changes in the pulp
 This may cause painful symptoms or adversely effect the
response of pulp to restorative procedures
 After infection spreads from pocket through PDL, involvement of
pulp in periodontal disease occurs through :
Lateral canals in the root Apical
foramen
 RELATIONSHIP OF ATTATCHMENT LOSS
& BONE LOSS TO POCKET DEPTH

 Positive correlation, but not always

 Degree of attachment loss depends on location of base

of pocket

 Pockets of same depth may be associated with different

degrees of attachment loss & vice versa

 Slight bone loss can occur with deep pockets

 Extensive attachment & bone loss may be associated

with shallow pockets if there is recession of gingival
margin
 RELATIONSHIP OF ATTATCHMENT LOSS
& BONE LOSS TO POCKET DEPTH

Different PDs with same Same PD with different

amount of attachment amounts of recession
loss
 AREA BETWEEN BASE OF POCKET & ALVEOLAR
BONE

 Distance between apical end of JE &

alveolar bone is relatively constant
 Distance between apical extent of
calculus & alveolar crest –
constant
 Mean length – 1.97mm (±33.16%)
-
Stanley & Wade

 Distance from attached plaque to

bone is never less than 0.5 and
never more than 2.7 mm - Wade
 Isolated bacteria on c.t. & bone surface
may modify these considerations
DIAGNOSING POCKETS
 DETECTION OF PERIODONTAL POCKETS

 Probing - Gold standard

method for assessment of
periodontal breakdown – World
workshop of periodontics, 1989

 Radiographs indicate areas

where presence of pockets may
be suspected.

 Guttapercha points /
caliberated silver points +
Radiographs – Level of
attachment in periodontal
pockets.
 HOW TO PROBE

Probe inserted parallel to long axis of tooth & “walked”

circumferentially around each surface of all teeth – The walking
stroke

Plastic periodontal probe

around implants
ADAPTATION
PARALLELISM
Full Millimeter Measurements:

Probing depths are recorded to the nearest full

millimeter.
Round measurements to the next higher whole
number.
A reading of 3.5 mm is recorded as 4 mm, and a
5.5 mm reading is recorded as 6mm.
 PROBING DEPTH

 Depth of penetration of probe into connective tissue apical to JE

is
0.3 mm – Listgarten, 1976
 Force of 0.75 NBIOLOGIC/
is well tolerated – Tibbets, 1969
CLINICAL
 25grams - HISTOLOGIC
PROBING
PROBING
Armitage et al DEPTH
DEPTH
Distance to
Gingival
which
margin to
probe
base of
penetrates
pocket
into pocket

Depends on
Histological
many
sections
factors
 LEVEL OF ATTACHMENT Vs PROBING DEPTH

POCKET DEPTH • Gingival margin to

base of pocket
• Susceptible to
changes

LEVEL OF • Base of pocket to CEJ

ATTACHMENT • Better indicator of
periodontal
destruction
 BLEEDING ON PROBING

Insert probe into bottom of pocket wall

Gently move probe laterally along pocket

wall

Wait for 30 – 60 sec & check for bleeding

TREATMENT
 POCKET THERAPY

PURPOSE OF POCKET THERAPY

 To eliminate changes in pocket wall.

 To create a stable, maintainable state.
 To promote periodontal regeneration.

CRITERIA FOR METHOD SELECTION

 Characteristics of pocket
 Accessibility to instrumentation
 Existence of mucogingival problems
 Response to Phase I therapy
 Patient’s age & general health
 Previous periodontal treatment
 Esthetic considerations
 DEPENDING ON POCKET
TYPE

GINGIVAL PERIODONTAL
POCKET POCKET

Phase I therapy : SRP & Re-evaluation

IF POCKET PERSISTS
PHASE II
• Flap surgery
Gingivectomy • Removal of
pocket wall
• Removal of
tooth side of
pocket wall
 NON-SURGICAL TECHNIQUES

For pockets <5mm :

 Scaling & root planing

 Good oral hygiene with adjunctive therapies

 ADJUNCTIVE THERAPIES

ANTI-MICROBIAL AGENTS & FORM

2%
Minocycline 10% 25% 2.5mg
microsphere Doxycycline Metronidazol Chlorhexidine
s gel e gel in gelatin
matrix
Powder Biodegradab Biodegradabl Biodegradabl
le mixture e mixture e device
 SURGICAL TECHNIQUES

 Increase accessibility to root deposits

 Eliminate or reduce pocket depth by resection of pocket wall
 Expose the area to perfom regenerative methods

Suprabony pockets Infrabony pockets

Pocket Pocket
reductio eliminati
Gingivectomy n on

Internal bevel Modified

Kirkland
Gingivectomy widman
flaps
flap,
ENAP Apically
Undisplace
repositione
d flaps
d flap
 SURGICAL MANAGEMENT OF SUPRABONY
POCKETS

Gingivectomy
Glickman and Prichard (1957)

ENAP
ENAP
Excisional New Attachment Procedure
U.S. Naval Dental Corps
 SURGICAL MANAGEMENT OF INFRABONY
POCKETS

POCKET REDUCTION

Conventional flap technique (Kirkland flap)

Undisplaced
flap – Morris
 SURGICAL MANAGEMENT OF INFRABONY
POCKETS

POCKET
ELIMINATION
Apically repositioned
flap - Nabers
 It eliminates pocket depth

 Increases attached

gingiva

Open flap debridement

(Modified widman flap)
- Ramjford & Nissle
 Exposes root surface for

instrumentation &
removal of pocket lining.
 REMOVAL OF TOOTH SIDE OF POCKET WALL

Bicuspidization

 Splitting of two rooted teeth

into two separate portions
 Removal of involved part

Root resection

In multirooted teeth with

grade III or IV furcation
 LASER THERAPY

Better improvement of clinical parameters at 6 months after

pocket treatment with the laser, compared to SRP treatment
– Swartz, 2006

A one-time use of the laser in periodontal pockets did not

sterilize or substantially reduce subgingival bacterial
populations compared to negative controls – Stephanie,
2007

No significant difference in reduction of PD & BOP between

subjects treated with SRP + lasers & only SRP however
showed significant reduction in bacterial counts following
laser application – Beatriz Maria, 2010
 ANTIMICROBIAL PHOTODYNAMIC THERAPY

PDT and SRP showed similar clinical results in the non-surgical

treatment of aggressive periodontitis – Olivera et al, 2007

At 3 and 6 months after treatment, there were no statistically

significant differences between the groups with regard to CAL,
PD, FMPS, or microbiologic changes. At 3 and 6 months, a
statistically significantly greater improvement in FMBS was found
in the test group – Nicoas, 2008

Reduction in Porphyromonas gingivalis, Fusobacterium

nucleatum, and Capnocytophaga gingivalis counts following SPR
+ PDT when compared to SRP alone – Anne Pfitzner, 2004
 OUTCOMES TO POCKET THERAPY

NEW
NEW
ATTACHMENT EPITHELIAL PERSISTENCE
ATTACHMENT LONG JE ANKYLOSIS ADAPTATION OF POCKETS
 CONCLUSION

Periodontitis is stated as one of the worldwide health

hazards – WHO.

Periodontal pockets are a classic sign of periodontal

diseases.

However, its very simple to diagnose and the correct

treatment plan would result in elimination or
reduction of pockets thereby reducing the severity
of the periodontal disease.