Periodontal Pocket

1. Periodontal Pocket
PRESENTED BY
DR ASIF
DEPARTMENT OF PERIODONTICS

2. Def : Pathological deepening of gingival sulcus.
Classification :
•Gingival : Relative or false
•Periodontal: True

3. Classification of periodontal pockets
i. Depending on base of the pocket:
A. Suprabony : Supra crestal, Supra alveolar
B. Infrabony : Intrabony, Intra alveolar

5. ii. Based on involved tooth surfaces :
A. Simple
B. Compound
C. Complex

6. 6
Depending upon nature of soft tissue wall of
pocket :
Pockets
Edematous Fibrotic

7. 7

8. 8
Depending upon the disease activity :
Pockets
Active Inactive

10. CLINICAL FEATURES :
Bluish red thickened marginal gingiva.
Bluish red vertical zone from gingival margin to alveolar
mucosa.
Suppuration with gingival bleeding.
Tooth mobility with diastema formation.
Generally asymptomatic, but less frequently associated with
localized deep dull pain
sensitivity
Urge to bite on the affected area
Urge to use toothpick or needles
relief after bleeding is induced

13. POCKET CONTENTS :
Micro organisms and their byproducts
Dental plaque
GCF, Salivary mucin
Food remnants
Desquamated epithelial cells
Leukocytes
DIAGNOSIS :
Williams graduated periodontal probe.

14. Difference between Suprabony and Infrabony pockets :
•Base of the pocket
•Type of bone loss
•Transeptal fibers arrangement
•Remaining PDL fibers

15. Pathogenesis of pocket formation:
Pockets are caused by bacteria and their toxic byproducts.
Toxic byproducts cross the epithelial barrier and produce pathological changes in
the connective tissue, ultimately leading to deepening of gingival sulcus
Sequence of events in progression of periodontal pockets:
•Bacterial byproducts induce inflammatory changes in connective tissue of gingival
sulcus.
•The cellular and fluid inflammatory exudate causes degeneration of connective
tissue.
•Just apical to JE an area of destroyed collagen fiber develops and gets occupied by
inflammatory cells and exudates.

17. •Destruction of collagen fibers take place by two mechanisms :
An enzyme collagenase is released by PMN’s and Macrophages
Bacterial enzymes induce cytotoxic changes in fibroblasts
These altered fibroblasts phagocytose collagen and resorb gingival fibers
•Due to continuous loss of collagen the apical JE proliferates along the root.
•Hence the coronal JE detaches from the root.
•More no of PMN’s from connective tissue invade the coronal end of JE.
•Once the relative volume o PMN’s exceed by 60%, the tissue looses cohesiveness
and detaches from tooth surface.
•Thus the sulcus shifts apically.
Plaque  Gingival inflammation  Pocket formation More plaque
formation

18. 18
Due to inflammation
PMNs invade coronal end of the junctional epithelium
Relative volume of PMNs reaches approximately 60% or more of the
junctional epithelium
Tissue loses cohesiveness and detaches from the tooth surface.
--- detaches from the root
--- migrates, resulting in its apical shift
--- gradually occupies an increasing
portion of the sulcus lining
Coronal portion
Apical portion
Oral sulcular
epithelium

19. 19
 Extension of junctional epithelium along root requires presence of
healthy epithelial cells.
Continued inflammation
Gingiva increases in bulk
Crest of gingival margin extends coronally
Apical cells of junctional epithelium continue to migrate along root
Coronal cells continue to separate from it
Epithelium of lateral wall of the pocket proliferates to form bulbous,
cordlike extensions into inflamed connective tissue
Leukocytes and edema from inflamed connective tissue infiltrate the
epithelium --- resulting in degeneration and necrosis.

20. HISTOPATHOLOGY
1. Soft tissue wall
2. Root surface wall

21. 1. Soft tissue wall (CT) :
 CT is edematous, densely infiltrated with plasma cells, lymphocytes,
scattering of PMN’s.
 Blood vessels are increased, dilated and engorged.
 CT exhibits varying degrees of degeneration and proliferation of
endothelial cells, newly formed capillaries and collagen fibers.
 JE is usually much shorter with coronoapical length of 50-100 micro
meters.
 Cells of JE are in good condition or show slight vacuolar degeneration.

22.  The lateral wall (sulcular epithelium) shows severe degenerative changes.
 Epithelial cells undergo vacuolar degeneration and necrosis of epithelium.
 This leads to ulceration of lateral wall, exposure of inflamed CT and
suppuration.
 Bacterial invasion is seen in the apical and lateral wall of pocket.
 Bacterial invasion is active or by passive translocation.
 They invade Intercellular spaces Deeper epithelial cells Basement
laminaSubepithelial CT.
 Prominent microorganisms are GM –ve like PG, PI, AA.

23. 3. Root surface changes:
cause pain, perpetuate infection, complicate periodontal treatment.
Structural changes:
•Degeneration of collagen fibrils.
•Penetration of bacteria.
•Presence of pathologic granules(incomplete mineralization)
•Necrotic cementum.

24. Chemical changes:
•Areas of increased mineralization(ca,mg,po,fl.)increased hardness.
•Areas of decreased mineralization Root caries.
•Root caries appears as yellowish or light brown.
•Progression is around root rather than into root.
•Aa is dominant microorganism.

25. Cytotoxic changes:
•Bacterial endotoxins are present on root surfaces.
•Prevents attachment of normal fibroblasts.
•Induce inflammatory reaction, when re implanted in mucosa even when
autoclaved.

26. Periodontal disease activity:
Related to specificity of plaque.
Periods of exacerbation:
Increased inflammatory response.
Increased bleeding and exudate.
Increased bone,CT, PDL loss.
Periods of quiescence:
Decreased above conditions.
Site specificity:
Affected and non affected sites coexist.
Periodontal pockets and pulp changes:
Produce significant pulp changes through lateral canals or periapically.
Severe pain.

28. Periodontal pockets as healing lesions:
•These are chronic lesions.
•Constantly undergo repair
•Presence of plaque does not allow complete healing.
•Clinical presentations of gingival features are dependent on predominance
of destructive or repair phase.

29. Relation of CAL and bone loss with pocket depth.
CAL is distance between CEJ to base of pocket.
Pocket depth is distance between gingival margin and base of pocket.

31. Periodontal Abscess : (Lateral or Parietal abscess)
Localized purulent inflammation in periodontal tissues.

32. Periodontal abscess :
An acute destructive process in the periodontium resulting in localized
collection of pus and not arising from pulp
Classification
Location
Onset & course of action
Number of Abscess

34. Symptoms :
Pain
Gingival and mucosal pain
Red to reddish blue gingiva
Teeth are tender on chewing and sensitive to percussion
Mobility
May have sinus tract and already draining
Lymphadenopathy and slight elevation of body temperature
Purulent exudate

35. Microscopic features :
•Presence of viable and non viable PMN’s.
•PMN’s liberates enzymes that digest cells and other
tissue structures.
•Liquid pus is formed.
•Acute inflammation surrounds this purulent area.
•Epithelium exhibits intra and extra cellular edema and
invasion of leucocytes.

37. ETIOLOGY :
Periodontitis related cases
Pockets with tortuous course.
Incomplete removal of calculus during periodontal treatment.
Partial treatment resulting in coronal occlusion and purulent bacteria
remain deep inside the pocket particularly deep narrow and tortuous
pocket
Use of oral irrigation devices that may push bacteria deep into
tissues
Antibiotics without debridement in advanced periodontitis

38. Etiology : Non periodontitis related
Perforation during endodontic therapy
Cracked tooth, vertical tooth fracture, external root resorption
Impaction of tooth brush bristle, ortho elastics, dental floss, fish or chicken bone
Microbial picture
Anaerobic microorganisms, gm –ve like bacteroides melaninogenicus,
capnocytophaga, PG, PI fungi spirochetes, AA
Microbial picture is similar to chronic periodontitis

39. Differential diagnosis:
Periapical abscess:
Deep caries, restorations, crowns, nonvital pulp
Radiolucency at apex
Pain in the apex of root
Absence of periodontal pocket
Severe pain on percussion
Pain is sharp, intermittent ,severe and diffuse, not able to recognize
affected teeth

40. Acute pulpitis:
Most of the symptoms of periodontal abscess are
absent except pain
No soft tissue swelling are or purulent drainage
Pain in opp arch affected by thermal changes
Incomplete tooth fracture
Pain or sensitivity on biting and sensitivity to cold

41. Treatment :
Drainage through incision or through gingival sulcus
Use of antimicrobial agents
Open approach with flap surgery and osseous correction
Irrigation with sterile saline, 0.1 % povidone iodine or 3 % hydrogen
peroxide
For systemic symptoms antibiotics and analgesics

42. Use of antibiotics:
Culture and sensitivity
250 mg of tetracycline every six hours for 10 days
100 mg doxy once for 10days
500mg azithromycin single dose on first day followed by 250 mg once
for 3 days
500/ 125 amox + clavulinic acid every 8 hour for 8 days
500mg metronidazole every 8 hour for 10 days
150 to 300 mg clindamycin 3 times for 7 days