pockets

2. Content
 Introduction
 Classification
 Clinical features
 Theories of pathogenesis
 Pathogenesis
 Histopathology
 Periodontal Disease Activity
 Site Specificity
 Relation of Attachment Loss to Pocket Depth
 Conclusion
 References

3. Introduction
Pathologically deepened gingival sulcus

4. Classification
 Gingival pocket (pseudo pocket)
 Periodontal pocket

5. Classification
 Suprabony / Supracrestal / Supraalveolar
 Intrabony/ Infrabony / Subcrestal / Intraalveolar

6. Classification
Suprabony Pocket Intrabony Pocket
Base of
pocket
Pattern of
destruction

7. Classification
Suprabony Pocket Intrabony Pocket
Transseptal
fibers
PDL fibres
(Facial &
Lingual)

8. Classification
Simple Compound Complex

9. Clinical Features
Extrusion & migration
Diastema
Enlarged, bluish-red marginal gingiva
“Rolled” edge
Reddish-blue vertical zone
Shiny & puffy gingiva
Gingival bleeding
Purulent exudate

10. Clinical Features
Localized pain/
Sensation of
pressure
Foul taste
Tendency to suck
material
Radiating pain
“Deep in the bone”
Gnawing feeling Urge to dig
Foods sticks
between teeth
Sensitivity to heat &
cold
Tooth ache

11. Theories of Pathogenesis
 Two stage pocket formation (James & Counsell, 1927)
Proliferation of subgingival epithelium
Loss of superficial layers of proliferated epithelium
Space or pocket

12. Theories of Pathogenesis
 Pocket formation : Initiated in a defect in sulcus wall
(Becks,1929)
 Between oral & enamel epithelium

13. Theories of Pathogenesis
 Pathologic destruction of epithelial attachment due to infection
or trauma : Initial histologic change in pocket formation
(Skillen, 1930)
o Epithelial attachment : Area of low resistance
Infection / Trauma
Pathologic dissolution of epithelial attachment
Pocket formation
Accumulation of debris in pocket

14. Theories of Pathogenesis
 Proliferation of the epithelium of lateral wall is the initial
change in formation of the periodontal pocket (Wilkinson, 1935)
o Proliferation & down growth of oral epithelium Thickening of
epithelial lining of sulcus Cells along inner aspect of sulcus
deprived of nutrition Degeneration & necrosis
Calcification of necrotic cells Separation of calcified masses
from adjacent normal epithelium Pocket or trough

15. Theories of Pathogenesis
 Periodontal pocket is initiated by invasion of bacteria at base of
the sulcus or absorption of bacterial toxins through epithelial
lining of sulcus (Box,1941)
o Initial invasion of bacteria at base of sulcus Inflammation in
underlying CT Ulceration at base Sloughing of
epithelium Loss of attachment to cementum Progressive
loss of CT & penetration of pocket into deeper tissues

16. Theories of Pathogenesis
 Orban & Weinmann,1942
o Subgingival bacterial growth : Secondary to pocket

17. Theories of Pathogenesis
 The initial change in pocket formation occurs in the cementum.
(Gottlieb 1926, 1946)
o Continuous eruption of teeth : Down growth of epithelial
attachment
o Continues deposition of new cementum : Prevents accelerated
migration of epithelial attachment
o Normal deposition of cementum impaired : Dissolution of
organic connection between cementum & gingiva

18. Theories of Pathogenesis
 Destruction of gingival fibers : Pre-requisite for initiation of
pocket formation (Fish, 1948)
Top most fibers digested & absorbed
Epithelium proliferates until healthy fiber is reached

19. Theories of Pathogenesis
 Simulation of the epithelial attachment by inflammation :
Prerequisite for initiation of the periodontal pocket (Aisenberg
& Aisenberg, 1948)
o Inflammation Epithelium migrates along root Epithelial
cells burrow between intact gingival fibers Enmesh
connective tissue fibers in epithelial network Secondary fiber
degeneration

20. Theories of Pathogenesis
 Inflammation is the initial change in the formation of the
periodontal pocket (Nuckolls & Dienstein, Bell & Rule, 1950)
o Inflammation in connective tissue
 ↑ Mitotic activity
 ↑ Keratin
 Cellular desquamation

21. Theories of Pathogenesis
o Basal epithelial cells at bottom of sulcus : Proliferate into
connective tissue
o Open lesion
o Repair of lesion : Periodontal pocket

22. Theories of Pathogenesis
 Waerhaug, 1976
o Bacteria spreading subgingivally Pocket formation

23. Theories of Pathogenesis
 Schroeder and Attstrom (1980)
Microbial invasion of subgingival dentogingival junction
Destroy coronal epithelial attachment
Pathological pockets

24. Theories of Pathogenesis
 Takata & Donath (1988)
o Early & established lesion
Degenerative changes in most coronal part of JE
Intraepithelial cleavage
Degeneration of cells lining the cleavage
Deep crevice formation

25. Theories of Pathogenesis
o Advanced lesions
Deep pocket epithelium
Toxic bacterial products
Mechanical irritation of calculus
Thin and ulcerated
Typical periodontal pocket

26. Pathogenesis
 Initial lesion : Inflammation of gingiva
 Not a predictor of future attachment & bone loss
Hillman 1998

27. Pathogenesis
 Cellular & inflammatory exudate : Degeneration of CT & fibers
 Apical Cells of JE : Fingerlike projections
 Coronal portion : Detaches from the root
 60% PMNs : Loss of tissue cohesiveness
 Sulcus shifts apically
Matrix Metalloproteinases
Taichman 1968, Takada 1988
Phagocytosis
Deporter 1980

28. Pathogenesis
 Gingival sulcus Periodontal pocket Plaque removal impossible
 Rationale for pocket reduction : Eliminate areas of plaque
accumulation
Plaque
Gingival
Inflammation
Pocket
formation
More plaque
formation

29. Histopathology
 Soft tissue wall
o Connective tissue
Exudative
ProliferativeDegenerative

30. Histopathology
o Junctional epithelium
 50-100 µm
 Cells : Well formed & in good condition
Slight to marked degeneration

31. Histopathology
o Lateral wall
 Most severe degenerative changes
 Epithelial buds or interlacing cords of epithelial cells
 Dense infiltration
 Cells : Vacuolar degeneration & form vesicles
 Ulceration & suppuration

32. Histopathology
 Severity of degenerative changes : Not related to pocket depth
 Epithelium of gingival crest : Intact with prominent retepegs
 Predominant gram-negative filaments, rods & cocci
? Bacterial invasion
? Passive translocation of plaque bacteria

33. Histopathology
 Microtopograghy
o Irregular oval/elongated areas : 50 - 200 microns
Saglie et al 1975
 Relative quiescence
 Bacterial accumulation
 Emergence of leucocytes
 Leucocytes bacterial interaction
 Intense epithelial desquamation
 Ulceration
 Haemorrhage

34. Histopathology

35. Histopathology
 Periodontal pocket as a healing lesion
Chronic inflammatory lesions
Persistence
bacterial attack
Repair
Degeneration of
new tissue
elements

36. Histopathology
Destructive
tissue
changes
Constructive tissue
changes
Edematous
pocket
Fibrotic
pocket

37. Histopathology
 Pocket contents
o Debris
o Microorganisms & products
o Gingival fluid
o Food remnants
o Salivary mucin
o Desquamated epithelial cells
o Leukocytes
o Plaque-covered calculus
o Purulent exudate

38. Histopathology
o Significance of Pus Formation
 Secondary sign
 Nature of the inflammatory changes
Not an indication of depth of pocket / severity of destruction

39. Histopathology
 Root surface wall
Structural Chemical
Cytotoxic

40. Histopathology
 Structural Changes
Pathologic
granules
Areas of increased
mineralization
Areas of
demineralization

41. Histopathology
o Pathologic granules : Collagen degeneration / Incompletely
mineralized collagen fibrils
Bass 1951
o Areas of increased mineralization : Exchange of minerals &
organic components at cementum-saliva interface
Selvig 1969
 Perfection of crystal
 Subsurface cuticle
 10-20µm thick

42. Histopathology
o Areas of demineralization: Root carries
Herting 1967
Oral fluid & bacteria plaque
Proteolysis of embedded remnants
of sharpeys fibers
Cementum softened
Fragmentation & cavitation
Progress around the tooth

43. Histopathology
Active root
caries lesions
Inactive root
caries lesions

44. Histopathology
 Severe Cases
 Actinomyces viscosus
 Caries Pulpitis
Involvement
of
cementum
Bacterial
penetration
of dentinal
tubules
Destruction
of
dentin

45. Histopathology
 Necrotic cementum : Removed by scaling & root planing
 Areas of cellular resorption of cementum & dentin : Roots
unexposed by periodontal disease

46. Histopathology
 Chemical Changes
o Mineral content increased
o Calcium, Magnesium, Phosphorus, Fluoride
o Microhardness : Unchanged
o Exposed cementum : Resistant to decay
Selvig 1966

47. Histopathology
 Cytotoxic Changes
o Bacterial penetration : Cemento-dentinal Junction
o Endotoxins
o Diseased root fragments : Prevents in-vitro attachment of
human gingival fibroblasts

48. Histopathology
 Surface Morphology of Tooth Wall

49. Periodontal Disease Activity
 Models of Disease Progression
o Continuous
o Random / Episodic burst
o Asynchronous multiple burst
o Synchronous burst
o Epidemiologic
o Brownian motion / Stochastic
o Fractural

50. Periodontal Disease Activity
• Exacerbation
Episodic bursts
of activity
• Quiescence
Periods of
remission
 Bone loss in untreated periodontal disease occurs in episodic
manner
McHenry 1981

51. Periodontal Disease Activity
Periods of quiescence Period of exacerbation
Reduced inflammatory
response
Little or no bone & CT
attachment loss
Build-up of unattached
plaque
Bone & connective tissue
attachment lost
Pocket deepens
Bleeding & Gingival exudate
Epithelium thin & ulcerated
Inflammatory infiltrate
Motile organisms & spirochetes

52. Site Specificity
 Some aspects of some teeth at any given time
 New site : Increased severity

53. Relation of Attachment loss to Pocket Depth

54. Conclusion
 Understanding the etiopathogenesis, histopathology and
progression of periodontal pockets is essential to provide the
patient with the successful treatment outcomes and monitoring the
response to therapy.

55. References
 Newman MG, Takei HH, Klokevold PR, Carranza FA. Carranza’s
Clinical Periodontology. Saunders Elsevier;10th Edition.
 Glickman I. Clinical Periodontology. WB Saunders Co; 4th Edition.
 Greenstein, Lamster. Changing Periodontal Paradigms: Therapeutic
Implications. Int J Periodontics Restorative Dent 2000;20:337-357.
 Takada, Donath. Mechanism of pocket formation. J Periodontol 1988;
59; 215-221.
 Grant, Stern, Listgarten. Periodontics. CV Mosby Co; 6th ed.