3. CONTENTS
• Introduction
• Classification
• Clinical features
• Old theories of pocket formation
• Mechanism of pocket formation
• Histopathology of periodontal pocket
• Periodontal disease activity
• Site specificity
• Pulpal changes associated with pockets
• Relationship of attachment loss & bone loss to pocket depth
• Relationship of pocket to bone
• Examination
• Conclusion
• References
4. INTRODUCTION
• Periodontal pockets are caused by microorganism so and their
products, which produces pathological tissue changes that lead to
the deepening of the gingival sulcus.
• One of the most important clinical features of periodontal disease.
The periodontal pocket is defined as a pathologically deepened gingival
sulcus due to apical migration of junctional epithelium
5. CLASSIFICATION
Relation between the base of the pocket & the crest of the
remaining alveolar bone
Suprabony
Supracrestal /
Supraalveolar
Intrabony/ Infrabony/
Subcrestal/
Intraalveolar
Morphology
Gingival/ False/
Relative
Combined
Periodontal/
Absolute/ True
6. The number of surface involved
Simple ComplexCompound
Nature of the soft tissue trail of the pocket
Edematous Fibrotic
8. CLASSIFICATION OF INFRABONY POCKET
Number of walls
One-walled Three-walledTwo-walled
Combined/
Crater defect
Depth & width
Type I
Shallow narrow
Type III
Deep narrow
Type II
Shallow wide
Type IV
Deep wide
Goldman & Cohen,
1980
9. CLINICAL FEATURES: signs
Bluish-red thickened marginal gingiva
Bluish-red vertical zone from the gingival margin to
the alveolar mucosa
Gingival bleeding and suppuration
Tooth mobility
Diastema formation
Localized pain or pain “deep in the bone.”
10. SYMPTOMS
Localized pain or sensation of pressure after eating which gradually diminishes
A foul taste in localized area
A tendency to suck material from interproximal spaces
A gnawing feeling or itchiness in the gums
An urge to dig a pointed instrument into the gums with relief from resultant
bleeding
Sensitivity to heat and cold
Toothache in absence of caries
12. The initial change in pocket formation occurs in cementum
-Gottlieb, 1926
Two stage pocket formation:
a. Proliferation of the subgingival epithelium.
b. Loss of superficial layers of proliferated epithelium, which produces
space or pocket.
-James & Counsell, 1927
Pocket formation is initiated as a defect in sulcus
- Becks, 1929
Pathologic destruction of the epithelial attachment due to infection or
trauma is the initial histologic changes in pocket formation.
-Skillen, 1930
Proliferation of the epithelium of the lateral wall, rather than epithelium at
the base of the sulcus, is the initial change in the formation of periodontal
pocket
- Wilkinson, 1935
13. The periodontal pocket is initiated by invasion of bacteria at the base of the
sulcus or the absorption of bacterial toxins through the epithelial lining of the
sulcus
-Box, 1941
Destruction of gingival fibers is a prerequisite for the initiation of pocket
formation
-Fish, 1948
Stimulation of the epithelial attachment by inflammation rather than
destruction of gingival fibers is the prerequisite for the initiation of
periodontal pocket
-Aisenberg, 1948
Inflammation is the initial change in the formation of periodontal pocket
-J. Nuckolls, 1950
Early & established lesion
-Takata & Donath, 1988
15. Plaque formation and gram +ve bacteria in the supragingival tooth
surface
Extends to subgingival area
Plaque maturation
Microbial shift towards gram –ve bacteria
Change in subgingival environment
Virulent factors produce by bacteria stimulates host immune response
Metabolic acids, bacterial LPS, Volatile sulphur compounds,
extracellular enzymes & fatty acids
16. JE produce various proiinflammatory mediators: IL-8, PGE2, TNF α & MMP
Along with neuropeptides & histamine produced by free nerve endings causes
vascular effect in that area. This mediators cause increase vascular permeability
Perivascular mast cell produces histamine
Endothelium to release IL-8
PMN cell recruitment
Neutrophils transmigrate into CT under chemoattractant gradient
Rapidly pass through the JE into the gingival sulcus
Variably thick layer over the subgingival plaque
17. As the inflammation intensifies
Degradation of CT & gingival fibers
Collagen fibers
Collagenases & other
enzymes of host &
bacterial origin
Fibroblasts which
phagocytize collagen
fibers
JE cells proliferate & form finger like projections in the CT
Apical extension of JE along the root surface
The increasing number of transmigrating neutrophils interferes with epithelial
attachment
When volume increases approx. 60% of JE there is disruption of epithelial
barrier
Open communication between pocket & underlying tissue
18. Chemoattractant gradient is hampered
Neutrophil move randomly in the CT
Microorganisms get access to the CT
Battlefield for host bacterial interaction
Neutrophils perform their phagocytic function & release their granules
because of which various enzymes accumulate in that area & execute
their destructive functions
Activated macrophages produce various chemical mediators which
further intensify the inflammatory reaction
19. As the duration of
lesion prolongs
Antigen presenting
cells activates T-cell
response
Further activates B-
cell response
Host bacterial
interaction continues
till there is bacterial
infiltration
Alveolar bone
resorption starts
Deepening of
periodontal pocket
22. 1. CHANGES IN SOFT TISSUE WALL
• The connective tissue is edematous and densely infiltrated with
plasma cells (approximately 80%), lymphocytes, and a scattering of
PMNs.
• The blood vessels are increased in number, dilated, and engorged.
• The CT exhibits varying degrees of degeneration.
• Single or multiple necrotic foci are occasionally present.
• The CT shows proliferation of the endothelial cells, with newly formed
capillaries, fibroblasts, and collagen fibers
• The JE at the base of the pocket is usually much shorter than that of a
normal sulcus.
• The coronoapical length of the JE is reduced to only 50 to 100 μm.
23. 2. CHANGES IN LATERAL WALL
• Epithelial buds or interlacing cords of epithelial cells project from the
lateral wall into the adjacent inflamed CT, and they may extend farther
apically than the JE.
• Densely infiltrated by leukocytes and edema from the inflamed CT
• Vacuolar degeneration and rupture to form vesicles
• Ulceration of the lateral wall, exposure of the underlying inflamed CT,
and suppuration.
24. These observations demonstrated numerous structural features
indicative of more pronounced degenerative changes in Rapid
Progressive Periodontitis than in Adult Periodontitis.
25. • Ulceration of the lateral wall may occur in shallow pockets, and
deep pockets are occasionally observed in which the lateral
epithelium is relatively intact or shows only slight degeneration.
• The epithelium at the gingival crest of a periodontal pocket is
generally intact and thickened, with prominent rete pegs.
26. 3. BACTERIAL INVASION
• The bacterial penetration are reported to be a mixture of bacterial
morphotypes within the tissues rather than homogenous populations in
single or multiple colonies.
• Filaments, rods, and coccoid organisms with predominant gram -ve cell
walls have been found in intercellular spaces of the epithelium.
• Hillmann et al: the presence of P. gingivalis and P. intermedia in the
gingiva of aggressive periodontitis cases.
• Actinobacillus actinomycetemcomitans has also been found in the
tissues.
27. • Bacteria intercellular space under exfoliating epithelial cells,
also found between deeper epithelial cells as well as accumulating on
the basement lamina transverse basal lamina
subepithelial CT.
28. 4. MICROTOPOGRAPHY OF THE GINGIVAL WALL
Areas of relative quiescence: relatively flat surface with minor
depressions and mounds and occasional shedding of cells.
Areas of bacterial accumulation: depressions on the epithelial
surface, with abundant debris and bacterial clumps penetrating into
the enlarged intercellular spaces.
Areas of emergence of leukocytes: leukocytes appear in the pocket
wall through holes located in the intercellular spaces.
Areas of leukocyte–bacteria interaction: numerous leukocytes are
present and covered with bacteria in an apparent process of
phagocytosis. Bacterial plaque associated with the epithelium is seen
either as an organized matrix covered by a fibrin like material in
contact with the surface of cells or as bacteria penetrating into the
intercellular spaces
Areas of intense epithelial desquamation: semi-attached and folded
epithelial squames.
Areas of ulceration
Areas of hemorrhage
29. 5. PERIODONTAL POCKET AS HEALING LESIONS
• Complete healing does not occur.
Destructive
Constructive
Edematous pocket wall
Fibrotic pocket wall
Fibrotic pocket walls may be misleading,
because they do not necessarily reflect what is
taking place throughout the pocket wall
Externally the pocket appears pink and fibrotic, despite the inflammatory
changes occurring internally
30. 6. POCKET CONTENTS
• Debris that consists principally of microorganisms and their products,
gingival fluid, food remnants, salivary mucin, desquamated epithelial
cells, and leukocytes.
• Plaque covered calculus
• Purulent exudate: living, degenerated, and necrotic leukocytes, living
and dead bacteria, serum, and a scant amount of fibrin.
• It is not an indication of the depth of the pocket or the severity of the
destruction of the supporting tissues.
• However, it represents a period of active tissue breakdown.
• Abscess formation usually occurs due to marginal closure of a deep
periodontal pocket that prevents proper drainage.
Pus is a common feature of periodontal disease, but it is only a
secondary sign
31. 7. ROOT SURFACE WALLS
Pocket deepens
Collagen fibers embedded in the cementum are destroyed
Exposed to the oral environment.
Collagenous remnants of Sharpey fibers in the cementum undergo
degeneration
Creating an environment favourable to the penetration of bacteria
Bacterial penetration into the cementum can be found as deep as
the cementodentinal junction and it may also enter the dentinal
tubules
Penetration and the growth of bacteria leads to fragmentation and
breakdown of the cementum surface
Areas of necrotic cementum that are separated from the tooth by
masses of bacteria
32. When placed in oral mucosa of the patient, diseased
root fragments induce an inflammatory response even
if they are autoclaved
33. A. DECALCIFICATION & REMINERALIZATION OF CEMENTUM
Areas of increased mineralization: a result of an exchange of minerals
and organic components at the cementum–saliva interface after
exposure to the oral cavity.
- The mineral content of exposed cementum increases.
- minerals that are increased in diseased root surfaces include Ca,
Mg, P and F.
- Microhardness, however, remains unchanged.
Areas of demineralization: related to root caries.
Exposure to oral fluid and bacterial plaque
proteolysis of the embedded remnants of Sharpey fibers
the cementum softened
undergo fragmentation and cavitation
34. Root caries lesion
Active lesions
• Yellowish or light-brown areas
• Frequently covered by plaque
• Softened or leathery consistency on
probing
Inactive
lesions
• Well-defined darker lesions
• Smooth surface and a harder
consistency on probing
Caries of the cementum requires special attention when the pocket is
treated. The necrotic cementum must be removed by scaling and root
planing until firm tooth surface is reached, even if this entails extension into
the dentin
Dominant microorganism: A. viscosus.
Other: A. naeslundii, S. mutans, S. salivarius, S. sanguis, B. cereus.
35. Areas of cellular resorption of cementum and dentin:
- common in roots that are unexposed by periodontal
disease
- These areas are of no particular significance because they
are symptom free, and, as long as the root is covered by the PDL, they
are likely to undergo repair
- if the root is exposed by progressive pocket formation
before repair occurs, these areas appear as isolated cavitations that
penetrate into the dentin.
36. B. SURFACE MORPHOLOGY OF TOOTH WALL
Cementum covered by calculus
Attached plaque
The zone of unattached plaque
The zone of attachment
of the JE to the tooth
A zone of semidestroyed
connective tissue fibers
“Plaque-free zone”
38. Periods of
Quiescence/
Inactivity
• Reduced inflammatory response and little or no
loss of bone and CT attachment.
Period of
Exacerbation/
Activity
• Bone and CT attachment are lost and the pocket
deepens.
• Last for days, weeks, or months, followed by a
period of remission or quiescence during which
gram +ve bacteria proliferate and a more stable
condition is established.
• Bleeding, either spontaneously or with probing,
and greater amounts of gingival exudate.
• Histologically, the pocket epithelium appears thin
and ulcerated, and an infiltrate composed
predominantly of plasma cells, PMNs, or both is
seen.
• Bacterial samples from the pocket lumen
analyzed with dark-field microscopy show high
proportions of motile organisms and spirochetes
39. SITE SPECIFICITY
• Periodontal destruction occurs on a few teeth at a time or even only
on some aspects of some teeth at any given time.
• This is referred to as the site specificity of periodontal disease.
• Sites of periodontal destruction are often found next to sites with
little or no destruction.
• Therefore, the severity of periodontitis increases with the
development of new disease sites and with the increased breakdown
of existing sites.
40. PULP CHANGES ASSOCIATED
WITH PERIODONTAL POCKETS
• The spread of infection from periodontal pockets may cause pathologic
changes in the pulp.
• Such changes may give rise to painful symptoms, or they may adversely
affect the response of the pulp to restorative procedures.
• Involvement of the pulp in periodontal disease occurs through either
the apical foramen or the lateral pulp canals after pocket infection
reaches them.
41. RELATIONSHIP OF ATTACHMENT LOSS AND BONE
LOSS TO POCKET DEPTH
• The severity of the attachment loss in pocket formation is generally but
not always correlated with the depth of the pocket.
• The degree of attachment loss depends on the location of the base of
the pocket on the root surface, whereas pocket depth is the distance
between the base of the pocket and the crest of the gingival margin.
• Pockets of the same depth may be associated with different degrees of
attachment loss.
• pockets of different depths may be associated with the same amount
of attachment loss
• The severity of bone loss is generally but not always correlated with
pocket depth
42.
43. AREA BETWEEN BASE OF POCKET AND ALVEOLAR
BONE
• The distance between the apical extent of calculus and the alveolar
crest in human periodontal pockets is most constant, having a mean
length of 1.97 mm (±33.16%).
• The distance from attached plaque to bone is never < 0.5 mm and
never > 2.7 mm
• These finding suggest that the bone-resorbing activity induced by the
bacteria is exerted within these distances.
46. DETECTION OF POCKETS
Careful exploration with a periodontal probe.
Periodontal probe and its use was first described by: F.V Simoton of the
university of California, San Francisco, 1925
Goldman et al stated that “clinical probing with suitable periodontal
instruments such as William calibrated probe is a prime necessity in
delineating the depth, topography & character of the periodontal
pocket”
47. Pockets are not detected by radiographic examination.
Radiographs indicate areas of bone loss in which pockets may be
suspected, but they do not show pocket presence or depth, and
consequently they show no difference before and after pocket
elimination unless bone has been modified.
Gutta-percha points or calibrated silver points can be used with the
radiograph.
48. POCKET PROBING
•The distance between the gingival margin and
the base of the pocket
•This can be measured only in carefully prepared
and adequately oriented histologic sections
The biologic
depth
•The distance to which a probe penetrates into
the pocket
Probing
depth
49. PROBE PENETRATION
Probe penetration can vary, depending on the force of introduction, the shape and
size of the probe tip, the direction of penetration, the resistance of the tissues, the
convexity of the crown, and the degree of tissue inflammation & the accuracy of
the examiner in reading the probe measurement.
50. • Probe penetration varies with the degree of health and disease at the
probing site.
• For example:
a) In healthy specimens, the probe tends to fall short of the apical
termination of the epithelial attachment by an average of 0.4mm
b) In experimental gingivitis, the probe tends to fall short of apical
termination of the epithelial attachment by an average of 0.2 mm
c) In periodontitis specimen, the probe tends to go past the apical
termination of the epithelial attachment by an average of 0.2mm.
The depth of penetration of the probe in the CT apical to JE
in a periodontal pocket is about 0.3mm
51. PROBING FORCE
• Probing is performed with very light pressure of not more than one
or two ounces of force.
• It has been suggested that probe forces between 20 and 25 g (i.e.,
0.20–0.25 N) cause minimal discomfort and still enable accurate
diagnostic readings
Polson et al., 1980; Garnick et al., 1989; Armitage et al., 1977
2nd generation probes: pressure sensitive probes (20gm)
Forces of up to 30 g, the tip of the probe remains within the junctional
epithelium, whereas forces of up to 50 g are necessary to reach the bone
level.
52.
53. PROBING TECHNIQUE
The probe should be inserted parallel to the vertical axis of the tooth and
“walked” circumferentially around each surface of each tooth to detect the
areas of deepest penetration
54. - Rose, Mealey, Genco, Cohen
Probing involves “stepping” a calibrated periodontal probe
around the tooth and recording the deepest point at each of 6
tooth surfaces
55. • To detect an interdental crater, the probe should be placed obliquely
from both the facial and lingual surfaces to explore the deepest point
of the pocket located beneath the contact point.
• Furcation involvement: Nabers probes
58. BLEEDING ON PROBING
• To test for bleeding after probing, the probe is carefully introduced to
the bottom of the pocket and gently moved laterally along the pocket
wall.
• Sometimes bleeding appears immediately after the removal of the
probe
• It may be delayed for a few seconds. Therefore, the clinician should
recheck for bleeding 30 to 60 seconds after probing.
• When bleeding is present in multiple sites of advanced disease,
bleeding on probing is a good indicator of progressive attachment loss
59. WHEN TO PROBE?
• The purpose of this initial probing, together with the clinical and
radiographic examination, is to determine whether the tooth should be
saved or extracted.
• After the patient has performed adequate plaque control for some
time and the calculus has been removed, the major inflammatory
changes disappear, and an accurate probing of the pockets can be
performed
• The purpose of this second probing is to accurately establish the level
of attachment and the degree of involvement of roots and furcations.
• Later during periodontal treatment, probings are done to determine
changes in pocket depth and to ascertain healing progress after
different procedures
60. PROBE ANGULATION
• Standardization of the probe tip (i.e., <1 mm) and the addition of
registration stents to maintain reproducible probe angulation
• The Florida Probe System: 3rd generation probe (15gms & precision
of 0.2mm)
The end of the probe is 0.4 mm, and it reciprocates through a sleeve
that provides a reference by which measurements are made.
61. • The automatic probe appears to underestimate deep probing depths
but to show less variability than conventional probing.
• The automatic probe also has the problem of providing little tactile
sensitivity, thereby making it more difficult to “walk” the probe.
• INTER PROBE: Flexible probe tip which curves
with the tooth as the probe enters the pocket area.
62. 5th generation probe: US PROBE
Accurately measure the attachment levels without penetrating the JE
Small intraoral ultrasound beam projection area gives the image of the
periodontal ligament space
THERMAL PROBE: Perio Temp probe
Sensitive diagnostic devices used for measuring early inflammatory changes in
the gingival tissue.
Enables the calculation of temperature differential between pocket probed &
its subgingival temperature.
Subgingival temperature at diseased site is increased compared with healthy
sites
Mandibular sites were reported to be warmer than maxillary sites
Temperature increases with increase in probing depth
64. CONCLUSION
• Periodontal pocket formation is the first step in periodontal
breakdown cascade.
• Periodontal breakdown is dependent on rate of disease
progression which varies among individuals.
• Understanding the etiopathogenesis, histopathology & progression
of periodontal pockets is essential to provide the patient with the
successful treatment outcomes and monitoring the response to
therapy
65. REFERENCES
• Carranza’s clinical periodontology, 11th & 12th edition
• Grant, Stern, Listgarten. Periodontics. 6th edition
• K.H & E.M Ratietschak, H.F Wolf, T.M Hassell; Clour atlas of
periodontology
• Takashi Takata and Karl Donath; The Mechanism of Pocket Formation A
Light Microscopic Study on Undecalcified Human Material; J. Periodontol.
April, 1988
• Georg Hillmann, Somi Dogan, and Werner Geurtsen. Histopathological
Investigation of Gingival Tissue From Patients With Rapidly Progressive
Periodontitis; J Periodontol, February 1998.
• Jerry J Garnick & Lee Silverstein. Periodontal probing: probe tip diameter; J
of Periodontol, Jan 2000
• Louis F Rose, Brian L. Mealey, Robert J. Genco, D. Walter Cohen:
Periodontics: medicine, surgery & implants.
• Internet sources
