PERIODONTAL POCKET

1. PERIODONTAL POCKET
MOHAMED HARIS. P.M.
READER
MALABAR DENTAL COLLEGE

2. Contents
• Introduction
• Definition
• Classification
• Clinical features
• Pathogenesis
• Histopathology
• Microtopography of gingival wall
• Periodontal pockets as healing lesions
• Root surface wall
• Pocket contents
• Periodontal disease activity

3. • Relation of attachment loss and bone loss to pocket depth
• Periodontal abscess
• Periodontal cyst
• Detection of pocket
• Conclusion
• References

4. Introduction
• Chronic periodontitis is defined as plaque induced inflammation of
periodontal tissue which has resulted in destruction of periodontal
ligament,loss of crestal alveolar bone,and apical migration of epithelial
attachment (junctional epithelium).
• These process are usually collectively known as loss of attachment.
• Periodontitis is characterized by the presence of inflammation at the
marginal gingiva,together with loss of attachment, which normally results
in the formation of periodontal pocket and often reffered to as destructive
periodontal disease.
• It is always preceeded by gingivitis,but not all gingivitis progresses to
periodontitis.
• If the sulcus depth extends beyond 3mm it is known as pocket.
• It is one of the most important clinical feature in periodontal diseases

5. • Periodontal pocket is defined as pathologically deepened gingival sulcus.
• Deepening of gingival sulcus may occur by coronal movement of the
gingival margin,apical displacement of gingival attachment or combination
of both.
• It is bordered by the tooth on one side,by ulcerated epithelium on the other
and has the junctional epithelium at its base

6. CLASSIFICATION
Depending upon its morphologic characteristics:
• Gingival pocket (pseudo pocket) : formed by gingival enlargement
without destruction of the underlying periodontal tissues.
The sulcus is deepened because of the increased bulk of the gingiva
• Periodontal pocket(absolute/true pocket): This type of pocket
occurs with destruction of the supporting periodontal tissues.
Progressive pocket deepening leads to destruction of the supporting
periodontal tissues and loosening and exfoliation of the teeth.

7. Depending upon its relationship to crestal bone periodontal pocket classified as:
Suprabony/Supracrestal/Supra-alveolar pocket
Infrabony/intrabony/subcrestal/intra-alveolar pocket
Gingival pocket Suprabony pocket Infrabony pocket

8. Compound pocket
- Two or more tooth surfaces were involved.
- Base of the pocket in direct communication
with the gingival margin along each of
the involved surfaces .
• Depending upon the number of surfaces involved
Simple pocket
- It involves only one tooth surface

9. Complex pocket
- Spiral pocket that orginates on one tooth surface
and twists around the tooth to involve one or
more additional surfaces.
- Their only communication with the gingival margin
is at the surface where pocket originates.
- More commonly observed in furcation areas
• Depending upon nature of soft tissue wall of pocket
- Edematous pocket
- Fibrotic pocket
• Depending upon the disease activity
- Active pocket
- Inactive pocket

10. DIFFERENCES BETWEEN SUPRABONY & INFRABONY
POCKETS
Suprabony
• Base of the pocket is coronal to the
crest of alveolar bone
• Pattern of bone destruction is
Horizontal
• Inter proximally the transseptal
fibers are restored horizontally
during progressive periodontal
disease in the space between the
base of the pocket and crest of the
alveolar bone
Infrabony
• Base of the pocket is apical to the
crest of the alveolar bone so that the
bone is adjacent to soft tissue wall
• Pattern of bone destruction is
angular/vertical
• Inter proximally the transseptal
fibers are restored obliquely and
they extend from the cementum
below the base of the pocket along
alveolar bone over the crest of the
cementum of the adjacent tooth

11. • On the facial and lingual surfaces
the principal fibers beneath the
pocket follow their normal
horizontal oblique course between
the tooth and the bone
• On the facial and lingual surfaces
the principal fibers beneath the
pocket follow angular pattern of
the adjacent bone

12. CLINICAL FEATURES
Signs
- Enlarged bluish red marginal gingiva with a rolled edge separated from the
tooth
- Reddish blue vertical zone extending from the marginal gingiva to attached
gingiva and sometimes into alveolar mucosa
- Break in the faciolingual continuity of the interdental gingiva
- Shiny, discolored, and puffy gingiva
- Gingival bleeding
- Purulent exudate of the marginal gingiva in response to digital pressure
- Mobility, extrusion, and migration of teeth
- Development of diastema

13. Symptoms
- Periodontal pockets are generally painless but may give rise to the following
symptoms
- Localized pain or sensation of pressure after eating which gradually
diminishes
- Foul taste in localized areas
- Tendency to suck material in the interproximal spaces
- Radiating pain deep in the bone
- A gnawing feeling or feeling of itchiness in the gums and urge to dig
pointed instrument into gums and relief obtained from resultant bleeding
- Food stick between teeth or teeth feel loose or preference to eat on the other
side
- Sensitivity to heat and cold
- Toothache in the absence of caries

14. CORRELATION OF CLINICAL AND HISTOLOGIC
FEATURES OF PERIODONTAL POCKET
The gingival wall of periodontal
pocket presents:
• Varying degrees of bluish red
discoloration
• Flaccidity
• Smooth , shiny surface
• Pitting on pressure
Circulatory stagnation
Destruction of gingival fibers and
surrounding tissues
Atrophy of epithelium and edema
Edema and degeneration of connective
tissue

15. • Gingival wall may be pink and
firm
• Bleeding is elicited by gently
probing the soft tissue wall of
pocket
• When explored with a probe
inner aspect of pp generally
painful
Fibrotic changes predominate over
exudation and degeneration
particulatly in relation to outer
surface of the pocket wall.
Increased vascularity
Thinning and degeneration of epithelium
Proximity of engorged vessels to inner
surface
Pain upon tactile stimulation
due to Ulceration of the inner
aspect of the pocket wall

16. • Pus may be expressed by
applying digital pressure Pockets with suppurative inflammation of
the inner wall

17. Theories of the pathogenesis of periodontal pockets
1) Destruction of the gingival fibers is a prerequisite for the initiation of
pocket formation. (Fish)
2) The initial change in pocket formation occurs in the cementum.
(Gottlieb)
3) Stimulation of the epithelial attachment by inflammation rather than
destruction of gingival fibers is a prerequisite for the formation of
periodontal pocket.(Aisenberg)
4) Pathologic destruction of epithelial attachment due to infection or trauma
is the initial histologic change in pocket formation.(Skillen)
5) 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)

18. 6) Pocket formation initiated with defect in the sulcus wall.(Becks)
7) 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)
8) Two – stage pocket formation (James and Counsell)
- Proliferation of the subgingival epithelium (epithelial attachment)
- Loss of superficial layers of proliferated epithelium which produces
space or pocket.
9) Inflammation is the initial change in the formation of periodontal
pocket.(J. Nuckolls)
10) Pathologic epithelial proliferation occurs secondary to non inflammatory
degenerative changes in the periodontal membranes.

19. Most accepted recent concept is that the apical migration of apical cells of
junctional epithelium and deattachment of coronal portion of junctional
epithelium leads to intraepithelial cleft and pocket formation and
deepening.

20. Pathogenesis
• The initial lesion in the development of periodontitis is the inflammation of
the gingiva in response to a bacterial challenge.
• Changes involved in the transition from the normal gingival sulcus to the
pathologic periodontal pocket are associated with different proportions of
bacterial cells in dental plaque.
• Healthy gingiva is associated with few microorganisms, mostly coccoid
cells and straight rods.
• Pathologic changes that leads to the deepening of the gingival sulcus may
occur by:
- Movement of gingival margin in the direction of crown(produces gingival
pocket).
- Migration of junctional epithelium apically and its seperation from the
tooth surface.
- Combination of above processes.
• Diseased gingiva is associated with increased numbers of spirochetes and
motile rods.

23. • Pocket formation starts as an inflammatory change in the connective tissue wall
of the gingival sulcus.
• The cellular and fluid inflammatory exudate causes degeneration of the
surrounding connective tissue, including the gingival fibers.
• Just apical to the junctional epithelium, collagen fibers are destroyed and the
area becomes occupied by inflammatory cells and edema.
• Immediately apical to this is a zone of destruction and an area of normal
attachment.
• Earlier concept assumed that after the initial bacterial attack ,periodontal tissue
destruction continued to be linked to bacterial action.
• Recently it was established that host immunoinflammatory response to the
initial and persistant bacterial attack unleashes mechanism that lead to collagen
and bone destruction.
• These mechanism are related to various cytokines,some produced normally by
cells in noninflammed tissue and others by cells involved in the inflammatory
process such as polymorphonuclear leukocytes (PMNs),monocytes and other
cells leading to collagen and bone destruction.

25. • The two mechanism associated with collagen loss are:
(1) Collagenases and other enzymes secreted by various cells in healthy and
inflamed tissue such as fibroblasts ,polymorphonuclear leukocytes, and
macrophages become extra cellular and destroy collagen(these enzymes
that degrade collagen and other matrix macromolecules into small peptides
are called matrix metalloproteinases) and
(2) Fibroblasts phagocytize collagen fibers by extending cytoplasmic
processes to the ligament-cementum interface and degrade the inserted
collagen fibrils and the fibrils of the cementum matrix .
• As a consequence of the loss of collagen, the apical cells of the junctional
epithelium proliferate along the root, extending fingerlike projections 2-3
cells in thickness.
• As a result of inflammation, polymorphonuclear neutrophils (PMNs)
invade the coronal end of the junctional epithelium in increasing numbers.
• When the relative volume of PMNs reaches approximately 60% or more of
the junctional epithelium, the tissue loses cohesiveness and detaches from
the tooth surface.

26. • Thus the coronal portion of the junctional epithelium detaches from the
root as the apical portion migrates sulcus bottom shifts apically, and the
oral sulcular epithelium occupies a gradually increasing portion of the
sulcular (pocket) lining.
• Extension of the junctional epithelium along the root requires the presence
of healthy epithelial cells.
• Marked degeneration or necrosis of the junctional epithelium retards rather
than accelerates pocket formation.
• Degenerative changes seen in the junctional epithelium at the base of
periodontal pockets are usually less severe than those in the epithelium of
the lateral pocket wall.
• Because migration of the junctional epithelium requires healthy, viable
cells, it is reasonable to assume that the degenerative changes seen in this
area occur after the junctional epithelium reaches its position on the
cementum.

27. • With continued inflammation, the gingiva increases in bulk, crest of the
gingival margin extends coronally and the junctional epithelium continues
to migrate apically along the root and seperates from it.
• The transformation of a gingival sulcus into a periodontal pocket creates an
area where plaque removal becomes impossible.
• The rationale for pocket reduction is based on the need to eliminate areas of
plaque accumulation.

28. Histopathology
Soft Tissue Wall
• The connective tissue is edematous and densely infiltrated with plasma
cells (approximately80%),lymphocytes, and a scattering of PMNs.
• The blood vessels are increased in number, dilated, and engorged,
particularly in the sub epithelial connective tissue layer.
• It exhibits varying degrees of degeneration.
• Single or multiple necrotic foci are occasionally present.
• Connective tissue also shows proliferation of the endothelial cells with
newly formed capillaries,fibroblasts and collagen fibers.
• The junctional epithelium at the base of the pocket is usually much shorter
than that of a normal sulcus.
• Marked reduction in the length width and condition of epithelial cells,
usually the coronoapical length of the junctional epithelium is reduced to
only 50 to 100μm.

29. • The most severe degenerative changes in the periodontal pocket occur
along the lateral wall and the epithelium of the lateral wall of pocket
presents striking proliferative and degenerative changes.
• Progressive degeneration and necrosis of the epithelium lead to ulceration
of the lateral wall, exposure of the underlying inflamed connective tissue,
and suppuration.
• Ulceration of lateral wall may occur in shallow pockets and deep pockets
are occasionally observed in lateral epithelium is relatively intact or shows
only slight degeneration.
• Epithelium at the gingival crest of periodontal pocket is generally intact
and thickened with prominent rete pegs.

30. Bacterial invasion
• Filaments, rods, and coccoid organisms with predominant gram-negative cell
walls have been found in intercellular spaces of the epithelium.
• Presence of P gingivalis and Prevotella intermedia in the gingiva of
aggressive periodontitis cases and A a has also been found in the tissues.
• Bacteria may invade the intercellular space under exfoliating epithelial cells,
but they are also found between deeper epithelial cells and accumulating on
the basement lamina.
• Some bacteria may traverse the basement lamina and invade the subepithelial
connective tissue.
• The presence of bacteria in the gingival tissues has been interpreted by
different investigators as bacterial invasion or as passive translocation of
plaque bacteria.
• It has significant clinicopathologic implications and has not yet been
clarified.

31. Microtopography of the Gingival Wall of the Pocket
• These areas are irregularly oval or elongated and adjacent to one another
and measure about 50 to 200 µm.
• These findings suggest that the pocket wall is constantly changing as a
result of the interaction between the host and the bacteria.
Following areas are:
• Areas of relative quiescence, showing a relatively flat surface with minor
depressions and mounds and occasional shedding of cells.
• Areas of bacterial accumulation, These bacteria are mainly cocci, rods,
and filaments, with a few spirochetes.
• Areas of emergence of leukocytes, where leukocytes appear in the pocket
wall through holes located in the intercellular spaces.
• Areas of leukocyte-bacteria interaction, where numerous leukocytes are
present and covered with bacteria in an apparent process of phagocytosis.
-Bacterial plaque associated with epithelium is seen either as an organized
matrix covered by a fibrinlike material in contact with surface of cells or as
bacteria penetarting into the intercelleular spaces.

32. • Areas of intense epithelial desquamation,shows semi attached and folded
epithelial squames with one end attached to the pocket wall surface and other
other end free towards the pocket space
• Area of ulceration, occasionally seen surrounded by areas of
hemorrhage.Bottom of ulcer shows exposed collagen fibers and various
connective tissue cells.
• Areas of hemorrhage, with numerous erythrocytes seen.

33. A= Area of quiescence
B= Area of bacterial accumulation
C= Areas of leukocyte – bacteria interaction
D=Areas of intense epithelial desquamation

34. • The transition from one area to another could be postulated as follows:
- Bacteria accumulate in previously quiescent areas, triggering the
emergence of leukocytes and the leukocyte-bacteria interaction.
- This would lead to intense epithelial desquamation and finally to ulceration
and hemorrhage

35. Mechanism of tissue destruction
• Inflammatory response triggered by bacterial plaque unleashes a complex
cascade of events aimed at destroying and removing bacteria,necrotic cells
and deletorious agents.
• This process is non specific and in the attempt to restore health,hosts
cell,such as neutrophils,macrophages,fibroblats,epithelial cells and produce
proteinases,cytokines and prostoglandins that can damage or destroy the
tissues.

36. Periodontal Pockets as Healing Lesions
• Periodontal pockets are chronic inflammatory lesions and as are constantly
undergoing repair.
• Complete healing does not occur because of the persistence of the bacterial
attack, which continues to stimulate an inflammatory response, causing
degeneration of the new tissue elements formed in the continuous effort at
repair.
• The condition of the soft tissue wall of the periodontal pocket results from the
interplay of the destructive and constructive tissue changes.
• Their balance determines clinical features such as color, consistency, and
surface texture of the pocket wall.
• If the inflammatory fluid and cellular exudate predominate, the pocket wall is
bluish red, soft, spongy, and friable, with a smooth, shiny surface at the clinical
level known as edematous pocket wall.
• If there is a relative predominance of newly formed connective tissue cells and
fibers, the pocket wall is more firm and pink and clinically known fibrotic
pocket wall

37. • Edematous and fibrotic pockets represent opposite extremes of the same
pathologic process, not different disease entities.
• They are subject to constant modification, depending on the relative
predominance of exudative and constructive changes.
• Fibrotic pocket walls may be misleading because they do not necessarily
reflect what is taking place throughout the pocket wall.
• The most severe degenerative changes in periodontal tissues occur adjacent
to the tooth surface and subgingival plaque.
• In some cases, inflammation and ulceration inside of the pocket are walled
off by fibrous tissue on the outer aspect.
• Externally the pocket appears pink and fibrotic, despite the inflammatory
changes occurring internally.

38. Root Surface Wall
• The root surface wall of periodontal pockets often undergoes changes that
are significant because they may perpetuate the periodontal infection, cause
pain, and complicate periodontal treatment.
• As the pocket deepens, collagen fibers embedded in the cementum are
destroyed creating an environment favorable to the penetration of bacteria.
• Viable bacteria have been found in the roots of 87% of periodontally
diseased noncarious teeth.
• Bacterial penetration into the cementum can be found as deep as the
cementodentinal junction and may also enter the dentinal tubules.
• Penetration and growth of bacteria leads to fragmentation and breakdown
of cementum surface and results in areas of necrotic cementum ,seperated
from the tooth by masses of bacteria.
• Bacterial products such as endotoxins,have been detected in the cementum
wall of periodontal pockets.

39. • These changes are manifested clinically by softening of the cementum
surface, which is usually asymptomatic but painful when a probe or
explorer penetrates the area.
• They also constitute a possible reservoir for reinfection of the area after
treatment.
• During the treatment, these necrotic areas are removed by root planning
until a hard smooth surface is reached.

40. Root cementum suffers
• Structural
• Chemical and
• Cytotoxic changes
Structural changes –
• Presence of pathologic granules: may represent areas of collagen
degeneration or areas where collagen fibrils have not been fully
mineralized initially.
• Decalcification and Remineralization of Cementum.
- Areas of increased mineralization
- Areas of demineralization
- Areas of cellular resorption and dentin

41. • Areas of increased mineralization are probably a result of an exchange, on
exposure to the oral cavity,of minerals and organic components at the
cementum saliva interface.
• Chemical changes:The mineral content of exposed cementum increases .
• Minerals are increased in diseased root surfaces: calcium," magnesium
phosphorus, and fluoride .
• Microhardness, remains unchanged.
• The development of a highly mineralized superficial layer may increase the
tooth resistance to decay.
• Absorption property of cementum could be harmful if absorbed materials
are toxic to the surrounding tissues

42. • The hypermineralized zones are detectable by electron microscopy and are
associated with increased perfection of the crystal structure and organic
changes suggestive of a subsurface cuticle .
• No decrease in mineralization was found in deeper areas, indicating that
increased mineralization does not come from adjacent areas.
• A loss of, or reduction in, the cross-banding of collagen near the cementum
surface and a subsurface condensation of organic material of exogenous
origin are seen

43. • Areas of demineralization are commonly related to root caries.
• Exposure to oral fluid and bacterial plaque results in proteolysis of the
embedded remnants of Sharpey's fibers; the cementum may be softened and
may undergo fragmentation and cavitation.
• Active root caries lesions appear as well-defined yellowish or light-brown
areas, are frequently covered by plaque, and have a softened or leathery
consistency on probing.
• Inactive lesions are well-defined darker lesions with a smooth surface and a
harder consistency on probing.
• The dominant microorganism in root surface caries is Actinomyces viscosus,
although its specific responsibility in the development of the lesion has not
been established and other bacteria such as Actinomyces naeslundii,
Streptococcus mutans, Streptococcus salivarius, Streptococcus sanguis, and
Bacillus cereus have been found to produce root caries in animal models.

44. Quirynen et aI (1999) reported that when plaque levels and pocket depths
fall after periodontal therapy (both conservative and surgical), a shift in oral
bacteria occurs, leading to a reduction in periodontal pathogens and an
increase in S. mutans and the development of root caries.
Katz RV (1984) conducted an prevalence rate study of root caries in 20- to
64-year-old individuals and revealed that 42% had one or more root caries
lesions and that these lesions tended to increase with age

45. • The tooth may not be painful, but exploration of the root surface reveals the
presence of a defect, and penetration of the involved area with a probe causes
pain.
• Caries of the root, may lead to pulpitis, sensitivity to sweets and thermal
changes, or severe pain.
• Pathologic exposure of the pulp occurs in severe cases.
• Root caries may be the cause of toothache in patients with periodontal disease
and no evidence of coronal decay.
• 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.
• Bacterial endotoxins may penetrate deep into the cementum of untreated
periodontally involved teeth.
• Endotoxins limits the proliferation and attachment of fibroblasts to the
diseased root surfaces.
• Thus this cementum may act to perpetuate the destructive effects of periodontal
disease,by acting as a reservoir for potentially destructive products.

46. • Areas of cellular resorption of cementum and dentin are common in roots
unexposed by periodontal disease .
• These areas are of no particular significance because they are asymptomatic
and as long as the root is covered by the periodontal ligament, they are apt
to undergo repair.
• If the root is exposed by progressive pocket formation before repair of such
areas occurs, these appear as isolated cavitations that penetrate into the
dentin.
• These areas can be differentiated from caries of the cementum by their
clear-cut outline and hard surface.
• They may be sources of considerable pain, requiring the placement of a
restoration.

47. Surface morphology of tooth wall
Following zones are:
1.Cementum covered by calculus
2. Attached plaque, which covers calculus and extends apically from it to a
variable degree, probably 100 to 500 µm.
3. The zone of unattached plaque that surrounds attached plaque and extends
apically to it.
4. The zone where the junctional epithelium is attached to the tooth.
The extension of this zone, which in normal sulci is more than 500 µm, is
usually reduced in periodontal pockets to less than 100 µm.
5. Apical to the junctional epithelium, there may be a zone of semidestroyed
connective tissue fibers.

48. • Areas 3, 4, and 5 compose the so-called plaque-free zone seen in extracted
teeth.
• The total width of the plaque-free zone varies according to the type of tooth
(it is wider in molars than in incisors) and the depth of the pocket (it is
narrower in deeper pockets).
• It is important to remember that the term plaque-free zone refers only to
attached plaque because unattached plaque contains a variety of gram-
positive cocci and various gram-negative morphotypes including cocci,
rods, filaments, fusiforms, and spirochetes.
• The most apical zone contain predominantly gram-negative rods and cocci

50. Pocket Contents
• Periodontal pockets contain debris consisting principally of
microorganisms and their products (enzymes, endotoxins, and other
metabolic products), gingival fluid, food remnants, salivary mucin,
desquamated epithelial cells, and leukocytes.
• Plaque-covered calculus usually projects from the tooth surface.
• Purulent exudate, if present, consists of living, degenerated, and necrotic
leukocytes; living and dead bacteria; serum; and a scant amount of fibrin.
• The contents of periodontal pockets filtered free of organisms and debris
have been demonstrated to be toxic when injected subcutaneously into
experimental animals

51. • Pus is a common feature of periodontal disease, but it is only a secondary
sign.
• It merely reflects the nature of the inflammatory changes in the pocket
wall.
• It is not an indication of the depth of the pocket or the severity of the
destruction of the supporting tissues.
• Extensive pus formation may occur in shallow pockets, whereas deep
pockets may exhibit little or no pus.

52. Periodontal disease activity
• More recently, as a result of studies on the specificity of plaque bacteria,
the concept of periodontal disease activity has evolved.
• According to this concept, periodontal pockets go through periods of
exacerbation and quiescence, resulting from episodic bursts of activity
followed by periods of remission.
• Periods of quiescence are characterized by a reduced inflammatory
response and little or no loss of bone and connective tissue attachment.
• Buildup of unattached plaque, with its gram-negative, motile, and
anaerobic bacteria,starts a period of exacerbation in which bone and
connective tissue attachment are lost and the pocket deepens.
• This period may last for days, weeks, or months and is eventually followed
by a period of remission or quiescence in which gram-positive bacteria
proliferate and a more stable condition is established.
• These periods of quiescence and exacerbation are also known as periods of
inactivity and periods of activity

53. • Clinically, active periods show 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,polymorphonuclear
leukocytes,or both are seen.
• Bacterial samples from the pocket lumen, analyzed with darkfield
microscopy, show high proportions of motile organisms and spirochetes.
• Over time, bone loss detected radiographically.

54. Episodic pattern of chronic periodontitis
Socransky et al (1984) had conducted a longitudinal clinical study and
recorded clinical attachment loss at individual sites in different subjects
over time periods ranging from 2-5 years.
They have revealed that despite the presence of inflammation,most sites
showed no progression during the study period.
Instead,attachment loss occurred at only a few sites and even at these sites
was interspersed with long periods of stability or quiscence.
This type of episodic,site specific attachment loss has given rise to burst
theory of chronic periodontitis.
It has further proposed that these bursts might occur randomly through out
an individuals life(random burst) or there may be periods when bursts of
periodontal breakdown in many sites are more likely (asynchronous
multiple burst).

55. Implications of burst theories are:
1. Gingival inflammation at a site may not indicate that further periodontal
breakdown is occuring or that it will occur at a later date.
2. Periodontal disease is site-specific and may affect different teeth in the same
mouth at different rates.
3. Full-mouth periodontal charting on a regular basis is necessary to identify
sites with attachment loss,to determine the pattern and rate of progression and
to determine the patients susceptibility.
4. Individual serial radiograph based on findings in periodontal charting may be
needed to confirm disease progression but radiographs must not be repeated
without a sound cause and therefore must be based on clinical evidence.
5. Each tooth must be considered seperately for treatment.
In these studies ,only large changes ≥ 3mm of clinical attachment level could
be reliably measured and smaller changes could not be detected.
These studies show clearly that site specific,episodic disease progression does
occur they do not preclude other patterns of progression including slow
regular progression also occuring.
Episodic progression would predominate in susceptible patients with more
rapid rates of progression

56. Site specificity
• Periodontal destruction does not occur in all parts of the mouth at the same time but
rather on a few teeth at a time or even only some aspects of some teeth at any given
time.
• This is referred to as the site specificity of periodontal disease.
• It is most commonly found on the sites of periodontal destruction next to sites with
little or no destruction.
• Severity of periodontitis increases by the development of new disease sites and
with the increased breakdown of existing sites.
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 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 canals in the root after infection spreads from the pocket
through the periodontal ligament.
• Atrophic and inflammatory pulpal changes occur in such cases
• Servere breakdown of pulp is seen only when periodontal pocket extends to the
pocket.

57. Relation of attachment loss and bone loss to pocket depth
• Pocket formation causes loss of attachment of the gingiva and
denudation of the root surface.
• The severity of the attachment loss is generally, but not always,
correlated with the depth of the pocket.
• This is because the degree of attachment loss depends on the
location of the base of the pocket on the root surface, whereas the
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 and pockets of different depths may be associated
with the same amount of attachment loss.
• Severity of bone loss is generally, but not always, correlated with
pocket depth.
• Extensive attachment and bone loss may be associated with shallow
pockets if the attachment loss is accompanied by recession of the
gingival margin, and slight bone loss can occur with deep pockets.

59. Area between the base of the pocket and the alveolar bone
• Normally, the distance between the apical end of the junctional epithelium
and the alveolar bone is relatively constant.
• 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%.
• Distance from attached plaque to bone is never less than 0.5 mm and not
more than 2.7 mm.
• These findings suggest that the bone-resorbing activity induced by the
bacteria is exerted within these distances.
• Finding of isolated bacteria, clumps of bacteria, or both in the connective
tissue and on the bone surface may modify these considerations

60. Relationship of the periodontal pocket to bone
• The inflammatory, proliferative,and degenerative changes in intrabony and
suprabony pockets are the same, and both lead to destruction of the
supporting periodontal tissues.
• The principal differences between intrabony and suprabony pockets are the
relationship of the soft tissue wall of the pocket to the alveolar bone, the
pattern of bone destruction, and the direction of the transseptal fibers of the
periodontal ligament.

62. PERIODONTALABSCESS
• A periodontal abscess is a localized purulent inflammation in the
periodontal tissues .
• It is also known as a lateral or parietal abscess.
• Abscesses localized in the gingiva, caused by injury to the outer surface of
the gingiva, and not involving the supporting structures are called gingival
abscesses.
• They may occur in the presence or absence of a periodontal pocket.
• Periodontal abscess formation may occur in the following ways:
1. Extension of infection from a periodontal pocket deeply into the
supporting periodontal tissues and localization of the suppurative
inflammatory process along the lateral aspect of the root.
2. Lateral extension of inflammation from the inner surface of a periodontal
pocket into the connective tissue of the pocket wall.
Localization of the abscess results when drainage into the pocket space is
impaired.

63. 3. Formation of pocket that with a tortuous course around the root, a
periodontal abscess may form in the cul-de- sac, the deep end of which is
shut off from the surface.
4. Incomplete removal of calculus during treatment of a periodontal pocket.
Gingival wall shrinks, occluding the pocket orifice, and a periodontal
abscess occurs in the sealed-off portion of the pocket.
5. A periodontal abscess may occur in the absence of periodontal disease
after trauma to the tooth or perforation of the lateral wall of the root in
endodontic therapy.

64. • Periodontal abscesses are classified according to location as follows:
1. Abscess in the supporting periodontal tissues along the lateral aspect of the
root. In this condition, a sinus generally occurs in the bone that extends
laterally from the abscess to the external surface.
2. Abscess in the soft tissue wall of a deep periodontal pocket
• Bacterial invasion of tissues seen in abscesses; the invading organisms
were identified as gram negative cocci, diplococci, fusiforms, and
spirochetes.
• Invasive fungi were also found and were interpreted as being opportunistic
invaders.
• Microorganisms that colonize the periodontal abscess have been reported to
be primarily gram-negative anaerobic rods.
• Based on the nature/or duration:
Acute & Chronic

65. MICROSCOPIC FEATURES
• An abscess is a localized accumulation of viable & nonviable PMNs within
the periodontal pocket wall.
• The PMNs liberate enzymes that digest the cells and other tissue structures,
forming the liquid product known as pus, which constitutes the center of
the abscess.
• An acute inflammatory reaction surrounds the purulent area, and the
overlying epithelium exhibits intracellular and extracellular edema and
invasion of leukocytes.
• The localized acute abscess becomes a chronic abscess when its purulent
content drains through a fistula into the outer gingival surface or into the
periodontal pocket and the infection causing the abscess is not resolved.

66. ACUTE PERIODONTAL ABSCESS
SIGNS:
• An ovoid elevation of the gingiva along the lateral aspect of the root.
• Red & edematous gingiva with a smooth, shiny surface.
• Varied shape & consistency- dome like and relatively firm, or pointed and
soft.
• In most cases pus may be expressed from the gingival margin with gentle
digital pressure.
SYMPTOMS:
• Throbbing, radiating pain
• Exquisite tenderness of the gingiva to palpation
• Sensitivity of the tooth to palpation
• Tooth mobility
• Lymphadenitis
• Less frequently systemic effects such as-
fever, leukocytosis, malaise.

67. CHRONIC PERIODONTAL ABSCESS
SIGNS:
• A sinus opening onto the gingival mucosa seen along the length of the root.
• The orifice of the sinus may appear as a difficult-to-detect pinpoint
opening, which, when probed, reveals a sinus tract deep in the
Periodontium.
• The sinus may be covered by a small, pink, bead like mass of granulation
tissue.
SYMPTOMS:
• Usually asymptomatic.
• May have a history of intermittent exudation.
• Patient may report episodes of-
dull, gnawing pain,
slight elevation of the tooth,
a desire to bite down on and grind
the tooth.
• Chronic periodontal abscess often undergoes acute exacerbations with all
the associated symptoms.

68. Diagnosis: of the periodontal abscess requires correlation of the history and
clinical and radiographic findings.
• The suspected area should be probed carefully along the gingival margin in
relation to each tooth surface to detect a channel from the marginal area to
the deeper periodontal tissues.
• Continuity of the lesion with the gingival margin is clinical evidence that
the abscess is periodontal.
• The abscess is not necessarily located on the same surface of the root as the
pocket from which it is formed.
• Pocket at the facial surface may give rise to a periodontal abscess
interproximally.
• It is common for a periodontal abscess to be located at a root surface other
than that along which the pocket originated, because drainage is more
likely to be impaired when a pocket follows a tortuous course

69. PERIODONTAL CYST
It is an uncommon lesion that produces localized destruction of the periodontal
tissues along a lateral root surface, most often in the mandibular canine
premolar area .
The following possible etiologies have been suggested:
1.Odontogenic cyst caused by proliferation of the epithelial rests of
Malassez;the stimulus initiating the cellular activity is not known.
2. Lateral dentigerous cyst retained in the jaw after tooth eruption.
3. Primordial cyst of supernumerary tooth germ.
4. Stimulation of epithelial rests of the periodontal ligament by infection from
a periodontal abscess or the pulp through an accessory root canal.
• A periodontal cyst is usually asymptomatic and without grossly detectable
changes, but it may present as a localized tender swelling.
• Radiographically, an interproximal periodontal cyst appears on the side of
the root as a radiolucent area bordered by a radiopaque line.
• Its radiographic appearance cannot be differentiated from that of a
periodontal abscess

70. DETECTION OF POCKETS
• The only accurate method of detecting and measuring periodontal pockets
is careful exploration with a periodontal probe.
• They are are not detected by radiographic examination.
• Periodontal pocket is a soft tissue change.
• Radiographs indicate areas of bone loss where pockets may be suspected;
they do not show pocket presence or depth, and consequently they show no
difference before or after pocket elimination unless bone has been
modified.
• Gutta percha points or calibrated silver points can be used with the
radiograph to assist in determining the level of attachment of periodontal
pockets.
• They may be used effectively for individual pockets or in clinical research,
but their routine use throughout the mouth would be difficult to manage.
• Clinical examination and probing are more direct and efficient

71. POCKET PROBING
• The two different pocket depths are (1) biologic or histologic depth and (2)
clinical or probing depth.
• The biologic depth is the distance between the gingival margin and the base
of the pocket (the coronal end of the junctional epithelium).
• This can be measured only in carefully prepared and adequately oriented
histologic sections.
• The probing depth is the distance to which an instrument (probe) penetrates
into the pocket.
• The depth of penetration of a probe in a pocket depends on factors such as
size of the probe,force with which it is introduced, direction of penetration,
resistance of the tissues, and convexity of the crown.
• Probe penetration can vary depending on the degree of tissue inflammation.

72. • In humans, the probe tip penetrates to the most coronal intact fibers of the
connective tissue attachment .
• The depth of penetration of the probe in the connective tissue apical to the
junctional epithelium in a periodontal pocket is about 0.3 mm.
• This is important in evaluating differences in probing depth before and
after treatment, as the reduction in probe penetration may be a result of
reduced inflammatory response rather than gain in attachment .
• The probing forces have been explored by several investigators forces of
0.75 N have been found to be well tolerated and accurate.
• Interexaminer error (depth discrepancies between examiners) was reported
to be as much as 2.1 mm, with an average of 1.5 mm, in the same areas.

73. 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.
• special attention should be directed to detecting the presence of interdental
craters and furcation involvements.
• To detect an interdental crater, the probe should be placed obliquely from
both the facial and lingual surfaces so as to explore the deepest point of the
pocket located beneath the contact point.
• In multirooted teeth the possibility of furcation involvement should be
carefully explored.
• The use of specially designed probes (e.g., Nabers probe) allows an easier
and more accurate exploration of the horizontal component of furcation
lesions.

75. Level of attachment versus pocket depth.
• Pocket depth is the distance between the base of the pocket and the gingival
margin.
• It may change from time to time even in untreated periodontal disease
owing to changes in the position of the gingival margin, and therefore it
may be unrelated to the existing attachment of the tooth.
• The level of attachment is the distance between the base of the pocket and a
fixed point on the crown, such as the cementoenamel junction.
• Changes in the level of attachment can be due only to gain or loss of
attachment and afford a better indication of the degree of periodontal
destruction.
• Shallow pockets attached at the level of the apical third of the root connote
more severe destruction than deep pockets attached at the coronol third of
the roots

76. Determining the level of attachment
• When the gingival margin is located on the anatomic crown, the level of
attachment is determined by subtracting from the depth of the pocket the
distance from the gingival margin to the cementoenamel junction.
• If both are the same, the loss of attachment is zero.
• When the gingival margin coincides with the cementoenamel junction, the
loss of attachment equals the pocket depth.
• When the gingival margin is located apical to the cementoenamel junction,
the loss of attachment is greater than the pocket depth, and therefore the
distance between the cementoenamel junction and the gingival margin
should be added to the pocket depth.

77. BLEEDING ON PROBING.
• The insertion of a probe to the bottom of the pocket elicits bleeding if the
gingiva is inflamed and the pocket epithelium is atrophic or ulcerated.
• Noninflamed sites rarely bleed.
• In most cases, bleeding on probing is an earlier sign of inflammation than
gingival color changes"
• Depending on the severity of inflammation, bleeding can vary from a
tenuous red line along the gingival sulcus to profuse bleeding.
• After successful treatment, bleeding on probing ceases.
• 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 removal of the probe; other
times it may be delayed a few seconds.
• Therefore the clinician should recheck for bleeding 30 to 60 seconds after
probing.

78. • As a single test, bleeding on probing is not a good predictor of progressive
attachment loss; however its absence is an excellent predictor of
periodontal stability.'
• When present in multiple sites of advanced disease, bleeding on probing is
a good indicator of progressive attachment loss.'"
• Armitage (1996), performed a meta-analysis of the various studies and
concluded that the presence of bleeding on probing in a "treated and
maintained patient population" is an important risk predictor for increased
loss of attachment.

79. WHEN TO PROBE:
• Probing of pockets is done at various times for diagnosis, and for monitoring
the course of treatment and maintenance.
• The initial probing of moderate or advanced cases is usually hampered by the
presence of heavy inflammation and abundant calculus and cannot be done
very accurately.
• The purpose of this initial probing, together with the clinical and radiographic
examination is done, however, with the main purpose of determining whether
the tooth can be saved or should be extracted.
• After the patient has performed an adequate plaque control for some time and
calculus has been removed, the major inflammatory changes disappears, and a
more accurate probing of the pockets can be performed.
• This second probing is for the purpose of accurately establishing the level of
attachment and degree of involvement of roots and furcations.Data obtained
from this probing provides valuable information for treatment decisions.
• Periodontal treatment probings are done to determine changes in pocket depth
and to ascertain healing progress after different procedures

80. PROBING AROUND IMPLANTS
• Since periimplantitis can create pockets around implants, probing around
them becomes part of examination and diagnosis.
• To prevent scratching of the implant surface, plastic periodontal probes
should be used instead of the usual steel probes used for the natural
dentition.

81. Matuliene G et al (2008) conducted a retrospective cohort study , 172
patients were examined after Active periodontol therapy and supportive
periodontal therapy (SPT) for 3-27 years (mean 11.3 years ) and
investigated the influence of residual PPD >or=5 mm and bleeding on
probing (BOP) after active periodontal therapy on the progression of
periodontitis and tooth loss.
Results showed that the number of residual PPD increased during SPT.
Compared with PPD<or=3 mm, PPD=5 mm represented a risk factor for
tooth loss.
At patient level, heavy smoking, initial diagnosis, duration of SPT and
PPD>or=6 mm were risk factors for disease progression, while PPD>or=6
mm and BOP>or=30% represented a risk for tooth loss.
They concluded that residual PPD>or=6 mm represent an incomplete
periodontal treatment outcome and require further therapy.

82. Armitage et al (1977) evaluated the penetration of probe in healthy
beagle,dogs specimen using a standardized force of 25gms.
They concluded that probe penetrated the epithelium to about 2/3 rd of its
length in healthy specimens, it stopped 0.1 mm short of its apical end in
gingivitis specimens and in periodontitis specimens probs tips went past the
most apical cells of the junctional epithelium.
Thus penetration varies depending on the force of introduction and degree
of tissue inflammation.

83. Glauser WM et al (1982) conducted a study on block biopsies comprising
dental and gingival tissues taken from the buccal side of 8 beagle dogs
between the age of 1-4 years following the application of cotton floss
ligatures for periods of 4 to 21 days or upto 5 months.
The tissues were processed for light and electromicroscopic examination.
The observation revealed that the pocket epithelium:
1.does not attach to the tooth
2.forms irregular ridges and over connective tissue paipllae,thin covering
which occasionally ulcerate
3.consisits of cells only some of which show a tendency to differentiate
4.presents a basal lamina complex which discontinuities and multiplications
5.infiltrated mainly by T and B lymphocytes and plasma cells and is
transmigrated by neutrophilic granulocytes.

84. Methods of pocket therapy
The methods for pocket therapy can be classified under three main headings:
1. New attachment techniques offer the ideal result because they eliminate
pocket depth by reuniting the gingiva to the tooth at a position coronal to
the bottom of the preexisting pocket.
- New attachment is usually associated with filling in of bone and
regeneration of periodontal ligament and cementum.
2. Removal of the pocket wall is the most common method.
The wall of the pocket consists of soft tissue and may also include bone in
the case of intrabony pockets. It can be removed by the following:
• Retraction or shrinkage, in which scaling and root planing procedures
resolve the inflammatory process and the gingiva therefore shrinks,
reducing the pocket depth.

85. Surgical removal performed by the gingivectomy technique or by means of
an undisplaced flap.
• Apical displacement with an apically displaced flap.
3. Removal of the tooth side of the pocket, which is accomplished by tooth
extraction or by partial tooth extraction (hemisection or root resection)

86. Conclusion
• Periodontal pocket is an area that is inaccessible for plaque removal resulting
in the establishment of following feedback mechanism for further plaque
buildup:
Plaque gingival inflammation periodontal inflammation
periodontal pocket formation more plaque build up.
• Bacterial factors which might result in disease progression include an
increase in total no of bacteria,the presence or overgrowth of specific
pathogenic bacteria in the flora or direct invasion of the tissues by bacteria.
• The rationale of treatment of a pocket ( reduction or elimination) is to
establish a periodontal environment where bacterial plaque can be easily
removed and free form plaque.

87. References
• Clinical Periodontology ( Carranza 8th,10th and 11th edition.)
• Pathology of periodontal diseases.David.M.Williams.
• Periodontics.Grant , Stern & Everett .5th edition
• Contemporary periodontics.Genco,Goldman and Cohen
• Outline of periodontics.JD Manson and BM Eley.5th Edition
• Armitage GC,Svanberg GK,Loe H.Microscopic evaluation of clinical
measurements and connective tissue attachment levels.J Clin Periodontol
1977;4:173.

88. • Glauser WM,Schroeder HE.The Pocket Epithelium.A Light and
Electronmicroscopic Study.J Periodontol 1982;53:133.
• Matuliene G,Pjetursson BE,Schmidlin K, Bragger U,Zwahlen M,Lang
NP.Influence of residual pockets on progression of periodontitis and tooth
loss:Results after 11 years of maintenance.J Clin Periodontol 2008;35:685-
695.

89. Thank you