periodontics

1. PERIODONTAL POCKET
PRESENTED BY
DR AKHIL.S
FIRST YEAR POSTGRADUATE

2. CONTENTS
 INTRODUCTION
 CLASSIFICATION
 CLINICAL FEATURES
 PATHOGENESIS
 HISTOPATHOLOGY
 PERIODONTAL DISEASE ACTIVITY
 SITE SPECIFICITY
 PULP CHANGES ASSOCIATED WITH PERIODONTAL POCKET
 RELATIONSHIP OF ATTACHMENT LOSS AND BONE LOSS TO POCKET
DEPTH
 AREA BETWEEN BASE OF THE POCKET AND ALVEOLAR BONE
 RELATIONSHIP OF POCKET TO BONE
 PERIODONTAL ABSCESS
 LATERAL PERIODONTAL CYST
 PERIODONTAL POCKET PROBING
 CONCLUSION
 REFERENCES

3. INTRODUCTION
DEFINITION
The periodontal pocket is defined as a pathologically
deepened gingival sulcus, is one of the most important
clinical features of the periodontal disease.
-Fermin A. Carranza

4. CLASSIFICATION
Deepening of the gingival sulcus occur by coronal
movement of gingival margin, apical displacement of the
gingival attachment, or a combination of the two
processes.
Pockets can be classified as:
1. Gingival Pocket (Pseudopocket) – formed by gingival
enlargement without destruction of the underlying
tissues. The sulcus is deepened because of the increased
bulk of the gingiva.
2. Periodontal Pocket– it occurs with destruction of
supporting periodontal tissues leading to loosening and
exfoliation of the teeth.

5. Two types of periodontal pockets exist :
a) Suprabony (Supracrestal or Supraalveolar) - In this,
bottom of the pocket is coronal to the underlying
alveolar bone.
b) Intrabony (Infrabony, Subcrestal or intraalveolar) -
In this, bottom of the pocket is apical to the level of
the adjacent alveolar bone and the lateral pocket wall
lies between the tooth surface & alveolar bone.

6. Periodontal pockets can also be classified-
According to involved tooth surface
a) Simple
b) Compound
c) Complex or Spiral – originating on one surface and
twisting around the tooth to involve one or more
additional surfaces ( most commonly found in
furcation area)

7. Depending upon the nature of the soft tissue wall of the
pocket
a) Edematous Pocket
b) Fibrotic Pocket
Depending upon disease activity
a) Active Pocket
b) Inactive Pocket

9. CLINICAL FEATURES
SIGNS
1) Bluish red, thickened marginal gingiva.
2) A bluish red vertical zone from the gingival margin to
alveolar mucosa.
3) Gingival bleeding and suppuration.
4) Tooth mobility.
5) Diastema formation.
6) A rolled edge separating the gingival margin from the
tooth surface.
7) A break in the facio-lingual continuity of interdental
gingiva.
8) Shiny, puffy gingiva leads to exposed root surface.

10. SYMPTOMS
1) Localized pain or “pain deep in the bone”.
2) Usually painless but may give rise to localized /
radiating pain or sensation of pressure after eating
which gradually reduces.
3) A foul taste in localized areas.
4) Sensitivity to hot & cold.
5) Toothache in the absence of caries is also sometimes
present.
6) A tendency to suck material inter proximally.
7) Feeling of itching in the gums.
8) Urge to dig a pointed instrument in the gums.
9) Feeling of loose teeth.

11. CORRELATION OF CLINICALAND HISTOPATHOLOGIC
FEATURES OF PERIODONTAL POCKETS
CLINICAL FEATURES
1. Bluish red discoloration of gingival
pocket wall
2. Flaccidity
3. Smooth and shiny surface
4. Pitting on pressure
5. Less frequently gingival wall may
be pink and firm
6. Bleeding on gentle probing
7. Inner wall of pocket is painful
8. Pus discharge on applying digital
pressure
HISTOPATHOLOGIC FEATURES
1. Circulatory stagnation
2. Destruction of gingival fibers and
surrounding tissue
3. Atrophy of epithelium
4. Edema and degeneration
5. Fibrotic changes predominate over
exudation and degeneration
6. Increased vascularity, thinning of
epithelium and proximity of engorged
vessels to inner surface
7. Ulceration of inner aspect of pocket wall.
8. Suppurative inflammation of inner wall

12. PATHOGENESIS
The initial lesion in the development of Periodontitis in
response to a bacterial challenge is inflammation of the
gingiva.
Changes involved in the transition from the normal
gingival sulcus to pathologic periodontal pocket are as
follows:
 The local inflammatory reaction, in response to bacteria in the
dental biofilm, is characterized by an initial increase in blood flow.
This enhances vascular permeability and the influx of cells from
the peripheral blood to the gingival crevice.

13. PMNs or neutrophils are attracted to the area by other
bioactive molecules (e.g., IL-8) migrate through the
epithelial lining of the gingival sulcus to be the initial
defense .
There is an increase in the number of monocytes
/macrophages, as well as an influx of T and B cells to the
area.

14. Once activated by cytokines, bioactive molecules and
MAMPs (microbial-associated molecular pattern) present
in the area, infiltrating cells produce other inflammatory
mediators that modulate and affect homeostasis of
nonmineralized and mineralized tissues in the
periodontium.
Cytokines responsible for early responses to microbial
aggression include IL-1α, IL-1β,IL-6, and TNF-α.

15. Patients with periodontal inflammation have high
concentrations of TNF-α, IL-1β, RANKL, and MMP-13
in the gingivalcrevicular fluid (GCF).
To destroy potential intruders, polymorphonuclear
leukocytes release proteases, prostaglandins and other
inflammation-enhancing molecules.
Plasma cells develop from B cells and produce
antibodies in response to bacterial antigens and
mitogens.

16. In a typical gingival lesion, T cells predominate.
T-helper cell subsets (Th1 or Th2) develop from T cells
depending on the types and amount of cytokines released.
Th1 cells predominate in stable periodontal lesions, but a
strong presence of Th2 cells indicates a shift towards
lesion progression, with a predominance of plasma cells.

17. MMPs are a family of neutral proteases that are
zinc/calcium-dependent with an essential role in
extracellular matrix (ECM) turnover and degradation.
MMP-13 expression was positively correlated with the
severity of inflammation.

18. As periodontal disease progresses, the collagen fibers and
connective tissue attachment to the tooth are destroyed.
The junctional epithelial cells proliferate apically along
the root surface.

19. There are two mechanisms of collagen loss
1) Collagenases & other enzymes secreted by various cells
such as fibroblasts, PMNs, leukocyte & macrophages,
becomes extracellular and destroy collagen; these
enzymes that degrade collagen and other matrix macro
molecules into small peptides are called matrix
metalloproteinases.
2) Fibroblasts phagocytize collagen fibers by extending
cytoplasmic process to the ligament-cementum interface
and degrade the inserted collagen fibrils and the fibrils of
the cementum matrix.

20. After collagen loss, apical cells of Junctional Epithelium
proliferate along the root, extending finger like projections
two or three cells in thickness
↓
Coronal portion of Junctional Epithelium detaches from the
roots as the apical portion migrates
↓
As a result of inflammation PMNs invades the coronal end
of Junctional Epithelium and when relative volume
becomes approx. 60% or more of the Junctional
Epithelium, the tissue looses cohesiveness & detaches
from the tooth surface

21. The transformation of a gingival sulcus into a
periodontal pocket creates an area where plaque removal
becomes impossible and following feedback mechanism
is established:-
Plaque
Accumulation
Gingival
Inflammation
Pocket
Formation
Area difficult
to clean

22. HISTOPATHOLOGY
Once the pocket is formed, several microscopic features
are present:
Changes in the soft tissue wall
The connective tissue is edematous & densely infiltrated
with plasma cells, lymphocytes & a scattering of PMNs.
Blood vessels are increased in number, dilated and
engorged particularly in the subepithelial connective
tissue layer.
Connective tissue exhibit varying degrees of
degeneration.

23. The connective tissue shows proliferation of endothelial
cells with newly formed capillaries, fibroblasts and collagen
fibres.
The Junctional Epithelium at the base of the pocket is
usually much shorter than that of a normal sulcus and
usually coronoapical length of junctional epithelium is
reduced to only 50-100 m.

24. Changes along the lateral wall
The epithelium presents striking proliferative &
degenerative changes .
Epithelial buds or interlacing cords of epithelial cells
project from lateral wall into adjacent inflamed
connective tissue & may extend farther apically to
Junctional Epithelium.
These epithelium projection and remainder of lateral
epithelium are densely infiltrated by Leukocytes and
edema from the inflamed connective tissue.

25. These cells can undergo degeneration and rupture to
form vesicles.
Progressive degeneration & necrosis of epithelium lead
to Ulceration of lateral wall,Exposure of inflamed
connective tissue and suppuration.

26. The severity of degenerative changes are not necessarily
related to pocket depth.
Ulceration may occur in shallow pockets and deep
pockets with intact lateral epithelium.
The Epithelium at the gingival crest of a periodontal
pocket is generally intact & thickened, with prominent rete
pegs.

27. Bacterial Invasion
Occurs along the lateral & apical areas of the pocket in
cases of chronic periodontitis.
Filaments, Rods & coccoid organisms with predominent
gram-negative cell walls have been found in intercellular
spaces of epithelium.

28. Hillmann et al reported presence of Porphyromonas
gigivalis and Prevotella intermedia in the gingiva of
Aggressive Periodontitis cases.
Actinobacillus actinomycetumcomitans (AA) has also
been found in the tissues.

29. Bacteria may invade intercellular space under
exfoliating epithelial cells but also found between deeper
epithelial cells and accumulating on the basement
lamina.
Some bacterial traverse the basement lamina and invade
the subepithelial connective tissue.

30. Microtopography of the gingival wall
SEM reveals several areas in the soft tissue wall of the
pocket where different types of activity take place.
These areas are irregularly oval or elongated and adjacent
to one another and measure about 50-200 micrometer.

31. The pocket wall is the constantly changing as a result of
interaction between host and bacteria. Following areas
have been noted-:
1) Area of relative quiescence
2) Area of bacterial accumulation
3) Areas of emergence of leukocyte
4) Areas of Leukocyte-bacteria interaction
5) Areas of intense epithelial desquamation
6) Areas of ulcerations
7) Areas of haemorrhage

32. Scanning electron frontal micrograph of the periodontal pocket wall. Different areas
can be seen in the pocket wall surface. A, Area of quiescence; B, bacterial
accumulation; C, bacterial-leukocyte interaction; D, intense cellular desquamation

33. 1) Area of relative quiescence: Shows relatively flat surface
with minor depressions & mounds and occasional
shedding of cells.
2) Area of bacterial accumulation: which appear as
depression on the epithelial surface with abundant debris
and bacterial clumps penetrating into the enlarged
intercellular spaces. These Bacteria are mainly rods, cocci,
filamentous & a few spirochetes.
3) Areas of emergence of leukocyte: leucocyte appear in the
pocket wall through holes located in the intercellular
spaces.

34. 4) Areas of Leukocyte-bacteria interaction:
Numerous leukocytes are present & covered with bacteria
in an apparent process of phagocytosis.
Bacterial plaque associated with the epithelium is seen
either as an organised matrix covered by a fibrin like
material in contact with the surface of cells or as bacteria
penetrating into the intercellular spaces.
5) Areas of intense epithelial desquamation: consist of
semi-attached & folded epithelial squames, sometimes
partially covered with bacteria.

35. 6) Areas of ulcerations with exposed connective tissue.
7) Areas of haemorrhage with numerous erythrocytes.

36. The transition from one area to another could result from:
Bacterial accumulation in previously quiescent areas
↓
Triggering the emergence of leukocytes
↓
Leukocyte-bacteria interaction
↓
Lead to intense Epithelial desquamation
↓
Finally to ulceration & haemorrhage

37. PERIODONTAL POCKET AS A HEALING LESIONS
Periodontal pocket are chronic
inflammatory lesion and thus
constantly undergoing repair.
Complete healing does not occur
because of persistence of the
bacterial attack which continues to
stimulate an inflammatory
response, causing degeneration of
the new tissues formed in
continuous effort at repair.

38. There are destructive and constructive tissue changes and
their balance determines the clinical features as color,
consistency & surface texture of the pocket wall.
If Inflammatory fluid & cellular exudate predominate, the
pocket wall is bluish-red, soft, spongy and friable, with a
smooth, shiny surface, at the clinical level and this is
referred to as an edematous pocket wall.

39. If there is predominance of
newly formed connective
tissue cells & fibers, the
pocket wall is more firm and
pink, and known as fibrotic
pocket wall.

40. 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 & subgingival
plaque.

41. In some cases inflammation and ulceration on inside of
the pocket are walled off by fibrous tissue on the outer
aspects.
Externally the pocket appears pink and fibrotic, despite
the inflammatory changes occurring internally.

42. POCKET CONTENTS
Periodontal pocket contains;
Debris (consisting of microorganism & their products
mainly enzymes, endotoxins and other metabolic product)
Gingival fluid
Food remnants
Salivary mucin
Desquamated epithelial cells & Leukocytes

43. Plaque covered calculus projects from tooth surface.
If purulent exudate present: consists of–
Living, degenerated and necrotic leukocytes
Living and dead bacteria
Serum
A scant amount of fibrin

44. Significance Of Pus Formation
Pus is common feature of periodontal diseases, but it is
only a secondary sign.
The presence of pus or ease with which it can be expressed
from the pocket merely reflects nature of the inflammatory
changes in the pocket wall.

45. 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.

46. ROOT SURFACE WALLS
The root surface wall of periodontal pocket often undergoes
changes that are significant because they may perpetuate the
periodontal infection, causing pain, and complicate
periodontal treatment.

47. As the pocket deepens, collagen fibers embedded in the cementum are destroyed
↓
Cementum become exposed to the oral environment
↓
Remanants of Sharpey’s fibers in the cementum undergo degeneration
↓
Creating a favorable environment for bacterial penetration
↓
Penetration and growth of bacteria leads to fragmentation and breakdown of the
cementum surface
↓
Result in area of necrotic cementum, separated from the tooth by mass of bacteria

48. Decalcification And Remineralisation Of Cementum
Areas of increased mineralization
Probably a result of an exchange, on exposure to the oral
cavity, of minerals and organic components at the
cementum- saliva interface.
The mineral content of exposed cementum increases.
The minerals that are increased in diseased root surfaces
include Ca, Mg, P & F.
Micro hardness remains unchanged.
The development of highly mineralized superficial layer
may increase the tooth resistance to decay.

49. Areas of demineralization/Root carries
Exposure to oral fluid and bacterial plaque results in
proteolysis of the embedded remnants of the Sharpey's
fibres.
The cementum may be softened & may undergo
fragmentation and cavitation.
Unlike Enamel caries, root surface caries tend to progress
around rather than into the tooth.

50. Active
Well defined yellowish/
Light brown areas
Frequently covered by
plaque have softened or
leathery consistency on
probing
Inactive
Well defined darken
lesion with a smooth
surface
Harder consistency on
probing
Root caries lesion

51. Caries of the cementum require 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 extended into dentin.
The dominant microorganism in root surface caries is
Actinomyces viscosus.
Quirynen et al reported that when plaque levels and
pocket depths decrease after periodontal therapy (both
nonsurgical 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.

52. Areas of cellular resorption of cementum and dentin
They are common in roots unexposed by periodontal
diseases.
They are of no significance because they are symptom
free and as along as the root is covered by the periodontal
ligament, they are likely to undergo repair.

53. Surface Morphology Of Tooth Wall
The following zones can be found in the bottom of a
periodontal pocket:
1.Cementum covered by calculus
2. Attached Plaque – covers calculus and extends apically
from it to a variable degree (100-500 m).
3.The zone of unattached plaque Surround attached plaque
& extends apically to it.

54. 4. The zone of attachment of Junctional Epithelium to the
tooth – this zone reduced to 100 m (in periodontal pocket)
from 500 m found in normal sulcus.
5. A zone of semi-destroyed connective tissue fibres – apical
to the JE.

56. PERIODONTAL DISEASE ACTIVITY
According to the concept of periodontal disease activity,
periodontal pockets go through;
1. PERIODS OF QUIESCENCE OR INACTIVITY
Characterized by a reduced inflammatory response & little
or no loss of bone and connective tissue attachment.
A build up of unattached plaque with its gram-negative,
motile and anaerobic bacteria.

57. 2. PERIODS OF EXACERBATION OR ACTIVITY
Bone and connective tissue attachment are lost and the
pocket deepens.
This period may lasts for days, weeks, months & eventually
followed by a period of remission or quiescence in which
gram-positive bacteria proliferate and a more stable
condition is established.

58. Clinical features: Shows bleeding spontaneously or on
probing and greater amount of gingival exudates.
Histological Features : Pocket epithelium appears thin and
ulcerated, infiltrate composed of plasma cells & PMN
leukocytes.

59. 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.
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 increased
breakdown of existing sites.

60. PULP CHANGES ASSOCIATED WITH
PERIODONTAL POCKET
Spread of infection from periodontal pockets may cause
pathologic changes to the pulp.
It may give rise to painful symptoms.
Involvement of the pulp may occur through either the
apical foramen or the lateral canals.
Atrophic and inflammatory pulpal changes may occur in
such cases.

61. RELATION OF ATTACHMENT LOSS & BONE
LOSS TO POCKET DEPTH
Pocket formation leads to loss of attachment of gingiva &
denudation of root surface.
The severity of attachment loss in pocket formation is
generally but not always correlated with the depth of the
pocket.

62. The degree of attachment loss depends on the location
of base of pocket on the root surface.
Whereas pocket depth is the distance between the base
of the pocket & the crest of the gingival margin.
Pockets of same depth may be associated with different
degrees of attachment loss and pockets of different
depths may be associated with same amount of
attachment loss.

64. Excessive attachment & bone loss may be associated
with shallow pocket if the attachment loss is
accompanied by recession of gingival margin, and slight
bone loss can occur with deep pockets.

65. AREA BETWEEN THE BASE OF THE
POCKET AND BONE
Normally the distance between the apical end of the
Junctional epithelium & alveolar bone is relatively
constant.
The distance between apical extent of calculus & alveolar
crest in periodontal pocket is most constant,having a
mean length of 1.97mm (± 33.16%).
The distance from attached plaque to bone is never less
than 0.5 mm and never more than 2.7 mm.

66. RELATIONSHIP OF POCKET TO BONE
INTRABONY POCKET
Base of the pocket is apical to the crest of alveolar bone,
and the pocket wall lies between the tooth and the bone.
Mostly occur interproximally but may be located on facial
and lingual tooth surfaces.
The bone destructive pattern is vertical/Angular.
On facial and lingual surface, the periodontal fibres follow
angular pattern of adjacent bone.

67. SUPRABONY POCKET
Base of pocket is coronal to the level of alveolar bone.
Pattern of destruction of underlying bone is horizontal.
The transseptal fibers are arranged horizontal in space
between base & alveolar bone.
On the facial and lingual surface, PDL fibers beneath pocket
follow their normal horizontal-oblique pattern.

68. PERIODONTAL ABSCESS
 A periodontal abscess is a localized purulent
inflammation in the periodontal tissue. It is also known
as lateral abscess or parietal abscess.

69. Abscess localized in gingiva, caused by injury to the outer
surface of the gingiva, and not involving the supporting
structure are called gingival abscesses.

70. 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. Formation of the abscess results when
drainage into the pocket space is impaired.

71. 3. Formation in a pocket 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. The gingival wall shrinks, occluding
the pocket orifice, and a periodontal abscess occurs in the
sealed-off portion of the pocket.
5. After trauma to the tooth or with perforation of the
lateral wall of the root in endodontic therapy.

72. Periodontal abscesses are classified according to location as
follows:
1. Abscess in the supporting periodontal tissues along the
lateral aspect of the root.
2. Abscess in the soft tissue wall of a deep periodontal
pocket.

73. Microscopically, an abscess is a localized accumulation of
viable and 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.

74. 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.

75. LATERAL PERIODONTAL CYST
The periodontal cyst is an uncommon lesion.
 Localized destruction of the periodontal tissues along a
lateral root surface.
Most often in the mandibular canine-premolar area.
It is considered to be derived from rests of Malassez or
other proliferating odontogenic rests.
usually asymptomatic, without grossly detectable
changes, but it may present as a localized, tender
swelling.

76. 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.

77. Microscopically, the cystic lining may be
1. A loosely arranged, thin, nonkeratinized, epithelium,
sometimes with thicker proliferating areas or
2. An odontogenic keratocyst.

78. PERIODONTAL POCKET PROBING
The only reliable method of locating periodontal pockets
and determining their extent is careful probing along each
tooth surface. There are two different pocket depths:-
Biologic or Histologic depth :- is the distance between the
gingival margin and the base of the pocket (the coronal
end of the junctional epithelium.
Clinical or probing depth :- Is the distance from the
gingival margin to which a probe penetrates in to the
pocket.

79. The probing force of 0.75 N or 25 gm have been
found to be well tolerated and accurate

80. In normal sulcus, the probe penetrates about one third to
one half the length of junctional epithelium.
In periodontal pocket with a short junctional epithelium
the probe penetrates beyond the apical end of junctional
epithelium.

81. “Walking” the probe to explore the entire pocket

82. Vertical insertion of the probe (Left) may not detect
interdental craters, oblique positioning of the probe
(Right) reaches the depth of the crater.
Vertical Oblique

83. The depth of penetration of a probe in a pocket
depends on:
1. Size of the probe
2. Force with which it is introduced
3. Direction of penetration
4. Resistance of the tissues
5. Convexity of the crown

84. LIMITATIONS OF RADIOGRAPH
The 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.

85. Gutta Percha points or Calibrated Silver points can be
used with radiograph to assist in determining the level of
attachment of periodontal pocket.

86. CONCLUSION
Increased probing depth and loss of clinical attachment level
are pathognomonic of periodontitis and therefore pocket
probing is crucial and mandatory procedure in diagnosing
periodontal disease and treating it.
Currently the gold standard is measuring longitudinal
attachment from CEJ or relative attachment level from a
fixed reference point ,reduction of pocket depth or gain in
clinical attachment is used to determine the success of
treatment .
Thus the periodontal treatment should be aimed at removal
or elimination of the periodontal pocket thus creating a
maintainable environment for the patient and prevent further
progression of the disease.

87. REFERENCES
 Carranza’s Clinical periodontology, 11th edition.
Hefti AF. Periodontal probing. Critical Reviews in Oral
Biology & Medicine. 1997 Jul; 8(3):336-56.
Armitage GC, Svanberg GK, Loe H. Microscopic
evaluation of clinical measurements of connective tissue
attachment levels. Journal of Clinical Periodontology
1977; 4:173.
Solanki G. A General Overview of Periodontal Pockets
International Journal of Biomedical Research 3[03]
[2012]127‐130.
Essentials of Clinical Periodontology and Periodontics-
Shantipriya Reddy, Third Edition.
Periodontics Revisited -Shalu Bathla, First Edition.