GOOD MORNING

PERIODONTAL POCKET
 CONTENTS

 Definition  Pulp changes associated with

 Classification
 Clinical Features
 Theories of pocket formation
 Pathogenesis
 Histopathology
 Periodontal Disease Activity
periodontal pockets
 Relationship Of attachment loss
and bone loss to pocket depth
 Area between base of the
pocket and alveolar bone
 Conclusion
 References
 INTRODUCTION
 The anatomic space between the tooth's neck and the circumferential gingival tissue is known as the
gingival sulcus.
 Pathologically deepened pocket referred to as periodontal pocket occurs when this shallow crevice deepens
due to apical migration of junctional epithelium accompanied by attachment loss as a result of the
periodontal disease process.
 In order to establish better preventive measures and therapeutic outcomes for the treatment of this disease
process, a comprehensive insight into the development and advancement of periodontal pockets is
necessary.
 DEFINITION

 Pocket is derived from French word ; Pochette; a cul- de-sac or

pouch like cavity.

 Periodontal pocket is defined as a pathologically deepened gingival

sulcus and is one of the most important clinical features of
periodontal disease. -Carranza 13th edition
 Gingival pocket: A pathologically deepened gingival crevice that does
not involve loss of connective tissue attachment. Frequently observed
when there is gingival enlargement.
- (Glossary of Periodontal terms, 2001)

 Periodontal Pocket is defined as “A pathologic fissure between a tooth

and the crevicular epithelium, and limited at its apex by the junctional
epithelium. It is an abnormal apical extension of the gingival crevice
caused by migration of the junctional epithelium along the root as the
periodontal ligament is detached by a disease process.
-(Glossary of Periodontal terms, 2001)
Deepening of gingival sulcus may be due to :
1. Coronal movement of the gingival margin
2. Apical displacement of the gingival attachment
or
3. Combination of the two processes.
Classification
1. ACCORDING TO THE MORPHOLOGY:
 GINGIVAL POCKET
 (PSEUDOPOCKET/FALSE/RELATIVE):
 Formed by gingival enlargement
without destruction of the underlying
periodontal tissues.
 Pathological changes are confined to
the gingival compartment.
 Sulcus is deepened because of the
increase bulk of the gingiva.
 PERIODONTAL POCKET :
 (TRUE POCKET OR ABSOLUTE POCKET)
 Forms with the destruction of the
supporting periodontal tissues.
 Progressive pocket deepening leads to
destruction of the supporting periodontal
tissues and loosening and exfoliation of
the teeth.
 The pathological changes have reached
beyond the confines of the gingival
compartment; its base has advanced
apically.
v
 Detachment of junctional epithelial cells and inflammation : gingival and
periodontal pockets.

 In a gingival pocket inflammation and destruction of the

underlying periodontal tissues together with coronal detachment of
junctional epithelial cells but without bone destruction.

 In a periodontal pocket, bone destruction by osteoclastic resorption

is a characteristic feature beyond inflammation, tissue destruction and
detachment of junctional epithelium.
2. BASED ON THE LOCATION OF THE BASE OF THE
POCKET IN RELATION TO THE UNDERLYING BONE:

Suprabony (Supracrestal or supraalveolar):

 The bottom of the pocket is coronal to the alveolar bone crest.
 It is seen along with horizontal bone loss.
Intrabony (Infrabony, subcrestal or intraalveolar):
 In which the bottom of the pocket is apical to the level of the adjacent
alveolar bone.
 The lateral pocket wall lies between the tooth surface and alveolar bone.
Different types of periodontal pockets

Gingival
Suprabony pocket Intrabony pocket
pocket
 DISTINGUISHING FEATURES OF SUPRABONY AND INTRABONY POCKETS

Suprabony pocket Intrabony pocket

1. Base of the pocket 1. Base of the pocket
is coronal to the level of the alveolar is apical to the crest of the alveolar
bone. bone so that the bone is adjacent to
the soft tissue wall.

2. Pattern of bone destruction is 2. Pattern of bone destruction is

horizontal. vertical (angular).
3. Interproximally: transseptal fibres
are arranged horizontally in the space
between the base of the pocket and the
alveolar bone.
3. Interproximally: transseptal fibres
are oblique rather than horizontal.
Extend from the cementum beneath the
base of the pocket along the bone and
over the crest of the cementum of the
adjacent tooth.

4. On the facial and lingual surfaces:

the PDL fibres beneath the pocket 4. On the facial and lingual surfaces:
follow their normal horizontal-oblique the PDL fibres beneath the pocket
course between the tooth and the bone. follow the angular pattern of the
adjacent bone.
3. According to the involvement of tooth surfaces:

1. Simple Pocket: Pocket may involve only one tooth surface. (free
communication between the base of the pocket and the surface.)

2. Compound Pocket: Two or more tooth surfaces are involved.

• direct communication between the base of the pocket and the gingival
margin on each of the involved surface.

3. Complex Pocket: It is a spiral originating on one tooth surface and

twisting around the tooth to involve one or more additional surfaces. The
only communication with the gingival margin is at the surface where the
pocket originates.
• most common in furcation areas.
 Classification of pockets according to involved tooth surfaces

Simple pocket Compound pocket Complex pocket

4. Depending on the disease activity, there are

• Active pockets.
• Inactive pockets.
NOMENCLATURE OF DEFORMITIES OF THE ALVEOLAR
PROCESS(KARN ET AL 1984)
The proposed system of nomenclature for bony deformities caused by nonuniform loss of bone is based on the
following basic terms:

crater—A crater is formed as a result of loss of alveolar bone and a portion of the contiguous
supporting alveolar bone from only one surface of a tooth.

trench—when such bone loss (see above) affects two or three confluent surfaces of the same tooth.

moat—involves all four surfaces of a tooth, it is described as a moat.

ramp—describes a deformity that results when both alveolar bone and its supporting bone are lost to
the same degree in such a manner that the margins of the deformity are at different levels.

plane—This term is applied when both alveolar bone and supporting bone is lost to the same degree
such that the margins of the deformity are at the same level.
Karn KW, Shockett HP, Moffitt WC, Gray JL. Topographic classification of
deformities of the alveolar process. J Periodontol. 1984 Jun;55(6):336-40.
 CLINICAL FEATURES

Clinical signs
1. Enlarged bluish red marginal gingiva with a rolled edge separated from
the tooth surface.
2. A reddish-blue discoloration of the gingival margin seen extending upto
the attached gingiva.
3. A break in the continuity of the interdental gingiva.
• Shiny, discoloured, puffy gingiva
associated with exposed root surface.

• Gingival bleeding on gentle probing.

• Purulent exudate (pus) appears

spontaneously or on application of
digital pressure.

• Looseness, extrusion and migration of

the teeth.
 Symptoms:

 8. Localized pain or sensation of pressure after eating which gradually decreases.

 9. Foul taste in localized areas.
 10. A tendency to suck material from the interproximal surfaces.
 11. Radiating pain deep into the bone.
 12. A gnawing pain or feeling of itchiness in the gums.
 13. An urge to dig a pointed instrument into the gums with the relief obtained
from the resultant bleeding.
 14. Complains that the food sticks between the teeth and preference to eat on the
other side.
 15. Sensitivity to heat and cold, toothache in the absence of caries.
 CORRELATION OF CLINICAL AND
HISTOPATHOLOGIC FEATURES OF POCKET

Clinical features Histopathologic features

• Bluish-red discoloration; • Circulatory stagnation, destruction

• Flaccidity, of gingival fibers, atrophy of
• A smooth, shiny surface; and epithelium and oedema.
•Oedema and degeneration
• Pitting on pressure.
Clinical features
Less frequently the gingival wall
may be pink and firm.
Histopathologic features
• Fibrotic changes predominate over
exudation and degeneration,
particularly in relation to the outer
surface of the pocket wall.
• Despite the external appearance of
health, the inner wall of the pocket
invariably presents some degeneration
and is often ulcerated.
•Bleeding is elicited by gently
probing the soft tissue wall of the
pocket.
When explored with a probe, the
inner aspect of the probe is
generally painful
Ease of bleeding results from:
•Increased vascularity
•Thinning and degeneration of
the epithelium, and
•The proximity of the engorged
vessels to the inner surface.
Due to ulceration of the inner
aspect of the pocket wall.
Clinical features Histopathologic features

Pus may be expressed by Pus occurs in the pockets with

applying digital pressure. suppurative inflammation of the
inner wall.
 Detection of Periodontal Pockets

 The only accurate method of detecting and measuring periodontal pocket

is by careful exploration with a periodontal probe.

 Periodontal Pockets are not detected by radiographic examination.

 Periodontal pocket is a soft tissue change and Hence, clinical

examination and probing are more direct and efficient.
 Periodontal pocket Probing

There are two different pocket depths

1. Biological or histological depth
 The biological depth is the distance between gingival margin and the
base of the pocket.This can be measured only in carefully prepared and
adequatetely oriented histologic section.

2.The clinical or probing depth

 The probing depth is the distance to which a probe penentrates in to the
pocket
 The following land marks has to be borne in mind while
probing
 1 The crest of the gingival margin
 2 The base of the sulcus
 3The cementoenamel junction
 4 The crest of the alveolar bone
 5 The mucogingival junction
 Probing depth is generally ≤3 mm in gingival health and >3 mm in the
presence of gingival inflammation.
 Armitage and colleagues used beagle dogs to evaluate the penetration of
a probe with the use of a standardized force of 25 g.
 It has been suggested that probe forces between 20 and 25 g cause minimal discomfort and
still enable accurate diagnostic readings (Polson et al., 1980; Garnick et al., 1989; Armitage
et al., 1977). A number of periodontal probes have been developed and modified to achieve
that force setting(Polson et al., 1980; Garnick et al., 1989; Armitage et al., 1977).

 A probing force of 0.75 N has been found to be well tolerated and accurate. (Tibbetts LS,
1969)

 With forces of up to 30 g, the tip of the probe remains within the junctional epithelium.
(Armitage GC, Jeffcoat MK, Chadwick DE, et al. 1994)

 Forces of up to 50 g are necessary to reach the bone level. (Kalkwarf KI, Kahldal WD, Patil
KD, 1986).
 Gutta-percha points or calibrated silver points (Hirschfeld L. 1953)
can be used with the radiograph to assist with determining the level
of attachment of the periodontal pockets.
PATHOGENESIS

 As the conversion of junctional epithelium to pocket epithelium is

regarded as a hallmark in the development of periodontitis.

 Microorganisms are the primary etiologic cause of periodontal

disease and there is good evidence that pocket formation is related to
bacterial colonization of the subgingival tooth surface.

Bosshardt, D.D. (2018), The periodontal pocket: pathogenesis,

histopathology and consequences. Periodontol 2000, 76: 43-50.
 Healthy gingiva is associated with few microorganisms, mostly coccoid cells
and straight rods. Diseased gingiva is associated with increase in the number
of spirochetes and motile rods. (Listgarten 1978).
 Pocket formation starts as an inflammatory change in the connective tissue
wall of the gingival sulcus.
 The cellular and fluid inflammatory exudates 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. (Schroeder 1970)
• Several possibilities intra-epithelial cleavage in the junctional
epithelium.

• With degree of inflammation, an increase in both migration of

polymorphonuclear neutrophils and passage of gingival crevicular fluid
through the intercellular spaces occurs .

• An increased number of leukocytes is, however, considered as a

contributing factor that eventually leads to focal disintegration of the
junctional epithelium. This is in line with the concept that the host itself is
the driving force behind decomposition of the junctional epithelium.
• Indeed, it has been hypothesized that pocket formation results from the
subgingival spread of bacteria under impaired defense conditions.

• In this context, the cysteine proteinases, referred to as gingipains have been

the focus of intense research. As a result, a new effect of gingipains was
discovered

• Gingipains specifically proteolytically degrade components of cell-to-cell

junctional complexes in epithelial cells.

• In addition, gingipains also cleave intercellular adhesion molecule-1 on oral

epithelial cells, which consequently leads to disruption of the interaction
between polymorphonuclear neutrophils and epithelial cells, a sort of
immune evasion by P. gingivalis.
• Intercellular adhesion molecule-1, also known as CD54 mediates cell-to-cell
interactions in inflammatory reactions by functioning as a ligand for the b2 integrins
present on leukocytes and thus has an important function in the control of leukocyte
migration to inflammatory sites.

• Thus, specific degradation of cell junctional complexes and disturbance of the

intercellular adhesion molecule-1-dependent adhesion of polymorphonuclear
neutrophils to epithelial cells through gingipains point to the importance of these
virulence factors in the breakdown of the junctional epithelium, which eventually leads
to pocket development.

• In an apical direction, the pocket epithelium remains contiguous with a junctional

epithelium of reduced height.

• To maintain an epithelial attachment, the residual junctional epithelium proliferates

further apically, as the pocket deepens : best demonstrated histopathologically.
• The periodontal pocket formation is initiated by the microbial assault on the
tissues along with the susceptible host response.
 Mechanism of collagen loss

I. Collagenases and other enzymes secreted by various cells in healthy and

inflamed tissues such as fibroblasts, PMN’s and macrophages become
extracellular and destroy collagen; these enzymes that degrade collagen and
other matrix molecules are called as MMP’s. (Tencate AR 1994)
II. Fibroblasts phagocytise collagen fibers by extending cytoplasmic processes to
their ligament-cementum interface and degrade the inserted collagen fibrils and
the fibrils of the cementum matrix. (Deporter A, Tencate AR 1980)
The transformation of the gingival sulcus into a periodontal pocket
creates an area where plaque removal becomes impossible. The
following feedback mechanism is established:

Plaque  Gingival inflammation  Pocket formation 

More plaque formation.
 Detachment of the DAT cells from the tooth
surface

Role of the gingival crevicular fluid:

In the healthy sulcus, the amount of GCF is very small and participate in
the normal maintenance of function of the JE.
During inflammation the GCF flow increases and its composition starts to
resembling that of an inflammatory exudate.
 The increased GCF flow contributes to host defense by flushing bacterial
colonies and their metabolites away from the sulcus, thus restricting their
penetration into the tissue.

 Changes in the composition of the GCF caused either by bacteria, bacterial

metabolites or inflammatory reaction is maximum at the most coronal JE cells.
 A considerable number of bacteria and host-derived products found in the
GCF have been associated with the initiation and progression of
periodontal disease.
THE BACTERIAL AGENTS HOST-DERIVED AGENTS

 Endotoxins  Factors of the complement

 Hydrogen system
sulfide
 Prostaglandins,
 Butyric and propionic acids
 Different cytokines
 Bacterial collagenases
 Intracellular enzymes
 Other proteases (e.g. trypsin-
 Products of tissue breakdown-
like)
lactate dehydrogenase, aspartate
 Enzymes such as hyaluronidase
aminotransferase, polyamines,
and neuraminidase. and collagen peptides.
 Antimicrobial agents and leukocyte-derived enzymes such as
lysozyme, alkaline phosphatase, b-glucuronidase, cathepsin D,
elastase, collagenase, and lactoferrin as well as osteonectin and
fibronectin are also found in the GCF.

 Indeed, the GCF contains a wide variety of biologically active

molecules with the potential capacity to affect the growth of junctional
epithelium/DAT cells as well as oral bacteria, both competing for the
tooth surface at the dentogingival interface
 The GCF passing through the
junctional epithelium determines the
environmental conditions and provides
sufficient nutrients for the DAT cells to
grow.
 At the gingival margin the GCF may
become contaminated so that agents
from the oral cavity and the plaque
bacteria challenge the most coronal
DAT cells.
Role of the polymorphonuclear leukocytes

 Form the most important line of defense against bacterial plaque at the
gingival margin.
 Have two main types of granules that contain agents effective in killing
the bacteria.
 The azurophilic (primary) granules contain myeloperoxidase, lysozyme,
elastase, cathepsin G, urokinase, acid hydrolases, and defensins,
 Specific (secondary) granules contain lactoferrin, elastase, and lysozyme.
 Activated polymorphonuclear leukocytes also generate hydrogen peroxide
(H2O2) and highly reactive oxygen radicals with the potential to destroy
bacteria and gingival cells.
 Effects of the secondary granule contents esp. lactoferrin on gingival
epithelium are of special interest in formation of periodontal pockets.
 High concentrations of lactoferrin hamper epithelial cell growth by
interfering with their adhesion and spreading thus, have a role in delaying
the repair of the junctional epithelium/DAT cell population during severe
inflammation.
 Role of host proteinases and inflammatory mediators

 In response to the bacteria and inflammatory cytokines, fibroblasts,

junctional epithelial cells, osteoblasts/ osteoclasts, macrophages, and
polymorphonuclear leukocytes release proteinases that are involved in
the defense against microbes.
 Matrix metalloproteinases are able to degrade all extracellular matrix
proteins.
 Collagenases: Degrade interstitial type collagen fibrils (I, II, III)
 Gelatinases, stromelysins, and membrane-type
metalloproteinases :
Degrade fibronectin and gelatin (denatured collagen)
Basement membrane components including type IV collagen,
entactin, nidogen, and laminin.
 Neutrophil elastase and cathepsin G: Degrades basement
membrane type IV collagen and laminin, and type VIII collagen
found in the internal basal lamina.
 ROLE OF BACTERIAL PRODUCTS

 Lipopolysaccharides have the ability to increase epithelial permeability

and penetrate healthy gingival sulcular epithelium.

 Bacterial collagenases, gelatinases, and trypsin- and chymotrypsin- like

enzymes have indirect effect on epithelial detachment and DAT cell
viability/degeneration because of changes in the living conditions of
these cells.
 Butyric and propionic acids are short-chain fatty produced by periodontopathogenic
bacteria, such as Porphyromonas, Fusobacterium, Prevotella and Treponema.
 It is found that the concentrations of butyric and propionic acids in human plaque and
GCF correlate directly with the degree of gingival inflammation and periodontal pocket
depth.

 Ammonium has been shown to cause cell vacuolization and to inhibit collagen secretion.

 Hydrogen sulfide is a highly toxic compound and found to cause significant damage to
the junctional epithelium.
 THEORIES REGARDING THE
MICROSCOPIC TISSUE CHANGES IN
THE INITIATION OF POCKET
FORMATION
I. Destruction of the gingival fibres is a prerequisite for the initiation of
pocket formation:( Fish 1948)
 This concept is focused on the migration of the epithelial attachment along
the root.
 Proliferation of the epithelial attachment along the root can take place only if the
attachments of the underlying gingival fibres into the cementum are destroyed.
 These fibres are a barrier to the normal
migratory tendency of the epithelium at the base
of the sulcus.
 Degeneration and necrosis of these fibers occur
secondary to gingival inflammation or the action
of the bacterial enzymes such as hyaluronidase.
 As soon as the top most fiber is get digested and
absorbed the epithelium proliferates along the
root until a healthy fiber is reached.
•Gottlieb and Orban questioned this concept.

I. They point to areas of repaired idiopathic tooth resorption immediately

subjacent to the epithelial attachment

•Since the resorption of the tooth means detachment of the PDL fibers from

that area and repair of those areas means that epithelium had not

proliferated in those areas even after destruction of fibers.

II. They also referred to the condition in which the epithelial attachment is
attached to the enamel and is separated from the cementum by the
unattached connective tissue rather than the fibers embedded in the tooth.
•In such instances pathologic migration of the epithelial attachment does

not occur.
II. The initial change in pocket formation occurs in
the cementum (Gottlieb 1946)

•Gottlieb stressed the changes in tooth surface rather than the gingiva for
pocket formation.

•Acc. to him down growth of the epithelial attachment is a physiologic

phenomenon, and is part of the process of continuous eruption of the teeth,
which occurs throughout life.
•Under physiologic conditions, the continuous deposition of new cementum
acts as a barrier and prevents an acceleration in the rate of migration of the
epithelial attachment As long as continuous cemental deposition is not
disturbed, migration of the JE occurs at physiologic rate.

•Nothing can induce the epithelial attachment to move apically in the

presence of a highly developed cementum barrier.
• If the normal deposition of cementum disturbed and connective tissue fibers
destroyed:
• Low resistance
• Inflammation or
• Trauma
•Organic connection between cementum and fibers will be dissolved.
•Epithelium will proliferate along the root, according to its natural tendencies,
until it meets undisturbed cementum and connective tissue fibers.
Continuous deposition of new cementum acts as a barrier

Prevents accelerated migration of the epithelial

attachment.

Injury to cementum and fiber connection

Epithelial migration
III. Stimulation of the epithelial attachment due to
infection or trauma is the initial histological change in
pocket formation. (Aisenberg 1948)
•Destruction of the underlying gingival fibres is not a prerequisite for

epithelial migration.
•Stimulated by inflammation, the epithelium will migrate along the root

without preceding destruction of the gingival fibers

 Underlying fibres may remain intact, the epithelial cells will enmesh
between the fibres. and attach themselves further apically along the
cementum.

 Epithelial attachment enmeshes fiber bundles in epithelial network,

producing secondary degeneration of the connective tissue fibres.
In support of this hypothesis:
•There are findings of epithelial cells attached to the cementum between

individual fiber bundles.

•In certain areas, the cementum is bundle-free.
 Initially neither destruction of fibers nor cementum

Inflammation stimulates epithelium

Epithelial moves apically and enmeshes through intact

bundle fibers

Secondary destruction of fibers

IV. Pathologic destruction of the epithelial attachment due
to infection or trauma is the initial histological change in
pocket formation. (Skillen 1930)

•According to Skillen, the epithelial attachment has few protective qualities

for safeguarding the underlying connective tissue against spread of infection.

•But the epithelial attachment is an area of low resistance, which is subject to

infection.

•In experimental animals, pocket formation occurs because of pathologic

destruction of the epithelial attachment due to infection or trauma or both.

V. The periodontal pocket is initiated by the invasion of bacteria at
the base of the sulcus or the absorption of bacterial toxins
through the epithelial lining of the sulcus. ( Box 1941)

• According to Box, either because of

• Imperfect junction of the epithelial cells and the cementum or
• Extreme thinness of the epithelium,
the base of the sulcus offers a poor defense against bacteria.
•In the evolution of a “ pus-pocket” the following stages follows:
• An initial invasion of bacteria at the base of the sulcus
• Inflammation in the underlying connective tissue,
• Ulceration at the base of the crevice,
• Sloughing of the epithelium, and
• Loss of attachment to the cementum,
• Progressive loss of connective tissue, and
• Penetration of the pocket into the deeper tissues.
 Box also suggested that the specific infective agents possibly
related to the Leptothrix falciformis are capable of deepening
the pocket.
VI. Pocket formation is initiated in a defect in the sulcus
wall. (Becks 1929)
•According to Becks, the formation and maintenance of the normal sulcus
results from the coordination of the degeneration of the enamel epithelium,
proliferation of the oral epithelium, and atrophy of the gingival papilla.

•Disturbance of this correlation, whether by inflammation or injury, induces

pathologic pocket formation.
•If degeneration of the enamel epithelium from the cuticle takes place
rapidly without being covered by the oral epithelium, a defect occurs in
the lateral sulcus wall.

•This defect constitutes a “ locus minoris resistentiae” which is a portal of

entry for bacteria with resultant inflammation .

VII. Proliferation of the epithelium of the lateral wall, rather than
the epithelium at the base of the sulcus, is the initial change in the
formation of the periodontal pocket. (Wilkinson 1935)
• Wilkinson regards epithelial proliferation as the primary change in the
pocket formation.
He describes the following sequence of changes:
• Proliferation and downgrowth of the oral epithelium or proliferation of
the epithelial attachment results in thickening of the epithelial lining of the
sulcus.
Because of the increased thickness, the cells along the inner aspect of the
sulcus, in relation to the tooth are deprived of their nutrition and undergo
degeneration and necrosis.
The degenerated and necrotic epithelial cells become calcified (serumal

calculus).
Separation of the calcified masses from the adjacent normal epithelium

produces a pocket or trough.

 These changes are followed by proliferation of the epithelium along the

cementum, and detachment of its coronal portion from the root surface.
•Destruction of the underlying periodontal membrane fibres and alveolar
bone is subsequent to and dependent upon the primary epithelial changes.
•The epithelial changes, which initiate pocket formation, are not caused by
infection.
•Inflammatory changes in the pocket formation are secondary to the
epithelial changes.
•Wilkinson suggested that vitamin A deficiency may be an important factor
in initiating pocket formation.
Proliferation & thickening of the epithelial lining of the
sulcus.

The cells inner aspect get deprived of their nutrition

Degeneration and necrosis epithelial cells and their

calcification
Separation of the calcified masses from adjacent
epithelium

Proliferation of the epithelium along the cementum

VIII. Two stage pocket formation. (James & Counsell 1927)
James and Counsell Instead they felt pocket formation occurs in two
stages:
The first stage is proliferation of the subgingival epithelium.
The second stage is loss of superficial layers of proliferated epithelium
which produces space or pocket. The rate of proliferation of the
epithelium at the base is such that it precedes the destruction of the
superficial epithelium, and the pocket is therefore always lined with
epithelium.
IX. Inflammation is the initial change in the formation of the
periodontal pocket. (Nuckolls 1950)
•“Periodontal lesions of purely local origin have their beginnings in
inflammation”.
•According to Nuckolls the first reaction is an imperceptible one, and
consists of a nerve reflex in the epithelium, which stimulates a vascular
change in the underlying connective tissue.
 Vascular change in the connective tissue stimulates the following changes in
the epithelial lining of the sulcus.
 Increased mitotic activity in the basal epithelial layer, and sometimes in the
prickle cell layer
 Increased production of keratin with desquamation.
 Cellular desquamation adjacent to the tooth surface, tends to deepen the pocket.
The epithelial cells at the bottom of the sulcus proliferate downward, invade
and break up gingival fibres.
The dissolution of connective tissue results in the formation of “open
lesion”.
Granulation tissue fills in the defect created by the open lesion, and the
epithelium proliferates inward.
This forms a lining of the repaired open lesion to a point where the
connective tissue is attached to the root.
X. Pathologic epithelial proliferation occurs secondary to
noninflammatory degenerative changes in the periodontal
membrane:

Noninflammatory degenerative changes in the periodontal membrane has

been described as “periodontosis” – under such conditions the normal
barrier afforded by the gingival fibres is diminished, this facilitates the
migration of the epithelial attachment along the root and pocket formation,
in the presence of local irritation.
 Recently, Schroeder and Attström proposed a new hypothesis of the development
of the gingival pocket .
 They suggested that pathological pockets are formed by microbial invasion of the
subgingival dentogingival junction, thus destroying the coronal epithelial
attachment.
 Schroeder and Attström pointed out that almost none of the earlier studies related
pocket formation to the presence of bacterial deposits.
 They hypothesized that pocket formation is the result of a split in the junctional
epithelium from its attachment to the tooth surface through the action of bacteria.
HISTOPATHOLOGY
Conversion of Junctional Epithelium to
Pocket Epithelium

Significant changes occur in the junctional epithelium at an

early stage of gingivitis.
These include:
An increase in the amount of extra cellular space
probably reflecting increased permeability,
A loss of intercellular junctions,
Beginning proliferation of the basal cells with rete ridge
formation, and
The pattern of cell maturation changes.
Patches of cells may under go keratinisation, a process that is completely
abnormal for this tissue.
Where as adjacent patches may die and slough, resulting in ulceration,
converting JE into pocket epithelium.
Though the mechanisms that underlie the alterations are not clearly
understood, there are several possibilities.
Rapidly growing bacteria requires space, this fact may relate to the
striping of the JE cells from the tooth surface in an apical direction.

Stripping could be achieved either by enzymes released from the

extending bacteria or through the induced inflammatory response.

 On the other hand a large population of non epithelial cells including

many emigrating neutrophils resides on the JE as the disease evolves.
 These streams of neutrophils may become so large that they disrupt the structure and
they create ulcer in the pocket wall.

 Finally, Barnett has suggested that the mast cells that comprise a portion of the non-
epithelial cell proliferation may play a destructive role by releasing potent trypsin
like neutral proteases which dissociates epithelial cells one from another.

 All these events in the JE or pocket epithelium lead to an influx of serum proteins
and leucocytes in defense against bacterial substances but the reverse passage of
bacterial substances into the connective tissues from the pocket also occurs leading
 SOFT TISSUE WALL

 The connective tissue is edematous and densely infiltrated with plasma

cells (approximately 80%) lymphocytes, and a scattering of PMNs.
(Wittwer JW, Dickler EH, Toto PD )
 The blood vessels are increased in number, dilated, and engorged,
particularly in the subepithelial connective tissue layer.(Bonakdar MPS,
Barber PM, Newman HN.1997 )
 The connective tissue exhibits varying degrees of degeneration.
 Single
or multiple necrotic foci are occasionally present. (Orban B, Ray
HG,1948 )
 The connective tissue 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.
 Although marked variations are found as to length, width, and condition
of the epithelial cells, (Schroeder HE 1986 ) usually the corono-apical
length of the junctional epithelium is reduced to only 50 to 100 m.
(Carranza FA Jr 1987 )

 The most severe degenerative changes in the periodontal pocket occur

along the lateral wall.
 Epithelial buds or interlacing cords of epithelial cells project from the
lateral wall into the adjacent inflamed connective tissue and may extend
farther apically than the junctional epithelium.

 The cells undergo vacuolar degeneration and rupture to form vesicles.

 Progressive degeneration and necrosis of the epithelium lead to ulceration

of the lateral wall, exposure of the underlying inflamed connective tissue,
and suppuration.
The severity of the degenerative changes is not necessarily related to
pocket depth.
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 periodontal pocket is generally
intact and thickened, with prominent rete pegs.
A detailed electron microscopic study of the pocket epithelium in
experimentally induced pockets in dogs has been performed by Mliller-
Glauser and Schroder.
 Bacterial Invasion

 Bacterial invasion of the apical and lateral areas of the pocket wall has been
described in chronic periodontitis.
 Filaments,rods, and coccoid organisms with predominant gram-negative cell have
been found in intercellular spaces of the epithelium. (Frank RM. 1980 )
 Hillmann et al have reported the presence of Porphyromonas gingivalis and
Prevotella intermedia in the gingiva of aggressive periodontitis cases.
 Actinobacillus actinomycetemcomitans has also been found in the tissues.
(Christersson LA, Albini B, Zambon JJ, et al.1987, Meyer DH, Screenivasan PK, Fives-Taylor PM,
1991; Saglie FR, Marfany A, Camargo P.1988)
 Bacteria may invade intercellular space and found
 Under ex-foliating cells
 Between deeper epithelial cells and
 On the basement lamina.
 Traverse the basement lamina and invade the subepithelial
connective tissue. (Saglie FR, Newman MG, Carranza FA Jr, et
al.,1982)
 Different investigators believe presence of bacteria due to
 Active bacterial invasion or
 Passive translocation of plaque bacteria. (Listgarten MA, 1986)
Scanning electron micrograph of a section of pocket wall in
advanced periodontitis in a human specimen showing bacterial
penetration into the epithelium and connective tissue.
 Microtopography of the Gingival Wall of the Pocket

 Scanning electron microscopy revealed several areas with different types

of activity. (Saglie FR, Carranza FA Jr, Newman MG, et al.,1982)
 These areas are irregularly oval or elongated and adjacent to one another
and measure about 50 to 200 m.
 These findings suggest that the pocket wall is constantly changing as a
result of the interaction between the host and the bacteria.
 The following areas have been noted:
The following areas have been noted:
1. Areas of relative quiescence, showing a relatively flat surface with minor
depressions and mounds and occasional shedding of cells .
2.Areas of bacterial accumulation, which appear as depressions, with abundant
debris and bacterial clumps penetrating into the enlarged intercellular spaces.
These bacteria are mainly cocci, rods, and filaments, with a few spirochetes.
3.Areas of emergence of leukocytes, where leukocytes appear in the pocket
wall through holes located in the intercellular spaces.
4.Areas of leukocyte-bacteria interaction, where 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.
5. Areas of intense epithelial desquamation, which consist of semi-
attached and desquamating cells sometimes partially covered with
bacteria.
6. Areas of ulceration, with exposed connective tissue.
7. Areas of hemorrhage, with numerous erythrocytes.
The transition from one area to another could be postulated as follows:
Bacteriaaccumulate 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.
 Periodontal Pockets as Healing Lesions

 Periodontal pockets are chronic inflammatory lesions and as such 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 exudates predominate, the pocket wall
is bluish red, soft, spongy, and friable, with a smooth, shiny surface.

 Ifthere is a relative predominance of newly formed connective tissue cells

and fibers, the pocket wall is more firm and pink.
At the clinical level, the former condition is generally referred to as an
edematous pocket wall and the latter as a fibrotic pocket wall.
Edematous and fibrotic pockets represent opposite extremes of the same
pathologic process, not different disease entities.
 Theyare subject to constant modification, depending on the relative
predominance of exudative and constructive changes.
In some cases, inflammation and ulceration on the inside of the pocket
are walled off by fibrous tissue on the outer aspect.
Outwardly the pocket appears pink and fibrotic, despite the inflammatory
changes occurring within.
 Pocket Contents

Periodontal pockets contain debris of :

 Microorganisms and
 Microbial products (enzymes, endotoxins, and other metabolic products)
 Gingival fluid
 Food remnants
 Salivary mucin
 Desquamated epithelial cells
 Leukocytes
 Plaque-covered calculus
 Pocket Contents

 Purulent exudate if present consists of living, degenerated, and necrotic

leukocytes; living and dead bacteria; serum; and a scant amount of
fibrin. (McMillan L, Burrill DY, Fosdick LS, 1958 )
 The contents of periodontal pockets filtered free of organisms and
debris have been demonstrated to be toxic when injected

subcutaneously into experimental animals. (Graham JW.1937)

Pus Formation

 The presence of pus expressed from the pocket merely reflects the nature of the
inflammatory changes in the pocket wall.
 It is a clinical finding and only a secondary sign.
 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.
 Localized accumulation of pus constitutes an abscess.
 Root Surface Wall

 The root surface wall of periodontal pockets undergoes significant

changes because they may perpetuate the periodontal infection, cause
pain, and complicate periodontal treatment.(Bosshardt DD, Selvig KA,
1997)
 As the pocket deepens, collagen fibres embedded in the cementum are
destroyed and cementum becomes exposed to the oral environment.
 Collagenous remnants of sharpey’s fibers in the cementum undergo
degeneration, creating an environment favorable to the penetration of
bacteria.
 Viable bacteria have been found in the roots of 87% of periodontally
diseased noncarious teeth.(Adriaens PA, DeBoever JA, Loesche
WJ,1988)
 Bacterial penetration into the cementum can be found as deep as the
cementodentinal junction (Adriaens PA, DeBoever JA,1986; Davenport
RH Jr, Simpson DM, Hassell TM,1982) and may also enter the dentinal
tubules. (Giuliana G, Ammatuna P, Pizzo G, et al, 1997; Graham JW.
1937)
 Penetration and growth of bacteria leads to fragmentation and
breakdown of the cementum separated from the tooth by masses of
bacteria.
 Pathologic granules (Bass CC.1951) have been observed with light and
electron microscopy,(Armitage GC, Christie TM. 1973) and they may
represent areas of collagen degeneration or areas in which collagen
fibrils have not been fully mineralized initially.
 Bacterial products such as endotoxins (Aleo JJ, DeRenzis FA,
Farber PA, et al,1974) have also been detected in the cementum
wall of periodontal pockets.
 When root fragments from teeth with periodontal disease are
placed in tissue culture, they induce irreversible morphologic
changes in the cells of the culture. Such changes are not
produced by normal roots. (Hatfield CG. Baumhammers A,1971)
 Diseased root fragments prevent the in vitro attachment of human
gingival fibroblasts (Aleo JJ, DeRenzis FA, Farber PA., 1975) and can
induce an inflammatory response in the oral mucosa even when
autoclaved (Lopez NJ, Belvederessi M, de la Sotta R, 1980)

 Clinically
there is 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 course of treatment, these necrotic areas are removed by root
planing until a hard, smooth surface is reached.

 Cementum is very thin in the cervical areas, and scaling and root planing
often remove it entirely, exposing the underlying dentin.

 Sensitivity to cold may result until the pulp tissue forms secondary
dentin.
 CHANGES ON ROOT SURFACE WALL OF PERIODONTAL POCKETS:

Areas of increased mineralization (Selvig KA, 1969) are probably a

result of exposure and exchange minerals and organic components at the
cementum saliva interface.
The mineral content of exposed cementum increases.(Selvig KA, 1966)
Minerals increased are: calcium, magnesium, phosphorus, and fluoride.
Micro hardness remains unchanged. (Rautiola CA, Craig RG, 1961;
Warren EB, Hanse NM, Swartz ML, et al, 1964)
 The development of a highly mineralized superficial layer may increase
the tooth resistance to decay.

 The hypermineralized zones associated with increased perfection of the

crystal structure, organic changes suggestive of a subsurface cuticle
(Selvig KA, 1966) and 10 to 20 m thick with area as thick as 50 mm.
(Selvig KA, Hals E.,1977)
• No decrease in mineralization was found in deeper areas, thereby
indicating that increased mineralization does not come from deeper
tissues.

• A loss of or reduction in the crossbanding of collagen near the

cementum surface (Furseth R.,1971; Furseth R, Johanson E. 1970 )
and a subsurface condensation of organic material of exogenous
origin (Selvig KA,1966) have also been reported.
 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. (Herting HC., 1967)

 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. (Fejerskov O, Nyvad B,1986).

 The dominant microorganism in root surface caries is Actinomyces

viscosus, (Syed SA, Loesche WJ, Pape HL, et al,1975) other bacteria
such as Streptococcus mutans, Streptococcus salivarius, Streptococcus
sanguis, and Bacillus cereus have been found to produce root caries in
animal models.
Quirynen et al reported that when plaque levels and pocket depths fall
after periodontal therapy 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.

Caries of the root may lead to pulpitis, sensitivity severe pain and
exposure of the pulp.
 Areas of cellular resorption of cementum and dentin are common in roots
unexposed by periodontal disease. (Sottosanti JS.,1977)
 These areas are of no particular significance because they are symptom free and
undergo repair. However, if the root is exposed by progressive pocket formation
before repair these appear as isolated cavitations.
 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.
 Zones in the bottom of periodontal pocket

 Cementum covered by calculus

 Attached plaque: covers calculus, and extends apically from it to a variable degree
typically 100-500µ
 Unattached plaque that surrounds the attached plaque and extends apically to it.
 Attachment of junctional epithelium to 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.
 Semi destroyed connective tissue fibers may be apical to the junctional epithelium.
(Saglie FR, Newman MG, Carranza FA Jr, et al.,1982).
 Zones3, 4, and 5 make up the “plaque-free zone” seen in extracted teeth.
(Bass CC., 1946; Brady JM, 1973; Hoffman ID, Gold W., 1971; Saglie
FR, Johansen JR, Tollefsen T.,1975; Waerhaug J.,1952)

 The total width of the plaque-free zone varies according to the type of
tooth (i.e., it is wider in the molars than in the incisors) and the depth of
the pocket (i.e., it is narrower in deeper pockets).(Saglie FR, Johansen
JR, Flotra L, 1975)
Plaque free zone
 plaque-free zone refers only to attached plaque, because
unattached plaque contains a variety of gram-positive and
gram-negative morphotypes, including cocci, rods, filaments,
fusiforms, and spirochetes.
 The most apical zone contains predominantly gram negative
rods and cocci. (Vrahopoulos TP, Barber PM, Newman
HN.,1995)
 Periodontal Disease Activity

 In recent studies, the concept of periodontal disease activity has evolved.

 According to this concept, periodontal pockets go through periods of
exacerbation and quiescence as a result of 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.
A buildup of unattached plaque, with its gram-negative, motile, and
anaerobic bacteria starts a period of exacerbation during which bone and
connective tissue attachment are lost and the pocket deepens.

 This period may last for days, weeks, or months, and it is eventually
followed by a period of remission or quiescence during which gram-
positive bacteria proliferate and a more stable condition is established.
 On the basis of a study of radioiodine125I absorptiometry,
McHenry and colleagues confirmed that bone loss in
patients with untreated periodontal disease occurs in an
episodic manner.
 These periods of quiescence and exacerbation are also
known as periods of inactivity and periods of activity.
 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,
(Davenport RH Jr, Simpson DM, Hassell TM, 1982; ) PMNs,(Page
RC, Schroeder HH; 1977) or both is seen.

 Bacterial samples from the pocket lumen that are analyzed with
dark-field microscopy show high proportions of motile organisms
and spirochetes.(Listgarten MA, Hellden L; 1978).
 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.
 Atrophic and inflammatory pulpal changes occur in such cases.
 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.
 This is because 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 , and pockets of different depths may be associated with
the same amount of attachment loss.
Area Between Base of Pocket and
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%).
(Stanley HR, 1955; Wade AB, 1960)
 The distance from attached plaque to bone is never less than 0.5 mm and
never more than 2.7 mm. (Waerhaug J.1952,1979)
 These findings suggest that the bone-resorbing activity induced by the
bacteria is exerted within these distances.
 However, the finding of isolated bacteria or clumps of bacteria in the
connective tissue(Saglie FR, Newman MG, Carranza FA Jr, et al,1982)
and on the bone surface (Frank RM, Voegel RC, 1978) may modify these
considerations.
 Relationship of Pocket to Bone

 In infrabony pockets, the base of the pocket is apical to the crest of the
alveolar bone, and the pocket wall lies between the tooth and the bone.
 The bone loss is in most cases vertical.
 Alternatively, in suprabony pockets, the base is coronal to the crest of
the alveolar bone, and the pocket wall lies coronal to the bone.
 The type of bone loss is always horizontal.
Radiographic and microscopic features
of intrabony pockets.
• In suprabony pockets, the alveolar crest gradually attains a more apical position in
relation to the tooth, but it retains its general morphology and architecture.

• The interdental fibers that run over the bone from one tooth to the other maintain
their usual horizontal direction. In infrabony pockets, the morphology of the alveolar
crest changes completely, with the formation of an angular bony defect. The
interdental fibers in this case run over the bone in an oblique direction between the
two teeth of the interdental space.

• This may affect the function of the area and also necessitate a modification in
treatment techniques.
 Finally periodontal pocket go through periods of exacerbation and
quiescence resulting from episodic bursts of activity followed by periods
of remission.

 These periods of activity and in-activity alternates and process of

deepening of periodontal pocket goes on.
 Treatment:

♦ Residual pockets with Pocket depth ≥ 6mm were risk factors for both
disease progression and tooth loss. Practical implications: Residual Pocket
depth ≥ 6mm represent an incomplete periodontal treatment outcome and
need further therapy.
♦ BOP at the same site during supportive periodontal therapy (SPT) was
found to be a parameter with a limited, but statistically significant positive
predictive value for attachment loss.
 ♦ Clinical attachment loss (CAL) is a reliable measurement to detect the
changes in periodontal status than the probable pocket depth.
CONCLUSION

 Residual pockets are associated with progression of periodontal

disease and tooth loss. Nonsurgical retreatment of these sites rarely
proved to be effective in closing the pockets. Thus, surgical
treatment of residual pockets is a treatment option that should not
be underestimated by the clinician. However, differences in terms of
patient, site or technique selection, may greatly affect the final
outcome.
 References

 Periodontology 2000, Vol. 31, 2003, 12–31.

 Periodontology 2000, Vol. 13, 1997 , 41–57.
 Carranza’s clinical periodontology: 13 th edition.