Periodontal pocket

PERIODONTAL POCKETPERIODONTAL POCKET
Presented by :
Dr Gaurav Girdhar
IInd Year P.G.

CONTENTS
– Introduction
– Definition
– Classification
– Clinical features
– Pathogenesis
– Histopathology
– Bacterial invasion
– Contents of pocket
– References

INTRODUCTIONINTRODUCTION
 Periodontitis is defined as “an inflammatory disease
of the supporting tissues of the teeth caused by
specific organisms or groups of specific organisms,
resulting in progressive destruction of the
periodontal ligament and alveolar bone with pocket
formation, recession or both.”
 Pocket formation is one of the characteristic feature
of periodontitis.

DEFINITIONDEFINITION
• The periodontal pocket, defined as “a pathologically
deepened gingival sulcus.”
Deepening of the gingival sulcus
by coronal movement apical displacement combination
of the gingival margin of the gingival attachment

CLASSIFICATION OF POCKETS:CLASSIFICATION OF POCKETS:
1. Gingival pocket
(pseudo pocket)
2. Periodontal
pocket:
a. Suprabony pocket:
bottom of the pocket is coronal
to the underlying alveolar bone
b. Intrabony pocket:
bottom of the pocket is apical
to the level of the adjacent
alveolar bone.

Differences between Intrabony and
Suprabony Pockets
Suprabony Pockets Infrabony Pockets
Base of pocket is coronal to
alveolar bone
Base of pocket is apical to the crest
of alveolar bone
Bone destructive pattern is horizontal Pattern of bone destruction is vertical
Interproximally, transseptal fibers
restored during progressive
periodontal disease are arranged
horizontally.
Transseptal fibers are oblique
On facial and lingual surfaces, PDL
fibers beneath the pocket follow
normal horizontal-oblique course
between tooth and bone.
PDL fibers follow angular pattern of
adjacent bone

According to involved tooth surfaces
1. Simple: Involves one tooth
surface.
2. Compound: Involves 2 or
more tooth surfaces.
3. Complex: Spiral type of
pocket -most common in
furcation areas.

CLINICAL FEATURESCLINICAL FEATURES
SIGNS OF PERIODONTAL POCKET:
1. Enlarged bluish-red marginal gingiva with rolled edge
separated from the tooth surface.
2. A reddish blue vertical zone extending from the gingival
margin to the attached gingiva and sometimes into alveolar
mucosa.
3. A break in the faciolingual continuity of interdental gingiva.
4. Shiny, discolored and puffy gingiva associated with exposed
root surface.
5. Gingival bleeding.
6. Purulent exudate or its appearance in response to digital
pressure on lateral aspect of gingival margin.
7. Looseness, extrusion and migration of teeth.
8. Diastema formation.

CLINICAL FEATURESCLINICAL FEATURES
SYMPTOMS OF PERIODONTAL POCKET:
1. Localized pain or sensation of pressure after eating.
2. Foul taste in localized area.
3. Tendency to suck material from interproximal space.
4. Radiating pain deep in bone.
5. A gnawing feeling or feeling of itchiness into the gums.
6. Urge to dig a pointed instrument into the gums with relief
obtained from the resultant bleeding.
7. Complain that food sticks between the teeth.
8. Teeth feel loose, preference to eat on the other side.
9. Sensitivity to heat and cold and toothache in absence of
caries.

 The only reliable method of locating periodontal pockets
and determining their extent is careful probing of the
gingival margin along each tooth surface.
 On the basis of depth alone, however, it is sometimes
difficult to differentiate between a deep normal sulcus
and a shallow periodontal pocket.
 In such borderline cases, pathologic changes in the
gingiva distinguish the two conditions.

CORRELATION OF CLINICAL ANDCORRELATION OF CLINICAL AND
HISTOPATHOLOGIC FEATURES OF POCKETHISTOPATHOLOGIC FEATURES OF POCKET
CLINICAL FEATURES HISTOPATHOLOGY
Bluish red discoloration circulatory stagnation.
Flaccidity destruction of gingival fibres & CT.
Smooth, shiny surface atrophy of epithelium & edema.
Pitting on pressure edema & degeneration.
Firm & pink fibrotic changes.
Bleeding on probing ↑ed vascularity, thinning &
degeneration of epithelium, proximity
of engorged vessels.
Inner aspect of pocket painful ulceration of inner aspect of pocket.
Expression of pus from pocket suppurative inflammation of inner wall.

PATHOGENESISPATHOGENESIS
• There are many hypotheses on pocket formation.
– Some imply that the subgingival bacterial growth is
secondary to the opening of the pocket, others suggest that
the pocket formation is a result of bacteria spreading
subgingivally.
• Schroeder and Attstrom proposed a hypothesis of the
development of the gingival pocket using experimentally
produced neutropenic dogs.
• They suggested that pathological pockets are formed by
microbial invasion of the subgingival dentogingival junction, thus
destroying the coronal epithelial attachment.

• In addition to the bacterial factors, the mechanism of
deepening of the sulcus, along with its pathological
counterparts, is also the subject of long standing interest.
• The deepening has been considered to be initiated at the
interface between
– (1) the junctional epithelium and tooth, and
– (2) at the line of fusion between the junctional
epithelium and the reduced enamel epithelium within the
junctional epithelium.

THEORIES ON THE PATHOGENESIS OFTHEORIES ON THE PATHOGENESIS OF
PERIODONTAL POCKETSPERIODONTAL POCKETS

I. Destruction of the Gingival Fibers is a PrerequisiteI. Destruction of the Gingival Fibers is a Prerequisite
for the Initiation of Pocket Formation.for the Initiation of Pocket Formation.
• This concept focuses attention upon the migration of gingival fibers.
• The contention is that proliferation of the junctional epithelium along
the root can take place only if the underlying gingival fibers are
destroyed.
• These fibers are considered a barrier to the normal migratory
tendency of the epithelium at the base of the sulcus, and it is believed
that their degeneration and necrosis occur secondary to gingival
inflammation or the action of bacterial enzymes such as hyaluronidase.
• As soon as the topmost fiber is digested and absorbed, the epithelium
proliferates along the root until a healthy fiber is reached.

• Gottlieb and Orban have questioned this concept.
• They pointed to areas of repaired idiopathic tooth resorption
immediately beneath the junctional epithelium, and noted that since the
resorption of the tooth entailed detachment of the gingival fibers,
repair would not have been possible had the epithelium proliferated
simply because the fibers had been destroyed.
• They also point out that when the junctional epithelium is attached to
the enamel and is separated from the cementum by unattached
connective tissue rather than fibers embedded in the tooth, so
pathologic migration of the epithelium does not occur.

II. The Initial Change in Pocket FormationII. The Initial Change in Pocket Formation
Occurs in the CementumOccurs in the Cementum
• In seeking an explanation for pocket formation, Gottlieb stresses the
changes in tooth surface rather than in the gingiva.
• He envisions downgrowth of the junctional epithelium as a physiologic
phenomenon that is part of the process of continuous eruption of teeth
throughout life.
• Under physiologic conditions, the continuous deposition of new
cementum acts as a barrier that prevents accelerated migration of the
junctional epithelium.
• So long as continuous cementum deposition is not disturbed, migration
of the junctional epithelium at a pathologic rate cannot occur.

• However, if the tooth surface is of low resistance, or if the normal
deposition of cementum is impaired, inflammation or trauma can do
additional harm by destroying either the cementum or the gingiva,
or both.
• This dissolves the organic connection between the two, and the
epithelium proliferates along the root until it meets undisturbed
connective tissue fibers and cementum.
• Death of the cementum does not necessarily occur under such
circumstances, as evidenced by the fact that epithelium attaches
itself to cementum after its organic connection with the periodontal
ligament fibers is destroyed.

III. Stimulation of the Junctional Epithelium by Inflammation Rather
than Destruction of Gingival Fibers is the Prerequisite for the
Initiation of the Periodontal Pocket.
• Destruction of the underlying gingival fibers is not a prerequisite for
epithelial migration.
• Stimulated by inflammation, the epithelium migrates along the root
without preceding destruction of the gingival fibers.
• In such instances the epithelial cells burrow between the intact
gingival fibers and attach themselves farther apically on the cementum
in bundle free areas.
• The junctional epithelium may move between healthy connective tissue
fibers, enmesh them in an epithelial network, and produce secondary
fiber degeneration.

IV. Pathologic Destruction of the junctionalIV. Pathologic Destruction of the junctional
Epithelium due to Infection or Trauma is the InitialEpithelium due to Infection or Trauma is the Initial
Histologic Change in Pocket FormationHistologic Change in Pocket Formation
• According to Skilien, the junctional epithelium has few protective qualities for
safeguarding the underlying connective tissue against spread of infection.
• It is the normal down growth of the oral epithelium behind the junctional
epithelium that protects the underlying connective tissue.
• The junctional epithelium is an area of low-resistance subject to infection.
– In experimental animals, pocket formation occurs because of pathologic
dissolution of the junctional epithelium due to infection or trauma, or both.
Accumulation of debris in the pocket may be secondary after the pocket is
formed by dissolution of the junctional epithelium.

V. The Periodontal Pocket is Initiated by Invasion of BacteriaV. The Periodontal Pocket is Initiated by Invasion of Bacteria
at the Base of the Sulcus or the Absorption of Bacterialat the Base of the Sulcus or the Absorption of Bacterial
Toxins Through the Epithelial Lining of the Sulcus.Toxins Through the Epithelial Lining of the Sulcus.
• 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 pocket, initial invasion of bacteria at the base of
the sulcus leads to the following changes: inflammation in the
underlying connective tissue, ulceration at the base of the crevices,
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.
• Specific infective agents possibly related to Leptothrix falciformis
are capable of deepening the periodontal pocket.
• Also Holt considers the epithelial lining of the sulcus a poor barrier
against bacterial toxins, which initiate inflammatory changes leading
to pocket formation.

VI. Pocket Formation is initiated in a Defect in theVI. Pocket Formation is initiated in a Defect in the
Sulcus Wall.Sulcus Wall.
• According to Becks," the formation and maintenance of the
normal 1 mm deep sulcus results from the coordination of
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, leads to pathologic pocket formation.
• Pocket formation occurs between the oral epithelium and the
enamel epithelium, rather than by separation of enamel
epithelium from the cuticle.
• If degeneration of the enamel epithelium 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.
• This induces proliferation of the basal cells of the enamel
epithelium and the oral epithelium, a protective mechanism for
the connective tissue.
• Inflammation is a stimulant to oral epithelium proliferation,
which shuts off nutrition from enamel epithelium, hastens its
degeneration, and increases the pocket
• In some cases, pathologic pocket formation may be initiated
without inflammation appearing to play a role.
• In such instances there is an accelerated degeneration of the
enamel epithelium, possibly of systemic origin. This is followed
by proliferation of the oral epithelium to cover the defect.

Vll. Proliferation of the Epithelium of the lateral Wall, ratherVll. Proliferation of the Epithelium of the lateral Wall, rather
than the Epithelium at the Base of the Sulcus, is the Initialthan the Epithelium at the Base of the Sulcus, is the Initial
change in the Formation of the Periodontal pocket.change in the Formation of the Periodontal pocket.
• Wilkinson regards epithelial proliferation as the primary change in
pocket formation.
• He describes the following sequence of changes:
– Proliferation and down growth of the oral epithelium or
proliferation of the junctional epithelium result in a thickening of
the epithelial lining of the sulcus.
– The cause of this proliferation is not known. Because of the
increased thickness, the cells along the inner aspect of the sulcus
are deprived of 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.
• The epithelial changes that initiate pocket formation are not caused by
infection. Inflammatory changes in pocket formation are secondary to
the epithelial changes.
– Wilkinson suggests that vitamin A deficiency may be an important
factor in initiating pocket formation.

VIII. Two-stage Pocket Formation.VIII. Two-stage Pocket Formation.
• James and Counsel disagree with the concept that proliferation of
junctional epithelium followed by separation from cementum forms a
pocket.
• Instead, they feel pocket formation occurs in two stages:
– The first stage is proliferation of the sub-gingival epithelium
(junctional epithelium).
– The second stage is loss of the superficial layers of the
proliferated epithelium, which produces a 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 theIX. Inflammation is the Initial Change in the
Formation of the Periodontal Pocket.Formation of the Periodontal Pocket.
• According to this concept periodontal pockets start as inflammatory
lesions. The first reaction is a vascular change in the underlying
connective tissue.
• Inflammation in the connective tissue stimulates the following changes
in the epithelial lining of the sulcus and in the junctional epithelium:
increased mitotic activity in the basal epithelial layer, and sometimes in
the prickle cell layer; increased production of keratin with
desquamation.’
• The cellular desquamation adjacent to the tooth surface tends to
deepen the pocket.

• The epithelial cells of the basal layer at the bottom of the sulcus and in
the area of attachment proliferate into the underlying connective
tissue and break up the gingival fibers.
• It is the repair of the lesion in the absence of treatment that
establishes the periodontal pocket. Granulation tissue fills in the
defect created by the open lesion, and the epithelium proliferates
inward.
• In pocket formation, the epithelium does not proliferate along the root;
instead it proliferates from the gingival surface to cover the
connective tissue lesion created by inflammation, and thereby forms
the lining of the pocket.

X. Pathologic Epithelial Proliferation Occurs Secondary to Non-X. Pathologic Epithelial Proliferation Occurs Secondary to Non-
inflammatory Degenerative Changes in the Periodontal Ligament.inflammatory Degenerative Changes in the Periodontal Ligament.
• Under the term "periodontosis" a condition has been described which is
characterized by generalized non-inflammatory degeneration of the
collagen fibers embedded in the cementum.
• Under such conditions, the normal barrier afforded by the gingival
fibers is diminished.
• This facilitates the migration of the junctional epithelium along the
root and pocket formation in the presence of local irritation.

EARLY LESIONEARLY LESION
• the degenerative changes occur first in the second or third
cell layer from the innermost cell layer of the most coronal
part of the junctional epithelium, which faces the microbial
plaque.
• an intraepithelial cleavage is formed followed by the
degeneration of the cells lining the cleavage, resulting in a
deep crevice formation.
• Schroeder and Attstrom 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 cocci.

THE ESTABLISHED LESIONTHE ESTABLISHED LESION
• As bacterial plaque spreads apically into the
deepened crevice,
– the preceding cellular degeneration of the
junctional epithelium,
– the intraepithelial cleavage formation, and
– the subsequent cell desquamation in the gingival
pocket occur at the bottom of the deepened
crevice in the same manner as described in the
early lesion.

THE ADVANCED LESIONTHE ADVANCED LESION
• The pocket becomes so deep with the pocket epithelium being
exposed for such a long periods to the subcrevicular plaque
and calculus, that the epithelium is easily and directly
affected by toxic bacterial products and mechanical irritation
by the calculus.
• While the pocket epithelium proliferates reactively in some
areas, it also become very thin and often ulcerates.
• Concomitant destruction of the periodontium and alveolar bone
provides access for the apical migration of the junctional
epithelium.

• 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.

Two mechanisms are considered to beTwo mechanisms are considered to be
associated with collagen loss:associated with collagen loss:
• (1) Collagenases and other enzymes secreted by various cells in
healthy and inflamed tissue such as fibroblasts,
polymorphonuclear leukocytes, and macrophages become
extracellular and destroy collagen (matrix metalloprpteinases)
• (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 two or three cells in
thickness.

• The coronal portion of the junctional epithelium detaches from
the root as the apical portion migrates.
• As a result of inflammation, polymorphonuclear neutrophils
(PMNs) invade the coronal end of the junctional epithelium in
increasing numbers.
• The PMNs are not joined to one another or to the remaining
epithelial cells by desmosomes. 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.
• Thus the 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.
• 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 on to the cementum.

• The transformation of a gingival sulcus into a periodontal pocket
creates an area where plaque removal becomes impossible, and
the following feedback mechanism is established:
– Plaque Gingival inflammation Pocket formation
More plaque formation
• The rationale for pocket reduction is based on the need to
eliminate areas of plaque accumulation.

HISTOPATHOLOGICAL FEATURESHISTOPATHOLOGICAL FEATURES
• The connective tissue is edematous and densely infiltrated
with plasma cells (approximately 80%), lymphocytes, and a
scattering of PMNs.
• The blood vessels are increased in number, dilated, and
engorged, particularly in the subepithelial connective tissue
layer.
• The connective tissue exhibits varying degrees of
degeneration and shows proliferation of the endothelial cells,
with newly formed capillaries, fibroblasts, and collagen fibers.
Soft Tissue Wall

• 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, usually the coronoapical length
of the junctional epithelium is reduced to only 50 to 100 μm.
• The cells may be well formed and in good condition or may
exhibit slight to marked degeneration.

• The most severe degenerative changes in the periodontal pocket
occur along the lateral wall.
• The epithelium of the lateral wall of the pocket presents
striking proliferative and degenerative changes.
• 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 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 a periodontal pocket is
generally intact and thickened, with prominent rete pegs.

The SEM studies have shown the following
features in the lower part of pocket epithelium.
– Widening of intercellular spaces.
– Epithelial cell degeneration which mainly occurred in the
supra basal and superficial layers of the epithelium and in
nuclei and RER.
– Reduction in cell contacts was clear and enzymatic digestion
of desmosomes by trypsin in vitro proved this point.
– increased pocket wall permeability due to disruption of
intercellular spaces and basal lamina.

Bacterial Invasion
• Bacterial invasion of the apical and lateral areas of the pocket
wall has been described in human chronic periodontitis.
• Filaments, rods, and coccoid organisms with predominant gram-
negative cell walls have been found in intercellular spaces of
the epithelium.
• 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 traverse the basement lamina and invade
the subepithelial connective tissue.
• direct bacterial invasion or as passive translocation of
plaque bacteria.

Microtopography of the Gingival
Wall of the Pocket
• SEM has shown various areas of activity:
– 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 on the epithelial surface, 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.

• 5. Areas of intense epithelial desquamation, which consist of
semiattached and folded epithelial squames, some times partially
covered with bacteria.
• 6. Areas of ulceration, with exposed connective tissue.
• 7. Areas of hemorrhage, with numerous erythrocytes.

CONTENTS OF THE PERIODONTAL
POCKET
• Periodontal pockets contain debris consisting principally of:
• Microorganisms and their products (enzymes, endotoxins,
and other metabolic products),
• Food remnants,
• Salivary mucin,
• Gingival fluid,
• 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.

Importance of Pus Formation
• There is a tendency to overemphasize the importance of the
purulent exudate and to equate it with severity of periodontal
disease.
• Pus is a common feature of periodontal disease, but it is only a
secondary sign.
• The presence of pus expressed from the pocket is not an
indication of the depth of the pocket or the severity of the
destruction of the supporting tissues.
– It merely reflects the nature of the inflammatory changes in
the pocket wall. Extensive pus formation may occur in shallow
pockets, whereas deep pockets may exhibit little or no pus

Healing of Periodontal Pockets
• Periodontal pockets are chronic inflammatory lesions where
complete healing does not occur because of the persistence of
the bacterial attack, which continues to stimulate an
inflammatory response, causing degeneration of elements
formed at the time of repair.
• The status of the lateral wall of the periodontal pocket depends
upon the interplay between destructive and constructive tissue
changes which 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 (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
(Fibrotic pocket wall).
• Fibrotic pocket walls may be misleading because they
do not necessarily reflect what is taking place
throughout the pocket wall.

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.
Exposure of the cementum to oral environment
proteolysis of Sharpeys fibres
fragmentation & cavitation.

• Bacterial products such as endotoxins have been
detected in the cementum wall of periodontal
pockets.
• Cementum is very thin in the cervical areas and
scaling and root planing often removes it entirely,
exposing the underlying dentin.
– Sensitivity to cold may result until secondary
dentin is formed by the pulp tissue

Areas of increased mineralization
• an exchange of minerals and organic components.
• The following minerals are increased in diseased root
surfaces: calcium, magnesium, phosphorus, and fluoride.
– Micro hardness, however, remains unchanged.
– The development of a highly mineralized superficial layer
may increase the tooth resistance to decay.
• The hypermineralized zones 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,
thereby indicating that increased mineralization does not
come from adjacent areas.

Areas of demineralization
• These 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.
• Other associated bacteria are:
– Actinomyces naeslundii,
– Streptococcus mutans,
– Streptococcus salivarius,
– Streptococcus sanguis, and
– Bacillus cereus
• 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, however, may lead to pulpitis, sensitivity to
sweets and thermal changes, or severe pain. Pathologic exposure of
the pulp occurs in severe cases.

Areas of cellular resorption of cementum and
dentin
• These are common in roots unexposed by periodontal disease. These
areas are symptom free, and as long as the root is covered by the
periodontal ligament, they are apt to undergo repair.
• However, 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.

Surface Morphology of the Tooth
Wall of Periodontal Pockets
• The following zones can found in the
bottom of a periodontal pocket:
1. Cementum covered by calculus
2. Attached plaque, which covers calculus
and extends apically from it to a
variable degree, probably 100 to
500µm.
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.

PERIODONTAL DISEASE
ACTIVITY
• For many years the loss of attachment produced by periodontal disease
was thought to be a slow but continuously progressive phenomenon.
• 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.
• Period of exacerbation starts with a buildup of unattached plaque, with
its gram-negative, motile, and anaerobic bacteria in which bone and
connective tissue attachment are lost and the pocket deepens.
• These periods of quiescence and exacerbation are also known as periods
of activity and inactivity.
– 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.

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.
• Therefore the severity of periodontitis increases by the
development of new disease sites, the increased breakdown of
existing sites, or both.

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.

Different Pocket Depths with same
amount of attachment loss

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%.
• The distance from attached plaque to bone is never less than 0.5 mm
and never more than 2.7 mm.
– These findings suggest that the bone resorbing activity induced by
the bacteria is exerted within these distances.

Comment regarding pocket formationComment regarding pocket formation
• The following salient facts regard pocket formation are worthy of
special note:
• Local irritation is required for the initiation and progress of
pocket formation.
• Proliferation of the junctional epithelium along the root
and degeneration of underlying gingival fibers are
prim changes in pocket formation.
• Proliferation of the junctional epithelium is
stimulated by local irritation, inflammation caused by local
irritation produces degeneration of the gingival fibres.

References:
• Clinical Periodontology, 10th Ed. Carranza.
• Clinical Periodontology and implant dentistry; 4th Ed. Jan Lindhe.
• Takashi Takata, Karl Donath. “The mechanism of pocket formation” J
Periodontol 1988; 59:215-221.
• Listgarten MA “Pathogenesis of Periodontitis” J Clin Periodontol 1986;
13: 418-425.
• Muller GW, Schroeder HE, “The Pocket Epithelium: A light and
electron microscopy study” J Periodontol 1982; 53: 133-144.
• Hiroshi Takarada et al. “Ultrastructural studies of human gingiva part
I & II.” J Periodontol 1974; 45: 155-169.

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