Periodontology 2000, Vol. 0, 2017, 1–8 © 2017 John Wiley & Sons A/S.
Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Printed in Singapore. All rights reserved
The periodontal pocket:
pathogenesis, histopathology and
consequences
D I E T E R D. B O S S H A R D T
As the formation of a periodontal pocket is the funda-
mental feature of progressive periodontal disease
(41), knowledge about factors contributing to the ini-
tiation of pocket formation and its progression is
important and may add to the development of better
preventive measures and improve healing outcomes
after therapeutic interventions.
Definition and classification
The periodontal pocket is defined as a pathologically
deepened gingival sulcus around a tooth at the gingi-
val margin. Accordingly, the space between the
pathologically detached gingiva and the tooth is
called a pocket. A gingival sulcus depth of up to
0.5 mm may be considered clinically healthy. Differ-
ent classification types of pocket exist (18, 19, 46).
Pseudopockets develop because of gingival
enlargement. The causes of this enlargement com-
prise gingival hyperplasia, edema, drugs or hormones
(51). Characteristic features are absence of loss of
supporting periodontal tissues, absence of loss of
connective tissue attachment to the tooth root and
absence of apical migration of the epithelium, which
means that the gingival margin migrates coronally.
Some authors distinguish true gingival pockets
from periodontal pockets – the former being related
to gingivitis, whereas the latter is found in periodonti-
tis. Detachment of junctional epithelial cells and
inflammation are part of both gingival and periodon-
tal pockets. In a gingival pocket there is, in contrast to
a pseudopocket, inflammation and destruction of the
underlying periodontal tissues together with coronal
detachment of junctional epithelial cells but without
bone destruction (Fig. 1). In a periodontal pocket,
bone destruction by osteoclastic resorption is a
PERIODONTOLOGY 2000
characteristic feature beyond inflammation, tissue
destruction and detachment of junctional epithelium
(Fig. 2). Two types of periodontal pockets exist:
suprabony pockets; and intrabony pockets (19, 46). In
a suprabony (supracrestal or supra-alveolar) pocket,
the bottom of the pocket is coronal to the alveolar
crest (Fig. 2A). When the bottom of the pocket is api-
cal to the alveolar crest, which means that bone is
present lateral to the pocket wall, the pocket is called
an intrabony (infrabony, subcrestal or intra-alveolar)
pocket (Fig. 2B) (19, 46).
Another type of classification takes into considera-
tion the pocket morphology according to the number
of surfaces involved. A simple pocket involves one
tooth surface only, a compound pocket involves more
than one surface and a complex (or spiral) pocket
means that the base of the pocket is not in direct
communication with the gingival margin. Finally,
depending on the disease activity, there are active
and inactive pockets.
Pathogenesis
In a clinically healthy situation, there is a shallow
gingival sulcus around teeth. Histologically, the gin-
gival sulcus is lined by the sulcular epithelium, the
coronal end of the junctional epithelium at the sul-
cus bottom and the tooth surface (33). The sulcular
epithelium is structurally different from and less
permeable than the junctional epithelium. The free
surface of the junctional epithelium is very perme-
able, allowing fluid and cells to leave the junctional
epithelium and enter the oral cavity, thereby ensur-
ing normal defense mechanisms against constantly
present microorganisms and their products (6, 37,
43, 44). This open system, which lacks a physical
1
Bosshardt
A B
A B
barrier in the form of a keratinized cell layer, may,
however, allow microorganisms and their products
to invade the junctional epithelium. Normally, the
junctional epithelium masters this difficult task as a
result of its very sophisticated structural and func-
tional properties that provide potent antimicrobial
mechanisms (6, 44). In this defense system, the
junctional epithelium provides a structural frame-
work through which mainly neutrophilic granulo-
cytes migrate to reach the sulcus bottom. These
transmigrating neutrophils provide the first line of
defense around teeth.
2
Fig. 1. Light micrographs illustrating
early gingival pocket formation
around a porcine tooth. The rectan-
gle in A is enlarged in B. (A) Subgin-
gival calculus with biofilm is present
on the enamel. (B) Note the inflamed
gingival connective tissue adjacent
to the pocket epithelium (PE).
Fig. 2. Light micrographs illustrating
a suprabony (A) and an intrabony
(B) periodontal pocket from dog
teeth. Subgingival calculus and sub-
and supragingival biofilm are seen
in both pockets. PE, pocket epithe-
lium. (Fig. 2B from Bosshardt &
Lang. Dental Calculus. In: Clinical
Periodontology and Implant Den-
tistry. J Lindhe, NP Lang, eds. Wiley
Blackwell. 2015.)
The nature of the dento–gingival junction is very
heterogeneous and consists of: (i) cell attachment to
the tooth surface via hemidesmosomes and basal
lamina; (ii) cell-to-cell attachment within the junc-
tional epithelium, primarily via desmosomes (macu-
lae adherentes); and (iii) attachment to the
surrounding gingival connective tissue via a base-
ment membrane (6, 44). Knowledge of this complex
dento–gingival junction is key to understanding the
initiation of pocket formation. Epithelial cell attach-
ment to the tooth surface is first established by ame-
loblasts and later maintained by the innermost cells

of the junctional epithelium (6). The epithelial attach-
ment mechanism is considered to be of high strength.
Of equal importance are the cell-to-cell contacts con-
necting neighboring epithelial cells. In fact, intact
cell-to-cell connectivity is an absolute requirement
for the correct functioning of cells, tissues and entire
organisms (9). Cell-to-cell adherence and communi-
cation between cells is mediated by the so-called
intercellular junction complexes consisting of desmo-
somes, adherens junctions, tight junctions and gap
junctions. Compared with other types of epithelia,
junctional epithelial cells are interconnected by a few
desmosmes only and occasional gap junctions (44).
The low number of desmosomes and wide intercellu-
lar spaces enable sulcular fluid and inflammatory and
immune cells to transmigrate through the junctional
epithelium. The importance of proper functioning of
intercellular junctions can be demonstrated in a wide
spectrum of inherited, infectious and autoimmune
diseases. Direct or indirect disruption of desmosomes
results in one group of diseases by virtue of their great
importance in maintaining tissue integrity. Among
these pathologies are cardiomyopathy, epidermal and
mucosal blistering, palmoplantar keratoderma,
woolly hair, keratosis, epidermolysis bullosa, ectoder-
mal dysplasia and alopecia (9). On the other hand,
microorganisms and inflammatory stimuli are known
to increase transepithelial permeability by inducing
disassembly of epithelial junctions, as seen in inflam-
matory bowel disease (24). Crohn’s disease, one
major type of bowel disease, falls into the class of
autoimmune diseases and is associated with peri-
odontitis (8, 20, 52).
As the conversion of junctional epithelium to
pocket epithelium is regarded as a hallmark in the
development of periodontitis, the potential factors
contributing to the initiation of pocket formation
need to be critically analyzed. 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. Nevertheless, there is a lack of experi-
ments evaluating the mechanisms of pocket forma-
tion. Previous discussions on the initiation of pocket
development centered around whether: (i) the
epithelial cells first recede and later, as a consequence
of this, biofilm can migrate apically; or (ii) bacterial
products force the epithelial cells to migrate apically.
Degenerative changes, such as loss of cellular conti-
nuity and detachment from the tooth, are first
observed in the coronal-most portion of the junc-
tional epithelium (i.e. at the sulcus bottom) (22, 36,
41, 44, 48). Whether detachment of junctional
Periodontal pocket formation
epithelial cells from the tooth surface or destruction
of cell junctional complexes is more important for
pocket development remains unclear. However, the
important question is why does loss of cellular conti-
nuity, and thus loss of structural integrity, occur at all
at this site? Are host-derived factors associated with
inflammation (such as cytokines) the primary cause
or do microbial products directly trigger destruction
of the junctional epithelium and thereby destabilize
the structure–function relationship?
Several possibilities have been proposed to explain
intra-epithelial cleavage in the junctional epithelium.
With increasing degree of inflammation, an increase
in both migration of polymorphonuclear neutrophils
and passage of gingival crevicular fluid through the
intercellular spaces occurs (1, 2, 27–29). A moderate
distension of intercellular spaces is not considered to
compromise the structural and functional integrity of
the junctional epithelium (44). An increased number
of leukocytes is, however, considered as a contribut-
ing factor that eventually leads to focal disintegration
of the junctional epithelium (44). This is in line with
the concept that the host itself is the driving force
behind decomposition of the junctional epithelium.
Apart from this view, direct influence of bacteria on
the breakdown of the coronal portion of the junc-
tional epithelium has to be taken into consideration.
Indeed, it has been hypothesized that pocket forma-
tion results from the subgingival spread of bacteria
under impaired defense conditions (41). In this con-
text, the cysteine proteinases, referred to as gingi-
pains (namely virulence factors produced by
Porphyromonas gingivalis, a species of bacterium
implicated as a major etiological agent of chronic
periodontitis), have been the focus of intense
research (7, 23, 35). As a result, a new effect of gingi-
pains was discovered. Gingipains specifically prote-
olytically degrade components of cell-to-cell
junctional complexes in epithelial cells (10, 25, 26, 32,
45, 53). In addition, gingipains also cleave intercellu-
lar adhesion molecule-1 on oral epithelial cells, which
consequently leads to disruption of the interaction
between polymorphonuclear neutrophils and epithe-
lial cells, a sort of immune evasion by P. gingivalis
(47). Intercellular adhesion molecule-1, also known as
CD54, a member of the immunoglobulin superfamily
of recognition molecules, mediates cell-to-cell inter-
actions 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 (11, 12, 16,
49, 50). Thus, specific degradation of cell junctional
complexes and disturbance of the intercellular
3
Bosshardt
adhesion molecule-1-dependent adhesion of poly-
morphonuclear neutrophils to epithelial cells through
gingipains point to the importance of these virulence
factors in the breakdown of the junctional epithe-
lium, which eventually leads to pocket development.
In an apical direction, the pocket epithelium remains
contiguous with a junctional epithelium of reduced
height (41). To maintain an epithelial attachment, the
residual junctional epithelium proliferates further
apically, as the pocket deepens. What the conse-
quences of this pathological situation are is probably
best demonstrated histopathologically.
Histopathology
Histopathologically, a pocket is ‘a pathologically
altered gingival sulcus, lined to a variable extent with
pocket epithelium’ (54). Furthermore, the pocket
epithelium, which lines the pocket wall facing peri-
odontal tissues, is defined as ‘unattached epithelial
lining of the pocket, which extends from the sulcular
epithelium to the junctional epithelium. It is charac-
terized by marked proliferation of retial ridges around
inflamed connective tissue papillae and by a ten-
dency to micro-ulceration’ (54).
Much of our knowledge on the histopathologic
appearance of gingival and periodontal pockets is
derived from observations made in animals, mainly
dogs, with ligature-induced periodontal diseases (38,
39, 42) or neutropenia (3, 40) and from ‘broken-
mouth’ periodontitis in sheep (13, 15). Studies
describing the histopathology of gingival and peri-
odontal lesions in humans were mainly focused on
the host response to microbial challenge (4, 14, 17, 31,
34, 56, 57).
At first view, the junctional epithelium (Fig. 3A)
and pocket epithelium (Figs 3B and 4) have some fea-
tures in common, such as formation of a barrier
against microorganisms and their products, passage
A B
4
of gingival fluid and leukocytes (in particular neu-
trophilic granulocytes) and concomitant infiltration
with mononuclear leukocytes (39). On closer inspec-
tion, however, the pocket situation demonstrates
characteristic features distinctly different from the
healthy conditions in a gingival sulcus environment
(Figs 3–5). The major differences can be summarized
as follows:
 definite detachment of junctional epithelium from
the tooth surface and conversion into pocket
epithelium, leading to formation of an intra-
epithelial cleft.
 proliferation of epithelial ridges into the inflamed
soft connective tissue with very thin regions
between these ridges.
 focal micro-ulcerations of the epithelial ridges and
at the free surface of the pocket epithelium.
 increased permeability of the pocket epithelium.
 high infiltration, particularly of the epithelial
ridges, with lymphocytes, including T- and B-cells
and plasma cells.
 increased migration of neutrophilic granulocytes
through the pocket epithelium.
 change in direction of the exudate from apico-cor-
onal to horizontal (i.e. toward the tooth root sur-
face).
 seamless transition from pocket epithelium to
junctional epithelium at the pocket fundus.
 significant reduction in height of the residual
junctional epithelium.
The condition of the soft connective tissue may
depend on the severity and duration of the disease.
Figure 4 shows a very active phase of destruction in
which all fibroblasts and collagen fibers around the
epithelial ridges are lost and replaced with inflamma-
tory and immune cells. More peripheral, residual col-
lagen fibers and fibroblasts demarcate the highly
infiltrated (former) connective tissue area from
healthy tissue. The morphology of the pocket can
vary greatly because extension of the pocket occurs
Fig. 3. Light micrographs demon-
strating (A) junctional epithelium
(JE) and (B) pocket epithelium (PE).
The JE adheres on the enamel sur-
face (ES, enamel space), while the PE
is separated from the biofilm (BF)-
covered tooth surface by the pocket
space (PS).
 Periodontal pocket formation

A B

C D

Fig. 4. Light micrographs showing

acute inflammation of a human
tooth affected by periodontitis. The
rectangles in A are enlarged in B, C
and D. (A) The area of the inflamed
connective tissue (ICT) is quite large
and demarcated by residual collagen
fibers (CF) seen in the lower left
right. The pocket epithelium (PE)
has proliferated deeply into the ICT.
(B) Higher magnification of the bor-
der region between ICT and intact
connective tissue. (C) The surface of
the PE facing the pocket space is
very thin. (D) Occasionally, the PE is
ulcerated and the adjacent ICT is
heavily infiltrated.

not only by apical deepening but also by widening in
a horizontal direction, which leads to undermining
pockets.
Pockets also occur in conditions of disease around
dental implants (Fig. 6). In recent reviews, it was con-
cluded that peri-implant mucositis and peri-implanti-
tis lesions do not differ fundamentally from gingivitis
and periodontitis lesions, respectively, from the per-
spectives of etiology, pathogenesis, risk assessment,
diagnosis and therapy (21, 30). However, there appear
to be histopathological differences in the host
response to infections around implants and teeth in
the sense that persistent biofilm may elicit a more
pronounced inflammatory response in mucosal tis-
sue around implants than around teeth (5, 21). Struc-
tural changes (in vascularity and the fibroblast-to-
collagen ratio) and, consequently, functional dispari-
ties may account for this difference. It is noteworthy
that the presence of excess cement at the abutment–
crown interface provides an ideal substrate for plaque
and calculus deposition and retention (Fig. 6) and is
associated with peri-implant disease (55). Overhang
at such sites may impede calculus and biofilm
removal. It has been shown that clinical and endo-
scopic signs of peri-implant disease are absent in the
majority of cases after excess cement removal (55).
Consequences
The defense mechanisms in a healthy periodontal sit-
uation are generally sufficient to control the constant
microbiological challenge through a normally func-
tioning junctional epithelium and a concentrated
powerful mass of inflammatory and immune cells
and macromolecules transmigrating through this
epithelium. In contrast, the destruction of the struc-
tural integrity of the junctional epithelium, which
includes disruption of cell-to-cell contacts and
detachment from the tooth surface, consequently
leading to pocket formation, disequilibrates this deli-
cate defense system. Deepening of the pocket and
apical, but also horizontal, expansion of the biofilm
puts this system to a grueling test. There is no more

5
Bosshardt
A B
C D
A B
this powerful concentration of defense cells and
macromolecules that are discharged at the sulcus
bottom and that face a relatively small biofilm surface
in the gingival sulcus. In a pocket situation, the
defense cells and the macromolecules are directly
6
Fig. 5. Transmission electron micro-
graphs showing higher magnifica-
tions of the tissue biopsy seen in
Fig. 4. (A) The pocket epithelial cells
(EC) are poorly connected to one
another in the epithelial ridges and
leukocytes are seen within and adja-
cent to the pocket epithelium. (B)
Other regions show better cell con-
nectivity within the pocket epithe-
lium. Total disappearance of
collagen fibers and fibroblasts is evi-
dent in the inflamed (former) con-
nective tissue. (C) Various leukocytes
are present in the inflamed former
connective tissue. (D) Towards the
margin of the inflamed region, colla-
gen fibers (CF) are present.
Fig. 6. Peri-implant mucositis with-
out (A) and with (B) the presence of
excess cement at the abutment–
crown interface. The excess cement
provides an ideal substrate for pla-
que and calculus deposition and
retention. Detachment of the epithe-
lium indicates peri-implant pocket
formation. The detachment of the
apical-most portion of the epithe-
lium, however, may be an artifact
caused by histological processing.
PE, pocket epithelium. (Fig. 6B from
Bosshardt & Lang. Dental Calculus.
In: Clinical Periodontology and
Implant Dentistry. J Lindhe, NP
Lang, eds. Wiley Blackwell. 2015.).
discharged into the periodontal pocket and the
majority of epithelial cells directly face the biofilm.
The thinning of the epithelium and its ulceration
increase the chance for invasion of microorganisms
and their products into the soft connective tissue and

aggravates the situation. Depending on the severity
and duration of disease, a vicious circle may develop
in the pocket environment, which is difficult or
impossible to break without therapeutic intervention.
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