Basic periodontology Topic, it is a part of gingiva attached with the tooth.

1. Clinical significance
of Junctional
Epithelium
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2. Introduction
 Current knowledge of the structure and function of
the junctional epithelium permits definition of the
anatomic boundaries of the gingival sulcus.
 The base of the gingival sulcus comprises the
coronalmost aspect of the junctional epithelium.
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3. Why maintaining normalcy (homeostasis) in the
gingival sulcular region is more important ?
 This is the site at which microbial accumulation (dental
plaque) takes place, inflammatory gingival and
ultimately, periodontal diseases originate.
 The gingival sulcus is the area in which dentists
determine whether disease is present in a patient, and
this is the locus where severity of disease is assessed.
 Treatment is aimed to maintain/restore healthy gingival
sulcus
 It is toward the sulcus that the patient must target
rigorous home care measures.
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4. Dynamic aspects of
the Junctional Epithelium
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 unique structural and functional
features that preventing pathogenic
bacterial flora from colonizing the
subgingival tooth surface
 1.epithelial barrier against the plaque
bacteria

5. 2. rapid turnover, which contributes to the host–
parasite equilibrium and rapid repair of damaged
tissue.
3. allows the access of GCF, inflammatory cells and
components of the immunological host defense to
the gingival margin.
4. Attachment to tooth and capacity to regenerate.
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6. Rapid turnover of the Junctional
epithelial cells
 Schroeder studied, area covered
by the dividing cells in the
junctional epithelium is at least
50 times larger than the area
through which the epithelial cells
desquamate into the gingival
sulcus, there is a strong
funnelling effect that contributes
to the flow of epithelial cells
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7.  Turnover times for different areas of the oral
epithelium in experimenting animals:
 Palate, tongue and cheek: 5-6 days
 Gingiva 10-12 days
 Junctional epithelium: 1-6 days
 Regarding JE, epithelial cells facing external
basal lamina are rapidly dividing.
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8. Antimicrobial defense
 The intercellular spaces provide a pathway for
GCF and transmigrating leukocytes. In the
absence of clinical signs of inflammation,
approximately 30,000 PMNs migrate per minute
through the junctional epithelia of all human teeth
into the oral cavity (Schiött and Löe, 1970).
 its flow rate corresponds to the degree of
inflammation.
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9. Expression of various Molecules
and their function
 Knowledge about structure and molecules
involved in the maintenance of cell-cell contact is
particularly important in view of the pathological
changes that the epithelium undergoes during its
conversion to a pocket lining.
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10.  Integrins – are cell surface receptors that mediate
interactions between cell and extracellular matrix,
and also contribute to cell to cell adhesion.
 Cells in contact with the internal basal lamina
(adjecent to enamel) express the integrins.
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11.  The cadherins are responsible for tight contacts
between cells.
 E-cadherin, an epithelium specific cell adhesion
molecule, plays a crucial role in maintaining the
structural integrity.
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Carcino-embryogenic Ag related cell adhesion
molecule – 1 (CEACAM)
 guidance of PMNs through JE, proliferation, stimulation & co-
regulation of T- Cells. - Odin et al & Öbrink et al
Intercellular adhesion molecule – 1 (ICAM-1)
 cell-cell interactions in inflammatory reactions- Crawford
and Hopp
Lymphocyte function antigen-3 (LFA-3)
 controls leukocyte migration to inflammatory site - Crawford

13.  Interleukin-8 (IL-8)
 Interleukin-1(IL-1)
 Tumour necrosis factor (TNF)
 Chemotaxis; guiding PMNs toward the sulcus bottom
 innate immune defense
Tonetti et al.
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14. Role of JE in the
initiation of pocket formation
 the conversion of the junctional epithelium to
pocket epithelium is regarded as a hallmark in the
development of periodontitis.
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15.  Schluger et al (1977): Pocket formation is
attributed to a loss of cellular continuity in the
coronal most portion of the JE
 Thus the initiation of pocket formation may be
attributed to the detachment of the DAT cells
from the tooth surface or to the development of
intraepithelial split.
 Takata and Donath (1988): observed
degenerative changes in the second or third
layer of the DAT cells in the coronal most portion
of the JE cells facing the biofilm.
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16.  Schroeder and Listgarten (1977):
An increased number of
mononuclear leukocytes (T and B
cells, macrophages) together with
PMNs are considered as factors
contributing to the disintegration
of the JE.
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The degeneration and detachment of
DAT cells exposes tooth surface and
creates a sub-gingival niche suitable
for the colonization of anaerobic gram-
negative bacteria and apical growth of
dental plaque.

17.  Hintermann et al 2002: Gingipains degrade the
epithelial cell-cell junctional complexes and cells
exposed to this cysteine proteinases derived from
P.gingivalis showed reduced adhesion to extracellular
matrix.
 Gingipains may also disturb the ICAM-1-dependent
adhesion of PMNs to oral epithelial cells, an immune
evasion mechanism by P. gingivalis, points to the
importance of these molecules for the disintegration of
the junctional epithelium (Tada et al., 2003).
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18. Regeneration of the
Junctional epithelium
 Injury of the junctional epithelium may occur
through accidental or intentional trauma,
toothbrushing, flossing, or clinical probing.
 a new and complete attachment indistinguishable
from that in controls was established 5 days after
complete separation of the junctional epithelium
from the tooth surface
(Taylor and Campbell, 1972)
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19.  re- establishment of the epithelial seal
around implants after clinical probing was
shown to occur within about the same time
period (Etter et al., 2002).
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20.  Waerhaug (1981) studied healing of the junctional
epithelium following the use of dental floss at
premolars in 12-year-old humans.
Detachment of cells persisted for 24 hrs after
flossing ceased.
 New attachment of junctional epithelial cells started 3
days after flossing ceased. After 2 wks, the cell
populations on the experimental and control surfaces
were again indistinguishable from each other.
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21.  In humans, a new junctional epithelium
after gingivectomy may form within 20 days
(Listgarten, 1972;
Schroeder and Listgarten, 1977).
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22. Biologic Width
 Biological width is defined as the
dimension of soft tissue which is
attached to the portion of the tooth
coronal to the crest of alveolar bone.
-Gargiulo et al (1961)
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23.  Gargiulo et al (1961) described the dimensions and
relations of dentogingival junction in humans.
The average histological width of connective tissue
attachment is 1.07mm. The mean average length of
epithelial attachment is 0.97mm.
 The average combined histological width of connective
tissue attachment and junctional epithelium was
2.04mm, which is referred to as the BIOLOGIC
WIDTH.
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 It is important from the restorative point of view
because its violation leads to complications like
gingival enlargement, chronic progressive
inflammation of gingiva around margins of
restoration, alveolar bone loss and improper fit of
the restoration.
 when the implant-abutment connection was placed
at the gingival level supracrestal to the alveolar
bone, the biologic width measurement was similar
to natural dentition.

25. JE AROUND IMPLANTS
 The junctional epithelium around implants always
originates from epithelial cells of the oral mucosa,
as opposed to the junctional epithelium around
teeth which originates by merging of REE and OE
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NATURAL TOOTH
 Epithelium tapers
towards the depth
 Large number of
cell organelles
 Fibers are
arranged
perpendicular
IMPLANT
Epithelium is thicker
Few organelles
Fibers are arranged
parallely

26. Concluding remarks
 The junctional epithelium is a unique tissue that fulfills
a challenging function at the border between the oral
cavity, colonized by bacteria, and the tooth attachment
apparatus.
 It is structurally and functionally very well-adapted to
control the constant presence of bacteria and their
products. However, its antimicrobial defense
mechanisms do not preclude the development of
inflammatory lesions in the gingiva.
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27.  These defense mechanisms may be overwhelmed
by bacterial virulence factors, and the gingival
lesion could progress to periodontitis.
 Recent studies have shed light on the role of
gingipains in this process. Such new information
may be used to develop therapeutic strategies
aimed at neutralizing the detrimental effects of
these cysteine proteinases.
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28. References
 DD Bosshardt and NP Lang. The Junctional Epithelium: from health to
disease. J Dent Res 2005, 84 (1): 9-20.
 Moon Cho & Philias R. Garant. Development and general structure of the
periodontium. Periodontology 2000, Vol. 24, 2000, 9–27.
 Mark Bartold, Laurence J. Walsh & A. Sampath Narayanan. Molecular and
cell biology of the gingiva.P. Periodontology 2000, Vol. 24, 2000, 28–55.
 Thomas M Hassell. Tissues and cells of the periodontium. Periodontology
2000, Vol. 3, 1993, 9-38
 Huberte . Schroede & R M Listgarten. The gingival tissues: The architecture
of periodontal Protection. Periodontology 2000, Vol. 13, 1997, 91-120.
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