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RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
• Epithelium has wide intercellular gaps, larger than those in either sulcular or
oral epithelium.
• Hence, even in healthy gingiva, numerous polymorphonuclear leukocytes are
evident.
• During inflammatory conditions, the numbers of these cells increases
dramatically.
• Lymphocytes are also found inside the epithelial lining in the junctional
epithelium.
• The junctional epithelium exhibits several characteristic features such as acting
as a barrier against plaque bacteria & allowing access of gingival fluid,
inflammatory cells & components of the immunologic host defence to the
gingival margin.
• It also possesses a rapid turnover contributing to the host–parasite equilibrium
& repair of injured tissue.
RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
A: An electron micrograph of junctional epithelium (JE) showing the attachment to the enamel surface
at the internal basal lamina (IBL) & to the connective tissue (CT) by the external basal lamina (EBL). The
lack of differentiation of the epithelium & the wide intercellular spaces are notable. ES, Enamel space.
B: An electron micrograph showing the fine structure of the attachment of a junctional epithelial cell to
the enamel surface via the internal basal lamina. Hemidesmosomes (HD) are evident at the surface of
the cell. TEN CATE’S ORAL HISTOLOGY 9TH EDITION
Bosshardt, D. D. & Lang, N. P. The junctional epithelium: from health to disease. J. Dent. Res. 2005; 84, 9–20.
Bosshardt, D. D. & Lang, N. P. The junctional epithelium: from health to disease. J. Dent. Res. 2005; 84, 9–20.
DEVELOPMENT OF THE JUNCTIONAL EPITHELIUM
• The enamel of the unerupted, fully formed crown is covered by a few layers of
flattened cuboidal cells called reduced enamel epithelium.
• Normally, it terminates at the cementoenamel junction.
• At this early stage, the epithelial attachment to the crown surface is by means of
hemidesmosomes.
• When the tooth breaks through the oral mucosa, the reduced enamel epithelium
fuses with the oral epithelium & is converted into the junctional epithelium,
forming a collar around the fully erupted tooth.
• Concurrently, gingival sulcus is also formed.
• This process takes 1–2 years to get completed.
• The junctional epithelium, like all squamous epithelia, is a continually renewing
structure with epithelial cells moving coronally to be shed off at the free surface
into the base of the sulcus.
RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
TEN CATE’S ORAL HISTOLOGY 9TH EDITION
MIGRATION OF THE JUNCTIONAL EPITHELIUM
• The position of the junctional epithelium varies with different stages of eruption.
• During the initial stages of eruption, the junctional epithelium covers most of the
crown portion of the tooth.
• Once the tooth reaches the occlusal plane, the junctional epithelium covers
about one-fourth of the crown.
• At this stage, the clinical crown is smaller than the anatomical crown.
• As age increases, the junctional epithelium migrates to the cementoenamel
junction, placing the clinical & the anatomical crown at the same level.
• In older age, it migrates to the cementum exposing the roots leading to a larger
clinical crown.
• This process occurs due to the detachment of the basal layer of cells.
• This basal layer of cells further get reattached at a more lower/apical level.
RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
RAJKUMAR’S TEXTBOOK OF ORAL ANATOMY, HISTOLOGY, PHYSIOLOGY AND TOOTH MORPHOLOGY 2ND EDITION
• Epithelial tissues form junctional
complexes to maintain a continuous
demarcation against the external INTRODUCTION
environment and prevent the invasion of
foreign substances inside the living body.
• Tooth eruption collapses the continuity
of epithelial tissue in the oral cavity.
• Erupted teeth are surrounded by the
gingival epithelium, which is one of the
most specialized tissues of the body
because the discontinuity of the gingival
epithelial sheath renders it susceptible
to bacterial infection from dental
plaques and periodontal disease.
THE GINGIVAL EPITHELIUM CONSISTS OF:
ORAL
ORAL GINGIVAL
GINGIVAL
EPITHELIUM
EPITHELIUM
ORAL
ORAL SULCULAR
SULCULAR
EPITHELIUM
EPITHELIUM
JUNCTIONAL
JUNCTIONAL EPITHELIUM
EPITHELIUM
•• The JE attaches to the tooth surface via hemidesmosomes, which forms the front-line
The JE attaches to the tooth surface via hemidesmosomes, which forms the front-line
of
of defense
defense against
against periodontal
periodontal bacterial
bacterial infection.
infection.
•• The JE originates from the enamel organ and constructs the gingival epithelium along
The JE originates from the enamel organ and constructs the gingival epithelium along
with
with OGE
OGE and
and OSE,
OSE, which
which are
are derived
derived from
from the
the oral
oral epithelium.
epithelium.
•• The OGE and OSE are keratinized squamous epithelial cells with narrow intercellular
The OGE and OSE are keratinized squamous epithelial cells with narrow intercellular
space.
space.
•• On the contrary, the JE is non-keratinized epithelium and has wide intercellular
On the contrary, the JE is non-keratinized epithelium and has wide intercellular
space.
space.
•• In addition, many migrating cells such as PMNs and lymphocytes are located within
In addition, many migrating cells such as PMNs and lymphocytes are located within
JE.
JE.
•• The JE shows rapid turnover, which might contribute to its defense against dental
The JE shows rapid turnover, which might contribute to its defense against dental
plaque.
plaque.
TEN CATE’S ORAL HISTOLOGY 9TH EDITION
Saha AP et al (2018) stated that junctional epithelium represents a dynamic seal
around the tooth, at a strategically important interface of oral cavity (flushed with oral
fluid containing in numerous pathogens) and delicate periodontal tissues. This is a
specialized unique tissue, capable enough to act as a barrier against the bacterial
challenge by adapting both structurally and functionally as per the requirement. The
integrity of this tiny tissue carries extreme importance for the health of supportive
periodontal structures, and virtually the tooth. Detachment of junctional epithelium
from tooth surface initiates formation of periodontal pocket, and hence periodontitis.
Saha AP, Saha Sananda, Mitra Somadutta. Junctional Epithelium: A dynamic seal around the tooth. Journal Of Applied Dental and Medical Sciences. 2018; 4(3).
• JE is classified as non-keratinized
stratified squamous epithelium.
• Intercellular junctions formed in JE are STRUCTURE
relatively loose and contain only few
desmosomes, adherens junctions, and
gap junctions, which allow tissue
exudate and inflammatory cells to
penetrate toward the gingival sulcus.
• JE has a true basement membrane towards the connective tissue of gingiva (called
the external basal lamina, EBL) and a simple ECM (called the internal basal lamina,
IBL) against the enamel.
• The EBL contains structures that are identical to those of a typical basement
membrane, with the lamina lucida against the basal keratinocytes and the lamina
densa towards the underlying connective tissue.
• The protein composition of the IBL differs significantly from that of a typical
basement membrane.
• The IBL does not contain any typical basement membrane-forming proteins such as
laminin 111, laminin 511, type IV and VII collagens, and perlecan.
• The main cell adhesion protein identified so far in the IBL is laminin 332.
TEN CATE’S ORAL HISTOLOGY 9TH EDITION
• Furthermore, reports show the presence of type VIII collagen and versican at the JE-
tooth interface.
• ICAM-1 expression is initiated during the formation of the papillary layer. However,
all stages of ameloblasts do not express ICAM-1.
• The papillary layer adheres to the oral epithelial tissue during tooth eruption. These
results indicate that the JE might have originated from papillary layer cells and not
the reduced ameloblasts.
• SLPI protects the intestinal epithelium from proteases secreted as part of the
inflammatory response and is associated with the maintenance of tissue integrity.
• KC and MIP-2 are potent chemo attractants for neutrophils. The expression of these
chemokines is up-regulated by bacterial stimulation.
• The JE also constitutively express follicular dendritic cell-secreted protein (FDC-SP)
and odontogenic ameloblast-associated protein (ODAM).
• Furthermore, the gene encoding FDC-SP lies adjacent to the cluster of genes encoding
C—X—C chemokines.
• The interaction of LFA-1 and ICAM-1 plays a key role in the migration of these cells in
JE.
• Endothelial cells and fibroblasts underlying the JE also express ICAM-1, which might
provide a pathway for granulocytic and lymphocytic migration into JE.
Yajima-Himuro S et al (2014) stated that the epithelium, called the junctional
epithelium (JE), is directly attached to the tooth surface (enamel) and has a defensive
role against continuous bacterial infection. After bacterial pathogenic components in
dental plaque, such as lipopolysaccharide, cause gingival inflammation, the defense
system is destroyed; furthermore, the JE is detached from the tooth surface and
transformed to the pocket epithelium and a small area remains attached to the root
(attachment loss). The periodontal tissue breakdown begins here. Therefore, the JE is
involved in the pathogenic mechanism of periodontitis.
Yajima-Himuro S, Oshima M, Yamamoto G, Ogawa M, Furuya M, Tanaka J, et al. The junctional epithelium originates from the odontogenic epithelium of an
erupted tooth. Sci Rep. 2014;4:4867.
• The commensal microflora plays a
ROLE OF
critical role in the postnatal COMMENSAL
development of the system, as the MICROFLORA
physiological inflammatory response in
the gut during early postnatal
ontogenesis is essential for the
development of the immune system and
its appropriate functioning.
• An interaction between commensal bacteria and the innate defense system of the
periodontal tissue has also been reported.
• Hayashi et al. observed the increased expression of SLPI in the JE compared to that in
oral gingival epithelium.
• Thus, the constitutive expression of these factors and the migration of neutrophils in
the JE might be induced by intrinsic genetic regulation rather than by bacterial
infection for the maintenance of the functional specificity of the JE.
• Histological examination indicated an increase in the JE area in conventional mice.
• Tsukamoto et al. evaluated the relationship between epithelial cell proliferation and
inflammation in clinically healthy and inflamed human gingival tissue and found that
epithelial cell proliferation and epithelial thickness were associated with gingival
inflammation. Similarly, chemokines were induced by bacterial lipopolysaccharide.
• In contrast, IELs produce growth factors to regulate the epithelial cell proliferation.
• Previous studies from laboratories
indicated that IELs in the duodenum EXPECTED
and jejunum induced enterocyte FUNCTION OF IELs
apoptosis within 30 min after activation
by anti-CD3 antibody treatment.
• Cytotoxic activity of IELs is inhibited by
immunosuppressive agents such as
cyclosporine A (CsA) and FK506, which
induce the elongation of intestinal villi
and decrease enterocyte activity.
• The JE plays an active role in the synthesis of a variety of molecules that are involved
in anti-bacterial defense.
• Therefore, the balance between cell death and mitotic activity is critical for
maintaining the number of JE cells, which affects the defensive properties of the JE,
and eventually, disease progression.
• The JE and OSE have a high rate of cell turnover. The JE shows higher proliferation
than the OSE.
• To maintain the structure of the inner gingival epithelium over time, either the cell
cycle of the two epithelial tissues must be identical or cells of the epithelium showing
high proliferative activity should be eliminated.
• Three weeks treatment with Cyclosporin A (25 mg/kg) induced the elongation of JE.
• In normal conditions, the tips of the JE are always located under the OSE, while the
tips of the JE are guided to a position higher than the OSE by CsA treatment, which
indicate that the cytotoxic activity of IELs expressing TCRγδ+ might be inhibited by
CsA.
• These results suggest that IELs in the JE regulate epithelial cell survival for
maintaining barrier function against bacterial stimulation similar to that in the
gastrointestinal tract.
• The inhibition of rapid turnover of JE might decrease the survival activity and the
barrier function of JE, and permit the easy penetration of bacterial LPS into the
gingival connective tissue.
• The JE is the only discontinuous epithelial
tissue in the body. The JE functions as a
front-line barrier against foreign antigens
with structural and functional features CONCLUSION
such as adhesion to tooth surface via
formation of basal lamina, large
intercellular space, expression of several
cytokines and chemokines, and the
penetration of neutrophils and
lymphocytes to play as the front-line innate
immune system and to maintain the JE
homeostasis. Further understanding of the
structure and function of the JE would
provide better understanding of systemic
host defense system and specificity of the
oral mucosal tissue.
• TEN CATE’S ORAL HISTOLOGY 9TH EDITION