12. ▪ Ground substance in the lamina propria contains glycoproteins and
proteoglycans.
* Heparin
* Hyaluronan
* Heparin sulfate
*Versican
* Decorin
*Biglycan
* Syndecan
▪ Collagen fibers are of type I & III. Presence of elastic fibers in the lining
mucosa helps to restore tissue form after stretching.
14. Permanently wet, warm, nutrient rich oral cavity
Perfect environment for microorganisms
Forms complex ecological system
Attaches to glycoprotein layer on solid/ non shedding surfaces
Tissue in vicinity are constantly challenged.
15. ▪ The tooth-epithelial interface thus call for a specialized structural and
functional adaptation called “Junctional epithelium”’.
16. JUNCTIONAL EPITHELIUM
▪ The Junctional epithelium consists of a collar like band of stratified
squamous non-keratinizing epithelium.
(Carranza’s 11th Edition)
• A single or multiple layers of non-keratinizing cells adhering to the
tooth surface at the base of the gingival crevice. Formerly called
epithelial attachment.
(Glossary of periodontal terms)
▪ JE is the epithelial component of the dento - gingival unit that is in
contact with the tooth surface. The innermost cells of the JE form
and maintain a tight seal against the mineralized tooth surface, the
so called “Epithelial attachment”.
(Schroeder and Listgarten,1977)
17.
18. ▪ Epithelial tissues form junctional complexes to maintain a continuous
demarcation against the external environment and prevent the
invasion of foreign substances inside the body.
▪ Tooth eruption collapses the continuity of the epithelial tissue in the
oral cavity.
19.
20. DENTO – GINGIVAL UNIT
▪ Dento-gingival unit refers to the functional unit comprising of
junctional epithelium and the gingival fibers.
21. HISTORICALASPECTS
▪ “Gottilieb”(1921) was the 1st to describe the junctional epithelium.
▪ “Schroeder” & “Listgarten” (1977) clarified the Anatomy and
Histology of the dento gingival junction in their monograph “Fine
structure of developing epithelial attachment of human teeth”.
22. GOTTILIEB 1921:
▪ His experimental and clinical observations led to the concept that the Soft
tissue of gingiva is organically united to enamel surface.
▪ He termed the epithelium contacting the tooth the “Epithelial attachment”.
▪ Primary enamel cuticle.
▪ Secondary enamel cuticle
23. ORBAN’s CONCEPT 1944:
Orban incorporated the views of ‘Meyer’, ‘Beck’ & ‘Weski’ by
stating that the separation of the epithelial attachment cells from the
tooth surface involved preparatory degenerative changes in the
epithelium.
▪ This statement was a sharp departure from the Gottilieb’s concept of
production of a cornified cuticle layer.
24. WAERHAUGH’s CONCEPT 1952:
▪ He presented the concept of “Epithelial cuff”.
▪ This concept was based on the insertion of thin blades between the
surface of tooth and the gingiva.
▪ Blades could be easily passed apically to the CT attachment at CEJ
without resistance.
▪ It was concluded that gingival tissue and tooth are closely adapted
but not organically united.
25. SCHROEDER & LISTGARTEN CONCEPT 1971:
▪ The previous controversy was resolved after evolution of
transmission electron microscopy.
▪ ‘Primary epithelial attachment’
26. ▪ Secondary epithelial attachment
▪ Based on Transmission electron microscopic studies, he proved the
existence of a hemidesmosomal basal lamina attachment between
the tooth and the cells of the so called the cells of epithelial
attachment.
28. DEVELOPMENT OF JE
▪ The JE forms as the tooth crown erupts into the oral cavity.
▪ Steps-
i) Formation of REE
ii) Union of REE & oral epithelium
iii) As the tooth erupts, REE is converted into JE.
29.
30.
31. Ameloblasts
become reduced
in height,(basal
lamina) + OEE
REE
REE surrounds the
crown of the tooth
until the tooth
erupts
Eruption cells of
outer layer of REE &
basal layer of oral
epithelium mitotic
activity & migrates
into CT
Epithelial mass
between oral
epithelium & REE
When crown
breaches the oral
mucosa a slow cell
transformation
process develops.
REE gradually
converts into JE
32. STRUCTURE OF JE
▪ JE tapers off in the apical direction, and it consists of 15-30 cell layers
coronally and only 1-3 layers at its apical termination.
▪ It is a stratified squamous non-keratinizing epithelium that is made of
2 strata only-
i) a basal layer (Stratum basale)
ii) a supra basal layer (Stratum suprabasale)
33. ▪ The innermost suprabasal cells are also called DAT cells (directly
attached to the tooth).
▪ They form and maintain the “Internal basal lamina” that faces the
tooth surface.
34.
35. MICROSCOPIC STRUCTURE:
▪ Lysosomal bodies
▪ Cytokeratin bundles
▪ Golgi bodies
▪ Cisternae of RER
▪ Polyribosomes
▪ Cytokeratins No. 5,13,14&19 and occasionally weak activity for No.
8,16&18.
36. ▪ Few desmosomes and occasionally by gap junctions.
▪ Intercellular spaces may vary in width, but are wider in comparison
with the oral gingival or sulcular epithelium. These accounts for
permeability of JE.
▪ Mononuclear leucocytes & PMN’s -central region of JE and near tooth
surfaces.
▪ Lymphocytes and macrophages reside in and near the basal cell
layers.
37. ▪ Antigen presenting cells and Langerhans cells and other dendritic
cells are also present.
▪ Basal layer is well innervated by sensory nerve fibers.
38. EPITHELIAL ATTACHMENT APPARATUS:
▪ The attachment of JE to the tooth is mediated through an ultra
microscopic mechanism called as “Epithelial attachment apparatus”.
▪ It consists of hemidesmosomes at the plasma membrane and a basal
lamina-like extracellular matrix, termed the “Internal basal lamina”
on the tooth surface.
▪ While a basement membrane sometimes referred to as “External
basal lamina” (Schroeder,1996), is interposed between the basal
cells of the JE and the gingival CT.
41. ▪ They usually consists of - * Lamina lucida
* Lamina densa
* Lamina fibroreticularis
42. ▪ Typical matrix constituents of the basement membrane are
-Collagen types IV &VIII
- Laminin
- Heparin sulfate
- Fibronectin
- Nidogen
- Perlecan
43. ▪ Internal basal lamina proteins include laminin and typeVIII collagen.
▪ Laminin identified as type V (Ln332), is localized mainly to the electro
dense part of IBL.
▪ Characteristically, the IBL lacks laminin-1 and type IV collagen which
are components of true basement membranes.
44. HEMIDESMOSOMES:
▪ Hemidesmosomes have a decisive role in the firm attachment of the
cells to the IBL on the tooth surface.
▪ It may also act as specific sites of signal transduction and thus
participate in regulation of
*Gene expression
*Cell proliferation
*Cell differentiation.
45. ▪ The intracellular part of the hemidesmosomes consists of at-least 2
distinct proteins,
- BP 230 (230KDa bullous pemphigoid antigen)
- Plectin
46.
47. ▪ These proteins mediate the attachment of the cell cytoplasmic
keratin filaments to 2 trans membrane components of the
hemidesmosomes known as –
- 180KDa bullous pemphigoid antigen (BP180)
- a6b4 integrin
48. EXPRESSION OFVARIOUS MOLECULES &
THEIR FUNCTONS
▪ Numerous cell and extracellular molecules regulate maintenance of
normal tissue architecture and function.
▪ Cells have surface or cell membrane molecules that play a role in cell
matrix and cell-cell interactions.
▪ JE cells express numerous cell adhesion molecules (CAMs), such as
Integrins and Cadherins.
49.
50. ▪ Cadherins are responsible for tight contact between cells.
▪ E-cadherin, an epithelium specific CAM, plays a crucial role in
maintaining structural integrity.
▪ Intercellular adhesion molecule-1 (ICAM-1 or CD54) and lymphocyte
function antigen-3 (LFA-3) are additional cell adhesion moelcules.
▪ CEACAM-1, (Carcino embryogenic Ag cell adhesion molecule)
▪ High expression of IL-8, a chemotactic cytokine, is seen in the
coronal-most cells of JE.
51. ▪ IL-1α, IL-1β,TNF-α are strongly expressed in the coronal half of JE.
▪ N-acetyllactosamine, the type2 chain H precursor of the blood group
A-specific carbohydrate, which is usually associated with the lowest
level of cell differentiation.
▪ Anti microbial molecules – α,β defensins, cathelicidin family,
calprotectin
52. MATURATION:
The process of cell migration from the basal layer to the
surface is called “Maturation”.
DIFFERENTIATION:
During its migration as a keratinocyte, basal cells becomes
committed to various biochemical and morphological changes.
DESQUAMATION:
The process of shedding of surface epithelial cells is called
“Desquamation”.
53. TURNOVER RATE:
The time taken for a cell to divide and pass through the entire
epithelium is called as “Turn over rate”.
54.
55. DYNAMIC ASPECTS OF JE
▪ Coronal part of JE- DAT cells -Transferrin receptors.
▪ Structural or molecular changes in IBL
56. ▪ Changes in the cell metabolism
▪ Morphological studies of the IBL of teeth extracted because of
advanced periodontitis have shown that remnants of IBL can be
detected even adjacent to severely degenerated DAT cells.
57. MECHANISM OF JE CELLSTURNOVER:
i. The daughter cells produced by dividing DAT cells replace degenerating cells on the
tooth surface.
ii. The daughter cells enter the exfoliation pathway and gradually migrate coronally
between the basal cells and the DAT cells to eventually break off into the sulcus, or
iii. Epithelial cells move/migrate in the coronal direction along the tooth surface and are
replaced by basal cells migrating around the apical termination of the JE.
58. PERMEABILITY OF JE
▪ JE is the most permeable portion of the gingival epithelia.
▪ Because of its permeability to bacterial products and other assorted
antigens, the CT adjacent to the JE tends to become infiltrated with
chronic inflammatory cells, primary lymphocytes and plasma cells.
59. FUNCTIONS OF JE
Epithelial barrier
Permeability barrier
Rapid turnover rate
Anti-microbial defense
GCF flow
60. JE INTHE ANTI-MICROBIAL DEFENSE
▪ active populations of cells and anti-microbial functions
▪ barrier
61. ▪ The area covered by the dividing cells in the JE is at-least 50 times
larger than the area through which the epithelial cells desquamate
into the gingival sulcus, is a strong funneling effect that contributes
to the flow of epithelial cells.
▪ Rapid shedding and effective removal of bacteria adhering to
epithelial cells is therefore an important part of the anti-microbial
defense mechanisms at the dento-gingival junction.
62. ROLE OF ENZYMES INTHE ANTI-MICROBIAL DEFENSE OF JE:
▪ There is an increasing evidence that several specific antimicrobial
defense systems exist in the oral mucosa.
▪ enzyme-rich lysosomes. Their fusion with plasma membrane is
triggered by the elevation of the intracellular Ca concentration
(Rodriguez et al.1997).
▪ In rats, lysosomes have been demonstrated to contain cysteine
proteinases (Cathepsin B&H) active at acidic pH (Yamaza et al.1997).
63. ▪ It has been found that the JE cells lateral to DAT cells produce
“Matrilysin”(MMP-7) (UittoVJ et al.2002).
▪ Contributes to the mucosal defense by the release of bioactive
molecules from the cell surfaces.
64. ▪ Several anti-microbial mechanisms exist in JE. In the coronal part of JE, quick cell
exfoliation occurs due to-
i) Because of rapid cell-division
ii) Funneling of JE cells towards the sulcus hinder bacterial colonization.
iii) Active anti-microbial substances are produced in JE cells.
iv) Epithelial cells activated by microbial substances secrete chemokines like IL-8,
TNF-α that attract and activate professional defense cells.
65. JE IN DISEASE
DETACHMENT OF DAT CELLS FROMTHETOOTH SURFACE:
- Role of GCF
- Role of PMN’s
- Role of host proteinases & inflammatory mediators
- Role of bacterial products
- Role of risk factors for periodontal disease
66. ROLE OF GCF:
▪ GCF is an exudate of varying composition found in the sulcus/pocket
between the tooth and gingival margin.
▪ GCF contains components of serum, inflammatory cells, CT,
epithelium and microbial flora inhabiting the gingival margin of the
sulcus (Embery G et al.1992).
▪ GCF passing through the JE determines the environmental
conditions and provides sufficient nutrients for DAT cells to grow.
67. ▪ Main route of GCF diffusion is through the EBL and intercellular
spaces.
▪ At the gingival margin GCF may become contaminated so that
agents from the oral cavity/plaque challenge the most coronal DAT
cells.
68. ▪ In the healthy sulcus, the amount of GCF is very small. However, it
constituents participate in the normal functions of JE.
▪ During inflammation, GCF flow increases and its composition starts
to resemble that of an inflammatory exudate and have a flushing
action against the bacteria and bacterial products.
69. ROLE OF PMN’s:
▪ PMN’s are a major contributor in the host-parasite equilibrium.
▪ ‘Lactoferrin’ is an important anti-microbial protein present in the
PMN’s.
▪ High concentrations of lactoferrin, do, however, hamper the
epithelial cell growth by interfering with their adhesion and
spreading.
▪ The molecule may thus have a role in delaying the repair of JE/DAT
cell population during severe inflammation.
70. ROLE OF HOST PROTEINASES & INFLAMMATORY MEDIATORS:
▪ Degradation of extracellular matrix during periodontal inflammation
is a multi-step process that involves several proteolytic enzymes.
▪ MMP’s, plasminogen activator, cathepsins and elastase.
▪ Neutrophil elastase and cathepsin G are capable of degrading
basement membrane type IV collagen, laminin and also type VIII
collagen found in EBL.
▪ However, electron microscopic studies on DAT cells attached to teeth
extracted because of advanced periodontitis do not support the idea
that enzymatic degradation of the epithelial attachment apparatus
preceedes the degeneration of DAT cells.
71.
72. ROLE OF HOST:
▪ Factors include DM, smoking, immunosuppression, genetic factors,
stress and age.
▪ A sound inflammatory host response is needed for successful
periodontal defense.
73. ▪ If the JE is repeatedly or continuously exposed to bacterial
challenges, it may lead to-
* Degeneration of JE
* Sub gingival plaque formation
* Conversion of gingival sulcus into a periodontal pocket
* Increase in inflammatory focus in CT.
74. ROLE OF JE IN PASSIVE ERUPTION
▪ Passive eruption is the exposure of the teeth by apical migration of
gingiva.
▪ This concept distinguishes between anatomic crown and root and
between clinical crown and root.
▪ When teeth reach their functional antagonists, the gingival sulcus
and JE are still on enamel and the clinical crown is app.2/3rd of
anatomic crown.
▪ Passive eruption was originally thought to be a physiologic process, it
is now considered as a pathologic process.
77. JE IN POCKET FORMATION
▪ Conversion of JE into pocket epithelium is regarded as the hallmark
in the development of periodontitis.
Supra crestal
collagen
destruction
Apical
migration of
JE
Coronal
detachment
of JE
78.
79. ▪ 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.
80. ▪ 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.
▪ The degeneration and detachment of DAT cells exposes tooth
surface and creates a sub-gingival niche suitable for the colonization
of bacteria.
81. ▪ Hintermann et al 2002:
Gingipains degrade the epithelial cell- cell junctional
complexes and cells exposed to proteinases derived from P.gingivalis
showed reduced adhesion to extracellular matrix.
▪ Destruction of cell-cell and cell to ECM perturbs the structural and
functional integrity of the JE.
82. ▪ In pocket, JE-
* Cells are shorter than normal
* Cells are mostly in normal condition
* May exhibit slight degeneration
83. JE IN GINGIVITIS
▪ During the initial lesion of gingivitis, PMN’s leave the capillaries by
migrating through the walls.
▪ They can be see in increased quantities in CT, and JE and gingival
sulcus.
▪ JE becomes densely infiltrated with neutrophils and it may begin to
show development of rete pegs in the early lesion of gingivitis..
84.
85. JE in NUG
▪ Here the surface epithelium is destroyed and it is replaced by a
meshwork of fibrin, necrotic epithelial cells, PMN’s and neutrophils
and various types of microbes.
▪ The epithelium becomes edematous and there is infiltration of
PMN’s in the intercellular spaces.
86. KINDLER SYNDROME:
▪ A rare blistering disorder along with early onset of aggressive
periodontitis.
▪ Due to loss of kindlin-1 protein which is involved in integrin
activation.
▪ Here, JE fails to attach to the tooth surface.
87.
88. REGENERATION OF JE
▪ Injury of JE may occurs through accidental or intentional trauma,
tooth brushing, flossing or clinical probing.
▪ Clinical probing results in a mechanical disruption of JE cells from the
tooth.
89. ▪ In an experimental study in marmosets, following probing, a new and
complete attachment indistinguishable from that in controls was
established 5 days after complete separation of JE from the tooth
surface (Taylor & Campbell.1972).
90. ▪ The 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)
▪ Based on these 2 studies, probing around teeth and implants doesn’t
seem to cause irreversible damage to the soft tissue components.
91. ▪ Waerhaug 1987 studied healing of JE following the use of dental floss
at premolars in 12-year old patients.
▪ Detachment of cells persisted for 24 hrs after flossing ceased.
▪ New attachment of JE cells started 3 days after flossing ceased.
▪ After 2 weeks, cell populations on the experimental and control
surfaces were again indistinguishable from each other.
92. ▪ In above studies, JE was never completely removed from the tooth.
However, the gingivectomy would completely remove it.
▪ Subsequently, formation of new JE must occur from the basal cells of
the oral gingival epithelium (Listgarten,1967; Innes,1970).
▪ In humans, a new JE after gingivectomy may form within 2o days
(Listgarten,1972; Schroeder & Listgarten,1977).
93. JE AROUND IMPLANTS
▪ JE around implants always originates from the epithelial cells of oral
mucosa, as opposed to JE around teeth which originates form REE.
▪ Structurally, peri-implant epithelium closely resembles JE around the
teeth ( Berglundh et al.1991; Listgarten et al.1991).
▪ There is also evidence that several of the mentioned marker
molecules involved in the defense mechanisms against the bacterial
challenge are also expressed in peri-implant epithelium.
94. Natural tooth Implant
Epithelium tapers towards the
depth
epithelium is thicker
Large no. of cell organelles Few organelles
Fibers are arranged
perpendicularly
parallely
Numerous keratohyalin granules
96. BIBLIOGRAPHY
Carranza’s clinical periodontology-11th ed.
Jan Lindhe, Niklaus P. Lang -6th ed; Clinical periodontology and Implant
Dentistry.
Orban’s Oral Histology & Embryology-13th ed.
Bosshardt DD, Lang NP, The Junctional epithelium: from health to epithelium;
J Dent Res. 2005 Jan;84(1):9-20.
Stern IB, Current concepts of the dentogingival junction: the epithelial and
connective tissue attachments to the tooth; J Periodontol. 1981 Sep;52(9):465-
76.
Nakamura M, Histological and immunological characteristics of the junctional
epithelium; Japanese Dental Science Review (2018) 54, 59—65
Dynamics of Junctional epithelium, Periobasics.com
