1. The junctional epithelium is a specialized non-keratinized stratified squamous epithelium that attaches to the tooth surface and forms a collar around the cervical portion. 2. It develops from the reduced enamel epithelium during tooth eruption. The reduced enamel epithelium fuses with the oral epithelium and transforms into the junctional epithelium. 3. The junctional epithelium attaches firmly to the tooth surface through hemidesmosomes of the basal cells (called DAT cells) and an internal basal lamina. This structure is called the epithelial attachment apparatus.

1. Junctional
Epithelium
PRESENTED BY DR. SUNDARA VIKRAM B, 1ST YEAR PG, DEPT OF PERIODONTICS

2. Introduction:
 There are three types of mucous membranes
(masticatory, lining, and specialized) line the oral cavity
and form the structural boundary between the body
and the external environment.
 Epithelia exhibit considerable differences in their
histology, thickness and differentiation suitable for the
functional demands of their location

3.  The gingival epithelium around a tooth is divided into
three functional compartments– outer, sulcular, and
junctional epithelium
 The outer epithelium extends from the mucogingival
junction to the gingival margin where crevicular/sulcular
epithelium lines the sulcus
 At the base of the sulcus connection between gingiva
and tooth is mediated with JUNCTIONAL EPITHELIUM

4. Introduction:
 Mucosal epithelia are composed of continuously
dividing and shedding populations of keratinocytes.
 The junctional epithelium is attached to the tooth
surface by a distinct mechanism known as the epithelial
attachment apparatus.

5. Introduction:
 It is commonly accepted that the junctional epithelium
exhibits several unique structural and functional features
that contribute to preventing pathogenic bacterial flora
from colonizing the subgingival tooth surface

6. HISTORICAL ASPECTS

7. Historical aspects of JE:
 Gottlieb (1921) was the first to describe the junctional epithelium
 Schroeder and Listgarten (1977) clarified the anatomy and
histology of the dentogingival junction in their monograph: ‘Fine
structure of developing epithelial attachment of human teeth’.

8. GOTTLIEB -1921
Epithelial
attachment is
organically
united to the
tooth surface

9. WAERHAUG -1952
Based on his animal
experiments(in dogs)
he postulated that the
cells of the epithelial
attachment adhere
weakly to the tooth
surface and it forms the
lining of the physiologic
pocket

10. Orban’s concept (1953)
 He stated that the separation of the epithelial
attachment cells from the tooth surface involved
preparatory degenerative changes in the epithelium.

11. Waerhaug’s concept (1960)
 He presented the concept of epithelial cuff. This
concept was based on insertion of thin blades between
the surface of tooth and the gingiva
 Blades could be easily passed apically to the
connective tissue attachment at CEJ without resistance.
 It was concluded that gingival tissue and tooth are
closely adapted but not organically united.

12. Max Listgarten- 1966-67
Based on trasmission
electron micrscopic
studies he proved
the existence of a
hemidesmosomal
basement lamina
attachment between
the tooth and the
cells of the so called
cells of epithelial
attachment

13. Schroeder and Listgarten concept
(1971)
 The previous controversy was resolved after evolution of
transmission electron microscopy.
 Primary epithelial attachment refers to the epithelial
attachment lamina released by the REE. It lies in direct
contact with enamel and epithelial cells attached to it by
hemi-desmosomes.
 When REE cells transform into JE cells the primary epithelial
attachment becomes secondary epithelial attachment . It is
made of epithelial attachment between basal lamina and
hemi-desmosomes.

14. Terminologies:
Epithelial attachment – Gottlieb 1921
Epithelial cuff -Waerhaug 1952
Attached epithelial cuff- Orban 1956
Attachment epithelium- Grant, Stern 1968
Junctional epithelium- Anderson and Stern1967

15. What is Junctional Epithelium?
 It is the third (and most intriguing) component of the
epithelial integument of the periodontium, in addition to
the oral gingival epithelium and the oral sulcular
epithelium.
 It consists of collar like band of stratified squamous
nonkeratinizing epithelium.

16. What is Junctional Epithelium?
 It is 3 to 4 layers thick in early life, but the number of
layers increases with age to 10 or even 20 years.
 JE tapers from its coronal end, which may be 10 to 29
cells wide to 1 or 2 cells at its apical termination, located
at the cemento enamel junction in healthy tissue.

17. What is Junctional Epithelium?
 Those cells are grouped into two strata:
 THE BASAL LAYER facing the connective tissue and
 THE SUPRABASAL LAYER extending to the tooth surface.
 The length of the JE ranges from 0.25 to 1.35mm.

18. What is Junctional Epithelium?
 It provides the attachment mechanism of the epithelium
to the surface of tooth hard substance.
 It also provides a protective function relative to the
subjacent periodontal ligament.

19. Definitions for JE:
Junctinal epithelium is the non keratinised stratified
squamous epithelium which attaches and form a
collar around the cervical portion of the tooth that
follows CEJ
Carranza’s clinical periodontology
Epithelial attachment is the structural complex by
which junctional epithelium is attached to the tooth
surface

20. What are it’s functions?
 First, JE is firmly attached to the tooth and thus forms an epithelial
barrier against the plaque bacteria.
 Second, it allows the access of GCF, inflammatory cells and
components of the immunological host defense to the gingival
margin.
 Third, JE cells exhibit rapid turnover, which contributes to the host
parasite equilibrium and rapid repair of damaged tissue
Genco RJ et al AAP 1996

21. DEVELOPMENT OF JUNCTIONAL
EPITHELIUM
1. Formation of reduced enamel epithelium
2. Union of REE and Oral epithelium
3. As the tooth erupts REE is converted into JE
Changes during conversion
Cuboidal cells derived from ameloblast begin to flatten and
align parallel to tooth surface and take appearance of JE.
Since these cells which have lost capacity to divide get
exfoliated at base of sulcus and cells from stratum
intermedium which has proliferative capacity get
transformed into JE

23. Development of JE:
 When the ameloblasts finish formation of the enamel matrix,
they leave a thin membrane on the surface of the enamel
called the primary enamel cuticle.
 The ameloblasts shorten after the primary enamel cuticle has
been formed and the epithelial enamel organ is reduced to a
few layers of flat cuboidal cells called reduced enamel
epithelium.
Orbans oral histology and embryology

24. Development of JE:
 During eruption, the tip of the tooth approaches the oral
mucosa, and the reduced enamel epithelium and the
oral epithelium meet and fuse.
 The remnant of the primary enamel cuticle after eruption
is referred to as Nasmyth’s membrane.
Orbans oral histology and embryology

26. Development of JE:
 The epithelium that covers the tip of the crown
degenerates in its center and the crown emerges
through this perforation into the oral cavity.
 The REE remains organically attached to the part of the
enamel that has not yet erupted. Once the tip of the
crown has emerged, the REE is termed as Primary
attachment epithelium (Junctional epithelium).

27. Development of JE:
 At the margin of the gingiva, the junctional epithelium is
continuous with the oral epithelium.
 As the tooth erupts, the REE grows gradually shorter.
 Gingival sulcus may develop between the gingiva and
the surface of the tooth and extend around its
circumference.

28. Development of JE:
 It is bounded by the JE at its base and by the gingival
margin laterally. The gingiva encompassing the sulcus is
the free, or marinal gingiva.

29. Anatomical features:
 JE forms a collar peripheral to cervical region of tooth of about 0.75
to 1.35 mm
 Interproximally JE of adjacent teeth fuse to form the lining of the col
area
 Epithelial connective tissue interface is smooth (no rete pegs)
 JE is thickest at bottom of sulcus and tapers of in apical direction

30. Microscopic features
 It has 15-30 cell layers coronally and 1-3 layers at apical termination
 It has two strata- stratum basale and stratum suprabasale
 The basal and adjacent 1-2 suprabasal cells are cuboidal to slightly spindle
shaped and all the remaining cells are flat and oriented parallel to the tooth
surface
 The innermost suprabasal cells(facing the tooth surface) also called DAT
cells(Salonen et al 1994) form and maintain the epithelial attachment
apparatus
 It has two basal lamina – External basal lamina and internal basal lamina

32. Transmission electron microscopic
features:
 Lysosomal bodies are in large numbers
 Golgi fields are large
 Poly ribosomes are numerous
 Keratinosomes (Odland bodies) are absent
 Cytokeratin bundles are scarce
 Desmosomes are less
 Inter cellular spaces are more wider and occupied by
inflammatory cells

33. Photomicrograph demonstrating the junctional epithelial DAT cells on the tooth surface (a). When
the gingiva is displaced laterally the DAT cells are left on the enamel (E) surface. The degeneration
of the DAT cells appears to be a prerequisite for the apical advancement of bacterial plaque (P). D Ω
dentin. The junctional epithelium (JE) attached to tooth (to enamel or cementum (C) as in (b) forms a
structural barrier against the bacterial plaque. Polymorphonuclear leukocytes that cover the plaque
(P) have migrated through the junctional epithelium into the sulcus. At the apical part of the
junctional epithelium, cells (arrow) are seen to grow/proliferate into the connective tissue (CT). A
higher magnification (c) of the apical part of the junctional epithelium. Note the dark-stained DAT
cells along the cementum surface, the epithelial ‘finger’ proliferating apically and the absence of
inflammatory infiltrate. Gingival epithelial cells grown on decalcified dentin matrix (d) show
apparent ability to extracellular collagenolysis (e)

34. Characteristics Outer Oral
epithelium
Sulcular epithelium Junctional
epithelium
Origin Oral epithelium Oral epithelium Reduced enamel
epithelium
Keratinization Parakeratinized
Sometimes
orthokeratinized
Nonkeratinized Nonkeratinized
Stratification Well stratified Stratified but
granulosam and
corneum are
absent
Poorly stratified
Proliferation Lesser proliferation
among three
Higher than OEE
but lesser than JE
Higher proliferation
Permeability Not permeable to
water soluble
substances
Moderately
permeable
Highly permeable
Intercellular Space
Desmosomes&
tonofilaments
Narrowest
More than SE& JE
Narrower than JE
More than JE
Widest among
three
Least among three
Retepegs Present Normally absent,
appears in
inflammation
Normally absent,
appears in
inflammation

35. PRIMARY EPITHELIAL ATTACHMENT
Attachment of reduced enamel epithelium to
enamel of unerupted crown
SECONDARY EPITHELIAL ATTACHMENT
After the conversion of REE to JE the attachment is
referred as secondary epithelial attachment
EPITHELIAL ATTACHMENT APPARATUS
Mediated by hemidesmosomes of DAT (Directly
Attached to Tooth) cells and internal basal lamina

36. Epithelial Attachment Apparatus:
 The attachment of the JE to the tooth is mediated
through an ultramicroscopic mechanism defined as the
Epithelial Attachment Apparatus.
 It consists of hemidesmosomes at the plasma membrane
of the cells Directly Attached to Tooth (DAT cells) and a
basal lamina-like extra-cellular matrix, termed the internal
basal lamina on the tooth surface.

37. Epithelial Attachment Apparatus:
 By morphological criteria the internal basal lamina
between the junctional epithelial DAT cells and the
enamel is quite similar to the basement membrane
between the epithelium and the connective tissue.

38. Epithelial Attachment Apparatus:
 However, by bio-chemical criteria, the internal basal
lamina differs essentially from the established basement
membrane composition and thus form the external
basal lamina.
 The internal basal lamina proteins include laminin and
type VIII collagen.

39. Epithelial Attachment Apparatus:
 Laminin identified as type 5(Ln 332), is localized mainly to
the electrodense part of the internal basal lamina and it
seems to be associated with hemidesmosomes.
 Characteristically, the internal basal lamina lacks
laminin-1 and type IV collagen which are components
of true basement membranes

40. External Vs Internal Basal lamina
External basal lamina Internal basal lamina
Formation By basal cells with the
cross talk with
con.tissue
By DAT cells without
the influence of
fibroblast
Collagen IV Yes No
Collagen VII Yes No
Collagen VIII Not reported Yes
Perlecan Yes No
Tenascin Yes Yes(variable)
Versican Not reported Yes
Laminin 111 Yes No
Laminin 511 Yes No
Laminin 332 (Laminin
5)
Yes Yes(10 times more)

41. Hemidesmosomes:
 Hemidesmosomes have a decisive role in the firm
attachment of the cells to the internal basal lamina on
the tooth surface.
 It may also act as specific sites of signal transduction and
thus participate in regulation of gene expression, cell
proliferation and cell differentiation.

42. Hemidesmosomes:
 The intracellular part of hemidesmosomes consists of
atleast two distinct proteins,
- BP230 (230kDa bullous pemphigoid antigen)
- Plectin
These proteins mediate the attachment of the epithelial
cell cytoplasmic keratin filaments to two transmembrane
components of the hemidesmosome known as the
- 180kDa bullous pemphigoid antigen (BP180)

43. Hemidesmosomes:
 In general, the interaction between the different
components of the extracellular matrix and the cell
surface molecules linked to the intercellular cytoskeleton
is fundamental for cell adhesion, cell motility, synthetic
capacity, tissue stability, regeneration and responses to
external signals.

44. Hemidesmosomes:

45. A schematic illustration of a DAT cell shows the
structural and molecular composition of the
epithelial attachment apparatus (EAA). N = nucleus
of a DAT cell, IF = cytoplasmic keratin filaments
(intermediate size filaments). The hemidesmosomes
at the plasma membrane are associated with the
a6b4 integrin that communicates with Ln-5 = laminin
5 located mainly in the internal basal lamina, the
extracellular domain (?) for BP180 is a collagenous
protein (perhaps type VIII), that has not yet been
definitely characterized. LL =lamina lucida, LD =
lamina densa, SLL =sublamina lucida, IBL = internal
basal lamina.

46. Turnover of the JE cells with DAT
cells:
 The turnover of the junctional epithelium is exceptionally rapid.
 At the coronal part of the JE, the DAT cells typically express a high
density of transferrin receptors.
 DAT cells have more important role in tissue dynamics and
reparative capacity of the junctional epithelium than has previously
been thought.

47. Turnover of the JE cells with DAT
cells:
 Any structural or molecular changes in the internal basal lamina can
potentially influence the vital functions of the DAT cells and
contribute to the effectiveness or failure of the junctional epithelial
defense or vice versa.
 Changes in the cell metabolism may affect the Internal Basal
Lamina (IBL).
 Morphological studies of the internal basal lamina of teeth
extracted because of advanced periodontitis have shown that
remnants of the internal basal lamina can be detected even
adjacent to severely degenerated DAT cells (Overman DO et all)

48. The mechanism of DAT cell turnover is not fully
understood. Considering the fact that the DAT
cells are able to divide and migrate, three
possible mechanisms can be proposed. These
are
(1) the daughter cells produced
by dividing DAT cells replace degenerating cells
on
the tooth surface,
(2) 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
(3) epithelial cells move/migrate in the
coronal direction along the tooth surface and
are replaced by basal cells migrating round the
apical termination of the junctional epithelium.

49. JE in the Anti-Microbial Defense:
 Junctional epithelium consists of active populations of
cells and antimicrobial functions, which together form
the first line of defense against microbial invasion into
tissue.
 Even though junctional epithelial cell layers provide a
barrier against bacteria many bacterial substances, such
as lipopolysaccharide, pass easily through the epithelium
but have only limited access through the external basal
lamina into the connective tissue (Shwartz et al 1972).

50.  Rapid turnover, as such, is an important factor in the
microbial defense of junctional epithelium.
 The 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 (Schroder et al 1967).
 Rapid shedding and effective removal of bacteria adhering
to epithelial cells is therefore an important part of the
antimicrobial defense mechanisms at the dentogingival
junction.

51. Role of Enzymes in the Anti-
Microbial Defense of JE:
 There is increasing evidence indicating that several specific
antimicrobial defense systems exist in the oral mucosa.
 Junctional epithelium, have been found to contain enzyme-rich
lysosomes.
 Their fusion with plasma membrane is triggered by elevation of the
intracellular calcium concentration (Rodriguez et al 1997)
 In rats, the lysosomes have been demonstrated to contain cysteine
proteinases (cathepsin B and H) active at acidic pH (Yamaza T et al
1997).

52.  Recently, it has been found that the junctional epithelial
cells lateral to DAT cells produce matrilysin (matrix
metalloproteinase-7) (Uitto VJ et al 2002).
 Matrilysin contributes to the mucosal defense by the
release of bioactive molecules from the cell surfaces
which play a role in the inflammatory reaction.
Role of Enzymes in the Anti-
Microbial Defense of JE:

53. Several antimicrobial mechanisms exist in the
junctional epithelium. In the coronal part of
the junctional epithelium quick cell
exfoliation
(1)because of rapid cell division
(2)and funnelling of junctional epithelial cells
towards the sulcus hinder bacterial
colonization. Laterally, the (external)
basement membrane forms an effective
barrier against invading microbes
(3). Active antimicrobial substances are
produced in junctional epithelial cells. These
include defensins and
lysosomal enzymes

54. (4). Epithelial cells activated by microbial
substances secrete chemokines, e.g.
interleukin- 8 and cytokines, e.g. interleukins -
1 and -6, and tumour necrosis factor-a that
attract and activate professional defense
cells, such as lymphocytes (LC) and
polymorphonuclear leukocytes (PMN). Their
secreted product, in turn,
cause further activation of the junctional
epithelial cells.

55. Role of Junctional Epithelium in
Disease

56. Problems in JE:

57. THE DETACHMENT OF THE DAT CELLS
FROM THE TOOTH SURFACE:
 Role of the gingival crevice fluid
 Role of the polymorphonuclear leukocytes
 Role of host proteinases and inflammatory mediators
 Role of bacterial products
 Role of risk factors for periodontal disease

58. Role of GCF:
 GCF is an exudate of varying composition found in the
sulcus/periodontal pocket between the tooth and marginal gingiva.
 GCF contains components of serum, inflammatory cells, connective
tissue, epithelium, and microbial flora inhabiting the gingival margin
or the sulcus/pocket (Embery G et al 1994)

59. The GCF passing through the junctional epithelium
determines the environmental conditions and
provides sufficient nutrients for the DAT cells to grow.
At the gingival margin the GCF may become
contamined so that agents from the oral cavity
and/or the plaque bacteria challenge the most
coronal DAT cells. Obviously, the conditions
for DAT cell survival and adequate function at the
coronal part of the JE are different and more
susceptible of compromises than those for the basal
cells living in the vicinity of the connective tissue (CT)
and the blood circulation.

60. Role of GCF:
 In the healthy sulcus the amount of GCF is very small. However, its
constituents participate in the normal maintenance of function of
the junctional epithelium throughout its lateral and vertical
dimensions, including the most coronal DAT cells.
 During inflammation the GCF flow increases and its composition
starts to resemble that of an inflammatory exudate (Cimasoni et al
1983).

61. Role of GCF:
 Although all the junctional epithelial cells are constantly exposed to
the GCF and its various constituents, the nutritional and other vital
conditions in the different parts of the junctional epithelium depend
on a large number of local factors.

62. Role of GCF
 Main route of GCF diffusion is
through the EBL and inter cellular
spaces
 GCF passing through JE gives
nutrients to DAT cells
 Increased GCF flow during
inflammation will have a flushing
action against bacteria and its
products

63.  Biologically active molecules in
GCF have protective as well as
destructive role

64. Role of the polymorphonuclear
leukocytes:
 Polymorphonuclear leukocytes form the most important
line of defense against bacterial plaque at the gingival
margin (Page RC et al).
 Polymorphonuclear leukocytes are a major contributor in
the host–parasite equilibrium but have a limited
capacity to reclaim any tooth surface once lost to the
plaque bacteria.

65. Role of the polymorphonuclear
leukocytes:
 The polymorphonuclear leukocytes are most effective in
aerobic conditions close to the gingival margin
(Dennison et al 1997), suggesting a different role for them
in anaerobic periodontal lesions.
 Lactoferrin is an important antimicrobial protein present
in the secondary granules of polymorphonuclear
leukocytes.

66. Role of the polymorphonuclear
leukocytes:
 High concentrations of lactoferrin do, however, hamper
epithelial cell growth by interfering with their adhesion
and spreading. The molecule may, thus, have a role in
delaying the repair of the junctional epithelium/DAT cell
population during severe inflammation.

67. Role of host proteinases and
inflammatory mediators:
 Degradation of extracellular matrix during periodontal
inflammation is a multistep process that involves several
proteolytic enzymes.
 Different cell types of periodontal tissue produce matrix
metalloproteinases (collagenases, stromelysins, gelatinases,
membrane-type metalloproteinases), plasminogen activator,
cathepsins and elastase (Birkedal Hansen et al, Suomaleinin et
al).

68. Role of host proteinases and
inflammatory mediators:
 Neutrophil elastase and cathepsin G are capable of
degrading basement membrane type IV collagen and
laminin, and also type VIII collagen, found in the internal basal
lamina (Heck & Blackburn et al, Kittlecherger et al).
 However, electron microscopic studies on DAT cells attached
to teeth extracted because of advanced periodontitis do not
support the idea that

69. Role of host proteinases and
inflammatory mediators:
enzymatic degradation of the epithelial attachment
apparatus precedes the degeneration of DAT cells
(Overman et al).

70. Cytokines:
Cytokine Suggested function
Interleukin 8 (IL8) Chemotaxis-Guiding PMN
to the bottom of sulcus
IL1α Proinflammatory cytokine
IL1β Proinflammatory cytokine
TNF α Proinflammatory cytokine

71. Problems in Junctional Epithelium:
If the junctional epithelium is repeatedly or continuously exposed to
bacterial challenges, which may lead to
 the failure of JE,
 subgingival plaque formation,
 Conversion of the gingival sulcus into a periodontal pocket, and
 Increase in the inflammatory focus in the connective tissue.

72. Role of JE in passive eruption:

73. Role of JE in passive eruption:
 Passive eruption is the exposure of the teeth by apical
migration of the gingiva.
 This concept distinguishes between the anatomic crown
(the portion of the tooth covered by enamel) and the
anatomic root (the portion of the tooth covered by
cementum) and between the

74. Role of JE in passive eruption:
 clinical crown (the part of the tooth that has been
denuded of its gingiva and projects into the oral cavity)
and clinical root (the portion of the tooth covered by
periodontal tissues).

75. Role of JE in passive eruption:
 When the teeth reach their functional antagonists, the
gingival sulcus and junctional epithelium are still on the
enamel and the clinical crown is approximately two
thirds of the anatomic crown.
 Passive eruption is divided into four stages. Although this
was originally thought to be a normal physiologic
process, it is now considered a pathologic process.

76. Role of JE in passive eruption:
 Stage 1: The teeth
reach the line of
occlusion. The
junctional epithelium
and base of the
gingival sulcus are on
the enamel.

77. Role of JE in passive eruption:
 Stage 2: The junctional
epithelium proliferates
so that part is on the
cementum and part is
on the enamel. The
base of the sulcus is still
on the enamel.

78. Role of JE in passive eruption:
 Stage 3: The entire junctional
epithelium is on the cementum,
and the base of the sulcus is at the
cementoenamel junction. As the
junctional epithelium proliferates
from the crown onto the root, it
does not remain at the
cementoenamel junction any
longer than at any other area of
the tooth.

79. Role of JE in passive eruption:
 Stage 4: The junctional
epithelium has proliferated
farther on the cementum. The
base of the sulcus is on the
cementum, a portion of which is
exposed. Proliferation of the
junctional epithelium onto the
root is accompanied by
degeneration of gingival and
periodontal ligament fibers and
their detachment from the tooth.
The cause of this degeneration is
not understood. At present, it is
believed to be the result of
chronic inflammation and
therefore a pathologic process.

80. JE in pocket formation:
 Conversion of JE to pocket epithelium is regarded as the
hallmark in the development of periodontitis
Inflammation
Supracrestal
collagen
destruction
Lossofcontactinhibition,
OverexpressionofEGF
Apical
migration of
JE
Inflammatorycell
infiltration
Coronal
detachment
of JE

81. Apical migration of JE:
 Due to
- Loss of contact inhibition -due to supra crestal collagen destruction
-Increased expression of EGF and its receptors due to cytokine
stimulation
 Epithelial cell at apical end of migrating JE have no internal and
external basal lamina

82. Coronal detachment of JE:
 Due to
- More pooling of inflammatory cells at the coronal end
-Degeneration of cell adhesion molecules by inflammatory mediators
-Destruction of cell adhesion complexes directly by bacterial enzymes
such as gingipains

83. JE in pocket:
 Shorter than normal
 Cells are mostly in normal condition
 May exhibit slight degeneration

84. Role of JE in Gingivitis:
 During the initial lesion of gingivitis, Leukocytes, mainly
PMNs leukocytes leave the capillaries by migrating
trough the walls ( Lindhe J perio res)
 They can be seen in increased quantities in the
connective tissue, and the junctional epithelium and the
gingival sulcus.

85. Role of JE in Gingivitis:
 The junctional epithelium becomes densely infiltrated
with neutrophils and it may begin to show development
of rete pegs or ridges in the early lesion of gingivitis.
 During the established lesion of gingivitis, the junctional
epithelium reveals widened intercellular spaces filled
with granular cellular debris, including lysosomes derived
from disrupted neutrophils, lymphocytes and monocytes.

86. Role of JE in Gingivitis:
 JE forms rete pegs or ridges that protrude into the
connective tissue and the basal lamina is destroyed in
some areas.

87. JE in Necrotizing Ulcerative
Gingivitis:
 Surface epithelium is destroyed
 And it is replacd by a meshwork of fibrin, necrotic
epithelial cells, PMNs and neutrophils and various types
of microorganisms
 The epithelium becomes edematous and there is
infilteration of PMNs in the intercellular spaces.

88. JE in Necrotizing Ulcerative
Gingivitis:
 Surface epithelium is destroyed
 And it is replacd by a meshwork of fibrin, necrotic
epithelial cells, PMNs and neutrophils and various types
of microorganisms
 The epithelium becomes edematous and there is
infilteration of PMNs in the intercellular spaces.

89. What happens to JE in Trauma
From Occlusion:
 TFO causes widening of the marginal PDL space, a
narrowing of the interproximal alveolar bone.
 In case of TFO, the junctional epithelium will be intact
and there will be no degeneration of the epithelial
tissues unless there is any plaque accumulation.

90. Syndromes affecting JE:
 Kindler syndrome:
A rare skin blistering disorder along with early onset
aggressive periodontitis.
Due to loss of kindlin-1 protein which is involved in
integrin activation.
JE fails to attach to the tooth surface

91. Regeneration
of JE

92.  Injury to JE may occur due to intentional or
accidental trauma.
 Accidental trauma can occur during probing,
flossing or tooth margin preparations for
restorations.
 Intentional trauma occurs during periodontal
surgeries where the JE is completely lost.

93.  Many studies have been done to investigate the
renewal of JE. These include studies done on
renewal of JE on tooth and implant surface after
mechanical detachment by probing.
 Studies have been done on mechanical trauma
during flossing and on regeneration of JE after
gingivectomy procedure which completely
removes JE.

94.  Taylor and Campbell 1972: A new and complete attachment
indistinguishable from that in control was established 5 days after
complete separation of the JE from the tooth surface.
 Frank et al 1972: A study demonstrated that newly differentiated
attachment apparatus with normal hemidesmosomal attachment is
possible following surgery. This new attachment apparatus was seen
on cementum as well as dentin.

95.  Listgarten 1972:Hemidesmosomes appeared to form prior to
the basal lamina. The basal lamina is initially formed in close
proximity to the hemidesmosomes at both the tooth and
connective tissue interface. At 4 to 7 weeks, the basal lamina
appeared complete. Studies have shown that regeneration of JE
after procedure usually occurs within 20 days.

96. JE AROUND
IMPLANTS

97.  The junctional epithelium around implants always
originates from epithelial cells of the oral mucosa, as
opposed to the junctional epithelium around teeth
which originates from the reduced enamel epithelium.
 Despite different origins of the 2 epithelia, a functional
adaptation occurs when oral epithelia form an epithelial
attachment around implants.

98. 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
•Numerous kerato-hyalin granules

99. CONCLUSION
 Junctional Epithelium is important because of its anatomical
location.
 It is the site of host-bacterial interaction in initiation of periodontal
disease.
 There is a constant presence of bacteria and their products in the
gingival sulcus which makes this an important structural component
of periodontal defense mechanism.
 The conversion of the junctional epithelium to pocket epithelium is
regarded as hallmark in the development of periodontitis.

100. References
 Moon-Il 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.
 Huberte . Schroede & R M Listgarten. The gingival tissues: The
architecture of periodontal Protection. Periodontology 2000, Vol. 13,
1997, 91-120.
 Takashi Sawada1 and Sadayuki Inoue. Ultrastructure of
Dentogingival Border of Normal and Replanted Tooth and Dental
Implant, chapter 11 www.intechopen.com/books/implantdentistry
 Carranza’s clinical periodontology 11th edition
 Orban’s oral anatomy and histology

101. Thank you…….