Seminar

JUNCTIONAL
EPITHELIUM

S H A S H I K A N T C H AU D H A RY
JR II
DEPT OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
TS
Introduction

Development

Structure

Epithelial attachment

Expression of various molecules

Functions
Dynamic aspects of junctional
epithelium
Regeneration
Role of JE in initiation of pocket
formation
Junctional epithelium around
implants
Biologic width

Conclusion
INTRODUCTION
Teeth are trans-mucosal organs.

This is a unique association in the human body

where a hard tissue emerges through the soft
tissue.

The gingival epithelium around a tooth is

divided into threeSulcular
Oral or outer functional compartments
epithelium
Junctional
epithelium epithelium
 Oral cavity forms a perfect habitat in which micro-
organisms thrive.

Quickly form biofilm on tooth surface

Tissues in the vicinity of this biofilm are constantly

challenged

The tooth-epithelial interface thus call for a specialized

structural and functional adaptation
Listgarten MA, 1970:
Dento-gingival unit refers to the functional unit
comprising of junctional epithelium and the
gingival fibers

The junctional epithelium is the epithelial

component of the dento-gingival unit that is in
contact with the tooth surface.
 The innermost cells of the junctional epithelium
form and maintain a tight seal against the
mineralized tooth surface, the so-called epithelial
attachment (Schroeder and Listgarten, 1977).

Its interposition between the underlying soft and

mineralized connective tissues of the
periodontium
 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

The gingival 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
 HISTORY

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.
DEVELOPMENT OF
JUNCTIONAL EPITHELIUM
Formation of reduced enamel
1. epithelium

2.
Union of REE and Oral epithelium

As the tooth erupts REE is converted

3. into JE
DEVELOPMENT
When the enamel of the tooth is fully developed,
the enamel-producing cells (ameloblasts)
become reduced in height, produce a basal
lamina and form, together with cells from the
outer enamel epithelium, the so-called reduced
dental epithelium(RE).

The REE surrounds the crown of the tooth from

the moment the enamel is properly mineralized
until the tooth starts to erupt.
As the erupting tooth approaches the oral
epithelium, the cells of the outer layer of the
reduced dental epithelium, as well as the cells
of the basal layer of the oral epithelium, show
increased mitotic activity and start to migrate
into the underlying connective tissue.

The migrating epithelium produces an

epithelial mass between the oral
epithelium and the reduced dental
epithelium so that the tooth can erupt
without bleeding.
When the tips of the cusps or the incisal edge of the
crown breaches the oral mucosa a slow cell
transformation process develops

Beginning orally and ending at the cemento-enamel

junction
1 to 2 years (Schroeder and Listgarten, 1977) or
3 to 4 years (Ten Cate, 1998)

The reduced enamel epithelium gradually converts

into junctional epithelium
 STRUCTURE
ANATOMICAL ASPECT
Part of marginal free gingiva
JE is a collar-like band of nonkeratinised
stratified squamous epithelium
extending from cemento-enamel junction
to bottom of gingival sulcus
Interproximal area fuse to form epithelia
lining of interdentation col
The coronal termination of the junctional
epithelium corresponds usually to the
bottom of the gingival sulcus.
JUNCTIONAL EPITHELIUM
AND INTERSTITIAL CELLS
Coronally it is 15-30 cells thick & apically
narrows to 1-3 cells
JE is thickest at bottom of sulcus and tapers of in
apical direction
Its length varies from 0.25 1.35mm
Epithelial connective tissue interface is smooth
(no rete pegs)
made up of 2 strata
a basal layer (the stratum basale - towards
CT)
a suprabasal layer (the stratum suprabasale
 The innermost suprabasal cells (facing the tooth
surface) are also called DAT cells (= directly
attached to the tooth) (Salonen et al., 1989).

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
 Organelles- lysosomal bodies, golgi fields,
polyribosomes, cisternae of RER are abundant.

Unique set of cytokeratins 5, 13, 14, 19 &

occasionally 8, 16, 18.

few Desmosomes & occasionally gap junction - cell

connection

Intercellular spaces are wider in comparison with

the oral gingival or sulcular epithelium

Antigen presenting cells and Langerhans and other

dendritic cells are present
 HISTORICAL
CONCEPTS
GOTTLIEB -1921
Soft tissue of gingiva is organically united to
enamel surface
Ameloblast upon completion of enamel
matrix formation is the production of primary
enamel cuticle which is continuous with the
enamel matrix and attaches the cells of REE
to calcified tooth structure
As tooth erupts epithelial cells adjacent to
the enamel surface produce a cornified layer
of material referred as secondary enamel
cuticle and subsequently separated from
Orbans concept (1953)-
He stated that the separation of the epithelial
attachment cells from the tooth surface
involved preparatory degenerative changes in
the epithelium.
Waerhaugs concept (1960)-
He presented the concept of epithelial cuf.

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
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
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
TERMINOLOGIES:

Epithelial attachment Gottlieb 1921

Attached Epithelial cuff -Waerhaug 1952
Junctional epithelium or attachment
epithelium- Anderson and Stern1966;
Schroeder1969
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.
 The junctional epithelium faces both the
gingival connective tissue and the tooth
surface
While a basement membrane, sometimes
referred to as 'the external basal lamina'
(Schroeder, 1996), is interposed between the
basal cells of the junctional epithelium and the
gingival connective tissue
A basal lamina (also known as the internal
basal lamina) forms part of the interfacial
matrix between the tooth-facing junctional
epithelial cells (also known as DAT cells) and
the tooth surface
At the apical end of the junctional epithelium,
BASEMENT
MEMBRANES
Specialized extracellular matrices that are
interposed between connective tissues and
epithelia, endothelia, muscle fibers, and the
nervous system

Play roles in Consist

compartmentaliza
Lamina lucida
tion
( the lamina rara)
cell polarization
migration Lamina densa
adhesion Lamina
fibroreticularis
Differentiation (the sub-basal
lamina)
 By morphologically 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.

However, by bio-chemically, the internal basal

lamina differs essentially from the established
basement membrane composition (the external
basal lamina).

The internal basal lamina proteins include

laminin and type VIII collagen.
 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, VII collagen most
laminin isoforms, perlecan, and a lamina
fibroreticularis

The internal basal lamina of the junctional

epithelium has its own characteristics and
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.
 The intracellular part of hemidesmosomes
consists of at least 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)
- a6b4 integrin
 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.
 THE STRUCTURAL AND
MOLECULAR COMPOSITION OF
THE EPITHELIAL ATTACHMENT
APPARATUS
N AT DAT CELL
= 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.
EXPRESSION OF VARIOUS
MOLECULES &THEIR FUNCTIONS

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

Junctional epithelial cells express numerous cell

adhesion molecules (CAMs), such as integrins and
cadherins
 Integrins are cell-surface receptors that mediate
interactions between cells and the extracellular
matrix, and also contribute to cell-cell adhesion
The cadherins are responsible for tight contact
between cells
E-cadherin, an epithelium specific CAM, plays a
crucial role in maintaining the structural integrity
Intercellular adhesion molecule-1 (ICAM-1 or
CD54) and lymphocyte function antigen-3 (LFA-3)
are additional cell adhesion molecules.
(CEACAM1)a transmembrane cell-adhesion
molecule that is expressed on leukocytes,
epithelia, and blood vessel endothelia .
 high expression of interleukin-8 (IL-8), a
chemotactic cytokine, is seen in the coronal-
most cells of the JE
interleukin-1 (IL-1),
interleukin-1 (IL-1),
tumor necrosis factor- (TNF-)are strongly
expressed in the coronal half of the JE
N-acetyllactosaminethe type 2 chain H
precursor of the blood group A-specific
carbohydrate, which is usually associated with
the lowest level of cell differentiation.
Antimicrobial molecules--- and defensins
cathelicidin family calprotectin
DYNAMIC ASPECTS OF THE
JUNCTIONAL EPITHELIUM

Cell and extracellular dynamics of the

Junctional epithelium are essential for its
protective and regenerative functions.
DYNAMICS (TURNOVER
RATE) OF JE
The turnover rate of JE cells is exceptionally
rapid.
In non- human primates it is about 5 days
(twice that of oral epithelium).
The DAT cells express a high density of
transferrin receptors supporting the idea of
active metabolism and high turnover.
DAT cells have an important role in tissue
dynamics and reparative capacity of the JE.
The existence of a dividing population of DAT
cells in a suprabasal location in several layers
from connective tissue is a unique feature of
The mechanism of DAT cell turnover is not fully
understood. Considering the fact that the DAT
cells are able to divide and migrate, 3 possible
mechanisms
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
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.
PERMEABILITY OF JE

The junctional epithelium is the most

permeable portion of the gingival epithelia.

Because of its permeability to bacterial

products and other assorted antigens, the
connective tissue adjacent to the junctional
epithelium tends to become infiltrated with
chronic inflammatory cells, primarily
lymphocytes and plasma cells.
FUNCTIONS OF JE
Attached to the tooth surface ,forming an
epithelial barrier against plaque bacteria .

Access of gingival fluid , inflammatory cells, and

components of the immunologic host defense to
the gingival margin.
A rapid turnover , which contributes to the host-
parasite equilibrium and rapid repair of damaged
tissue .
Cells have endocytic capacity equal to that of
macrophages and neutrophils .

Genco RJ et al AAP 1996

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).
 Rapid turnover, as such, is an important factor in
the microbial defense of junctional epithelium.

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, 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
 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.
JE 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).
 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
JE IN ANTIMICROBIAL
DEFENSE
1 JE cells exfoliate because of rapid cell division

Funnelling of JE cells towards the sulcus hinder

2 bacterial colonization.

the (external) basement membrane forms an

3 effective barrier against invading microbes

Active antimicrobial substances are produced in

4 JE cells

Epithelial cells activated by microbial substances

secrete chemokines, that attract & activate
5 professional defense cells, PMN.
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

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)
 The GCF passing through the
JE 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
 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).
 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.

Biologically active molecules in GCF have

protective as well as destructive role
 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
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 hostparasite equilibrium but have a limited capacity to
reclaim any tooth surface once lost to the plaque bacteria.

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 (Schitt and Le, 1970).
 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.

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.
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).
 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
 Enzymatic degradation of the epithelial
attachment apparatus precedes the
degeneration of DAT cells (Overman et al).
 CYTOKINES:
Cytokine Suggested function
Interleukin 8 (IL8) Chemotaxis-Guiding PMN to
the bottom of sulcus
IL1
IL1 Proinflammatory cytokine
TNF
ROLE OF HOST
periodontal diseases are primarily caused by
bacterial infections and that a number of risk
factors contribute to the susceptibility of individuals
factors include smoking, diabetes,
immunosuppression, genetic factors, stress and age
a sound inflammatory host response is needed for
successful periodontal defense
Factors modify this response may either cause an
overwhelming reaction or an inadequate reaction,
both of which may accelerate tissue destruction
ROLE OF JUNCTIONAL EPITHELIUM
IN DISEASE

Problems in JE:
-permeability
-degeneration
-detachment
-lateral and apical
proliferation
PROBLEMS IN JUNCTIONAL EPITHELIUM :
REGENERATION OF JE

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.
 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.
 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.
 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.
ROLE OF THE JUNCTIONAL
EPITHELIUM
IN THE INITIATION OF POCKET
Role of JE in the initiation of pocket formation
FORMATION
Conversion of the JE to pocket epithelium is regarded
as a hallmark in the development of periodontitis.

Schroeder 1996 pointed to a biologically relevant

and clinically important question that still awaits
resolution: what happens to the JE under conditions
of sub-gingival microbial attack i.e. in context with
pocket formation and deepening?
 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.
Schroeder and Listgarten 1977: An increased
number of mononuclear leukocytes (T and B
 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.
 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.
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
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
JE IN POCKET:

Shorter than normal

Cells are mostly in normal condition
May exhibit slight degeneration
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.
 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.

JE forms rete pegs or ridges that protrude into the

connective tissue and the basal lamina is destroyed in
some areas.
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.
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.
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
JUNCTIONAL EPITHELIUM
ADJACENT TO ORAL
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 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.
Natural tooth Implant
Epithelium tapers Eithelium is thicker
towards the depth
Largre nuber of cell Fibers are arranged
organelles parallel
Large number of Numerous kerato-
cell arganelles hyaline granules
 BIOLOGIC WIDTH
The biologic width is defined as the physiologic
dimension of the junctional epithelium and
connective tissue attachment

It is important from the

restorative point of view
because its violation leads
to complications like
gingival enlargement
alveolar bone loss and
improper fit of the
restoration.
 Gargiulo et al (1961) in their study described
the dimensions and relations of dentogingival
junction in humans. The average histological
width of connective tissue attachment was
1.07mm. The mean average length of
epithelial attachment was 0.97mm with the
range of 0.71mm-1.35mm.

The average combined histological width of

connective tissue attachment and junctional
epithelium was 2.04mm, which is referred to
as the BIOLOGIC WIDTH.
 Vacek et al (1994) evaluated cadaver tooth
surfaces. They observed mean measuremnts
of 1.34mm for sulcus depth, 1.14 for epithelial
attachment and 0.77mm for connective tissue
attachment
CONCLUSION
JE 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 JE to pocket epithelium
is regarded as hallmark in the development of
periodontitis.
 REFERENCES
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health to disease. J Dent Res 2005, 84 (1): 9-20
Marja T Pollanen, jukka I Salone. Veli- Jukka UittioStructure
and function of the toothepithelial interface in health and
disease Periodontology 2000, Vol. 31, 2003, 1231
Moon-Il Cho & Philias R. Garant. Development and general
structure of the periodontium. Periodontology 2000, Vol. 24,
2000, 927.
Mark Bartold, Laurence J. Walsh & A. Sampath Narayanan.
Molecular and cell biology of the gingiva.P. Periodontology
2000, Vol. 24, 2000, 2855.
H E Schroeder & R M Listgarten. The gingival tissues: The
architecture of periodontal Protection. Periodontology 2000,
Vol. 13, 1997, 91-120.
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