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Dentogingival Junction:-
The dentogingival junction is a unique anatomic feature whose function is the attachment of the
gingiva to the tooth. It comprises an epithelial portion and a connective tissue portion, both of which
are of fundamental importance in periodontal pathogenesis. The epithelial portion can be divided into
three distinct epithelial structures, the gingival epithelium, sulcular epithelium, and junctional
epithelium. These epithelial structures are in continuity with each other but have distinct structures
and functions.
Three zones of the gingival epithelium
Oral
epithelium
Junctional
epithelium
Crevicular (or
sulcular)
epithelium


Characteristics of the Epithelial Component of the Dentogingival Unit

Gingival Epithelium
Stratified squamous keratinized epithelium.
Continuous with the sulcular epithelium at the gingival crest/gingival margin.
Covers the gingiva and forms the clinically visible gingival tissues.
Covers both the free and attached gingival tissues.
Sulcular Epithelium
Stratified squamous epithelium.
Nonkeratinized.
Faces the tooth surface but is not attached to it.
Forms the soft tissue lining of the gingival sulcus or periodontal pocket.
Junctional Epithelium
Forms the epithelial attachment between the gingiva and the tooth.
Nonkeratinized.
Forms the floor of the sulcus/pocket.

Wraps around the tooth like a collar, in health following the morphology of the
cementoenamel junction (CEJ).
Wider at the floor of the sulcus (15-30 cells thick) and tapers apically to 3-4 cells thick.
Comprised of layers of flattened squamous cells oriented parallel to the tooth surface.
The surface cells attach to the tooth surface via hemidesmosomes.

The basal lamina differs from other basal laminae that oppose connective tissue in that type
IV collagen is absent.
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The junctional epithelium is formed by the confluence of the oral epithelium and the reduced enamel
epithelium during tooth eruption However, the reduced enamel epithelium is not essential for its
formation; in fact, the junctional epithelium is completely restored after pocket instrumentation or
surgery, and it forms around an implant.
Cell layers not juxtaposed to the tooth exhibit numerous free ribosomes and prominent membrane-
bound structures, such as Golgi complexes, and cytoplasmic vacuoles, presumably phagocytic.
Lysosome-like bodies also are present, but the absence of keratinosomes (Odland bodies) and
histochemically demonstrable acid phosphatase, correlated with the low degree of differentiation, may
reflect a low defense power against microbial plaque accumulation in the gingival sulcus. Similar
morphologic findings have been described in the gingiva of germ-free rats. PMNs are found routinely
in the junctional epithelium of both conventional rats and germ-free rats. Research has shown that
although numerous migrating PMNs are evident and present around healthy junctional epithelium, a
considerable increase in PMN numbers can be expected with the accumulation of dental plaque and
gingival inflammation.
The different keratin polypeptides of junctional epithelium have a particular histochemical pattern.
Junctional epithelium expresses K19, which is absent from keratinized epithelia, and the stratification-
specific cytokeratins K5 and K14. Morgan et al.,1987 reported that reactions to demonstrate K4 or
K13 reveal a sudden change between sulcular and junctional epithelia; the junctional area is the only
stratified nonkeratinized epithelium in the oral cavity that does not synthesize these specific
polypeptides. Another particular behavior of junctional epithelium is the lack of expression of K6 and
K16, which is usually linked to highly proliferative epithelia, although the turnover of the cells is very
high.
Similar to sulcular epithelium, junctional epithelium exhibits lower glycolytic enzyme activity than
outer epithelium and lacks acid phosphatase activity.
Cell-Cell Attachments:-
1. Desmosomes,
2. Adherens junction
3. Tight junctions
4. Gap junctions
Desmosomes are molecular complexes of cell adhesion proteins and linking proteins that attach the
cell surface adhesion proteins to intracellular keratin cytoskeletal filaments. The cell adhesion proteins
of the desmosome, desmoglein and desmocollin, are members of the cadherin family of cell adhesion
molecules. They are transmembrane proteins that bridge the space between adjacent epithelial cells by
way of homophilic binding of their extracellular domains to other desmosomal cadherins on the
adjacent cell. Both have five extracellular domains, and have calcium-binding motifs. The
extracellular domain of the desmosome is called the Extracellular Core Domain (ECD) or the
Desmoglea, and is bisected by an electron-dense midline where the desmoglein and desmocollin
proteins bind to each other. These proteins can bind in a W, S, or manner.

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On the cytoplasmic side of the plasma membrane, there are two dense structures called the Outer
Dense Plaque (ODP) and the Inner Dense Plaque (IDP). These are spanned by
the Desmoplakin protein. The Outer Dense Plaque is where the cytoplasmic domains of the cadherins
attach to desmoplakin via plakoglobin and plakophillin. The Inner Dense Plaque is
where desmoplakin attaches to the intermediate filaments of the cell.
Adherens junctions (or zonula adherens, intermediate junction, or "belt desmosome") are protein
complexes that occur at cellcell junctions in epithelial tissues, usually more basal than tight
junctions. An adherens junction is defined as a cell junction whose cytoplasmic face is linked to
the actin cytoskeleton. They can appear as bands encircling the cell (zonula adherens) or as spots of
attachment to the extracellular matrix (adhesion plaques).

Tight junctions, or zonula occludens, are the closely associated areas of
two cells whose membranes join together forming a virtually impermeable barrier to fluid. Tight
junctions are composed of a branching network of sealing strands, each strand acting independently
from the others. Therefore, the efficiency of the junction in preventing ion passage increases
exponentially with the number of strands. Each strand is formed from a row of transmembrane
proteins embedded in both plasma membranes, with extracellular domains joining one another
directly. Although more proteins are present, the major types are the claudins and the occludins.
These associate with different peripheral membrane proteins located on the intracellular side of
plasma membrane, which anchor the strands to the actin component of the cytoskeleton. Thus, tight
junctions join together the cytoskeletons of adjacent cells.

A gap junction or nexus is a specialized intercellular connection between a multitude of animal cell-
types. It directly connects the cytoplasm of two cells, which allows various molecules and ions to
pass freely between cells.
Electron microscopy reveals that keratinocytes, the principle cell type of gingival epithelium, are
interconnected by structures on the cell periphery called desmosomes. These desmosomes have a
typical structure consisting of two dense attachment plaques into which tonofibrils insert and an
intermediate, electron-dense line in the extracellular compartment. Tonofilaments, which are the
morphologic expression of the cytoskeleton of keratin proteins, radiate in brushlike fashion from the
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attachment plaques into the cytoplasm of the cells. The space between the cells shows cytoplasmic
projections resembling microvilli that extend into the intercellular space and often interdigitate.
Less frequently observed forms of epithelial cell connections are tight junctions (zonae occludens), in
which the membranes of the adjoining cells are believed to be fused. Evidence suggests that these
structures allow ions and small molecules to pass from one cell to another.
The junctional epithelium is attached to the tooth surface (epithelial attachment) by means of an
internal basal lamina. It is attached to the gingival connective tissue by an external basal lamina that
has the same structure as other epithelialconnective tissue attachments elsewhere in the body.
The internal basal lamina consists of a lamina densa (adjacent to the enamel) and a lamina lucida to
which hemidesmosomes are attached. Hemidesmosomes have a decisive role in the firm attachment
of the cells to the internal basal lamina on the tooth surface.
Recent data suggest that the hemidesmosomes may also act as specific sites of signal transduction and
thus may participate in regulation of gene expression, cell proliferation, and cell
differentiation. Organic strands from the enamel appear to extend into the lamina densa.

The
junctional epithelium attaches to afibrillar cementum present on the crown (usually restricted to an
area within 1 mm of the cementoenamel junction) and root cementum in a similar manner.
Histochemical evidence for the presence of neutral polysaccharides in the zone of the epithelial
attachment has been reported. Data also have shown that the basal lamina of the junctional epithelium
resembles that of endothelial and epithelial cells in its laminin content but differs in its internal basal
lamina, which has no type IV collagen. These findings indicate that the cells of the junctional
epithelium are involved in the production of laminin and play a key role in the adhesion mechanism.
Renewal of Gingival Epithelium
The oral epithelium undergoes continuous renewal. Its thickness is maintained by a balance between
new cell formation in the basal and spinous layers and the shedding of old cells at the surface. The
mitotic activity exhibits a 24-hour periodicity, with the highest and lowest rates occurring in the
morning and evening, respectively. The mitotic rate is higher in nonkeratinized areas and is increased
in gingivitis, without significant gender differences. Opinions differ as to whether the mitotic rate is
increased or decreased with age.
The mitotic rate in experimental animals varies among different areas of the oral epithelium in
descending order: buccal mucosa, hard palate, sulcular epithelium, junctional epithelium, outer
surface of the marginal gingiva, and attached gingiva. The following have been reported as turnover
times for different areas of the oral epithelium in experimental animals: palate, tongue, and cheek, 5 to
6 days; gingiva, 10 to 12 days, with the same or more time required with age; and junctional
epithelium, 1 to 6 days.
Regarding junctional epithelium, it was previously thought that only epithelial cells facing the
external basal lamina were rapidly dividing. However, evidence indicates that a significant number of
the cells, such as the basal cells along the connective tissue, are capable of synthesizing
deoxyribonucleic acid (DNA), demonstrating their mitotic activity.
[226,227]
Rapid shedding of cells
effectively removes bacteria adhering to the epithelial cells and therefore is an important part of the
antimicrobial defense mechanisms at the dentogingival junction.
The junctional epithelium is a particularly unique epithelial structure because the surface cells are
specialized for the purpose of attachment to the tooth. Therefore, unlike other epithelial tissues
elsewhere in the body, there is no opportunity for sloughing of cells from the surface. Instead, cells at
the basal layer continually divide and move to within two or three cell layers of the tooth surface and
then migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus and be
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sloughed off into the gingival crevice. The extracellular spaces between the junctional epithelium are
also greater than other epithelial tissues, with intercellular spaces comprising approximately 18% of
the volume of the epithelium. This is a result of a lower density of desmosomes in the junctional
epithelium compared to the gingival epithelium, and the junctional epithelium is therefore intrinsically
leaky. This has great relevance in periodontal pathogenesis, since the widened intercellular spaces
in the junctional epithelium permit migration of neutrophils (polymorphonuclear [PMN] leukocytes)
and macrophages from the gingival connective tissues to enter the sulcus to phagocytose bacteria, as
well as the ingress of bacterial products and antigens.
In conclusion, it is usually 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. First, junctional epithelium is firmly attached to the tooth surface, forming
an epithelial barrier against plaque bacteria. Second, it allows access of gingival fluid, inflammatory
cells, and components of the immunologic host defense to the gingival margin. Third, junctional
epithelial cells exhibit rapid turnover, which contributes to the host-parasite equilibrium and rapid
repair of damaged tissue. Also, some investigators indicate that the cells of the junctional epithelium
have an endocytic capacity equal to that of macrophages and neutrophils and that this activity might
be protective in nature.
Gingival Connective Tissue
The major components of the gingival connective tissue are collagen fibers (about 60% by volume),
fibroblasts (5%), vessels, nerves, and matrix (about 35%).
The connective tissue of the gingiva is known as the lamina propria and consists of two layers: (1)
a papillary layer subjacent to the epithelium, which consists of papillary projections between the
epithelial rete pegs; and (2) a reticular layer contiguous with the periosteum of the alveolar bone.
Connective tissue has a cellular and an extracellular compartment composed of fibers and ground
substance. Thus the gingival connective tissue is largely a fibrous connective tissue that has elements
originating directly from the oral mucosal connective tissue, as well as some fibers (dentogingival)
that originate from the developing dental follicle.
The ground substance fills the space between fibers and cells, is amorphous, and has a high content of
water. It is composed of proteoglycans, mainly hyaluronic acid and chondroitin sulfate, and
glycoproteins, mainly fibronectin. Glycoproteins account for the faint PASpositive reaction of the
ground substance. Fibronectin binds fibroblasts to the fibers and many other components of the
intercellular matrix, helping mediate cell adhesion and migration. Laminin, another glycoprotein
found in the basal lamina, serves to attach it to epithelial cells.
The three types of connective tissue fibers are collagen, reticular, and elastic. Collagen type I forms
the bulk of the lamina propria and provides the tensile strength to the gingival tissue. Type IV
collagen (argyrophilic reticulum fiber) branches between the collagen type I bundles and is
continuous with fibers of the basement membrane and blood vessel walls.
The elastic fiber system is composed of oxytalan, elaunin, and elastin fibers distributed among
collagen fibers.
Therefore densely packed collagen bundles that are anchored into the acellular extrinsic fiber
cementum just below the terminal point of the junctional epithelium form the connective tissue
attachment. The stability of this attachment is a key factor in limiting the migration of junctional
epithelium.

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The attachment of the junctional epithelium to the tooth is reinforced by the gingival fibers, which
brace the marginal gingiva against the tooth surface. For this reason, the junctional epithelium and the
gingival fibers are considered a functional unit, referred to as the dentogingival unit.
The connective tissue component of the dentogingival unit contains densely packed collagen fiber
bundles (mixture of type I and III collagen fibers) that are arranged in distinct patterns that maintain
the functional integrity of the tissues and tight adaptation of the soft tissues to the teeth. These include
the following:
Dentogingival fibers (extend from the cementum into the free and attached gingiva)
Alveologingival fibers (extend from the alveolar crest into the free and attached gingiva)

Circular fibers (wrap around the tooth, maintaining close adaptation of the free gingiva to the
tooth, and interweaving with other collagen fiber bundles)

Dentoperiosteal fibers (run from the cementum, over the alveolar crest, and insert into the
alveolar process)

Transseptal fibers (run interdentally, from the cementum just apical to the junctional epithelium,
over the alveolar crest, and insert into the cementum of the neighboring tooth).


Page et al., 1972 also described (1) a group of semicircular fibers that attach at the proximal surface
of a tooth, immediately below the cementoenamel junction, go around the facial or lingual marginal
gingiva of the tooth, and attach on the other proximal surface of the same tooth; and (2) a group
of transgingival fibers that attach in the proximal surface of one tooth, traverse the interdental space
diagonally, go around the facial or lingual surface of the adjacent tooth, again traverse diagonally the
interdental space, and attach in the proximal surface of the next tooth.
Repair of Gingival Connective Tissue
Because of the high turnover rate, the connective tissue of the gingiva has remarkably good healing
and regenerative capacity. Indeed, it may be one of the best healing tissues in the body and generally
shows little evidence of scarring after surgical procedures. This is likely caused by rapid
reconstruction of the fibrous architecture of the tissues. However, the reparative capacity of gingival
connective tissue is not as great as that of the periodontal ligament or the epithelial tissue.
Even in clinically healthy gingiva, the gingival connective tissue contains at least some inflammatory
cells, particularly neutrophils. Neutrophils continually migrate through the connective tissues and pass
through the junctional epithelium to enter the sulcus/pocket. These findings were reported in the
classic investigations of the histology of periodontal disease reported by Page and Schroeder in 1976.

This low-grade inflammation occurs in response to the continued presence of bacteria and their
products in the gingival crevice. There is a continuous exudate of fluid from the gingival tissues that
enters the crevice and flows out as gingival crevicular fluid (GCF). In addition to the continuous
migration of neutrophils through the gingival tissues, lymphocytes and macrophages also accumulate.
The presence of leukocytes in the connective tissues results from the chemotactic stimulus created by
the subgingival biofilm and bacterial products, as well as chemoattractant factors produced by the
host.
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In clinically healthy tissues, this steady state equilibrium between low-grade inflammation in the
tissues and the continual presence of the subgingival microflora may persist for many years or indeed
for the lifetime of the individual. Overt clinical signs of gingivitis (redness, swelling, and bleeding on
probing) do not develop because of several innate and structural defense mechanisms, including the
following:
The maintenance of an intact epithelial barrier (the junctional and sulcular epithelium).
Outflow of GCF from the sulcus (dilution effect and flushing action).
Sloughing of surface epithelial cells of the junctional and sulcular epithelium.
Presence of neutrophils and macrophages in the sulcus, phagocytosing bacteria.
Antibodies in the GCF (although it is not clear whether these are effective).
After the accumulation of subgingival plaque bacteria, a variety of microbial substances, including
chemotactic factors such as lipopolysaccharide (LPS), microbial peptides, and other bacterial
antigens, diffuse across the junctional epithelium into the gingival connective tissues. The
periodontium is anatomically unique in that the junctional epithelium ends on the tooth surface, which
is nonliving tissue; there is no other such discontinuous lining over the entire surface of the body. The
dentogingival junction indicates a priori vulnerability to bacterial attack. Epithelial and connective
tissue cells are thus stimulated to produce inflammatory mediators that result in an inflammatory
response in the tissues. The gingival vasculature dilates (vasodilation) and becomes increasingly
permeable to fluid and cells. Fluid accumulates in the tissues, and defense cells migrate from the
circulation toward the source of the chemotactic stimulus (bacteria and their products) in the gingival
crevice. Neutrophils, or polymorphonuclear leukocytes (PMNs), predominate in the early stages of
gingival inflammation to phagocytose and kill plaque bacteria. Bacterial killing by PMNs involves
both intracellular mechanisms (after phagocytosis of bacteria within membrane-bound structures
inside the cell) and extracellular mechanisms (by release of PMN enzymes and oxygen radicals
outside the cell). As bacterial products enter the circulation, committed lymphocytes return to the site
of infection, and B lymphocytes are transformed to plasma cells, which produce antibodies against
specific bacterial antigens. Antibodies are released in the gingival tissues and, in the presence of
complement, facilitate and enhance PMN phagocytosis and bacterial killing.
However, if plaque accumulation increases so that these defense mechanisms are overwhelmed, then
inflammation and the classic clinical signs of gingivitis will develop. Even though the development of
gingivitis in response to the accumulation of plaque is fairly predictable, research has identified that a
spectrum of responses may be observed, with some individuals developing marked gingival
inflammation for a given plaque challenge and others developing minimal gingival
inflammation. These observations underscore the importance of variations in host responses between
individuals in terms of gingival inflammatory responses. Furthermore, many individuals may never
develop periodontitis despite having widespread gingivitis. The host's immune-inflammatory response
is fundamental in determining which individuals may progress to developing periodontitis, and it is
likely that inflammatory responses are markedly different in those individuals who develop
periodontitis compared to those who never progress beyond gingivitis. The challenge that this
presents clinically is that we do not know (yet) enough about susceptibility to periodontitis to identify
these individuals before they actually develop signs of the disease.