dentogingival junction

8/10/2019 Dentogingival Junction

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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 thecementoenamel 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 typeIV collagen is absent.


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The junctional epithelium is formed by the confluence of the oral epithelium and the reduced enamelepithelium during tooth eruption However, the reduced enamel epithelium is not essential for itsformation; in fact, the junctional epithelium is completely restored after pocket instrumentation orsurgery, 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) andhistochemically demonstrable acid phosphatase, correlated with the low degree of differentiation, mayreflect a low defense power against microbial plaque accumulation in the gingival sulcus. Similarmorphologic findings have been described in the gingiva of germ-free rats. PMNs are found routinelyin the junctional epithelium of both conventional rats and germ-free rats. Research has shown thatalthough numerous migrating PMNs are evident and present around healthy junctional epithelium, aconsiderable increase in PMN numbers can be expected with the accumulation of dental plaque andgingival 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 orK13 reveal a sudden change between sulcular and junctional epithelia; the junctional area is the onlystratified nonkeratinized epithelium in the oral cavity that does not synthesize these specificpolypeptides. Another particular behavior of junctional epithelium is the lack of expression of K6 andK16, which is usually linked to highly proliferative epithelia, although the turnover of the cells is veryhigh.

Similar to sulcular epithelium, junctional epithelium exhibits lower glycolytic enzyme activity thanouter epithelium and lacks acid phosphatase activity.

Cell-Cell Attachments:-

1. Desmosomes,2. Adherens junction3. Tight junctions4. Gap junctions

Desmosomes are molecular complexes of cell adhesion proteins and linking proteins that attach the

cell surface adhesion proteins to intracellularkeratincytoskeletal filaments. The cell adhesion proteinsof the desmosome, desmoglein and desmocollin, are members of thecadherin family of cell adhesionmolecules. They aretransmembrane proteins that bridge the space between adjacentepithelial cellsbyway ofhomophilic binding of their extracellular domains to other desmosomal cadherins on theadjacent 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 theDesmoglea, and is bisected by an electron-dense midline where the desmoglein and desmocollinproteins bind to each other. These proteins can bind in a W, S, or manner.
http://en.wikipedia.org/wiki/Keratinhttp://en.wikipedia.org/wiki/Cytoskeletonhttp://en.wikipedia.org/wiki/Cadherinhttp://en.wikipedia.org/wiki/Transmembrane_proteinhttp://en.wikipedia.org/wiki/Epithelial_cellhttp://en.wikipedia.org/wiki/Homophilic_bindinghttp://en.wikipedia.org/wiki/Homophilic_bindinghttp://en.wikipedia.org/wiki/Epithelial_cellhttp://en.wikipedia.org/wiki/Transmembrane_proteinhttp://en.wikipedia.org/wiki/Cadherinhttp://en.wikipedia.org/wiki/Cytoskeletonhttp://en.wikipedia.org/wiki/Keratin


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On the cytoplasmic side of the plasma membrane, there are two dense structures called the OuterDense Plaque (ODP) and the Inner Dense Plaque (IDP). These are spanned bytheDesmoplakinprotein. The Outer Dense Plaque is where the cytoplasmic domains of the cadherinsattach todesmoplakin viaplakoglobin and plakophillin. The Inner Dense Plaque iswheredesmoplakin attaches to theintermediate filaments of the cell.

Adherens junctions(or zonula adherens, intermediate junction, or "belt desmosome") are proteincomplexes that occur at cellcell junctions in epithelial tissues, usually more basal thantight

junctions.An adherens junction is defined as a cell junction whose cytoplasmic face is linked totheactin 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

twocells whosemembranesjoin together forming a virtually impermeable barrier to fluid. Tightjunctions are composed of a branching network of sealing strands, each strand acting independentlyfrom the others. Therefore, the efficiency of the junction in preventing ion passage increasesexponentially 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 anotherdirectly. Although more proteins are present, the major types are theclaudins and theoccludins.These associate with different peripheral membrane proteins located on the intracellular side ofplasma membrane, which anchor the strands to theactin component of thecytoskeleton.Thus, tightjunctions join together the cytoskeletons of adjacent cells.

A gap junctionor nexusis a specialized intercellular connection between a multitude of animalcell-

types. It directly connects the cytoplasm of two cells, which allows variousmolecules andions topass freely between cells.

Electron microscopy reveals that keratinocytes, the principle cell type of gingival epithelium, areinterconnected by structures on the cell periphery called desmosomes. These desmosomes have atypical structure consisting of two dense attachment plaques into which tonofibrils insert and an

intermediate, electron-dense line in the extracellular compartment. Tonofilaments, which are themorphologic expression of the cytoskeleton of keratin proteins, radiate in brushlike fashion from the
http://en.wikipedia.org/wiki/Desmoplakinhttp://en.wikipedia.org/wiki/Desmoplakinhttp://en.wikipedia.org/wiki/Plakoglobinhttp://en.wikipedia.org/wiki/Desmoplakinhttp://en.wikipedia.org/wiki/Intermediate_filamentshttp://en.wikipedia.org/wiki/Tight_junctionshttp://en.wikipedia.org/wiki/Tight_junctionshttp://en.wikipedia.org/wiki/Actinhttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Cell_membranehttp://en.wikipedia.org/wiki/Claudinshttp://en.wikipedia.org/wiki/Occludinhttp://en.wikipedia.org/wiki/Actinhttp://en.wikipedia.org/wiki/Cytoskeletonhttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Cytoplasmhttp://en.wikipedia.org/wiki/Moleculehttp://en.wikipedia.org/wiki/Ionhttp://en.wikipedia.org/wiki/Ionhttp://en.wikipedia.org/wiki/Moleculehttp://en.wikipedia.org/wiki/Cytoplasmhttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Cytoskeletonhttp://en.wikipedia.org/wiki/Actinhttp://en.wikipedia.org/wiki/Occludinhttp://en.wikipedia.org/wiki/Claudinshttp://en.wikipedia.org/wiki/Cell_membranehttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Actinhttp://en.wikipedia.org/wiki/Tight_junctionshttp://en.wikipedia.org/wiki/Tight_junctionshttp://en.wikipedia.org/wiki/Intermediate_filamentshttp://en.wikipedia.org/wiki/Desmoplakinhttp://en.wikipedia.org/wiki/Plakoglobinhttp://en.wikipedia.org/wiki/Desmoplakinhttp://en.wikipedia.org/wiki/Desmoplakin


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attachment plaques into the cytoplasm of the cells. The space between the cells shows cytoplasmicprojections resembling microvilli that extend into the intercellular space and often interdigitate.

Less frequently observed forms of epithelial cell connections are tight junctions (zonae occludens),inwhich the membranes of the adjoining cells are believed to be fused. Evidence suggests that thesestructures 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 aninternal basal lamina. It is attached to the gingival connective tissue by an external basal lamina thathas 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 towhich hemidesmosomes are attached. Hemidesmosomes have a decisive role in the firm attachmentof 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 andthus may participate in regulation of gene expression, cell proliferation, and celldifferentiation. 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 anarea 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 epithelialattachment has been reported. Data also have shown that the basal lamina of the junctional epitheliumresembles that of endothelial and epithelial cells in its laminin content but differs in its internal basallamina, which has no type IV collagen. These findings indicate that the cells of the junctionalepithelium 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 betweennew cell formation in the basal and spinous layers and the shedding of old cells at the surface. Themitotic activity exhibits a 24-hour periodicity, with the highest and lowest rates occurring in themorning and evening, respectively. The mitotic rate is higher in nonkeratinized areas and is increasedin gingivitis, without significant gender differences. Opinions differ as to whether the mitotic rate isincreased or decreased with age.

The mitotic rate in experimental animals varies among different areas of the oral epithelium indescending order: buccal mucosa, hard palate, sulcular epithelium, junctional epithelium, outersurface of the marginal gingiva, and attached gingiva. The following have been reported as turnovertimes for different areas of the oral epithelium in experimental animals: palate, tongue, and cheek, 5 to6 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 theexternal basal lamina were rapidly dividing. However, evidence indicates that a significant number ofthe cells, such as the basal cells along the connective tissue, are capable of synthesizingdeoxyribonucleic 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 arespecialized for the purpose of attachment to the tooth. Therefore, unlike other epithelial tissueselsewhere 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 andthen 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 arealso greater than other epithelial tissues, with intercellular spaces comprising approximately 18% ofthe volume of the epithelium. This is a result of a lower density of desmosomes in the junctionalepithelium compared to the gingival epithelium, and the junctional epithelium is therefore intrinsicallyleaky. This has great relevance in periodontal pathogenesis, since the widened intercellular spacesin the junctional epithelium permit migration of neutrophils (polymorphonuclear [PMN] leukocytes)and macrophages from the gingival connective tissues to enter the sulcus to phagocytose bacteria, aswell as the ingress of bacterial products and antigens.

In conclusion, it is usually accepted that the junctional epithelium exhibits several unique structuraland functional features that contribute to preventing pathogenic bacterial flora from colonizing thesubgingival tooth surface. First, junctional epithelium is firmly attached to the tooth surface, formingan epithelial barrier against plaque bacteria. Second, it allows access of gingival fluid, inflammatorycells, and components of the immunologic host defense to the gingival margin. Third, junctionalepithelial cells exhibit rapid turnover, which contributes to the host-parasite equilibrium and rapidrepair of damaged tissue. Also, some investigators indicate that the cells of the junctional epitheliumhave 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 propriaand consists of two layers: (1)apapillary layer subjacent to the epithelium, which consists of papillary projections between theepithelial rete pegs; and (2) a reticular layercontiguous 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 elementsoriginating directly from the oral mucosal connective tissue, as well as some fibers (dentogingival)that originate from the developing dental follicle.

Theground substancefills the space between fibers and cells, is amorphous, and has a high content ofwater. It is composed of proteoglycans, mainly hyaluronic acid and chondroitin sulfate, andglycoproteins, mainly fibronectin. Glycoproteins account for the faint PASpositive reaction of theground substance. Fibronectin binds fibroblasts to the fibers and many other components of theintercellular matrix, helping mediate cell adhesion and migration. Laminin, another glycoproteinfound 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 IVcollagen (argyrophilic reticulum fiber) branches between the collagen type I bundles and iscontinuous with fibers of the basement membrane and blood vessel walls.

The elastic fiber system is composed of oxytalan, elaunin, and elastin fibers distributed amongcollagen fibers.

Therefore densely packed collagen bundles that are anchored into the acellular extrinsic fibercementum just below the terminal point of the junctional epithelium form the connective tissueattachment. The stability of this attachment is a key factor in limiting the migration of junctionalepithelium.


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The attachment of the junctional epithelium to the tooth is reinforced by the gingival fibers, whichbrace the marginal gingiva against the tooth surface. For this reason, the junctional epithelium and thegingival fibers are considered a functional unit, referred to as the dentogingival unit.

The connective tissue component of the dentogingival unit contains densely packed collagen fiberbundles (mixture of type I and III collagen fibers) that are arranged in distinct patterns that maintainthe functional integrity of the tissues and tight adaptation of the soft tissues to the teeth. These includethe 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 thetooth, 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 ofsemicircular fibers that attach at the proximal surface

of a tooth, immediately below the cementoenamel junction, go around the facial or lingual marginalgingiva of the tooth, and attach on the other proximal surface of the same tooth; and (2) a groupof transgingival fibersthat attach in the proximal surface of one tooth, traverse the interdental spacediagonally, go around the facial or lingual surface of the adjacent tooth, again traverse diagonally theinterdental 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 healingand regenerative capacity. Indeed, it may be one of the best healing tissues in the body and generallyshows little evidence of scarring after surgical procedures. This is likely caused by rapidreconstruction of the fibrous architecture of the tissues. However, the reparative capacity of gingivalconnective 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 inflammatorycells, particularly neutrophils. Neutrophils continually migrate through the connective tissues and passthrough the junctional epithelium to enter the sulcus/pocket. These findings were reported in theclassic 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 theirproducts in the gingival crevice. There is a continuous exudate of fluid from the gingival tissues thatenters the crevice and flows out as gingival crevicular fluid (GCF). In addition to the continuousmigration 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 thehost.


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In clinically healthy tissues, this steady state equilibrium between low-grade inflammation in thetissues and the continual presence of the subgingival microflora may persist for many years or indeedfor the lifetime of the individual. Overt clinical signs of gingivitis (redness, swelling, and bleeding onprobing) do not develop because of several innate and structural defense mechanisms, including thefollowing:

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, includingchemotactic factors such as lipopolysaccharide(LPS), microbial peptides, and other bacterialantigens, diffuse across the junctional epithelium into the gingival connective tissues. Theperiodontium is anatomically unique in that the junctional epithelium ends on the tooth surface, whichis 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 connectivetissue cells are thus stimulated to produce inflammatory mediators that result in an inflammatoryresponse in the tissues. The gingival vasculature dilates (vasodilation) and becomes increasinglypermeable 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 gingivalcrevice. Neutrophils, or polymorphonuclear leukocytes (PMNs), predominate in the early stages ofgingival inflammation to phagocytose and kill plaque bacteria. Bacterial killing by PMNs involvesboth intracellular mechanisms (after phagocytosis of bacteria within membrane-bound structuresinside 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 siteof 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 ofcomplement, 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 ofgingivitis 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 gingivalinflammation for a given plaque challenge and others developing minimal gingivalinflammation. These observations underscore the importance of variations in host responses betweenindividuals in terms of gingival inflammatory responses. Furthermore, many individuals may neverdevelop 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 developperiodontitis compared to those who never progress beyond gingivitis. The challenge that thispresents clinically is that we do not know (yet) enough about susceptibility to periodontitis to identifythese individuals before they actually develop signs of the disease.

dentogingival junction

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