Development of the dentogingival junction: Early stages. In order to understand how the dentogingival junction comes into existence, it is necessary to review. Looking for online definition of dentogingival junction in the Medical Dictionary? dentogingival junction explanation free. What is dentogingival junction?. J Periodontol. Sep;52(9) Current concepts of the dentogingival junction: the epithelial and connective tissue attachments to the tooth. Stern IB.

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Undifferentiated epithelial cells form the stratum intermedium SIdirectly adjacent to the ameloblasts.

Two kinds of models have been used in our laboratory, Dentogingial 2 a and 2 b. Recently also gram-positive genera such as Peptostreptococcus and Filifactor have been suggested to play roles in periodontitis [ 4 ]. View at Google Scholar D. The wide intercellular spaces and permeability of the JE, even though beneficial for the host defense, also allow bacteria and their harmful products to penetrate epithelium, which thereby activate the inflammatory reaction.

Oral bacteria exert a constant challenge to the host cells and tissues at the dentogingival junction. In order to understand how the dentogingival junction comes into existence, it is necessary to review some aspects of tooth development and eruption. This has been later confirmed by several other studies.

A thin layer of enamel E can be seen on the outer dentin surface. Junctional epithelium, dark red. Host PRRs may be either soluble e. The Junctional Epithelium-Bacteria Interactions The first line of innate host defense in the periodontal region is the JE that hinders bacterial advancement into periodontal tissues, Figure 1 a. A third possibility is bacterial invasion into JE cells and formation of an intraepithelial split that then results in periodontal pocket formation. Microorganisms in Subgingival Biofilm The presence of the initial colonizers on the tooth surface is essential for the emergence of the gram-negative periodontopathogens Porphyromonas gingivalis, Tannerella forsythia Bacteroides forsythusAggregatibacter actinomycetemcomitans, and Fusobacterium, Dentoginhival, Campylobacter, and Treponema species [ 1 — 3 ].

International Journal denotgingival Dentistry. However, the most coronal part of the JE attached to the tooth appear to stand in first line of periodontal defense.

The nonspecific innate immune nunction provides an immediate response, recognizing the difference between self-components and foreign molecules in the periodontal region.


In dentogjngival to the protective structures of multispecies biofilm which inhibit the actions of host defense cells, the molecular interactions between different species [ 1314 ] in the oral junctiom could influence the virulence of the bacterial community.

Such experimental setups however lack important issues, for example, cell-cell contacts of the multilayered epithelium, the basement membranes and the epithelium-connective tissue interface as well as the microbial pathogenicity of the biofilm.

View at Google Scholar K.

Decreased mitosis and increased apoptosis of gingival epithelial cells has been shown at sites exhibiting severe inflammation [ 69 ]. As stated before in this paper, bacteria behave differently in biofilms, where some virulence genes are expressed due to the quorum sensing signaling. Moreover, by weakening the host defense, opportunistic periodontal pathogens, such as P. Proteases such as elastase, cathepsin G, and MMPs, of which MMP-8, and MMP-9 are mainly originated from neutrophils, are able to degrade a wide variety of host cellular and extracellular components [ ].

Gingipains are proteases secreted by P. Especially quorum sensing signal, autoinducer-2, is used in inter-species signaling between various periodontal pathogens, and it may enhance the formation of the biofilm as well as change the virulence gene expression [ 15 ].

This leads to the release of the proinflammatory cytokines e. Despite of a huge number of studies on periodontitis development, we still do not have a clear picture of the crucial events leading to the periodontal tissue destruction. Langerin is a transmembrane cell surface protein which plays a role in antigen recognition and uptake. The past 60 years are replete with fine contributions by distinguished workers. The PMNs are a major contributor in the host parasite equilibrium but when activated can also cause tissue damage due to excess of enzymes, reactive oxygen species, MMPs, and other components that are released from their granules during the battle against microbes [ 48— ].

Toll-like receptor-2 TLR-2that recognizes, for example, bacterial peptidoglycans PGNlipoproteins, and LTAs has been found in abundance in the membrane of pocket epithelial cells as compared to the gingival tissues of healthy controls [ 73 ].

Dentogingival junction | definition of dentogingival junction by Medical dictionary

This paper focuses on host-bacteria crosstalk at the dentogingival junction and the models studying it in vitro. Skip to main content. Improved methods to detect bacteria in periodontal biofilm have broadened our knowledge about pocket-associated microbes. In vitro experiments have shown that P. When biofilm is placed on the top of the model host-bacteria interaction can be studied.


The complement system is a biochemical cascade of the small plasma proteins that activate another in series. Separately grown bacterial biofilms can be added onto the cultures. View at Google Scholar L.

Dentogingival junction

This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any ddentogingival, provided the original work is properly cited.

The primary tissue culture model of JE Figure 2 ain which a piece of masticatory mucosa is placed on a permeable filter, allows studies, for example, bacterial components on the dentogingival junction in vitro.

C4 deficiencies have been previously associated with chronic mucosal infections and the authors suggested that it may also predispose to periodontal infections. The organotypic tissue culture models are convenient systems to study how periodontal pathogens penetrate not only dentoginbival the cells but also to the cell layers.

Host-Bacteria Crosstalk at the Dentogingival Junction

The other model, Figure 2 boriginally presented by Oksanen and Hormia [ ], uses cell lines of either oral or skin origin and further includes a piece of tooth onto which the JE is formed Figure 4. Degeneration and detachment of the DAT cells, loss of cellular continuity, and cell death dentkgingival the coronal part of the JE and development of an intraepithelial split have been suggested in the initial phase of periodontal pathology [ — ].

Although novel detection methods have allowed the recognition of new species that could be involved in the pathogenesis of periodontitis, recent studies suggest that the whole composition, rather than single species, influence the pathogenicity of the biofilm [ 1112 ]. Calprotectin, expressed in neutrophils, monocytes, and gingival keratinocytes, protects gingival dentogingiavl against binding and invasion by P.