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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There are three separate pathways of complement activation. 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. Increased amounts of MMP-1, -2, -3, -8, -9, and have been found in GCF and gingiva of periodontitis patients compared with samples from healthy controls [ 228593 — 99 ]. Although this model is a very delicate and excellent model, it is difficult to repeat and individual variation may influence the results.
Furthermore, complement activation increases vascular permeability and attracts phagocytes to the inflammatory site. This is further strengthened by the external basal lamina EBL and internal basal lamina IBL that function as barriers to bacterial advancement, yet allowing the passage of leukocytes and their antimicrobial agents and antibodies into the gingival crevice.
International Journal of Dentistry
Into this model planktonic bacteria or bacterial products can be added to the culture medium. The JE cells actively facilitate leukocyte recruitment to the site of inflammation by expressing chemotactic factors IL-8 and complement C5a and factors such as ICAM-1 that aid leukocyte course from the blood vessels [ 19 — 22 ]. Additional contributions continue to be made. Development of the dentogingival junction: International Journal of Dentistry. This dynamic group of tissues is well adapted for the healing of direct injuries produced during mastication.
The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo. 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 ].
Impaired PMN functions are generally considered to be related to periodontal tissue destruction and patients with reduced number of neutrophils or impaired neutrophil function show often severe periodontitis [ ]. However, the connection between the IL-1 gene polymorphism and the clinical manifestations of periodontal disease do not seem to be likewise certain in all populations .
This paper dentogingivao on host-bacteria crosstalk at the dentogingival junction and the models studying it in vitro. It is probably not a coincidence that some of the known periodontopathogens, that is, P.
Yet surprisingly small number of studies has been done on this early host-microbe interaction. Langerhans cells, identified by the C-type lectin langerin, are dendritic cells responsible for the presentation of antigens to T-lymphocytes. In periodontitis their number decreases intraepithelially and increases in connective tissue where antigen junctionn takes place.
Host-Bacteria Crosstalk at the Dentogingival Junction
View at Google Scholar A. Normally they are distributed throughout the body without adverse effects. The classical study of Slots showed that in the bacterial plaque, the most remarkable change is the shift from gram-positive aerobic and facultatively anaerobic flora to a predominantly gram-negative and anaerobic flora. In vitro experiments have shown that P.
MAC inhibitor, CD59, is expressed in gingival epithelium and thus gingival epithelium is probably well-protected against MAC mediated cell damage [ ].
The entire tissue is capable of regeneration after wounding. Two kinds of models have been used in our laboratory, Figures 2 a and 2 b. Within the bell-shaped ectodermal structure several distinct layers are visible.
The edntogingival do remarkably well, dentogingjval long periods, in their response to periodontal disease, whether due to direct bacterial or toxic damage, or to indirect damage via the migration of inflammatory cells into the lesion.
Interestingly, the action of periodontal bacteria on complement seems to be biphasic.
In addition to known periodontal pathogens, other bacterial species, such as Pseudoramibacter, Bacteroidetes, Sphorocytophaga, Shuttleworthia, Dialister, Mogibacterium, Mycoplasma, Synergistes, and Acidaminococcaceaeseem to exist at high levels in patients with refractory nature of periodontitis [ 6 ].
The past 60 years are replete with fine contributions by distinguished workers. Periodontal pathogens may also evade or escape the innate defense mechanisms and in such cases the cells of the adaptive immune response have an important role in recognizing the pathogens and initiating specific defense targeted to the pathogens involved. Even when they are pathologic, they can be reconstituted by repair.
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— ].
However, at least A. They degrade complement proteins. Smoking also impairs neutrophil functions, for example, phagocytosis [ ]. Dendritic cells form the crucial link between the innate and adaptive immunity.