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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Alternatively, degradation of IBL on dentoggingival tooth surface and consequently detachment of the JE takes place. When biofilm is placed on the top of the model host-bacteria interaction can be studied.
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 ]. Next to it is the stratum intermedium SI consisting of layers of undifferentiated epithelial cells. Complement system is the immediate and major humoral component of innate immune response [ ].
Bacterial antigens coupled with antigen presenting cells with major histocompatibility complex MHC class-I molecules are recognized by T-killer cells and B cells. They degrade complement proteins.
PARs are expressed in human neutrophils, gingival fibroblasts, and osteoblasts [ 74dentogintival ]. This has been later confirmed by several other studies.
The junctional epithelium can advance and retract.
Additional contributions continue to be made. However, some studies have indicated that, in contrast to impaired function, PMN hyperreactivity may play a role in periodontitis [ ]. The inner jjunction epithelium cells, in contact with the first-formed dentin, differentiate into pre-ameloblasts and then into ameloblasts that produce enamel on top of the already formed dentin.
In vitro experiments have shown that P. The fact, that when MMP activity is inhibited, tissue hunction is reduced, further emphasizes the role of MMPs on tissue destruction [ ].
The C3 fragment is important in all three pathways. This is thought to result from both host- and bacteria-derived agents, such as lipopolysaccharides LPSsinflammatory cytokines, for example, IL-1beta, and TNF-alpha and to a lesser fentogingival also by IL, growth factors and hormones [ 8085jjnction ] that activate leukocytes, fibroblasts, and epithelial cells leading to production of prostaglandins and MMPs and causing destruction of the CT [ 728788 ].
In addition to the protective structures of multispecies biofilm which inhibit the actions of host defense cells, the molecular interactions between different species [ 1314 ] dentogingifal the oral biofilm could influence the virulence of the bacterial community. They are stored and secreted as inactive proenzymes. The Junctional Epithelium-Bacteria Interactions The first line of innate host defense in the periodontal region is the JE that hinders bacterial juncttion into periodontal tissues, Figure 1 a.
Subscribe to Table of Contents Alerts. It is obvious, however, that many factors, including direct bacterial effects and response of the host cells are involved in this process. With this model F.
Neutrophils are viable and functional in the gingival crevice. At site denfogingival infection proenzymes become proteases and produce local inflammatory responses. Recently also gram-positive genera such as Peptostreptococcus and Filifactor have been suggested to play roles in periodontitis [ 4 dejtogingival. View at Google Scholar L. Both their cellular and extracellular components exhibit a high rate of turnover.
PMNs are essential in the first line of innate defense against plaque bacteria at the gingival margin. Shortly after the onset of amelogenesis, the stellate reticulum SR shrinks considerably so that the outer enamel epithelium OEE comes into close contact with the stratum intermedium cells top of Fig.
In health, the commensal bacteria and the host defense mechanisms are in a dynamic steady state.
Into this model planktonic bacteria or bacterial products can be added to the culture medium. Microorganisms other than bacteria have also been found in periodontitis patients.
In already early periodontitis a great number of PMNs are migrating through gingival epithelium. Denntogingival receptor is crucial for binding of JE to basement membrane.
Many proteinases secreted by PMNs are capable of degrading dentogjngival lamina components, including laminin [ ]. The cuticle width is alterable. The complete story is not yet developed. A thin layer of enamel E can be seen on the outer dentin surface.
The pathways include the classical pathway, the alternative pathway and the lectin-mediated pathway. The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo.
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
However, it seems that a certain threshold exists to inflammatory and bacterial challenge and the expression of hBDs, since in chronic advanced periodontitis the expression of hBDs-2 and -3 is reduced [ 28 ]. Smoking also impairs neutrophil functions, for example, phagocytosis [ ]. 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— ].
Host PRRs may be either soluble e. Undifferentiated epithelial cells form the stratum intermedium SIdirectly adjacent to the ameloblasts. Abstract The dentogingival junction is of crucial importance in periodontal host defense both structurally and functionally. View at Google Scholar M. View at Google Scholar S. Since pathologically elevated levels of active MMPs have been found in periodontal tissues during periodontitis, the MMPs may play a role in lateral and apical migration of the JE during pocket formation [ 95].
The inhibited or exaggerated inflammatory response results from an imbalance of pro- and anti-inflammatory cytokines. 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.
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 . Separately dentogingoval bacterial biofilms can be added onto the cultures. Moreover, by weakening the host defense, opportunistic periodontal pathogens, such as P. This leads to the release of the proinflammatory cytokines e.