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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Macrophages are efficient phagocytes and are abundant within the gingival tissues.
Thus the activation of PARs seems to be important for the protective host response at the periodontal region. A third possibility is bacterial invasion into JE cells and formation of an intraepithelial split that then results in periodontal pocket formation.
Abstract The dentogingival junction is of crucial importance in periodontal host defense both structurally and functionally. Junctional epithelium, dark red. Several activated complement components form a membrane attack complex MACwhich creates a transmembrane pore leading to the lysis of the target cell and may thus lead to destruction of both bacterial and host cells.
Two kinds of models have been used in our laboratory, Figures 2 a and 2 b. The inheritance from our predecessors has been used well and our expanded knowledge in this area now serves as the conceptual framework for further study.
The active role of the JE in the innate host defense is further demonstrated by the production of cytokines and the presence of natural antimicrobial peptides and proteins such dentogngival the defensins, the cathelicidin family members LLand calprotectin [ 23 — 25 ].
Bacteria at the gingival margin causes drastic changes in CT; vascular permeability and the amount of inflammatory cell infiltrate are increased. The inner enamel epithelium cells, in contact with the first-formed dentin, differentiate into pre-ameloblasts and then into dentogingivwl that produce enamel on top of the already formed dentin.
Shortly after the onset of amelogenesis, the stellate reticulum SR shrinks considerably so that the outer enamel epithelium OEE jujction into close contact with the stratum intermedium cells dentogingkval of Fig.
Dentogingival junction | definition of dentogingival junction by Medical dictionary
Decreased mitosis and increased apoptosis of gingival epithelial cells has been shown at sites exhibiting severe inflammation [ 69 ]. Complement system is the immediate and major humoral component of innate immune response [ ]. Host PRRs may be either dentoglngival e. Planktonic cells of opportunistic periodontal pathogens A. Once these events are better understood treatment modalities aiming at preventing periodontal pocket formation can be designed.
Cocultures with bacterial biofilms can be used to study host-microbe interactions with this model. As an example, HSP60 from A. Application of PAR agonist peptide to gingiva has induced periodontitis in rats radiographically assessed bone loss, myeloperoxidase MPO activity [ 79 ]. Neutrophils have surface receptors for both complement C5a-receptor and immunoglobulin Fc gamma-receptors and the interaction with opsonized bacteria leads to phagocytosis of the bacteria.
The inhibited or exaggerated inflammatory response results from an imbalance of pro- and anti-inflammatory cytokines.
The anti-inflammatory cytokine profile of the Th2 response, low levels of costimulatory molecules and B-cell dependent antibody production have been suggested to dominate in cases of commensal bacteria, nonsusceptible patients and protective immune junctioh whereas the periodontopathogenic bacteria are thought to trigger the proinflammatory Dentognigival cytokine response resulting in inflammatory periodontal bone resorption [ 88— ].
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.
The tissue homeostasis is turned into tissue destruction and progression of periodontitis. Many of the complement proteins are proteases. During periodontal disease progression, the dental bacterial plaque, junctional epithelium JEinflammatory cells, connective tissue, and bone all go through a series of changes.
However, various pathogenic bacteria including P. The initial events of periodontal pocket formation are likely to involve destruction of the dento-epithelial junction resulting in the failure of the epithelial barrier function. They degrade complement proteins. 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 ].
With this model F. Alpha-defensins secreted by neutrophils are bound to junctional and pocket epithelium serving as an additional antimicrobial function [ 33 ]. Furthermore, complement activation increases vascular permeability and attracts phagocytes to the inflammatory site.
Indexed in Web of Science. Furthermore, not only the shift of the bacterial flora to a more pathogenic one, but also bacterial growth as a biofilm on the tooth surface, allows the bacteria to communicate with each other and exert their virulence aimed at favoring their growth. However, at least A. However, this does not exclude the possibility that its molecular structures may be altered.
The tissues show a capacity for repair and regeneration following the elimination of plaque formation and the resultant resolution of the inflammatory infiltrate. Bacterial internalization in a tissue culture model and in vivo in severe periodontitis followed by epithelial cell apoptosis have also been demonstrated [ 7071 ].
The innate immune system is a crucial part of the defense at the early stages of infection and further controls the emergence of the adaptive immune response [ ] Table 2.
Van Der Velden, V. 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— ].