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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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— ]. The outermost layer consists of a single layer of cells, the outer enamel epithelium OEE.
Development of the Dentogingival Junction – Early Stages
TGF-beta is an anti-inflammatory cytokine that also inhibits epithelial cell proliferation. 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 extent also by IL, growth factors and hormones [ 808586 ] that activate leukocytes, fibroblasts, and epithelial cells leading to production of prostaglandins and MMPs jnuction causing destruction of the CT [ 728788 ].
Many of the complement proteins are proteases. During the bell stage of tooth development, the developing tooth consists of an ectodermal component, the enamel organderived from the oral ectoderm, that surrounds an ectomesenchymal component, the dental papilla DP. Bacterial internalization in a tissue culture model and in vivo in severe periodontitis followed by epithelial cell apoptosis have also been demonstrated [ 7071 ]. Oral bacteria exert a constant challenge to the host cells and tissues at the dentogingival junction.
A third possibility is bacterial invasion into JE cells and formation of an intraepithelial split that then results in periodontal pocket formation. If the PMN dependent defense is insufficient, the inflammation is prolonged and lymphocytes, macrophages, and plasma cells start to dominate the infiltrate.
Alternatively, degradation of IBL on the tooth surface and consequently detachment of the JE takes place. As stated before in this paper, bacteria behave differently in biofilms, where some virulence genes are expressed due to the quorum sensing signaling.
Neutrophils are viable and functional in the gingival crevice. The organotypic tissue culture models are convenient systems to study how periodontal pathogens penetrate not only to the cells but also to the cell layers.
The main role of PMNs, however is phagocytosis and the PMNs in the gingival tissues are the main controllers of the microbial ecology within the gingival crevice. Interestingly the composition of the IBL and EBL differs from each other and also seems to differ from the basement membrane of the outer gingival epithelium, suggesting a very different role for these basement membranes [ 18 ].
In the periodontal region T. Junctional epithelium, dark red. This leads to the release of the proinflammatory cytokines e.
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. Both their cellular and extracellular components exhibit a high rate of turnover.
The destruction of CT in the periodontal region seems to be the result of synergistic action of both bacteria and host derived proteinases leading to an imbalance of the proteinases over their inhibitors [ 80 ]. The cross-talk between neutrophils and immune cells is constant.
The dentogingival junction is of crucial importance in periodontal host defense both structurally and functionally. A simultaneous application of LPS and proteases to rat gingiva has been found to cause apoptosis of connective tissue and periodontal ligament fibroblasts followed by apical migration of the JE [ 72 junxtion.
Host-Bacteria Crosstalk at the Dentogingival Junction
The entire tissue is capable of regeneration after wounding. The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo. The cells are capable of movement and of positional change.
Once these events are better understood treatment modalities dentogingjval at preventing periodontal pocket formation can be designed. Both Immunoglobulin G and A IgG and IgA seem to be important to periodontal defense and are found in periodontal tissues and saliva [ — ].
The inhibited or exaggerated inflammatory response results from an imbalance of pro- and anti-inflammatory cytokines. In addition to activation, periodontal pathogens such as P. 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 dengogingival.
Alternatively the cytokines produced by Th1 cells can indirectly lead to bone resorption by inducing RANKL expression on osteoblasts that can bind to RANK on osteoclast precursor cells and activate osteoclast detogingival [ ].
The cells of the dental papilla in contact with the inner enamel epithelium differentiate into odontoblasts OB that proceed to form predentin PD and dentin D. In addition to the impaired pathogen-mediated complement activation, a clinical study has found partial gene deficiencies in complement C4 genes in patients suffering from chronic recurring periodontal inflammation [ ].
It is probably not a coincidence that some of the known periodontopathogens, that is, P. They are the first defense cells to respond to bacterial stimulus and dentoginbival are present within minutes after stimulus. Bacteria black, pocket epithelium light gray. However, various pathogenic bacteria including P.
It is activated immediately in the presence of a pathogen.