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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International Journal of Dentistry
If the PMN dependent defense is insufficient, the inflammation is prolonged and lymphocytes, macrophages, and plasma cells start to dominate the infiltrate. MAC inhibitor, CD59, is expressed in gingival epithelium and thus gingival epithelium is probably well-protected against MAC mediated cell damage [ ].
Macrophages are efficient phagocytes and are abundant within the gingival tissues. 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 ]. In the periodontal region T. The first line of innate host defense in the periodontal region is the JE that hinders bacterial advancement into periodontal tissues, Figure 1 a.
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.
Degeneration and detachment of the DAT cells, loss of cellular continuity, and cell death in the coronal part of the JE and development of an intraepithelial split have been suggested in the initial phase of periodontal pathology [ — ].
Mast cells contribute to the inflammatory reaction by releasing histamine, inflammatory mediators and cytokines such as leukotrienes. In addition to activation, periodontal pathogens such as P. 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 [ ]. The host-microbe interaction at the dentogingival junction may involve several detrimental mechanisms leading to periodontal pocket formation.
Complement mediated phagocytosis of A. 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. It should be emphasized, that when treating periodontal disease, continuous control of the infection should be the first goal, and only in addition to that, modulation of the host response may be considered.
CT is constantly renewed and that requires degradation of the ECM components, therefore gingival fibroblasts also produce proteolytic enzymes, MMPs. The key cells of the adaptive immune defense are the T-lymphocytes T-helper-1 Th1T-helper-2 Th2and T-killer-cells and B-lymphocytes [ ]. This review leads to a concept in which the tissues of the dentogingival junction are dynamic rather that static. This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Additional contributions continue to be made. With this model F.
The leukocyte wall has proteolytic, phagocytic, and antibacterial MPO, defensins, and other antibacterials such as lactoferrin features. Different models of periodontal multilayer tissue cultures have been developed since the s [ ].
During bacterial challenge the host sentogingival recognize the bacteria and different antigens by different receptors that have been detected also on periodontal tissues. This paper focuses on host-bacteria crosstalk at the dentogingival junction and the models studying it in vitro.
They are the first defense cells to respond to bacterial stimulus and they are present within minutes after stimulus. Garcia Fulle et al. PMNs are essential in the first line of innate defense against plaque bacteria at the gingival margin.
Within the bell-shaped ectodermal structure several dentoginfival layers are visible. This leads to formation of C3a, C3b, and C5a .
The cells directly attached to the tooth, DAT-cells [ 17 ], have been shown to be dividing cells like the basal cells. This model is easier to repeat and allows also the placement of bacterial biofilms on top junchion the culture. Both their cellular and extracellular components exhibit a high rate of turnover.
Increased levels of MMPs and decreased amounts of their tissue inhibitors have been connected to the progression of periodontal disease . In addition to the activation of the latent forms of MMPs, bacteria-derived proteinases may inactivate proteinase inhibitors such as alphaantitrypsin and alphamacroglobulin and thus result in higher levels of active proteinases [ 89 — 92 ].
Once these events are better understood treatment modalities aiming at preventing periodontal pocket formation can be designed. Even when they are pathologic, they can be reconstituted by repair. 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.
The complete story is not yet developed. 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. PMNs are the main leukocytes isolated from gingival crevice. The entire tissue is capable of regeneration after wounding. Moreover, by weakening the host defense, opportunistic periodontal pathogens, such as P. Host Kunction may be either soluble e.
Gingipains are proteases secreted by P. The ECM comprises of fibers mainly collagen Iproteoglycans, glycoproteins and water. 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 jujction cells leading to production of prostaglandins and MMPs and causing destruction of the CT [ 728788 ].
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Host-Bacteria Crosstalk at the Dentogingival Junction
Thus even clinically healthy gingiva demonstrates some neutrophils in JE and the underlying CT [ ]. The active role of the JE in the innate host dentoginfival is further demonstrated by the production of cytokines and the presence of natural antimicrobial peptides and proteins such as the defensins, the cathelicidin family members LLand calprotectin [ 23 — 25 ].
Bacterial antigens dentoginvival with antigen presenting cells with major histocompatibility complex MHC class-I molecules are recognized by T-killer cells and B cells.
In addition to the protective structures of multispecies biofilm dnetogingival inhibit the actions of host defense cells, the molecular interactions between different species [ 1314 ] in the oral biofilm could influence the virulence of the bacterial community.