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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Langerhans cells, identified by the C-type lectin langerin, are dendritic cells responsible for the presentation of antigens to T-lymphocytes.
Human beta-defensins hBDs are expressed in gingival epithelia, salivary glands, saliva, and GCF [ 26 — 28 ] as a response to bacterial challenge [ 29 — 31 ]. Increased levels of MMPs and decreased amounts of their tissue inhibitors have been connected to the progression of periodontal disease . Certain MMPs from dentogingivql cells are also able to cleave laminin, exposing a cryptic molecular site that triggers cell migration [ juncton.
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 [ ].
Thus the activation of PARs seems to be important for the protective host response at the periodontal region. The cross-talk between neutrophils and immune cells is constant. The innate nature of PMN hyperresponsiveness is supported by a study showing high levels of PMN oxygen radical production in periodontitis patients also after periodontal treatment [ 27 ]. Development of the dentogingival junction: 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.
However, the role of complement in periodontal diseases still needs further studies.
Smoking also impairs neutrophil functions, for example, phagocytosis [ ]. Copyright Send feedback about this site. 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 ]. In spite of the wide range of innate defense mechanisms at the dentogingival junction, the bacteria are able to surpass the host defense.
Primary JE culture treated with A. 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.
This enzyme is able to activate the precursor peptide of alpha-defensin, an important antimicrobial agent of mucosal epithelium [ 35 ].
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 ].
View at Google Scholar D. 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. The tissues show a capacity for repair and regeneration following the elimination of plaque formation and the resultant resolution of the inflammatory infiltrate. Some of the cells are specialized for specific functions, such as attachment formation, and do not generate additional cells, but generative pools are always nearby.
The collapse of the enamel organ results in the formation of the reduced enamel epithelium. Many of the complement proteins are proteases. Oral bacteria exert a constant challenge to the host cells and tissues at the dentogingival junction. 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 junctional epithelium can advance and retract. Mast cells contribute to the inflammatory reaction by releasing histamine, inflammatory mediators and cytokines such as leukotrienes.
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.
Host PRRs may be either soluble e. Host-microbe interaction leading to periodontal pocket formation is a complex process, involving the presence of pathogenic bacterial biofilm as well as a susceptible host defense system. 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 [ ].
In order to understand how the dentogingival junction comes into existence, it is necessary to review some aspects of tooth development and eruption.
Undifferentiated epithelial cells form the stratum intermedium SIdirectly adjacent to the ameloblasts. 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.
This review leads to a concept in which the tissues of the dentogingival junction are dynamic rather that static. However, this does not exclude the possibility that its molecular structures may be dentogigival. Calprotectin, expressed in neutrophils, monocytes, and gingival keratinocytes, protects gingival keratinocytes dentoginigval binding and invasion by P.
Cocultures with bacterial biofilms can be used to study host-microbe interactions with this model. As stated before in this paper, bacteria behave differently in biofilms, where some virulence genes are expressed due to the quorum sensing signaling.
JE is a unique epithelial structure firmly attached to the hard tissue of tooth via hemidesmosomes. Table of Contents Alerts.
Application of PAR agonist peptide to gingiva has induced periodontitis in rats radiographically assessed bone loss, myeloperoxidase MPO activity [ 79 ]. Dendritic cells form the crucial link between the innate and adaptive immunity. The C3 fragment is important in all three pathways.
Development of the Dentogingival Junction – Early Stages
Mast cells show MMP-1, -2, and -8 activity which is linked to periodontal tissue breakdown [ ]. In periodontitis their number decreases intraepithelially and increases in connective tissue where antigen presentation takes place. Van Der Velden, V.
In addition to the protective structures of multispecies biofilm which 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. Even when they are pathologic, they can be reconstituted by repair. In inflamed pocket epithelium, however, integrin is absent allowing high epithelial proliferation [ ].
When differentiated into dendritic cells macrophages participate in antigen presentation by expressing costimulatory molecules and MHC-II molecules [ 37 ]. Different models of periodontal multilayer tissue cultures have been developed since the s [ ]. Langerin is a transmembrane cell surface protein which plays a role in antigen recognition and uptake. The innermost layer, or inner enamel epithelium IEE is in intimate contact with the dental papilla.
They degrade complement proteins.