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 ectomesenchymal tissue that surrounds the enamel organ forms the dental dentogintival DF. The inner enamel 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. Although the immune response is primarily aimed dentoyingival protect the host from the bacteria, it also seems to be strongly involved in tissue destruction in the periodontal region, Figure 1 c.
The Molecular BasisH.
Bacterial antigens coupled with antigen presenting cells with major histocompatibility complex MHC class-I molecules are recognized by T-killer cells and B cells. The initial events of periodontal pocket formation are likely to involve destruction of the dento-epithelial hunction resulting in the failure of the epithelial barrier function.
Dentogingival junction | definition of dentogingival junction by Medical dictionary
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 response whereas the periodontopathogenic bacteria are thought to trigger the proinflammatory Th1 cytokine response resulting in inflammatory periodontal bone resorption [ jynction— ].
The coexistence of, for example, Epstein-Barr and human cytomegalovirus together with periodontopathogens has also been implicated to play a role in periodontal pathogenesis [ 10 ].
Microorganisms in Subgingival Biofilm The presence dentoginngival the initial colonizers on the tooth surface is essential for the emergence of the gram-negative periodontopathogens Porphyromonas gingivalis, Tannerella forsythia Bacteroides forsythusAggregatibacter actinomycetemcomitans, and Fusobacterium, Prevotella, Campylobacter, and Treponema species [ 1 — 3 ]. Studies have also reported apoptosis in cells of pocket epithelium caused by bacterial internalization [ ] and enhanced activation of intracellular proteases that regulate apoptosis caspases 3 and 7 [ ].
Different models of periodontal multilayer tissue cultures have been developed since the s [ ]. Junctional epithelium, dark red. C4 deficiencies have been previously associated with chronic mucosal infections and the authors suggested that it may also predispose to periodontal infections.
The collapse of the enamel organ results in the formation of the reduced enamel epithelium.
As stated before in this paper, bacteria behave differently in biofilms, where some virulence genes are expressed due to the quorum sensing signaling. 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 jhnction prostaglandins and MMPs and causing destruction of the CT [ 728788 ].
Alternatively the cytokines produced dentogignival Th1 cells can indirectly lead to bone resorption by inducing RANKL expression on osteoblasts dentogibgival can bind to RANK on osteoclast precursor cells and activate osteoclast differentiation [ ].
Host-Bacteria Crosstalk at the Dentogingival Junction
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 ]. Junvtion leads to the release of the proinflammatory cytokines e. Bacterial internalization in a tissue culture model and in vivo in severe periodontitis followed by epithelial cell apoptosis have also been demonstrated [ 7071 dentoginggival.
Undifferentiated epithelial cells form the stratum intermedium SIdirectly adjacent to the ameloblasts. Planktonic cells of opportunistic ddntogingival pathogens A. Connective tissue and periodontal ligament fibers green, and bone yellow. The microbial recognition is based on interaction between microbial ligands known as pathogen-associated molecular patterns PAMPs e. Furthermore, a recent study on experimental periodontitis showed dual changes in CT; simultaneous collagen fiber breakdown and fiber bundle thickening, and suggested a protective role for the inflammatory tissue breakdown in order to avoid the spreading of the infection into the deeper areas [ ].
Gingipains are proteases secreted by P. Impaired PMN functions are generally considered to be related to periodontal tissue destruction and patients with reduced number of neutrophils or impaired neutrophil function show often severe periodontitis [ ].
A third possibility is bacterial invasion into JE cells and formation of an intraepithelial split that then results in periodontal pocket formation. A thin layer of enamel E can be seen on the outer dentin surface.
Yet surprisingly small number of studies has dentogingivql done on this early host-microbe interaction. At site of infection proenzymes become proteases and produce local inflammatory responses. Cocultures with bacterial biofilms can be used to study host-microbe interactions with this model.
International Journal of Dentistry
Alternatively, degradation of IBL on the tooth surface and consequently detachment of the JE takes place. International Journal of Dentistry. However, some studies have indicated that, in contrast to impaired function, PMN hyperreactivity may play a role in periodontitis [ ]. The wide intercellular spaces and permeability of the JE, even though beneficial for the host defense, also allow bacteria and their harmful products to juncion epithelium, which thereby activate the inflammatory reaction.
Monolayers of epithelial and connective tissue cells as well as planktonic bacteria have been widely used in studies on periodontal host-microbe interactions. The junctional epithelium can advance and retract. Protease activated receptors PARs mediate cellular responses to extracellular proteinases such as thrombin and trypsin-like serine proteases.
Next to it is the stratum intermedium SI consisting of layers of undifferentiated epithelial dnetogingival. The action of the complement system affects both innate and adaptive immunity and thus has an important role in inflammatory and immune responses. In addition to activation, periodontal pathogens such as P.