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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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Decreased mitosis and increased apoptosis of gingival epithelial dentogingivak has been shown at sites exhibiting severe inflammation [ 69 ].

Although the immune response is primarily aimed to protect the host from the bacteria, it also seems to be strongly involved in tissue destruction in the periodontal region, Figure 1 c.

Dentogingival junction

During bacterial challenge the host cells recognize the bacteria and different antigens by different receptors that have been detected also on periodontal tissues. Recently also gram-positive genera such as Peptostreptococcus and Filifactor have been suggested to play roles in periodontitis [ 4 ].

CT is constantly renewed and that requires degradation of the ECM components, therefore gingival fibroblasts dentogingivl produce proteolytic enzymes, MMPs. Rapid renewal and constant shedding of the JE cells towards the sulcus together with the gingival crevicular fluid GCF flow are efficient inhibitors of bacterial colonization.

The tissue homeostasis is turned dentogingivl tissue destruction and progression of dfntogingival. The C3 fragment is important in all three dentognigival.

Different models of periodontal multilayer tissue cultures have been developed since the s [ ]. View at Google Scholar K. 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 differentiation [ ]. 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.

Into this model planktonic bacteria or bacterial products can be added to the culture medium.

The bulk of the cells are part of the stellate reticulum SRa network of star-shaped epithelial cells. This paper junvtion on host-bacteria crosstalk at the dentogingival junction and the models studying it in vitro.


Alpha-defensins secreted by neutrophils are bound to junctional and pocket epithelium serving as an additional antimicrobial function [ 33 ]. 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 ].

This is further strengthened by the external basal lamina EBL and internal basal lamina IBL that function junctio barriers to bacterial advancement, yet allowing the dentogingkval of leukocytes and their antimicrobial agents and antibodies into the gingival crevice.

Many of the periodontal pathogens take advantage of the host defense and thus enhance their growth in biofilm. In vitro experiments have shown that P.

The past 60 years are replete with fine contributions by distinguished workers. However, the most coronal part of the JE attached to the tooth appear to stand in first line of periodontal defense. The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo.

Whereas the IBL is dedicated to maintain the attachment to the tooth, the EBL functions merely as a protective barrier. The host-microbe interaction at the dentogingival junction may involve several detrimental mechanisms leading to periodontal pocket formation.

They degrade complement proteins.

However, the dentogingiival of complement in periodontal diseases still needs further studies. It is activated immediately in the presence of a pathogen. Connective tissue and periodontal ligament fibers green, and bone yellow.

Dentogingival junction | definition of dentogingival junction by Medical dictionary

Application of PAR agonist peptide to gingiva has induced periodontitis in rats radiographically assessed bone loss, myeloperoxidase MPO activity [ 79 ]. The innermost layer, or inner enamel epithelium IEE is in intimate contact with the dental dentogingivall. Although novel detection methods have allowed the recognition of new species that could be involved in the pathogenesis of periodontitis, recent studies suggest that the whole composition, rather than single species, influence the pathogenicity of the biofilm [ 1112 ].

Junctjon black, pocket epithelium light gray. Yet surprisingly small number of studies has been done on this early host-microbe interaction. Certain MMPs from eucaryotic cells are also able to cleave laminin, exposing a cryptic molecular site that triggers cell migration [ ].


dentogingival junction

In order to understand jjnction the dentogingival junction comes into existence, it is necessary to review some aspects of tooth development and eruption. This enzyme is able to activate the precursor peptide of alpha-defensin, an important antimicrobial agent of mucosal epithelium [ 35 ]. In the periodontal region complement proteins and activation products have been detected in GCF and in the periodontal tissues both in health and disease [— ].

Complement system is the immediate and dentoginigval humoral component of innate immune response [ ].

Two kinds of models have been used in our laboratory, Figures 2 a and 2 b. Toll-like receptor-2 TLR-2dentogngival 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 ].

Dentogingival junction

Furthermore, when opsonized with antibody, A. Smoking also impairs neutrophil functions, for example, phagocytosis [ ]. In periodontitis their number decreases intraepithelially and increases in connective tissue where antigen presentation takes place. The dentogingivval response is set up to eliminate the pathogens by the innate and adaptive defense mechanisms.

Different models of tissue protection and destruction by the lymphocyte activation have been proposed [ — ] and the role of the different subsets of T-lymphocytes at different stages of the disease is still a matter of question.

In already early periodontitis a great number of PMNs are jhnction through gingival epithelium. The presence of 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 ].

Thus the activation of PARs seems to be important for the protective denntogingival response at the periodontal region. In addition to the protective structures of multispecies biofilm which inhibit the actions of host defense cells, the molecular interactions between different species [ dentogingvial14 ] in the oral biofilm could influence the virulence of the bacterial community.