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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This enzyme is able to activate the precursor peptide of alpha-defensin, an important antimicrobial agent of mucosal epithelium [ 35 ].

In spite of the wide range of innate defense mechanisms at the dentogingival junction, the bacteria are able to surpass the host defense. The first line of innate host defense in the periodontal region is the JE that hinders bacterial advancement into periodontal tissues, Figure 1 a.

Once these events are better understood treatment modalities aiming at preventing periodontal pocket formation can be designed. Alpha-defensins secreted by neutrophils are bound to junctional and pocket epithelium serving as an additional antimicrobial function [ 33 ].

To receive news and publication updates junctoin International Journal of Dentoginhival, enter your email address in the box below. They degrade complement proteins.

Dentogingival junction

C4 deficiencies have been previously associated with chronic mucosal infections and the authors suggested that it may also predispose to periodontal infections.

Interestingly, the action of periodontal bacteria on complement seems to be biphasic. Separately grown bacterial biofilms can be added onto the cultures. C3a and also C5a in turn act as chemoattractants for phagocytes and activate mast cells.

The tissues do remarkably well, over long periods, in their response to periodontal disease, whether due to direct bacterial or toxic damage, or to indirect damage via the migration of inflammatory cells into the lesion.

With this model F.

Development of the Dentogingival Junction – Early Stages

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.

However, some studies have indicated that, in contrast to impaired function, PMN hyperreactivity may play a role in periodontitis [ ]. Especially quorum sensing signal, autoinducer-2, is used in inter-species signaling between various periodontal pathogens, and it may enhance the formation of the biofilm as well as change the virulence gene expression [ 15 ].


Degeneration and detachment of the DAT cells, loss of cellular dentogingivql, and cell death in the coronal part of the JE and development of an intraepithelial split have been suggested in the initial dentogingoval of periodontal pathology [ — ]. 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.

Dendritic cells form the crucial link between the innate and adaptive immunity. The complete story is not yet developed. Cocultures with bacterial biofilms can be used to study host-microbe interactions with this model. It is probably not a coincidence that some of the known periodontopathogens, that is, P.

In inflamed pocket epithelium, however, integrin is absent allowing high epithelial proliferation [ ]. The main role of PMNs, however is phagocytosis and the PMNs in the gingival tissues are the main controllers of the microbial ecology dentogingiva, the gingival crevice.

However, this does not exclude the possibility that its molecular structures may be altered. This leads to the release of the proinflammatory cytokines e.

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 dentogingical recognizing the pathogens and initiating specific defense targeted to the pathogens involved. Thus the activation of PARs seems to be important for the protective host response at the periodontal region. At site of infection proenzymes become proteases and produce local inflammatory responses.

Thus even clinically healthy gingiva demonstrates some neutrophils in JE and the underlying CT [ ]. This leads to formation of C3a, C3b, and C5a []. Next to it is the stratum intermedium SI consisting of layers of undifferentiated epithelial cells.

Dentogingival junction | definition of dentogingival junction by Medical dictionary

They are stored and secreted as inactive proenzymes. Increased amounts of MMP-1, -2, -3, -8, -9, and have been found in GCF and gingiva of periodontitis patients compared with samples from healthy controls [ 228593 — 99 ]. 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.

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Also osteoprotegerin OPGthe known decoy receptor for and inhibitor of RANKL may regulate and protect the host from inflammatory bone resorption, since interference with RANKL by systemic administration of OPG has resulted in abrogation of periodontal bone resorption in a rat model [ ]. 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 [ ].


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 jumction. 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.

It is activated immediately in the presence of a pathogen. Human beta-defensins hBDs are expressed in gingival epithelia, salivary glands, saliva, and GCF [ 26 — 28 ] as a response to bacterial challenge [ 29 — 31 ]. Several activated complement components form a membrane attack complex MACwhich creates a transmembrane pore leading to the lysis of the target cell and jubction thus lead to destruction of both bacterial and host cells.

Gingival CT is composed of extracellular matrix ECM and fibroblasts producing the ECM and participating immune and inflammatory responses of the gingiva.

The fact, that when MMP activity is inhibited, tissue destruction is reduced, further emphasizes the role of MMPs on tissue destruction [ ].

Both Immunoglobulin G and A IgG and IgA seem to be important to periodontal defense and are found in periodontal tissues and saliva [ — ]. Despite of a huge number of studies on periodontitis development, we still do not have a clear picture of the crucial events leading to the periodontal tissue destruction.

Impaired PMN functions are generally considered to be junctikn to periodontal tissue destruction and patients with reduced number denfogingival neutrophils or impaired neutrophil function show often severe periodontitis [ ]. However, the connection between the IL-1 gene polymorphism and the clinical manifestations of periodontal disease do not seem to be likewise certain in all populations [ dentogingkval, ].