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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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. However, the role of complement in periodontal diseases still needs further studies.
This is thought to result jhnction 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 of prostaglandins and MMPs and causing destruction of the CT [ 728788 ]. However, some studies have indicated that, in contrast to impaired function, PMN hyperreactivity may play a role in dentogimgival [ ].
When differentiated into dendritic cells macrophages participate in antigen presentation by expressing costimulatory molecules and MHC-II molecules [ 37 ]. Into this model planktonic bacteria or bacterial products can be added to the culture medium. Junctuon the IBL is dedicated to maintain the attachment to the tooth, the EBL functions merely as a protective barrier. Furthermore, a recent study on experimental periodontitis showed dual changes in Dentogingjval 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 denrogingival infection into the deeper areas [ ].
Once these events are better understood treatment modalities aiming at preventing periodontal pocket formation can be designed. 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. Since pathologically elevated levels of active MMPs have been found in periodontal tissues during periodontitis, the MMPs may play a role in lateral and apical migration of the JE during pocket formation [ 95].
It has been suggested that complement deposits in connective tissue may reflect disease-associated complement activation [ ]. Certain MMPs from eucaryotic cells are also able to cleave laminin, exposing a cryptic molecular site that triggers cell migration [ ]. 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 ].
The innermost layer, or inner enamel epithelium IEE is in intimate contact with the dental papilla. This leads to the release of the proinflammatory cytokines e. In the periodontal region complement proteins and activation products have been detected in GCF and in the periodontal tissues both in health and disease [— ]. The ectomesenchymal tissue that surrounds the enamel dentogingifal forms the dental follicle DF.
The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo. Human beta-defensins hBDs are expressed in gingival epithelia, salivary glands, saliva, and GCF [ 26 — 28 ] as a response to bacterial challenge [ 29 — 31 ]. However, it seems that a certain threshold exists to inflammatory and bacterial challenge and the expression of hBDs, since in junftion advanced periodontitis the expression of hBDs-2 and -3 is reduced [ 28 ].
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Indexed in Web of Science. 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.
A shift in the balance between anti-inflammatory and proinflammatory cytokines may be crucial for the progression of periodontitis. Bacteria black, pocket epithelium light gray. Microorganisms other than bacteria have also been found in periodontitis patients.
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 ]. Alpha-defensins secreted by neutrophils are bound to junctional and pocket epithelium serving as an additional antimicrobial function [ 33 ].
Alternatively, degradation of IBL on the tooth surface and consequently detachment of the JE takes place. PARs are expressed in human neutrophils, gingival fibroblasts, and osteoblasts [ 7475 ]. This is further strengthened by the external basal lamina EBL and internal basal lamina IBL that function as barriers to bacterial advancement, yet allowing the passage of leukocytes and their antimicrobial agents and antibodies into the gingival crevice.
To receive news and publication updates for International Journal of Dentistry, enter your email address in the box below. View at Google Scholar K. Calprotectin, expressed in neutrophils, monocytes, and gingival keratinocytes, protects gingival keratinocytes against binding and invasion by P. 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 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. The cells are capable of movement and of positional change.
Gingival CT is composed of extracellular matrix ECM and fibroblasts producing the ECM and participating immune and inflammatory responses of the gingiva. JE is a unique epithelial structure firmly attached to the hard tissue of tooth via hemidesmosomes.
View at Google Scholar D. The cuticle width is alterable. In already early periodontitis a great number of PMNs are migrating through gingival epithelium. Furthermore, complement activation increases vascular permeability and attracts phagocytes to the inflammatory site. Both Immunoglobulin G and A IgG and IgA seem to be important to periodontal defense and are found in periodontal tissues and saliva [ — ].
In periodontitis their number decreases intraepithelially and increases in connective tissue where antigen presentation takes place. The leukocyte wall has proteolytic, phagocytic, and antibacterial MPO, defensins, and other antibacterials such as lactoferrin features. Many of the dentohingival pathogens take advantage of the host defense and thus enhance their growth in biofilm. 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.
Application of PAR agonist peptide to gingiva has induced periodontitis in rats radiographically assessed bone loss, myeloperoxidase MPO activity [ 79 ].
Junctiln cells of opportunistic periodontal pathogens A.