DENTOGINGIVAL JUNCTION PDF

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.

Author: Kajikus Fenrigami
Country: Mayotte
Language: English (Spanish)
Genre: Spiritual
Published (Last): 3 January 2016
Pages: 200
PDF File Size: 18.42 Mb
ePub File Size: 6.40 Mb
ISBN: 758-6-48960-911-8
Downloads: 79793
Price: Free* [*Free Regsitration Required]
Uploader: Duzahn

The microbial recognition is based on interaction between microbial ligands known as pathogen-associated molecular patterns PAMPs e.

Cocultures with bacterial biofilms can be used to study host-microbe interactions with this dentogingivxl.

The C3 fragment is important in all three pathways. This has been later confirmed by several other studies.

JE is a unique epithelial structure firmly attached to the hard tissue of tooth via hemidesmosomes. The complement system is a biochemical cascade of the small plasma proteins that activate another in series. Subscribe to Table of Contents Alerts. Furthermore, when opsonized with antibody, A. 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 dentogongival antimicrobial agents and antibodies into the gingival crevice.

They degrade complement proteins. However, different models have also been proposed where the Th2 cell response has been connected to periodontal bone destruction by uncontrolled Dentogingivla production of IL-1 or B-cell expression of RANKL []. Two kinds of models have been used in our laboratory, Figures 2 a and 2 b. This leads to the release of the proinflammatory cytokines e. 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 [ ].

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. Planktonic cells of opportunistic periodontal pathogens A. Bacterial antigens coupled with antigen presenting cells with major histocompatibility complex MHC class-I molecules are recognized by T-killer cells and B cells.

  CONFUSION OF TONGUES FERENCZI PDF

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]. With this model F. The action of the complement system affects both innate and adaptive immunity and thus has an important role in inflammatory and immune responses.

Improved methods to detect bacteria in periodontal biofilm have broadened our knowledge about pocket-associated microbes. Application of PAR agonist peptide to gingiva has induced periodontitis in rats radiographically assessed bone loss, myeloperoxidase MPO activity [ 79 ]. Such experimental setups however lack important issues, for example, cell-cell contacts of the multilayered epithelium, the basement membranes and the epithelium-connective tissue interface as well as the microbial pathogenicity of the biofilm.

Complement mediated phagocytosis of A. The cells are capable of movement and of positional change.

Dentogingival junction

Whereas the IBL is dedicated to maintain the attachment to the tooth, the EBL functions merely as a protective barrier. This paper focuses 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 ].

View at Google Scholar D. The key cells of the adaptive immune defense are the T-lymphocytes T-helper-1 Th1T-helper-2 Th2and T-killer-cells dentoginglval B-lymphocytes [ ]. It is secreted by a layer of columnar fentogingival AB in the secretory stage. The collapse of the enamel organ results in the formation of the reduced enamel epithelium.

MAC inhibitor, CD59, is expressed in gingival epithelium and thus gingival epithelium is probably well-protected against MAC mediated cell damage [ ].

The interface between the filter and the epithelium shows morphologically similar hemidesmosomal attachment as the epithelium-tooth interface in vivo. The tissue homeostasis is turned into tissue destruction and progression of periodontitis. Yet surprisingly small number of studies has been done on this early host-microbe interaction.

  INSULARISMO ANTONIO PEDREIRA PDF

The entire tissue is capable of regeneration after wounding. The classical study of Slots showed that in the bacterial plaque, the most remarkable change is the shift from gram-positive aerobic and facultatively anaerobic flora to a predominantly gram-negative and anaerobic flora. Bacteria at the gingival margin debtogingival drastic changes in CT; junctoon permeability and the amount of inflammatory cell infiltrate are increased. The ectomesenchymal tissue that surrounds the enamel organ forms the dental follicle DF.

The inheritance from our predecessors has been used well and our expanded knowledge in this area now serves as the conceptual framework for further study.

Dentogingival junction | definition of dentogingival junction by Medical dictionary

However, this does not exclude the possibility that its molecular structures may be altered. Calprotectin, expressed in neutrophils, monocytes, and gingival keratinocytes, protects gingival keratinocytes against binding and invasion by P. Primary JE culture treated with A. C3a and also C5a in turn act as chemoattractants for phagocytes and activate mast dentogingoval.

Dentogingival junction

The dental papilla DP is on the left. The PMNs are a major contributor in the host parasite equilibrium but when activated can also cause tissue damage due to excess of enzymes, reactive oxygen species, MMPs, and other components that are released from their dentogignival during the battle against dentogngival [ 48— ].

It has been suggested that complement deposits in connective tissue may reflect disease-associated complement activation [ ]. The complete story is not yet developed.

However, at least A.