Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migration of leukocytes to inflammation sites through vascular endothelium is controlled by the interactions of adhesion molecules expressed on both endothelial cells and leukocytes, most of which are already covered by cluster of differentiation (CD) codes. We examined the expression of a variety of endothelial cell adhesion molecules in human dental pulp vasculature to obtain further evidence on the tissue distribution and function of these molecules by using an indirect immunoperoxidase technique. We obtained the pulp tissue samples from teeth extracted due to orthodontic reasons as controls and compared with those extracted due to chronic periodontitis. In all samples, both CD31 and CD146 were expressed by arterial, venous, and capillary endothelia. There was no significant difference between the staining intensity of normal and inflamed pulp tissues. CD102 expression on the endothelium was significantly stronger in chronic periodontitis pulp samples. CD106, CD62-E, CD62-P, CD105, and CD54 were variably expressed in control and chronic periodontitis groups. Our results indicate that CD102 represents the major endothelial cell adhesion molecule probably involved in the inflammatory reactions in chronic periodontitis.
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PMID:Endothelial cell adhesion molecules in human dental pulp: a comparative immunohistochemical study on chronic periodontitis. 1068 24

Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence determinants of this organism. As vascular expression of leukocyte adhesion molecules is a critical determinant of tissue response to microbial challenge, the objective of this study was to determine the capacity of gingipains to modulate the expression and function of these receptors. Given the potential multifunctional role of platelet endothelial cell adhesion molecule 1 (PECAM-1) in the vasculature, the effect of gingipains on PECAM-1 expression by endothelial cells was examined. Activated gingipains preferentially down-regulated PECAM-1 expression on endothelial cells compared with vascular cell adhesion molecule 1 and endothelial-leukocyte adhesion molecule 1, but the reduction in PECAM-1 expression was completely inhibited in the presence of the cysteine proteinase inhibitor TLCK (Nalpha-p-tosyl-l-lysine chloromethyl ketone). Endothelial monolayers treated with activated gingipains demonstrated progressive intercellular gap formation that correlated with reduced intercellular junctional PECAM-1 expression as determined by Western blotting and immunofluorescence microscopy. This was accompanied by enhanced transfer of both albumin and neutrophils across the monolayer. The results suggest that degradation of PECAM-1 by gingipains contributes to increased vascular permeability and neutrophil flux at disease sites.
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PMID:Functional implication of the hydrolysis of platelet endothelial cell adhesion molecule 1 (CD31) by gingipains of Porphyromonas gingivalis for the pathology of periodontal disease. 1573 Oct 36

Periodontitis is accompanied by the proliferation of small blood vessels in the gingival lamina propria. Specialized postcapillary venules, termed periodontal high endothelial-like venules, are also present, and demonstrate morphological and functional traits similar to those of high endothelial venules (HEVs) in lymphatic organs. The suggested role of HEVs in the pathogenesis of chronic periodontitis involves participation in leukocyte transendothelial migration and therefore proinflammatory effects appear. Recent observations suggest that chronic periodontitis is an independent risk factor for systemic vascular disease and may result in stimulation of the synthesis of acute phase protein by cytokines released by periodontal high endothelial cells (HECs). However, tissue expression of HEV-linked adhesion molecules has not been evaluated in the gingiva of patients with chronic periodontitis. This is significant in relation to potential therapy targeting expression of the adhesion molecules. In this review, current knowledge of HEV structure and the related expression of four surface adhesion molecules of HECs [CD34, platelet endothelial cell adhesion molecule 1, endoglin and intercellular adhesion molecule 1 (ICAM-1)], involved in the key steps of the adhesion cascade in periodontal diseases, are discussed. Most studies on the expression of adhesion molecules in the development and progression of periodontal diseases pertain to ICAM-1 (CD54). Studies by the authors demonstrated quantitatively similar expression of three of four selected surface markers in gingival HEVs of patients with chronic periodontitis and in HEVs of reactive lymph nodes, confirming morphological and functional similarity of HEVs in pathologically altered tissues with those in lymphoid tissues.
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PMID:Role of high endothelial postcapillary venules and selected adhesion molecules in periodontal diseases: a review. 2258 23