Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential of epithelial cells to degrade interstitial collagen was studied by culturing human masticatory mucosa on decalcified dentin matrix. Morphological changes were observed in the underlying collagen substratum and in the connective tissue of the explant. Degradation of the substratum was initiated two days after the first contact with epithelial cells exhibiting basal cell markers. Electron microscopic studies confirmed extensive collagen degradation in the vicinity of these cells. No collagen degradation was observed underneath the connective tissue portion of the explant. Experiments in which the explant was partially separated from the underlying substratum by a filter further showed that connective tissue was apparently not involved in the collagen degradation by the epithelial cells. Lysis of connective tissue of the explant was observed in association with epithelial cells that showed a disrupted basal lamina and release of vesicular material from the exposed cell membrane. Collagen fibers were visible inside some epithelial cells suggesting intracellular collagenolysis. Primary cultures of human gingival epithelial cells and porcine periodontal ligament epithelial cells (epithelial cell rests of Malassez) that expressed similar basal cell cytokeratins as the active cells of the mucosal explants secreted collagenase, gelatinase and TIMP to the culture medium. They also contained acid collagenolytic proteinases. When cultured on a porous polycarbonate membrane the epithelial cells secreted collagenolytic enzymes from the pores at cell membrane sites lacking basal lamina. These results provide evidence that proliferating basal epithelial cells have a strong capacity for collagen degradation. It seems that the absence of basement membrane is the signal for these cells to secrete matrix degrading enzymes.
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PMID:Proliferating oral epithelial cells in culture are capable of both extracellular and intracellular degradation of interstitial collagen. 170 53

This article briefly reviews the origin, classification and pathogenesis of the various odontogenic cysts. Keratocysts and follicular cysts are said to be developmental lesions arising from the remnants of the dental lamina and the cell rests of the dental follicle respectively. The radicular cysts are the most commonly occurring lesions associated with the apices of non-vital teeth. They are said to arise from proliferation of the cell rests of Malassez in chronically inflamed granulomata. It is noted that bone resorption is the major requirement for any bony lesion to expand; hence the interest in the role of diverse cellular and chemical mediators of bone resorption in disease. The current concepts of the role, in cyst initiation and growth, of enzymes including cellular metabolites and cytokines are presented. Evidence on the activities of collagenase, arachidonic acid metabolites, leukotrienes, hydroxyeicosatetraenoic acids, interleukin--1 and prostaglandins is cited. It is observed that the understanding of these cellular and molecular biological behaviour patterns may yield more appropriate information necessary for the development of more effective management modalities for such tissue degrading lesions as odontogenic cysts.
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PMID:Pathogenesis of odontogenic cysts: an update. 191 78

Seven dental cyst epithelia were cultured in vitro and the conditioned media were analyzed for periodontal ligament fibroblast collagenase production. All the cyst epithelium-conditioned media stimulated fibroblast collagenase production, indicating that dental cyst epithelium, which is considered to be identical to the cell rests of Malassez, might play a role in periodontal pocket formation.
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PMID:Effect of dental cyst epithelium-conditioned medium on collagenase production by periodontal ligament fibroblasts. 919 33