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

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

Periodontal cysts synthesize large amounts of prostaglandins and collagenase which probably cause the localized bone destruction essential for intraosseous cyst growth. Fragments of cyst wall, and fibroblasts cultured from them, synthesized prostacyclin (PGI2) in addition to prostaglandin E2 (PGE2), PGF2 alpha and collagenase in vitro. Soluble products from cultures of unstimulated and phytohaemagglutinin-stimulated blood mononuclear cells enhanced the synthesis of these prostaglandins in monolayer cultures of cyst-wall fibroblasts. It is therefore proposed that cyst capsule fibroblasts are the major source of these bone-resorbing factors, acting under the stimulus of lymphocytes and monocytes in chronically inflamed cysts. Cysts which were not infiltrated by chronic inflammatory cells (follicular cysts, a keratocyst, an ameloblastoma, and an aneurysmal bone cyst) also produced prostaglandins and collagenase, indicating that the stimulatory mechanism for the production of bone-resorbing factors in these cysts may differ from that in periodontal cysts.
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PMID:Evidence for fibroblasts as the major source of prostacyclin and prostaglandin synthesis in dental cyst in man. 632 48

Keratocyst antigen was demonstrated in the fluid of keratinizing odontogenic cysts (primordial cysts) but not in fluids of other cyst types. The antigen was not present in plasma or saliva. It resisted collagenase digestion and did not react with keratin antibodies. In gel filtration, the antigen migrated as a single peak and gave a molecular weight of about 50 000 when analyzed in SDS-polyacrylamide gel electrophoresis. In immunoelectrophoresis, it migrated in the prealbumin region and was localized in epithelial cells of the cyst capsule, when studied by a double-antibody fluorescence technique. The origin and function of the keratocyst antigen is unclear but it may be a soluble marker for keratocyst differentiation.
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PMID:Demonstration and partial characterization of a novel soluble antigen present in keratocysts. 681 28

Neutral salt extracts of 14 specimens of jaw cysts were prepared. Histopathological analysis showed that the specimens consisted of 6 radicular cysts, 6 dentigerous cysts, 1 residual cyst, and 1 odontogenic keratocyst. One periapical granuloma, 1 dental follicle and a sample of clinically healthy oral mucosa were similarly processed and used as controls. Measurement of collagenase activity by monitoring the formation of specific degradation products of type I and II collagen in solution by SDS-PAGE demonstrated that all the cyst extracts contained collagenase, some of which was endogenously activated. Cyst wall collagenase preferably degraded type I over type II collagen, which suggests that the degradation was due to MMP-1 (matrix metalloproteinase-1) rather than the MMP-8 type. This was further supported by the doxycycline-inhibition profile of cyst collagenase, which was similar to that of MMP-1. Part of the cyst wall collagenase was in latent proenzyme form and probably derived, at least in part, from the newly synthesized intracellular collagenase pool. Latent cyst collagenase was efficiently activated with phenylmercuric chloride and to a lesser extent by gold (I) thioglucose and NaOCl. Western-blotting, using specific antibodies against collagenase from human polymorphonuclear neutrophilic leukocytes (MMP-8) and from fibroblasts (MMP-1), revealed a typical 55/45 kDa doublet; also MMP-8 in the latent 80 kDa form and fragmented to 65 kDa active species were found. These results suggest the presence of MMP-1 and, to a lesser extent, MMP-8 type collagenase in the cyst wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of interstitial collagenases in jaw cyst wall. 763 29

Intracystic fluid pressure is thought to be involved in odontogenic cyst growth. In this study, we investigated the effects of positive pressure on the expression of interleukin-1alpha (IL-1alpha), matrix metalloproteinases (MMPs), and prostaglandin E2 (PGE2) in odontogenic keratocysts to determine whether this pressure stimulates inflammatory cytokine production and signaling of osteoclastogenic events. Positive pressure enhanced the expression of IL-1alpha mRNA and protein in odontogenic keratocyst epithelial cells, and increased the secretion of MMP-1, MMP-2, MMP-3, and PGE2 in a co-culture of odontogenic keratocyst fibroblasts and the epithelial cells. The pressure-induced secretions were inhibited by an interleukin-1 receptor antagonist. Recombinant human interleukin-1alpha (rhIL-1alpha) increased the secretion of MMP-1, MMP-2, MMP-3, and PGE2 in the fibroblasts. Furthermore, in the fibroblasts, rhIL-1alpha enhanced the expression of macrophage colony-stimulating factor (M-CSF) mRNA, and rhIL-1alpha-induced PGE2 increased the expression of nuclear factor kappaB ligand (RANKL) mRNA. Thus, positive pressure may play a crucial role in odontogenic keratocyst growth via stimulating the expression of IL-1alpha in epithelial cells.
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PMID:Effects of positive pressure in odontogenic keratocysts. 1618 90