Factors affecting IL-1-mediated collagen metabolism by fibroblasts and the pathogenesis of periodontal disease: a review of the literature.
Fibroblasts have been studied extensively for their contribution to connective tissue destruction in diseases where the metabolism of extracellular matrix components plays an essential part in their pathogenesis. A considerable dissolution, especially of collagen fibrils, is a well-known characteristic of the periodontal ligament and the gingival connective tissue in microbial-induced periodontal disease. Fibroblasts, responsible for the assembly of the extracellular matrix, are capable of responding directly to oral microbial challenges or indirectly, following activation of the host immune response, and can alter the composition of connective tissue in several ways: synthesis of inflammatory mediators, their receptors and antagonists; fibroblast proliferation; collagen synthesis; phagocytosis of collagen fibrils; and synthesis of proteolytic enzymes, including matrix metalloproteinases and their corresponding inhibitors. The contributions of these cellular fibroblastic properties to the pathogenesis of periodontal disease are reviewed in the context of the cytokine, interleukin-1, as the inflammatory regulator.
Havemose-Poulsen
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Department of Periodontology, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Denmark.
Holmstrup
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P
D018407:Bacterial Physiological Phenomena; D002455:Cell Division; D003094:Collagen / Q000096:biosynthesis / Q000276:immunology / Q000378:metabolism*; D003238:Connective Tissue / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005881:Gingiva / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism; D007375:Interleukin-1 / Q000502:physiology*; D008666:Metalloendopeptidases / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D010447:Peptide Hydrolases / Q000096:biosynthesis; D010510:Periodontal Diseases / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D010513:Periodontal Ligament / Q000378:metabolism; D010587:Phagocytosis; D011480:Protease Inhibitors / Q000378:metabolism; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors / Q000096:biosynthesis
D016326:Extracellular Matrix Proteins; D018836:Inflammation Mediators; D007375:Interleukin-1; D011480:Protease Inhibitors; D011971:Receptors, Immunologic; D003094:Collagen; D010447:Peptide Hydrolases; D008666:Metalloendopeptidases