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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Matrix metalloproteinases, their physiological inhibitors and osteoclast factors are differentially regulated by the cytokine profile in human periodontal disease

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Garlet, Gustavo P. [1] ; Martins Jr., Walter ; Fonseca, Benedito A. L. ; Ferreira, Beatriz R. ; Silva, João S.
Total Authors: 5
[1] Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia - Brasil
Total Affiliations: 5
Document type: Journal article
Source: Journal of Clinical Periodontology; v. 31, n. 8, p. 671-679, Aug. 2004.
Field of knowledge: Health Sciences - Dentistry

Inflammatory reactions raised in response to periodontopathogens are thought to trigger pathways of periodontal tissue destruction. We therefore investigated the expression of matrix metalloproteinases (MMPs) and the osteoclastogenic factor receptor activator of nuclear factor-kappaB ligand (RANKL), their respective tissue inhibitors of metalloproteinases (TIMPs) and osteoprotegerin (OPG) in different forms of human periodontal diseases (PDs), and the possible correlation with the expression of inflammatory and regulatory cytokines. Quantitative polymerase chain reaction (real-time PCR) was performed with gingival biopsies mRNA from aggressive (AP) and chronic periodontitis (CP) patients. Periodontitis patients exhibit higher expression of all analyzed factors when compared with healthy tissues. The expression of MMPs and RANKL were similar in AP and CP, as well as the expression of TNF-alpha. On the other hand, the expression of TIMPs and OPG was higher in CP, and was associated with lower IFN-gamma and higher IL-10 expression, compared with AP. It is possible that the pattern of cytokines expressed determines the stable or progressive nature of the lesions and regulates the severity of PD, driving the balance between MMPs and TIMPs, RANKL and OPG expression in the gingival tissues controlling the breakdown of soft and bone tissues and, consequently, the disease severity. (AU)