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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Periodontal Disease-Associated Compensatory Expression of Osteoprotegerin Is Lost in Type 1 Diabetes Mellitus and Correlates with Alveolar Bone Destruction by Regulating Osteoclastogenesis

Texto completo
Autor(es):
Silva, Juliete Aparecida F. [1] ; Ferrucci, Danilo Lopes [1] ; Peroni, Luis Antonio [1] ; Ishi, Eduardo de Paula [2] ; Rossa-Junior, Carlos [2] ; Carvalho, Hernandes F. [1, 3] ; Stach-Machado, Dagmar Ruth [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Estadual Campinas, Dept Anat, Campinas, SP - Brazil
[2] Sch Dent Araraquara, Dept Diag & Surg, Araraquara - Brazil
[3] Natl Inst Sci & Technol Photon Appl Cell Biol, Campinas, SP - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: Cells Tissues Organs; v. 196, n. 2, p. 137-150, 2012.
Citações Web of Science: 19
Resumo

Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD. Copyright (C) 2012 S. Karger AG, Basel (AU)

Processo FAPESP: 08/54958-2 - Expressão molecular das colagenases e citocinas pró-inflamatórias envolvidas na reabsorção óssea na indução da doença periodontal experimental em animais diabéticos
Beneficiário:Dagmar Ruth Stach - Machado
Linha de fomento: Auxílio à Pesquisa - Regular