Immunohistochemical analysis of bone resorption regulators (RANKL and OPG), angiogenic index, and myofibroblasts in syndrome and non-syndrome odontogenic keratocysts

• Autor(a) principal: Nonaka, Cassiano Francisco Weege
• Data de Publicação: 2012
• Outros Autores: Cavalcante, Roberta Barroso, Nogueira, Renato Luiz Maia, Souza, Lélia Batista de, Pinto, Leão Pereira
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRN
• Texto Completo: https://repositorio.ufrn.br/jspui/handle/123456789/23808; https://doi.org/10.1016/j.archoralbio.2011.08.002
• topic: Odontogenic keratocyst; Receptor activator of nuclear factor kappa B ligand; Osteoprotegerin; CD34; Myofibroblast; Immunohistochemistry

Objective The aim of this study was to immunohistochemically analyse bone resorption regulators (receptor activator of nuclear factor kappa B ligand [RANKL] and osteoprotegerin [OPG]), angiogenic index, and myofibroblasts in Gorlin syndrome-related odontogenic keratocysts (SOKCs) and non-syndrome odontogenic keratocysts (NSOKCs). Study design Twenty-two SOKCs, 22 primary NSOKCs, and eight recurrent NSOKCs were evaluated by immunohistochemistry using anti-RANKL and anti-OPG antibodies. The angiogenic index was determined by microvessel count (MVC) using anti-CD34 antibody. Anti-α-smooth muscle actin (α-SMA) antibody was used for the identification of myofibroblasts. Results Analysis of the expression of RANKL and OPG in the epithelial lining and fibrous capsule did not reveal significant differences between groups (P > 0.05). In the epithelial lining, the RANKL/OPG ratio was RANKL < OPG and RANKL = OPG in most primary NSOCKs (54.5%) and SOKCs (59.1%), respectively (P > 0.05). In the fibrous capsule, the ratio was RANKL = OPG in most primary (81.8%) and recurrent NSOKCs (75.0%) and in most SOKCs (45.5%) (P > 0.05). No significant differences in the angiogenic index or number of myofibroblasts were observed between primary NSOKCs, recurrent NSOKCs, and SOKCs (P > 0.05). Conclusions The present results suggest that differences in the biological behaviour of SOKCs and NSOKCs may not be related to the expression of RANKL and OPG, to the RANKL/OPG ratio, to the angiogenic index, or to the number of myofibroblasts in these lesions.