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The expressions of IGF‐1, BMP‐2 and TGF‐β1 in cartilage of condylar hyperplasia
Authors:Q MENG  X LONG  M DENG  H CAI  J LI
Institution:Department of Oral and Maxillofacial Surgery, Key Laboratory for Oral Biomedical Engineering of Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei, P.R. China
Abstract:Summary Condylar hyperplasia is a complex post‐natal growth abnormality of the mandible and condyle, which leads to facial asymmetry. We investigated the distributions of insulin‐like growth factors (IGF‐1), bone morphogenetic protein‐2 (BMP‐2) and transforming growth factor‐β1 (TGF‐β1) in cartilage of condylar hyperplasia and revealed relationships between age and the cartilaginous thickness. Twenty patients with condylar hyperplasia were divided into four histopathological types. The cartilaginous thickness and age in different histological types were analysed, and the localizations of IGF‐1, BMP‐2 and TGF‐β1 were detected by immunohistochemistry analysis. The cartilaginous thickness of condylar hyperplasia significantly increased. The cartilaginous thickness of type III was significantly thicker than type I and type II, Bivariate correlation revealed a significant correlations between age and the cartilaginous thickness (r = 0·68, P = 0·01). However, the expressions of IGF‐1, BMP‐2 and TGF‐β1 were the strongest in type I. In almost all types of condylar hyperplasia, the presence of IGF‐1 and BMP‐2 was found mainly in the proliferative chondrocyte layer and the hypertrophic chondrocyte layer, and only a few in the calcified chondrocyte layer. The presence of TGF‐β1 widely distributed from the fibrous articular surface to the calcified cartilage. These findings suggest that the proliferative activity of cartilage in condylar hyperplasia is strongly associated with age and cartilaginous thickness. Therefore, the four pathological types of condylar hyperplasia seem more likely to be four discontinuous stages.
Keywords:temporomandibular joint  condylar hyperplasia  IGF‐1  BMP‐2 and TGF‐β  1
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