Maruotti Nicola, Corrado Addolorata, Cantatore Francesco P
Rheumatology Clinic, Department of Medical and Surgical Sciences, University of Foggia Medical School, Foggia, Italy.
J Cell Physiol. 2017 Nov;232(11):2957-2963. doi: 10.1002/jcp.25969. Epub 2017 May 24.
Even if osteoarthritis pathogenesis is still poorly understood, numerous evidences suggest that osteoblasts dysregulation plays a key role in osteoarthritis pathogenesis. An abnormal expression of OPG and RANKL has been described in osteoarthritis osteoblasts, which is responsible for abnormal bone remodeling and decreased mineralization. Alterations in genes expression are involved in dysregulation of osteoblast function, bone remodeling, and mineralization, leading to osteoarthritis development. Moreover, osteoblasts produce numerous transcription factors, growth factors, and other proteic molecules which are involved in osteoarthritis pathogenesis.
尽管骨关节炎的发病机制仍未被充分理解,但大量证据表明成骨细胞失调在骨关节炎发病机制中起关键作用。在骨关节炎成骨细胞中已发现骨保护素(OPG)和核因子κB受体活化因子配体(RANKL)的异常表达,这导致了异常的骨重塑和矿化减少。基因表达的改变参与了成骨细胞功能、骨重塑和矿化的失调,从而导致骨关节炎的发展。此外,成骨细胞产生多种转录因子、生长因子和其他蛋白质分子,这些分子都参与了骨关节炎的发病机制。