假体周围骨溶解中成骨细胞自噬的信号通路.

BACKGROUND: Recent evidence suggests that autophagy, as a cell self-protection mechanism, plays an important role in regulating osteoblast function and maintaining osteoblast homeostasis. It has an important influence on the treatment and prognosis of periprosthetic osteolysis. OBJECTIVE: To provide new therapeutic ideas and potential therapeutic targets for periprosthetic osteolysis by summarizing previous studies on the autophagy mechanism of osteoblasts. METHODS: The first author used the computer to search the articles published from 2015 to 2022. In Chinese, the search terms “wear particles, periprosthetic osteolysis, osteoblasts, signal pathways, autophagy” were used to search the databases of CNKI, WanFang, and VIP. In English, the PubMed and Web of Science databases were retrieved with “wear debris, wear particles, peri*prosthetic osteolysis, PPOL, aseptic loosening, osteoblast, OB, signal path, autophagy”. A total of 98 articles were included according to the inclusion criteria. RESULTS AND CONCLUSION: In periprosthetic osteolysis, the changes in the autophagy ability of osteoblasts induced by wear particles play a key role in the development and outcome of the disease. A variety of signaling pathways jointly mediate autophagy in osteoblasts, among which the key pathways include AMPK/ULK1/mTOR, nuclear factor-κB, Pink1/Parkin, etc. AMPK, mTOR, and ULK1 can regulate each other and jointly maintain the stability of the autophagy level. There is a complex crosstalk between the nuclear factor-κB pathway and autophagy. PINK1 and Parkin are accumulated on the surface of the damaged mitochondrial membrane, inducing autophagy. There is crosstalk among multiple signaling pathways, which form a complex autophagy network under their mutual influence. Moreover, the activation of the same autophagy pathway in different cells may bring about completely opposite effects. Moderate autophagy induced by wear particles can reduce the apoptosis of osteoblasts, enhance their differentiation and mineralization ability, and improve the prognosis of osteolysis around the prosthesis. On the contrary, insufficient or excessive activation of autophagy will cause damage to osteoblasts and promote the progress of osteolysis. Therefore, targeting the level of autophagy of osteoblasts induced by wear particles through drugs or genes may be one of the directions for the treatment of periprosthetic osteolysis. [ABSTRACT FROM AUTHOR]