Bone metabolic homeostasis is dependent on coupled bone formation dominated by osteoblasts and bone resorption dominated by osteoclasts, which is a process of dynamic balance between bone formation and bone resorption. Notably, the formation of bone relies on the development of bone vasculature. Previous studies have shown that oxidative stress caused by disturbances in the antioxidant system of the whole organism is an important factor affecting bone metabolism. The increase in intracellular reactive oxygen species can lead to disturbances in bone metabolism, which can initiate multiple bone diseases, such as osteoporosis and osteoarthritis. Traditional Chinese medicine is considered to be an effective antioxidant. Cumulative evidence shows that the traditional Chinese medicine can alleviate oxidative stress-mediated bone metabolic disorders by modulating multiple signaling pathways, such as Nrf2/HO-1 signaling, PI3K/Akt signaling, Wnt/β-catenin signaling, NF-κB signaling, and MAPK signaling. In this paper, the potential mechanisms of traditional Chinese medicine to regulate bone me-tabolism through oxidative stress is summarized to provide direction and theoretical basis for future research related to the treatment of bone diseases with traditional Chinese medicine.

Bone metabolic diseases are typically caused by abnormal cell metabolism and cell death within the bone, involving cell types such as osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Bone metabolic diseases include autosomal recessive^{osteosclerosis} (ARO), osteosarcoma (OS), rheumatoid arthritis (RA), and osteoporosis (OP). However, there are other categories of bone metabolic disorders in addition to the four mentioned in this review, including, but not limited to, osteochondrosis, Paget’s disease, and hyperparathyroidism-associated bone disease, and others. The incidence of bone metabolism-related diseases has gradually increased over time and social changes, affecting a wider and wider group of people. Therefore, systematically analyzing the molecular pathological mechanisms of bone metabolic diseases, particularly the spatiotemporal dynamics of key regulatory nodes, has become an urgent need for developing novel therapeutic strategies. It is important to note that strictly speaking OS and RA are not usually categorized as bone metabolic disorders. However, this review categorizes them as bone metabolic diseases because of the pathological mechanisms, cellular metabolic abnormalities, and clinical evidence explored in OS and RA. Both OS and RA fit the basic profile of bone metabolic diseases. SNX10, as a member of the sorting nexin family, exerts unique regulatory functions in membrane transport through its phospholipid-binding properties mediated by the PX (phox homology) domain. Recent mechanistic analyses have shown that SNX10 exhibits multidimensional therapeutic potential in bone metabolic diseases by regulating pathways such as vesicle transport, lysosome maturation, and RANKL signal transduction. This review systematically integrates the latest research evidence on SNX10 in bone metabolic diseases, focusing on elucidating its molecular regulatory networks in conditions such as ARO, OS, RA, and OP, aiming to provide a theoretical basis for the application of SNX10-targeted precision therapeutic strategies in bone metabolic diseases.