Abstract:
Osteoporosis (OP) is a skeletal disease characterized by a decrease in bone strength and an increased risk of fractures, posing both medical and socioeconomic threats. Alcohol abuse is prevalent worldwide, and due to unique drinking cultures, alcohol-related diseases are highly prevalent in our country. Long-term alcohol abuse can lead to bone metabolism disorders, bone loss, and degradation of bone microstructure by directly affecting osteoblasts, osteoclasts, and their precursor cells, or indirectly influencing protein metabolism, liver function, and endocrine systems, thereby triggering osteoporosis. However, the pathogenesis of osteoporosis has not yet been fully elucidated. The immune system is a complex network composed of various molecules, cells, tissues, and organs, and it is a crucial system for maintaining human life, aimed at protecting the body from infections and malignant cells. Recent studies have shown a close relationship between alcohol and the immune system, particularly the effects of alcohol on innate and adaptive immunity, as well as the correlation of many immune cells, such as neutrophils, macrophages, T cells, and B cells, with osteoporosis. Therefore, this article discusses the impact of alcohol on the immune system to elucidate the pathogenesis of osteoporosis, aiming to provide new insights and evidence for the mechanistic research of osteoporosis, the development of new drugs, and new treatment strategies. It also finds that alcohol disrupts the dynamic balance of immune cells (such as inhibiting the generation of neutrophils, macrophages, T and B lymphocytes) and the activity of related signaling pathways (including OPG/RANKL/RANK, JAK/STAT3, NF-κB, and JNK signaling pathways), while abnormally regulating the secretion of pro-inflammatory factors (such as IL-1, IL-6, IL-17, TNF-α, and IFN-γ), thereby directly or indirectly disrupting the homeostatic balance between bone formation and resorption, ultimately leading to the occurrence of osteoporosis.