Exercise for osteoporosis: A literature review of pathology and mechanism

Abstract

Osteoporosis (OP) is a disease that weakens bones and has a high morbidity rate worldwide, which is prevalent among the elderly, particularly, women of postmenopausal age. The dynamic balance between bone formation and resorption is necessary for normal bone metabolism. Many factors, including aging, estrogen deficiency, and prolonged immobilization, disrupt normal apoptosis, autophagy, and inflammation, leading to abnormal activation of osteoclasts, which gradually overwhelm bone formation by bone resorption. Moderate exercise as an effective non-drug treatment helps increase bone formation and helps relieve OP. The possible mechanisms are that exercise affects apoptosis and autophagy through the release of exercise-stimulated myohormone and the secretion of anti-inflammatory cytokines via mechanical force. In addition, exercise may also have an impact on the epigenetic processes involved in bone metabolism. Mechanical stimulation promotes bone marrow mesenchymal stem cells (BMSCs) to osteogenic differentiation by altering the expression of non-coding RNAs. Besides, by reducing DNA methylation, the mechanical stimulus can also alter the epigenetic status of osteogenic genes and show associated increased expression. In this review, we reviewed the possible pathological mechanisms of OP and summarized the effects of exercise on bone metabolism, and the mechanisms by which exercise alleviates the progression of OP, to provide a reference for the prevention and treatment of OP.

Keywords: cytokines; exercise; inflammatory reaction; mechanical stress; osteoporosis.

Figure 1

The pathological mechanism of osteoporosis. Various internal and external factors, such as aging, sexual steroid deficiency, mechanical unloading, and overuse of glucocorticoids, can cause bone resorption to exceed bone formation, leading to osteoporosis. The pathological mechanisms of OP mainly include the abnormal activation of osteoclasts resulting from changes in apoptosis, inflammatory reaction, and autophagy. Besides, epigenetic changes, such as changes in non-coding RNA and DNA methylation, can also reduce the expression of osteogenic genes.

Figure 2

The mechanism of exercise improving osteoporosis. Exercise-induced changes in mechanical stress, hormones, and cytokines can regulate the pathological changes of osteoporosis. Mechanistically, exercise reduces the harmful osteoporosis alterations via affecting apoptosis, inflammatory response, and autophagy, and exercise may affect the epigenetic mechanisms of bone metabolism by regulating non-coding RNAs and DNA methylation.