Effects of Mechanical Stress on Bone and Cartilage Metabolism: How Mechanical Stress Affects Energy Metabolism in Bone and Cartilage Tissues (Our Research Overview): Mini Review

Bone resorption and formation are known to change in response to mechanical stress. The mechano-transduction mechanism by which bone tissue senses the stress, altering cellular activity in response via intracellular signaling pathways, ultimately leading to physiological and pathological changes, is beginning to be elucidated. Furthermore, excessive mechanical stress on bone and joints due to aging, obesity, overload, and overuse is thought to cause decreased chondrocyte activity, degeneration and destruction of the cartilage collagen matrix, degeneration of the subchondral bone, and joint dysfunction, contributing to the progression of osteoarthritis (OA). However, much remains unknown about how osteoblasts, responsible for bone formation, and chondrocytes, responsible for cartilage homeostasis, sense and respond to mechanical stress. Furthermore, whether there are mechanisms to protect against pathological and excessive mechanical stress in bone and cartilage tissue, their associated molecular mechanisms, and the relationship between mechanical stress responses and osteochondral degeneration, remain unknown. Understanding these mechanisms is considered essential for the development of new therapeutic strategies for osteochondral diseases. Our research aims to deepen our understanding of the etiology and pathophysiology of bone and cartilage diseases (osteoporosis, fragility fracture, and OA) and to develop new treatments from the perspective of mechanical stress response. In this paper we review the latest findings regarding the roles of cellular energy regulators (glucose transporters and energy sensors) and mechanical stress response factors, and the relationship between these factor-mediated changes in energy metabolism and osteochondral degeneration. This minireview discusses how energy metabolism regulators control the activity of both osteoblasts and chondrocytes in osteochondral tissue in response to mechanical stress.