The role of muscle tissue in the homeostasis and development of a joint
The articular joint as an “organ” is interlinked with other tissues via metabolic and endocrine pathways and interacts via vascularization with muscle, adipose, nervous tissue and the circulatory system. In this review article, the mechanical action of muscles on the joint is analysed as well as the biological and endocrine effect of muscle tissue on joints metabolism and homeostasis. Pathological conditions such as degenerative osteoarthritis and inflammatory arthritides are also explained through pathways related to sarcopenia and obesity.
Mechanical load is an important factor in cartilage homeostasis. Muscle tissue has the ability to distribute mechanical stress in a joint. When mechanical stress is applied onto the cartilage, physical, electrochemical and biological phenomena occur through hydraulic pressure changes, fluid flow, osmotic pressure, diffusion and changes in the concentration of extracellular molecules, ions and pH. Furthermore, chondrocytes have mechanical stress receptors such as integrin receptors, connexins and Ca 2+ ion channels, which induce the production and function of collagenases and aggrecans in the cartilage. It has also been found that low-intensity circular loading in joint prevents the production of inflammatory factors that induce articular cartilage catabolism. The role of proprioception through the muscular spindle regulate the function of the muscles around the joint providing articular stability through protective contraction.
Skeletal muscle, in addition to its basic function in motion, stance and stability of the body and joints, has a second role as an endocrine organ. Myokines belong to the family of cytokines. They are small peptides produced in muscle tissue either during normal conditions or in exercise and induce autocrine, paracrine and endocrine activity. The study of the role of myokines in the joint is recent and mainly focus on their action in the bone and subchondral bone. Some myokines have a negative effect on subchondral bone metabolism, such as IL-6, myostatin, activin and ciliary neurotrophic factor (CNTF). Other myokines have anabolic activity on bone metabolism such as IL-15, IGF-I, FGF-2, follistatin, and irisin. Finally, muscle contraction in fetal life, both biochemically and morphologically, determines joint growth, in terms of structure of articular surfaces, proliferation and differentiation of chondrocytes, expression of extracellular matrix components.
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