The world population is aging, so it is not uncommon that diseases associated with old age are steadily increasing. Osteoporosis and sarcopenia are two disorders that seriously impair the quality of life in the elderly. Different studies have shown that bones and muscles produce cytokines that affect each other. Bone produces sclerostin that decreases muscle mass. Muscle produces myokines, such as myostatin, interleukin-6, and monocyte chemoattractant protein-1 (MCP-1), which have a negative influence on bone metabolism. However, in recent years the paradigm of cellular senescence has developed, focusing on global aging, not only osteoporosis and sarcopenia but also multiple other chronic diseases. Senescent cells stop their growth, contributing to the depletion of stem cell proliferation and tissue aging. Senescent cells have an altered secretion pattern called senescence-associated secretory phenotype (SASP) that includes cytokines, growth factors, chemokines, matrix metalloproteinases, telomere shortening, and alterations in the desoxyribonucleic acid. SASP has been related with inflammation that leads to cellular transformation and chronic diseases. Cellular senescence has been found in bone, muscle, and other tissues. Treatment of musculoskeletal diseases involves changes in lifestyles and/or drugs that modify the pathogenesis of these diseases. Some experimental studies have shown that the elimination of senescent cells or their biochemical mediators can improve bone mass, muscle mass and function, osteoarthritis, insulin resistance, and other chronic diseases, pointing to a probable single therapy to treat old age in contrast to the many drugs that older people usually use. The future will show us if this paradigm becomes a reality.
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Conflicts of Interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this document.
Funding acknowledgement: None of the authors received funding for the creation of this paper.
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