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The primary risk factor for most musculoskeletal diseases, including osteoarthritis, osteoporosis and sarcopenia, is aging. To treat the diverse types of musculoskeletal diseases and pathologies, targeting their root cause, the aging process itself, has the potential to slow or prevent multiple age-related musculoskeletal conditions simultaneously. However, the development of approaches to delay onset of age related diseases, including musculoskeletal pathologies, has been slowed by the relatively long lifespan of rodent models of aging. Thus, to expedite the development of therapeutic approaches for age-related musculoskeletal disease, the implementation of mouse models of accelerated musculoskeletal aging are of great utility. Currently there are multiple genetically diverse mouse models that mirror certain aspects of normal human and mouse aging. Here, we provide a review of some of the most relevant murine models of accelerated aging that mimic many aspects of natural musculoskeletal aging, highlighting their relative strengths and weaknesses. Importantly, these murine models of accelerated aging recapitulate phenotypes of musculoskeletal age-related decline observed in humans.

Skeletal muscle is a highly interactive connective tissue that makes up a large portion of an adult's body mass. Muscles are integrated with tendons as well as other specialized structures to support physiologic and homeostatic functions. In the state of injury, muscles have the ability to innately repair themselves through various phases of tightly regulated healing that can result in fibrotic tissue development. However, during aging, these homeostatic processes are disrupted leading to sarcopenia and reduced muscle regeneration capacity. Several cell-based therapies and biologic therapies have been investigated to regenerate skeletal muscle tissue and reduce fibrosis following injury or during aging. These include platelet-rich plasma (PRP) and an acellular portion of blood known as platelet-poor plasma (PPP). However, current clinical practice recommendations for the utilization of different PRP preparations vs PPP are unclear. Recent efforts have strove to improve the understanding of the role of senescent cells and profiles in the presence of early to late stage skeletal muscle injury and fibrosis, yet targeted interventions to remove senescent cells and attenuate the secretory environment to improve muscle regeneration are still forthcoming. Therefore, the purpose of this article is to review the basic principles of skeletal muscle repair, the role of senescence in attenuated muscle regeneration, and discuss current standards and literature supporting PRP and PPP treatment for skeletal muscle repair. This review concludes with future directions to improve biologic therapies and ongoing initiatives to customize PRP and PPP preparations using Food and Drug Administration-approved medications.