Abstract

A holistic, up‐to‐date understanding of skeletal biology is a vital component of clinical practice in a variety of fields, including orthopedics, endocrinology, internal medicine, physical medicine and rehabilitation, physical & occupational therapy, and others. However, most entry‐level practitioners in these fields come out of their degree programs with only a cursory knowledge of skeletal biology, which does not adequately incorporate a bounty of research that has been conducted over the last several decades.One of the great difficulties in educating students in our current understanding of skeletal biology – as is the case for most physiological systems – is the overwhelming complexity and interconnectivity of the skeleton with other body systems, which we are only now fully beginning to appreciate. Since this interconnectivity is also what makes an understanding of skeletal biology so important for the clinic, it is important not to shy away from it in our curricula.Therefore, the objective of this paper is to present a skeletal homeostasis model developed to educate students in graduate clinical degree programs with a well‐rounded, current understanding of skeletal biology. This model incorporates numerous body systems and strives to adequately incorporate the last three decades of research. The model presented here emphasizes the interaction between different tissues and the skeleton, placing the diversity of humoral and nervous outputs known to affect skeletal biology within tissue‐specific contexts in an attempt to make the interconnectivity of skeletal homeostasis more digestible to students. Each interaction of the skeleton with other systems is approached piece‐by‐piece, incorporating some of the most important neuroendocrine factors sequentially to build up to a broad understanding. While not complete, this model provides the student a good basis for interpreting the influence of muscles, fat, loading, calcium homeostasis, metabolism, and the nervous system upon bone – as well as the reciprocal impact that bone has upon these factors. Is also provides a foundation for understanding how failures in these interconnected networks can lead to pathology such as osteoporosis.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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