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Inflammatory Bowel Diseases and Skeletal Health

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Abstract

While the skeleton is often thought only as a scaffold for soft tissue, it serves many other important functions including the production of blood cells, a reservoir for calcium, buffer and perhaps glucose homeostasis and fertility in males. The skeleton responds to systemic influences such as hormones, mechanical loading and signals from the central nervous system. Bone becomes stronger or weaker depending on these influences, thanks to carefully orchestrated events of its main cells osteocytes, osteoblasts, and osteoclasts. Bone has a build-in mechanism of self-repair called bone remodeling. It is estimated that the adult skeleton is completely renovated every 10 years thanks to bone remodeling.

During childhood bone not only adapts and remodels but also grows in length and width. The process of bone growth involves changing shape, mass and architecture. The mechanical properties of bone therefore change dynamically over time. Bone growth is complete when the growth plate disappears but bone calcification continues into early adulthood. Inflammatory bowel disease can potentially affect bone by multiple mechanisms including malnutrition, decreased physical activity, reduced muscle mass and power and delayed puberty, growth hormone resistance, effects of inflammatory factors on bone cells and medications. In this chapter we will briefly review basic bone biology and disease and treatment factors that may affect that skeleton in pediatric IBD.

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Sylvester, F.A. (2013). Inflammatory Bowel Diseases and Skeletal Health. In: Mamula, P., Markowitz, J., Baldassano, R. (eds) Pediatric Inflammatory Bowel Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-5061-0_13

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