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Inflammatory Bowel Diseases and Skeletal Health

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Pediatric Inflammatory Bowel Disease
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Abstract

The muscle-bone unit is frequently affected in children with inflammatory bowel disease (IBD), especially Crohn disease. Muscle mass is significantly reduced at diagnosis in children with Crohn disease. Muscle mass deficits persist despite adequate clinical response to anti-inflammatory therapy and catch-up weight gain. Bone mass and bone architecture are both compromised in pediatric Crohn disease. Linear growth and bone modeling and remodeling are affected as well. As a result, bones may be shorter in children with Crohn disease. Osteoclasts expand the bone marrow cavity of long bones, while osteoblasts do not expand the periosteal envelope at the same rate, producing a thinner cortex. The cortical bone density is, however, augmented, probably due to inhibited bone remodeling, which can make bones brittle. Trabecular bone mass may be reduced secondary to decreased bone formation. The muscle-bone unit in pediatric IBD can be affected by multiple mechanisms, including malnutrition (resulting in deficits of macro- and micronutrients), inflammatory cytokines and activated T-cells, inhibition of sex steroids and insulin-like growth factor-1, and inactivity. In addition, corticosteroids can directly cause muscle loss, inhibit bone formation, and indirectly increase bone resorption. Antitumor necrosis factor-α and exclusive enteral nutrition, on the other hand, can reconstitute linear growth and bone modeling and remodeling in children with IBD. In this chapter, we discuss in detail the muscle-bone phenotype in human IBD and animal models of IBD. We also present possible mechanisms by which IBD affects the muscle-bone unit and options to enable the achievement of peak bone mass in children with IBD.

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Sylvester, F. (2023). Inflammatory Bowel Diseases and Skeletal Health. In: Mamula, P., Kelsen, J.R., Grossman, A.B., Baldassano, R.N., Markowitz, J.E. (eds) Pediatric Inflammatory Bowel Disease. Springer, Cham. https://doi.org/10.1007/978-3-031-14744-9_13

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