ABSTRACT
Inflammatory bowel disease (IBD) is an idiopathic, destructive chronic inflammatory condition of the gastrointestinal tract. The prevalence of IBD in children below 15 years of age is 20/100,000 (Kim and Ferry, 2004). About 80 % of pediatric IBD patients have Crohn’s Disease (CD); the remainder have ulcerative colitis. Apart from the gastrointestinal tract, IBD affects many organ systems, including the skeleton. The aetiology of the bone mass deficit in CD remains incompletely understood (Burnham et al., 2004). The effect on the skeleton is often difficult to distinguish from the effect of osteotoxic medications that are used to control the inflammatory process, such as glucocorticoids. The development of bone is a complex process in healthy children and that complexity is heightened further in children with CD both by the disease itself, treatment, and its effects on diet and exercise. It is clear that IBD by itself has an effect on the skeleton even prior to treatment as ilial histomorphometric analyses indicate a disturbance in skeletal architecture (thinning of the cortices), and in skeletal metabolism (Ward et al., 2010). The serum of children with IBD contains factors that inhibit osteoblasts (Sylvester et al., 2002). Mechanical stress exerted by skeletal muscle increases bone mass (Schoneau et al., 2002) and strength (Rittweger et al., 2000) which suggest that the osteopenia seen at diagnosis may have partly resulted from a lack of muscle development (sarcopenia). Sarcopenia may in turn result from systemic inflammatory cachexia (Burnham et al., 2005). At this juncture the potential role of physical activity/inactivity on muscle/bone development in children with CD has not been explored and is therefore the focus of this report.
