Bone Abstracts

Pediatric inflammatory diseases are associated with low bone mass and fractures during childhood. In conditions such as inflammatory bowel disease and systemic lupus erythematosus, glucocorticoid therapy, and pro-inflammatory cytokines are key factors that impair bone accrual through specific effects on osteoblasts, osteoclasts, and osteocytes. Other factors may contribute to suboptimal skeletal maturation, including malnutrition, pubertal delay, low muscle mass, and physical inactivity. Studies performed in diverse patient populations have documented a greater risk of both appendicular and vertebral compression fractures. Recently, the steroid-induced osteoporosis in the pediatric population (STOPP) study demonstrated that 6% of children with inflammatory diseases receiving chronic glucocorticoid therapy had incident vertebral compression fractures over 1-year of follow up. Those participants with incident vertebral fractures had a greater decrease in lumbar spine aBMD Z-scores in the first 6 months. In general, bone strength in the appendicular skeleton is compromised because of thinner cortical bone, with a low periosteal circumference and a normal or expanded endosteal circumference. Low muscle mass likely contributes to, but does not fully account for bone deficits. In children and adolescents with systemic lupus erythematosus have used spine QCT and HR-pQCT to document prominent axial and appendicular bone strength deficits. HR-pQCT trabecular deficits were associated with prevalent vertebral fractures. Despite known effects of chronic inflammatory diseases and concomitant glucocorticoid therapy on bone health and publication of the International Society for Clinical Densitometry Pediatric Position Statement, comprehensive bone health assessments are often not performed as part of routine clinical care. Potential solutions to this implementation gap will be discussed.

Disclosure: The author declared no competing interests.