Purpose of review: Chronic pediatric inflammatory diseases are associated with low bone mass and fractures during childhood, and may hasten the onset of osteoporosis later in life. Proinflammatory cytokines and glucocorticoid therapy are likely key factors that impair bone accrual, along with downstream effects including malnutrition, pubertal delay, low muscle mass and physical inactivity.
Recent findings: Studies have used advanced imaging to characterize deficits in trabecular and cortical bone and have evaluated the 'functional muscle-bone unit'. 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. Systematic efforts to define the incidence and prevalence of bone fragility in children with inflammatory conditions demonstrated that vertebral fractures occur in a significant minority of patients in association with high disease activity, glucocorticoid use, and weight gain. Lumbar spine dual X-ray absorptiometry does not consistently distinguish children with and without vertebral fractures.
Summary: In children with inflammatory diseases, the documented elevated fracture risk and bone structural abnormalities highlight the need for additional research to better define methods for the assessment and prevention of bone fragility.