Purpose of review: Children with chronic rheumatic disease have decreased bone mass. In adults, lowered bone mineral density is associated with increased fracture risk. This morbidity is undetermined in pediatric rheumatic disease as osteoporosis has not been well-defined in children. This review compares methods for determining bone mass in children, examines insights into molecular mechanisms of bone metabolism, and discusses the prevention and treatment of decreased bone mass in children.
Recent findings: Peak bone mass, attained during adolescence and early adulthood, is critical in determining fracture risk. Studies of children with chronic rheumatic disease demonstrate decreased bone mineral density, and potentially lowered peak bone mass. Dual energy x-ray absorptiometry is the most commonly used technique for monitoring bone mineral density and should be interpreted utilizing age-appropriate Z-scores. Recent studies suggest quantitative ultrasound may be as reliable as dual energy x-ray absorptiometry and lacks radiation exposure. The molecular mechanisms by which inflammation alters bone mineral density involve receptor activator of nuclear factor kappaB ligand (RANKL)/osteoprotegerin, tumor necrosis factor-alpha, and interleukin-1. Limited data on the use of bisphosphonates and calcitonin in children suggest they are safe and effective, but should be used cautiously.
Summary: Children with chronic rheumatic disease should have bone mass monitored by dual energy x-ray absorptiometry Z-scores. Targeting the RANKL/osteoprotegerin pathway may lead to therapies that improve bone health in this population. More studies on the role of bisphosphonates and calcitonin must be pursued to establish guidelines for use in pediatric patients with chronic rheumatic disease. For now, supplemental calcium and vitamin D should be implemented in these children.