Conditions such as juvenile idiopathic arthritis, inflammatory bowel diseases, systemic lupus erythematosus and cystic fibrosis are now being targeted with therapies that have markedly improved outcome and survival. However, as the classical clinical features of these diseases become better controlled, the problem of bone damage determined by chronic inflammation during childhood comes to the fore. Prolonged disease activity leads to stunted linear growth with reduced final height and reduced peak bone mass, which is a crucial factor in determining premature osteoporosis. The mechanisms leading to these skeletal alterations are many, but clinical observations and experimental models show that inflammation itself plays a major role in bone remodeling in the growing skeleton. A better understanding of these clinical features, together with insight into what is currently known about their pathogenesis, is essential in developing correct strategies to prevent and treat them.