Molecular Mechanisms of Osteoporosis in Inflammatory Rheumatic Diseases

Bone remodelling in healthy persons is characterised by balanced bone resorption and bone formation. On the cellular level, bone remodelling is regulated by a balanced osteoclast and osteoblast activity. Osteoporosis is characterised by bone loss. On a cellular level, the balance is shifted towards the side of osteoclast activation and activity. The immune system is able to influence bone remodelling via the RANK/RANKL/OPG system. Inflammatory processes directly and indirectly modify the differentiation and function of osteoclasts and play a central role in most of the pathophysiological pathways active in osteoporosis. Inflammation and, especially, chronic inflammatory pathways contribute to the shift of the bone remodelling balance in the direction of bone resorpion, leading to osteoporosis.