Bone is a target in many inflammatory rheumatic diseases, such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). The generalized effect of inflammation on bone may result in a decreased quality of bone and is associated with an increased risk of fractures and deformities, both in RA and AS. RA is characterized by periarticular osteopenia, systemic osteoporosis and bone erosions. Periarticular osteopenia and bone erosions are mainly correlated with disease activity. Unlike postmenopausal osteoporosis, osteoporosis in RA is more characterised by marked loss of bone in the hip and the radius, while the axial bone is relatively preserved. In general, several cross-sectional studies documented a lower bone mineral density in patients with RA, with a two-fold increase in osteoporosis compared to age- and sex-matched controls and relates to an increased fracture risk. Several factors contribute to the increased risk: older age, little exercise, long-term use of corticosteroids, and high disability index. AS is characterized by an increase in bone fragility due to reduced bone mineral density. The reported prevalence of osteoporosis in AS patients varies largely. The large variation reflects the difficulties in assessing BMD in AS due to new bone formation. Bone fragility is also due to changes in structural properties resulting from inflammation-induced bone failure in the spine in combination with reduced capacity of shock absorption leading to vertebral fractures. Different types of spinal fractures in patients with AS are described, including wedging. Wedging vertebral fractures contribute to hyperkyphosis and impaired physical function. In contrast to RA , bone loss in AS is accompanied by new bone formation. The pathophysiology of osteoporosis in RA and AS probably is fundamentally similar, but with different clinical phenotypes. The implications for therapeutically intervening in its occurrence and progression might be fundamentally different.