Abstract
The concept of osteoimmunology is based on growing insight into the links between the immune system and bone at the anatomical, vascular, cellular, and molecular levels. In both rheumatoid arthritis (RA) and ankylosing spondylitis (AS), bone is a target of inflammation. Activated immune cells at sites of inflammation produce a wide spectrum of cytokines in favor of increased bone resorption in RA and AS, resulting in bone erosions, osteitis, and peri-inflammatory and systemic bone loss. Peri-inflammatory bone formation is impaired in RA, resulting in non-healing of erosions, and this allows a local vicious circle of inflammation between synovitis, osteitis, and local bone loss. In contrast, peri-inflammatory bone formation is increased in AS, resulting in healing of erosions, ossifying enthesitis, and potential ankylosis of sacroiliac joints and intervertebral connections, and this changes the biomechanical competence of the spine. These changes in bone remodeling and structure contribute to the increased risk of vertebral fractures (in RA and AS) and non-vertebral fractures (in RA), and this risk is related to severity of disease and is independent of and superimposed on background fracture risk. Identifying patients who have RA and AS and are at high fracture risk and considering fracture prevention are, therefore, advocated in guidelines. Local peri-inflammatory bone loss and osteitis occur early and precede and predict erosive bone destruction in RA and AS and syndesmophytes in AS, which can occur despite clinically detectable inflammation (the so-called 'disconnection'). With the availability of new techniques to evaluate peri-inflammatory bone loss, osteitis, and erosions, peri-inflammatory bone changes are an exciting field for further research in the context of osteoimmunology.
Highlights
The concept of osteoimmunology emerged more than a decade ago and is based on rapidly growing insight into the functional interdependence between the immune system and bone at the anatomical, vascular, cellular, and molecular levels [1]
Further research is needed to understand why non-steroidal anti-inflammatory drug (NSAID) could decrease fracture risk and syndesmophyte formation, why tumor necrosis factor (TNF) blockade prevents bone loss but not syndesmophyte formation, and new ways to prevent syndesmophyte formation. These data indicate that bone is a major target for inflammation and that bone loss and osteoporosis are common features that contribute to the increased fracture risk in rheumatoid arthritis (RA) and ankylosing spondylitis (AS)
Periarticular bone loss and osteitis coincide early in RA and AS and precede and predict the occurrence of visible erosions [76]. This raises the question of the mechanism by which these anatomical coincident changes in the joints, entheses, and bone marrow occur
Summary
The concept of osteoimmunology emerged more than a decade ago and is based on rapidly growing insight into the functional interdependence between the immune system and bone at the anatomical, vascular, cellular, and molecular levels [1]. Many risk factors, including baseline disease severity, RF, anti-CCP, baseline bone destruction, the RANKL/OPG ratio, and CTX-I and CTX-II, have been identified for the prediction of bone erosions in RA This pallet of predictors can be extended with measurement of changes in periarticular bone (by DXR) and osteitis (on MRI) early in the disease [73,81,82]. Advocate calcium and vitamin D supplements, bisphosphonates, and eventually teriparatide as a second choice because of its higher cost price in the prevention of GIOP in patients at high risk, such as those with persistent disease activity, high dose of GCs, or high background risk such as menopause, age, low BMD, and the presence of clinical risk factors [138,139] Taken together, these data indicate that control of inflammation is able to halt bone loss and suppress osteitis in RA. Further research is needed to understand why NSAIDs could decrease fracture risk and syndesmophyte formation, why TNF blockade prevents bone loss but not syndesmophyte formation, and new ways to prevent syndesmophyte formation
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