Osteoimmunology and osteoporosis

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]. In 1997, the receptor activator of the nuclear factor-kappa-B ligand (RANKL)/RANK/osteoprotegerin (OPG) pathway was identified as a crucial molecular pathway of the coupling between osteoblasts and osteoclasts [2]. It appeared that not only osteoblasts but also activated T lymphocytes, which play a crucial role in the pathogenesis of rheumatoid arthritis (RA), and many other inflammatory cells can produce RANKL, which stimulates the differentiation and activation of osteoclasts [3]. These findings have contributed to the birth of osteoimmunology as a discipline.Because of the multiple interconnections and interactions of bone and the immune system, bone is a major target of chronic inflammation in RA and ankylosing spondylitis (AS). Inflammation increases bone resorption and results in suppressed local bone formation in RA and locally increased bone formation in AS, causing a wide spectrum of bone involvement in RA and AS [4,5].Osteoporosis has been defined as a bone mineral density (BMD) of lower than 2.5 standard deviations of healthy young adults and in daily practice is measured by dual-energy x-ray absorptiometry (DXA) at the spine and hip [6]. However, the bone disease component in RA and AS is much more complex, especially around the sites of inflammation. We reviewed the literature on the quantification of local and general bone changes and their relation to the structural damage of bone, disease activity parameters, and fracture risk in the context of osteoimmunology, both in RA and AS. We have chosen to focus on RA and AS since these inflammatory rheumatic diseases have the highest prevalence and since, in both diseases, characteristic but different types of bone involvement may occur.Multiple anatomical and vascular conta