Division of Rheumatology, Department of Medicine, Maastricht University Medical Center, Maastricht, The Netherlands.
Clin Exp Rheumatol. 2009 Jul-Aug;27(4 Suppl 55):S62-7.
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.
骨骼是许多炎症性风湿病的靶点，如类风湿关节炎 (RA) 和强直性脊柱炎 (AS)。炎症对骨骼的普遍影响可能导致骨骼质量下降，并增加 RA 和 AS 患者骨折和畸形的风险。RA 的特征是关节周围骨质疏松、全身性骨质疏松和骨侵蚀。关节周围骨质疏松和骨侵蚀主要与疾病活动度相关。与绝经后骨质疏松症不同，RA 中的骨质疏松症更以髋关节和桡骨明显的骨量丢失为特征，而轴向骨骼相对保存。一般来说，几项横断面研究表明，RA 患者的骨矿物质密度较低，与年龄和性别匹配的对照组相比，骨质疏松症的发生率增加了两倍，与骨折风险增加相关。几个因素导致了这种风险的增加：年龄较大、运动较少、长期使用皮质类固醇和高残疾指数。AS 的特征是由于骨矿物质密度降低导致的骨脆性增加。AS 患者骨质疏松症的报道患病率差异很大。这种大的差异反映了由于新骨形成，评估 AS 中 BMD 的困难。骨脆性也归因于炎症引起的脊柱骨衰竭导致的结构特性变化，以及减震能力降低导致的椎体骨折。描述了 AS 患者的不同类型的脊柱骨折，包括楔形变。楔形变椎体骨折导致后凸畸形和身体功能受损。与 RA 不同，AS 中的骨丢失伴随着新骨形成。RA 和 AS 中骨质疏松症的病理生理学可能在根本上相似，但临床表现不同。在治疗上干预其发生和进展的意义可能在根本上不同。
