de Vlam Kurt, Lories Rik J U, Luyten Frank P
University Hospitals Leuven, Division of Rheumatology, Herestraat 49, B-3000 Leuven, Belgium.
Curr Rheumatol Rep. 2006 Oct;8(5):332-7. doi: 10.1007/s11926-006-0061-z.
Pathologic new bone formation occurs in response to a variety of stimuli. Heterotopic and orthotopic bone formation can interfere with the normal function of the joint and can contribute to disability in inflammatory joint diseases. Syndesmophyte formation and progressive ankylosis are characteristic features of spondyloarthropathies, including psoriatic arthritis and ankylosing spondylitis, and they can be regarded as abnormal bone remodeling. Successful blocking of inflammation in patients with spondyloarthropathy apparently fails to halt progression of ankylosis in cohort studies. This suggests that though they may be linked in some way, bone formation and inflammation are largely independent phenomena. Indeed, new bone formation also occurs in diseases such as osteoarthritis and diffuse idiopathic skeletal hyperostosis. Therefore, therapeutic strategies in spondyloarthropathy ideally should control both inflammation and bone formation.
病理性新骨形成是对多种刺激的反应。异位和原位骨形成会干扰关节的正常功能,并可能导致炎性关节疾病的残疾。韧带骨赘形成和进行性关节强硬是脊柱关节病的特征性表现,包括银屑病关节炎和强直性脊柱炎,它们可被视为异常的骨重塑。在队列研究中,成功阻断脊柱关节病患者的炎症显然未能阻止关节强硬的进展。这表明尽管它们可能在某种程度上有关联,但骨形成和炎症在很大程度上是独立的现象。事实上,新骨形成也发生在骨关节炎和弥漫性特发性骨肥厚等疾病中。因此,脊柱关节病的治疗策略理想情况下应同时控制炎症和骨形成。