Walsh D A, Bonnet C S, Turner E L, Wilson D, Situ M, McWilliams D F
Academic Rheumatology, University of Nottingham Clinical Sciences Building, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Osteoarthritis Cartilage. 2007 Jul;15(7):743-51. doi: 10.1016/j.joca.2007.01.020. Epub 2007 Mar 21.
We hypothesised that osteochondral and synovial angiogenesis in osteoarthritis (OA) are independent processes. We investigated whether indices of osteochondral and synovial angiogenesis display different relationships with synovitis, disease severity and chondrocalcinosis in patients with OA.
Synovium and medial tibial plateaux were obtained from 62 patients undergoing total knee joint replacement for OA (18 [29%] had chondrocalcinosis) and from 31 recently deceased people with no evidence of joint pathology post-mortem (PM). Vascular endothelium, proliferating endothelial cells (ECs) and macrophages were quantified by immunohistochemistry for CD34, CD31/Ki67 and CD14, respectively. Grades were assigned for radiographic and histological OA disease severity, clinical disease activity and histological synovitis (based on cellular content of the synovium).
Blood vessels breached the tidemark in 60% of patients with OA and 20% of PM controls. Osteochondral vascular density increased with increasing cartilage severity and clinical disease activity scores, but not with synovitis. Synovial EC proliferation, inflammation and macrophage infiltration were higher in OA than in PM controls. Synovial angiogenesis indices increased with increasing histological synovitis, but were not related to osteochondral vascular density or other indices of OA disease severity. OA changes were more severe in patients with concurrent chondrocalcinosis. Chondrocalcinosis was not associated with increased angiogenesis or histological synovitis beyond that seen in OA alone.
Osteochondral and synovial angiogenesis appear to be independent processes. Osteochondral vascularity is associated with the severity of OA cartilage changes and clinical disease activity, whereas synovial angiogenesis is associated with histological synovitis. Modulation of osteochondral and synovial angiogenesis may differentially affect OA disease.
我们假设骨关节炎（OA）中骨软骨和滑膜血管生成是独立的过程。我们研究了骨软骨和滑膜血管生成指标与OA患者滑膜炎、疾病严重程度和软骨钙质沉着症之间是否存在不同的关系。
从62例行全膝关节置换术治疗OA的患者（其中18例[29%]有软骨钙质沉着症）以及31例近期死亡且尸检无关节病变证据的人获取滑膜和胫骨内侧平台。分别通过免疫组织化学检测CD34、CD31/Ki67和CD14对血管内皮、增殖内皮细胞（ECs）和巨噬细胞进行定量。根据影像学和组织学OA疾病严重程度、临床疾病活动度和组织学滑膜炎（基于滑膜细胞含量）进行分级。
60%的OA患者和20%的尸检对照者血管突破潮线。骨软骨血管密度随软骨严重程度和临床疾病活动评分增加而升高，但与滑膜炎无关。OA患者滑膜EC增殖、炎症和巨噬细胞浸润高于尸检对照者。滑膜血管生成指标随组织学滑膜炎加重而升高，但与骨软骨血管密度或OA疾病严重程度的其他指标无关。并发软骨钙质沉着症的患者OA改变更严重。软骨钙质沉着症与血管生成增加或组织学滑膜炎增加无关，超出了单独OA所见。
骨软骨和滑膜血管生成似乎是独立的过程。骨软骨血管形成与OA软骨改变的严重程度和临床疾病活动度相关，而滑膜血管生成与组织学滑膜炎相关。调节骨软骨和滑膜血管生成可能对OA疾病产生不同影响。
