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兔膝骨性关节炎早期软骨下骨血管再生变化及二磷酸盐干预效应

Change of angiogenesis at osteochondral bone of knee and intervention of diphosphonate in rabbits with osteoarthritis
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摘要 目的研究兔膝骨性关节炎(OA)早期软骨下骨血管再生变化及二磷酸盐的保护作用。方法 60只新西兰大白兔随机分成模型组(A组,24只)、二磷酸盐组(B组,24只)和对照组(C组,12只)。术后4周、8周、12周处死兔子,切取手术侧膝关节,进行大体评分及Mankin评分,免疫组化染色测量骨软骨连接处的血管密度。结果与C组相比,A组4周时已出现软骨退变(P<0.01),8、12周时退变进一步加重(P<0.01),并且骨软骨连接区血管侵犯的密度增加(P<0.01);而B组的软骨退变轻于A组(P<0.05或P<0.01)。结论 OA早期关节软骨开始退变,软骨下骨与关节软骨交界区血管增生。二磷酸盐对关节软骨有明显的保护作用。 Objective To investigate the changes of angiogenesis at the osteochondral bone of the knee and the protective effect of diphosphonate on it in rabbits with osteoarthritis (OA) in the early stage. Methods Sixty New Zealand white rabbits were randomly divided into three groups of A (OA model, 24 rabbits), B(treated with diphosphonate 0. 01 mg/kg, 24 rabbits) and C(sham operated, 12 rabbits). On the 4th, 8th and 12th week after operation, the rabbits were sacrificed to take specimens of the knee joint. The gross morphologic examination and Mankin score were analyzed, and blood vessel density at the osteochondral junction was detected by immunohistochemistry. Results Compared with group C, cartilage regression was found on the 4th week and aggravated on the 8th and 12th week after operation (P〈0. 01), and blood vessel density at the osteochondral junction was increased in group A(P〈0. 01), which were significantly less in group B than those in group A (P〈0. 05 or P〈0. 01). Conclusion Cartilage degeneration and angiogenesis in border area of subchondral bone and articular cartilage are found in the early stage of OA, which may be effectively ameliorated by diphosphonate.
出处 《江苏医药》 CAS 北大核心 2014年第10期1117-1119,F0002,共4页 Jiangsu Medical Journal
基金 国家自然科学基金(81171730) 苏州市科技发展项目(SYS201065)
关键词 骨性关节炎 软骨下骨 二磷酸盐 血管再生 Osteoarthritis Subchondral bone Diphosphonate Angiogenesis
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参考文献8

  • 1Blom AB, van der Kraan PM, van den Berg WB. Cytokine targeting in osteoarthritis[J]. Curr Drug Targets, 2007,8 (2): 283-292.
  • 2Walsh DA, Bonnet CS, Turner EL, et al. Angiogenesis in the synovium and at the osteochondral junction in osteoarthritis[J]. Osteoarthritis Cartilage, 2007,15 (7) : 743-751.
  • 3Anderson-MacKenzie JM, Quasnichka HL, Starr RL, et al. Fundamental subehondral bone changes in spontaneous knee osteoarthritis[J]. Int J Biochem Cell Biol, 2005, 37 (1) : 224- 236.
  • 4Mapp PI, Avery PS, McWilliams DF, et al. Angiogenesis in two animal models of osteoarthritis[J]. Osteoarthritis Cartilage, 2008,16(1) :61-69.
  • 5Walsh DA, McWilliams DF, Turley MJ, et al. Angiogenesis and nerve growth factor at the osteochondral junction in rheuma- toid arthritis and osteoarthritis [J]. Rheumatology (Oxford), 2010,49 (10) : 1852-1861.
  • 6Mapp PI, Walsh DA. Mechanisms and targets of angiogenesis and nerve growth in osteoarthritis[J]. Nat Rev Rheumatol, 2012,8(7) : 390-398.
  • 7Saito M, Sasho T, Yamaguchi S, et al. Angiogenie activity of subchondral bone during the progression of osteoarthritis in a rabbit anterior cruciate ligament transection model[J]. Osteo- arthritis Cartilage,2012,20(12) : 1574-1582.
  • 8Blanquaert F, Pereira RC, Canalis E. Cortisol inhibits hepato- cyte growth factor/scatter factor expression and induees c-met transcripts in osteoblasts[J]. Am J Physiol Endocrinol Metab, 2000,278(3) :509-515.

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