Sakai Yoshihito, Matsuyama Yukihiro, Hasegawa Yukiharu, Yoshihara Hisatake, Nakamura Hiroshi, Katayama Yoshito, Imagama Shiro, Ito Zenya, Ishiguro Naoki, Hamajima Nobuyuki
Department of Orthopaedic Surgery, Nagoya University School of Medicine, Nagoya, Japan.
Spine (Phila Pa 1976). 2007 May 20;32(12):1279-86. doi: 10.1097/BRS.0b013e318059af8a.
Cross-sectional cohort study of elderly people.
To examine the factors influencing osteophyte formation without lumbar disc degeneration and to estimate the implications of osteophytes from the viewpoint of low back pain and gene polymorphisms.
The degenerative changes that occur in the intervertebral discs are the point of departure of osteophyte formation. Several studies on factors associated with genetic susceptibility to spinal osteophyte formation, such as VDR and TGF-beta1. However, there are no detailed studies concerning osteophytes not accompanied with disc degeneration.
A total of 387 elderly persons were recruited, and disc degeneration and osteophyte formation were evaluated. The cases with osteophyte formation were classified into 3 groups: osteophyte formation with disc height narrowing (n = 217), osteophyte formation without disc height narrowing (n = 99), and control group defined as the cases without osteophyte formation (n = 71). Twelve genotypes were characterized. Correlations between these degenerative factors and the polymorphisms were analyzed.
The prevalence of low back pain was significantly greater in the group of osteophyte formation with disc height narrowing than the other 2 groups. In the polymorphism of alcohol dehydrogenase (ADH2), prevalence of osteophyte formation without disc height narrowing was less in His/Arg (odds ratio = 0.57, P = 0.041) and Arg/Arg (odds ratio = 0.41, P = 0.18) than His/His.
Patients with osteophyte formation preceding intervertebral disc narrowing had a lower risk of low back pain compared with those without osteophytes. The 47Arg polymorphism in the ADH2 may act to suppress osteophyte formation unaffected by disc degeneration.
针对老年人的横断面队列研究。
探讨影响无腰椎间盘退变情况下骨赘形成的因素，并从腰痛和基因多态性角度评估骨赘的影响。
椎间盘发生的退行性改变是骨赘形成的起点。已有多项关于与脊柱骨赘形成遗传易感性相关因素的研究，如维生素D受体（VDR）和转化生长因子-β1（TGF-β1）。然而，尚无关于不伴有椎间盘退变的骨赘的详细研究。
共招募387名老年人，评估椎间盘退变和骨赘形成情况。骨赘形成的病例分为3组：伴有椎间盘高度变窄的骨赘形成组（n = 217）、不伴有椎间盘高度变窄的骨赘形成组（n = 99）以及定义为无骨赘形成的对照组（n = 71）。鉴定了12种基因型。分析这些退变因素与多态性之间的相关性。
伴有椎间盘高度变窄的骨赘形成组中腰痛的患病率显著高于其他两组。在乙醇脱氢酶（ADH2）的多态性方面，不伴有椎间盘高度变窄的骨赘形成组中，His/Arg（优势比 = 0.57，P = 0.041）和Arg/Arg（优势比 = 0.41，P = 0.18）基因型的骨赘形成患病率低于His/His基因型。
与无骨赘的患者相比，椎间盘狭窄之前出现骨赘形成的患者腰痛风险较低。ADH2基因的47Arg多态性可能起到抑制不受椎间盘退变影响的骨赘形成的作用。
