Premorbid knee osteoarthritis is not characterised by diffuse thinness: the Framingham Osteoarthritis Study
Premorbid knee osteoarthritis is not characterised by diffuse thinness: the Framingham Osteoarthritis Study
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DOI：
10.1136/ard.2007.076810
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发表时间：
2008-11-01
影响因子：
27.4
通讯作者：
Felson, D. T.
中科院分区：
文献类型：
--
作者：
Hunter, D. J.;Niu, J. B.;Felson, D. T.
目的：据推测，与低骨密度和骨折一样，薄软骨也容易患骨关节炎（OA）。关于软骨厚度对 OA 发展的影响，可以通过评估单侧 OA 患者未受影响的未患病对侧膝关节的状态来推断，我们将其标记为“病前膝关节”。该分析的主要目的是将病前膝关节的软骨厚度与取自没有任何膝关节 OA 的人的非 OA 膝关节进行比较，以确定病前膝关节中的软骨是否比取自某人的膝关节薄。方法：从 2002 年到 2005 年，弗雷明汉骨关节炎研究从社区中招募了与 OA 无关的受试者，我们获得了双膝的后前位、半屈位和外侧片以及膝关节磁共振成像，以量化一个膝关节的软骨体积，使用 3D 技术对髌骨、股骨内侧和外侧、胫骨内侧和外侧的软骨板进行量化。 FLASH-水激发序列（平面分辨率 0.360.3 毫米，512 矩阵，切片厚度 1.5 毫米）和数字后处理（涉及三维重建）用于定义膝关节的 OA 状态，该膝关节的疾病定义为外侧片上的 Kellgren 和 Lawrence 分级 >= 2 和/或髌股关节骨关节炎，其中 720 名参与者的任一膝关节都没有 OA。 （无膝 OA 样本），55 名受试者使用磁共振成像检查膝关节无 OA（病前膝关节 OA 样本），我们比较了这些组之间的软骨厚度和软骨覆盖率（软骨覆盖的总骨界面）。我们使用广义估计方程来解释软骨板之间的相关性，为了进一步确定软骨是否广泛变薄或仅增加了软骨裸露面积，我们从分析中删除了裸露面积（软骨覆盖率小于 95%）的板材。结果：55% 的受试者为女性。年龄、性别和体重指数，并从分析中去除覆盖率低于 95% 的钢板，我们发现与膝关节 OA 样本相比，病前膝盖的软骨相同甚至更厚。结论：病前膝盖没有弥漫性软骨变薄，而是软骨正常或较厚，有裸露区域，表明这可能是最初的病理学而不是弥漫性变薄。
Objective: It is hypothesised that, like low bone density and fracture, thin cartilage predisposes to osteoarthritis (OA). Inferences about the effects of cartilage thickness on the development of OA can be made by evaluating the status of an unaffected non-diseased contralateral knee, in persons with unilateral OA, which we shall label the "premorbid knee''. The primary objective of this analysis was to compare cartilage thickness in premorbid knees with non-OA knees drawn from persons without any knee OA to determine if cartilage in the premorbid knee was thinner than in the knee drawn from someone without OA in either knee.Methods: From 2002 to 2005, The Framingham Osteoarthritis Study recruited subjects without respect to OA from the community. We obtained posteroanterior, semiflexed and lateral films of both knees and knee magnetic resonance imaging to quantify cartilage volume in one knee. The cartilage plates of the patella, medial and lateral femur, medial and lateral tibia were quantified, using a 3D FLASH-water excitation sequence (in plane resolution 0.360.3 mm, 512 matrix, slice thickness 1.5 mm) and digital post-processing, involving three-dimensional reconstruction. Radiographs were used to define the OA status of knees with disease defined as Kellgren and Lawrence grade >= 2 and or patellofemoral OA on the lateral film. Of 1020 participants included in this analysis, 720 had no OA in either knee (no-knee OA sample), and 55 subjects had no OA in the knee that was examined using magnetic resonance imaging and OA in the contralateral knee (premorbid knee OA sample). We compared cartilage thickness and percentage of cartilage coverage (total bone interface covered with cartilage) between these groups. After initial plate-specific univariate comparisons we performed a multiple regression to assess the association between OA status (premorbid versus no OA knee) and cartilage thickness adjusting for age, sex and body mass index. We used the Generalised Estimating Equation to account for correlation between plates. To further determine if the cartilage was diffusely thinned or had only increased areas of denuded cartilage, we removed plates with denuded areas (less than 95% cartilage coverage) from the analysis.Results: 55% of subjects were women. There was no difference in cartilage thickness between the premorbid knees and the no-knee OA sample. After adjusting for age, sex and body mass index and removing plates with less than 95% coverage from the analysis, we found the same or even thicker cartilage in premorbid knees compared with the knee OA sample.Conclusions: Premorbid knees do not have diffuse cartilage thinness. Rather the cartilage is normal or thicker with denuded areas suggesting that this may be the initial pathology rather than diffuse thinning.