Cui Guanyu, Watanabe Kota, Miyauchi Yoshiteru, Hosogane Naobumi, Tsuji Takashi, Ishii Ken, Nakamura Masaya, Toyama Yoshiaki, Chiba Kazuhiro, Miyamoto Takeshi, Matsumoto Morio
Department of Orthopedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, 160-8582, Japan.
J Orthop Sci. 2011 Nov;16(6):785-90. doi: 10.1007/s00776-011-0135-2. Epub 2011 Aug 10.
Lumbar spinal canal stenosis (LSCS) is one of the most common spinal disorders in the elderly, and ligamentum flavum (LF) hypertrophy is an important cause of LSCS. Matrix metalloproteinase 13 (MMP13) can degrade fibrillar collagens and elastic microfibrils, and is involved in inflammation and fibrosis. The purpose of this study was to compare the expression of MMP13 in the LF from LSCS patients with diabetes mellitus [DM (+)] with that in the LF from patients without DM [DM (-)] and to analyze the relationship among DM, MMP13 expression, and LF hypertrophy.
LFs from 11 DM (+) and 24 DM (-) LSCS patients were analyzed in this study. Histology analysis using hematoxylin and eosin and Masson's trichrome stain was performed for each LF. The expression of MMP13 was analyzed by quantitative real-time PCR. The thickness of LF was measured by CT.
In the LF from DM (+) LSCS patients, the elastic fibers were more disorganized and had lower volumes than in the LF from DM (-) LSCS patients, while more fibrotic tissue was observed in the LF from DM (+) than from DM (-) LSCS patients. MMP13 expression was significantly higher in the LF from DM (+) LSCS patients (0.46 ± 0.61 vs. 0.05 ± 0.09, P = 0.002). The LF from the DM (+) LSCS patients was significantly thicker than that from the DM (-) LSCS patients (5.0 ± 0.9 vs. 3.1 ± 0.8 mm, P < 0.01), and the thickness was correlated with the expression of MMP13 (correlation coefficient = 0.43, P = 0.01, Pearson's correlation test).
DM-related MMP13 expression can be one of the factors contributing to fibrosis and hypertrophy of the LF. Further research on the mechanism of this process may lead to new therapies for LF hypertrophy.
腰椎管狭窄症(LSCS)是老年人中最常见的脊柱疾病之一,而黄韧带(LF)肥厚是LSCS的重要病因。基质金属蛋白酶13(MMP13)可降解纤维状胶原蛋白和弹性微纤维,并参与炎症和纤维化过程。本研究的目的是比较糖尿病患者[DM(+)]的LSCS患者LF中MMP13的表达与非糖尿病患者[DM(-)]的LF中MMP13的表达,并分析DM、MMP13表达与LF肥厚之间的关系。
本研究分析了11例DM(+)和24例DM(-)的LSCS患者的LF。对每个LF进行苏木精-伊红染色和Masson三色染色的组织学分析。通过定量实时PCR分析MMP13的表达。通过CT测量LF的厚度。
与DM(-)的LSCS患者的LF相比,DM(+)的LSCS患者的LF中弹性纤维更紊乱且体积更小,而DM(+)的LSCS患者的LF中观察到的纤维化组织比DM(-)的LSCS患者更多。DM(+)的LSCS患者的LF中MMP13表达明显更高(0.46±0.61对0.05±0.09,P = 0.002)。DM(+)的LSCS患者的LF明显比DM(-)的LSCS患者的LF厚(5.0±0.9对mm 3.1±0.8,P <0.01),并且厚度与MMP13的表达相关(相关系数= 0.43,P = 0.01,Pearson相关检验)。
DM相关的MMP13表达可能是导致LF纤维化和肥厚得因素之一。对这一过程机制的进一步研究可能会带来针对LF肥厚的新疗法。