Yabe Yutaka, Hagiwara Yoshihiro, Ando Akira, Tsuchiya Masahiro, Minowa Takashi, Takemura Taro, Honda Masahito, Hatori Kouki, Sonofuchi Kazuaki, Kanazawa Kenji, Koide Masashi, Sekiguchi Takuya, Itoi Eiji
*Department of Orthopaedic Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan †Division of Aging and Geriatric Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan ‡Nanotechnology Innovation Station, National Institute for Materials Science, Tsukuba, Japan §Department of Otrhopaedic Surgery, Takeda General Hospital, Aizuwakamatsu, Japan; and ¶Division of Advanced Prosthetic Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan.
Spine (Phila Pa 1976). 2015 Apr 1;40(7):429-35. doi: 10.1097/BRS.0000000000000795.
A histological, biological, and immunohisto-chemical study of human lumbar ligamentum flavum.
To analyze changes in the hypertrophied ligamentum flavum and clarify their etiology.
Hypertrophy of the ligamentum flavum has been considered a major contributor to the development of lumbar spinal canal stenosis (LSCS). Although previous studies have reported some factors related to ligamentum flavum hypertrophy, its etiology is still unclear.
Ligamentum flavum samples were collected from 20 patients with LSCS (LSCS group) and 10 patients with lumbar disc herniation (LDH group) as a control. The thickness of the ligamentum flavum was measured histologically. The amounts of elastic fibers and proteoglycans were assessed by Elastica-Masson staining and alcian blue staining, respectively. Gene and protein expressions related to fibrosis, inflammation, and chondrogenesis were analyzed by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. The total genes of the 2 groups were compared by DNA microarray analysis.
The ligamentum flavum was significantly thicker in the LSCS group, which had a smaller amount of elastic fibers and a larger amount of proteoglycans. The gene expression related to fibrosis was significantly higher in the LSCS group; however, the immunoreactivities of collagen types I and III were weaker on the dorsal side of the ligamentum flavum in the LSCS group. The gene expression related to chondrogenesis and proteoglycan synthesis was significantly higher in the LSCS group. There was no significant difference in the gene expression related to inflammation between the 2 groups.
Synthesis of the collagenous fibers and degradation of the elastic and collagenous fibers are both accelerated in the ligamentum flavum of patient with LSCS, which may be the reason for hypertrophy of the tissue. In addition, chondrogenesis and proteoglycan synthesis may have critical roles in the pathogenesis of the ligamentum flavum hypertrophy.
一项关于人腰椎黄韧带的组织学、生物学及免疫组织化学研究。
分析肥厚型黄韧带的变化并阐明其病因。
黄韧带肥厚被认为是腰椎管狭窄症（LSCS）发病的主要因素。尽管先前的研究报道了一些与黄韧带肥厚相关的因素，但其病因仍不明确。
从20例LSCS患者（LSCS组）和10例腰椎间盘突出症患者（LDH组）中收集黄韧带样本作为对照。通过组织学方法测量黄韧带厚度。分别采用弹力纤维染色和阿尔辛蓝染色评估弹性纤维和蛋白聚糖的含量。通过定量逆转录-聚合酶链反应和免疫组织化学分析与纤维化、炎症及软骨形成相关的基因和蛋白表达。采用DNA微阵列分析比较两组的全部基因。
LSCS组的黄韧带明显更厚，弹性纤维含量更少，蛋白聚糖含量更多。LSCS组中与纤维化相关的基因表达显著更高；然而，LSCS组黄韧带背侧I型和III型胶原蛋白的免疫反应性较弱。LSCS组中与软骨形成和蛋白聚糖合成相关的基因表达显著更高。两组之间与炎症相关的基因表达无显著差异。
LSCS患者的黄韧带中胶原纤维的合成以及弹性纤维和胶原纤维的降解均加速，这可能是组织肥厚的原因。此外，软骨形成和蛋白聚糖合成可能在黄韧带肥厚的发病机制中起关键作用。
5级。
