Sudhir G, Balasubramaniam Subalakshmi, Jayabalan Vignesh, Sundaram Sandhya, Kumar Venkatesh, Kailash Karthik
Sri Ramachandra Institute of Higher Education and Research, Chennai, Tamil Nadu, India.
Int J Spine Surg. 2020 Jun 30;14(3):341-346. doi: 10.14444/7045. eCollection 2020 Jun.
Diabetes mellitus is one of the leading causes of morbidity resulting in multi-organ dysfunction. Animal studies have shown that hyperglycemia results in stress-induced senescence through the p16-pRb pathway, thereby accelerating early disc degeneration. There is a paucity of literature on the effect of hyperglycemia in human intervertebral disc cells. We aimed to analyze the effect of diabetes mellitus in human intervertebral disc cells.
This is a prospective study done in patients with degenerative disc disease. Patients were categorized into a control group (no diabetes: 26 patients) and a study group (type 2 diabetes for > 3 years: 24 patients). All patients underwent either discectomy or transforaminal lumbar interbody fusion and the removed disc was transported to pathology department. Tissue was prepared and histopathological grading was done followed by immunohistochemistry studies using antibodies for MMP-1, p21, p16, and pRb.
Samples from diabetic patients had severe (grade 2) degenerative changes compared with the control group (grade 1). Changes were more intense in the nucleus pulposus with increased cellularity and clustering of chondrocytes, and disorganization and loss of nuclear matrix. Immunohistochemical staining for MMP1, p16, and pRb was more intense (Q score = 4) whereas the staining for p21 was less intense (Q score = 1) in the diabetic group compared with the control group.
Our study demonstrates that type 2 diabetes mellitus accelerates stress-induced senescence in human intervertebral discs resulting in early disc degeneration. Also, the severity of disc degeneration is severe compared with the normal subjects.
Hyperglycemia can affect the intervertebral discs similar to other organs and hence adequate control of blood glucose in diabetics can prevent the disc degeneration, which is the initiator of degeneration cascade in spine.
糖尿病是导致多器官功能障碍的主要发病原因之一。动物研究表明，高血糖通过p16-pRb途径导致应激诱导的衰老，从而加速早期椎间盘退变。关于高血糖对人椎间盘细胞影响的文献较少。我们旨在分析糖尿病对人椎间盘细胞的影响。
这是一项针对退行性椎间盘疾病患者的前瞻性研究。患者被分为对照组（无糖尿病：26例患者）和研究组（2型糖尿病病程>3年：24例患者）。所有患者均接受了椎间盘切除术或经椎间孔腰椎椎间融合术，切除的椎间盘被送至病理科。制备组织并进行组织病理学分级，随后使用针对MMP-1、p21、p16和pRb的抗体进行免疫组织化学研究。
与对照组（1级）相比，糖尿病患者的样本有严重（2级）退变改变。髓核中的变化更明显，细胞增多且软骨细胞聚集，核基质紊乱和丢失。与对照组相比，糖尿病组中MMP1、p16和pRb的免疫组织化学染色更强（Q评分=4），而p21的染色较弱（Q评分=1）。
我们的研究表明，2型糖尿病会加速人椎间盘的应激诱导衰老，导致早期椎间盘退变。此外，与正常受试者相比，椎间盘退变的严重程度更高。
高血糖可像影响其他器官一样影响椎间盘，因此糖尿病患者血糖的充分控制可预防椎间盘退变，而椎间盘退变是脊柱退变级联反应的起始因素。
