Laboratory for Soft Tissue Research, Hospital for Special Surgery, New York, NY 10021, USA.
J Shoulder Elbow Surg. 2010 Oct;19(7):978-88. doi: 10.1016/j.jse.2009.11.045. Epub 2010 Mar 19.
Studies have demonstrated a significant decrease in skeletal mass, bone mineral density, and impaired fracture healing in the diabetic population. However, the effect of sustained hyperglycemia on tendon-to-bone healing is unknown.
Forty-eight male, Lewis rats underwent unilateral detachment of the supraspinatus tendon followed by immediate anatomic repair with transosseous fixation. In the experimental group (n = 24), diabetes was induced preoperatively via intraperitoneal injection of streptozotocin (STZ, 65 mg/kg) and confirmed with both pre- and post-STZ injection intraperitoneal glucose tolerance tests (IPGTT). Animals were sacrificed at 1 and 2 weeks postoperatively for biomechanical, histomorphometric, and immunohistochemical analysis. Serum hemoglobin A1c (HbA1c) levels were measured at 2 weeks postoperatively. Statistical comparisons were performed using Student t tests with significance set at P < .05.
IPGTT analysis demonstrated a significant impairment of glycemic control in the diabetic compared to control animals (P < .05). Mean HbA1c level at 2 weeks postoperatively was 10.6 ± 2.7% and 6.0 ± 1.0% for the diabetic and control groups, respectively (P < .05). Diabetic animals demonstrated significantly less fibrocartilage and organized collagen, and increased AGE deposition at the tendon-bone interface (P < .05). The healing enthesis of diabetic animals demonstrated a significantly reduced ultimate load-to-failure (4.79 ± 1.33 N vs 1.60 ± 1.67 N and 13.63 ± 2.33 N vs 6.0 ± 3.24 N for control versus diabetic animals at 1 and 2 weeks, respectively) and stiffness compared to control animals (P < .05).
Sustained hyperglycemia impairs tendon-bone healing after rotator cuff repair in this rodent model. These findings have significant clinical implications for the expected outcomes of soft tissue repair or reconstructive procedures in diabetic patients with poor glycemic control.
研究表明，糖尿病患者的骨骼质量、骨密度和骨折愈合受损显著下降。然而，持续高血糖对肌腱-骨愈合的影响尚不清楚。
48 只雄性 Lewis 大鼠行单侧冈上肌腱分离术，术后立即行经骨固定的解剖修复。实验组（n=24）术前通过腹腔注射链脲佐菌素（STZ，65mg/kg）诱导糖尿病，并通过术前和术后 STZ 注射腹腔葡萄糖耐量试验（IPGTT）确认。术后 1 周和 2 周处死动物，进行生物力学、组织形态计量学和免疫组织化学分析。术后 2 周测量血清血红蛋白 A1c（HbA1c）水平。采用 Student t 检验进行统计学比较，显著性水平设为 P<.05。
IPGTT 分析表明，糖尿病组动物的血糖控制明显受损，与对照组相比（P<.05）。术后 2 周时，糖尿病组和对照组的平均 HbA1c 水平分别为 10.6±2.7%和 6.0±1.0%（P<.05）。糖尿病动物的肌腱-骨界面的纤维软骨和有序胶原明显减少，AGE 沉积增加（P<.05）。糖尿病动物的愈合附着点的最终失效负载明显降低（术后 1 周和 2 周时，对照组和糖尿病组的分别为 4.79±1.33N 与 1.60±1.67N 和 13.63±2.33N 与 6.0±3.24N；P<.05）和刚度较对照组降低（P<.05）。
持续高血糖会损害这种啮齿动物模型的肩袖修复后的肌腱-骨愈合。这些发现对血糖控制不佳的糖尿病患者软组织修复或重建手术的预期结果具有重要的临床意义。
