Delayed remodeling in the early period of fracture healing in spontaneously diabetic BB/OK rats depending on the diabetic metabolic state
Delayed remodeling in the early period of fracture healing in spontaneously diabetic BB/OK rats depending on the diabetic metabolic state
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DOI：
10.14670/hh-19.473
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发表时间：
2004-04-01
影响因子：
2
通讯作者：
Merk, H
中科院分区：
文献类型：
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作者：
Follak, N;Klöting, I;Merk, H
对胰岛素依赖型 1 型糖尿病 (IDDM) 患者骨折愈合进行分析的多个临床系列表明，延迟愈合、不愈合和假关节的发生率很高。本研究的目的是根据自发性糖尿病 BB/O(ttawa)K(arlsburg) 大鼠（一种与人类 IDDM 密切同源的大鼠品系）的糖尿病代谢状态，检查骨折愈合过程中骨形成和重塑的详细组织形态学和组织学。选择标准化骨折模型，并基于手术时血糖值 (mg%)、术后血糖过程 (mg%) 和术后胰岛素需求 (IU/kg)，将 100 只自发性糖尿病 BB/OK 大鼠分为代谢状态良好（n=50、167+/-77 mg%；244+/-68 mg%；1.8+/-1.9 IU/kg）或代偿不良（n=50、380+/-89 mg%；415+/-80 mg%；6.0+/-1.0 IU/kg）代谢状态组。五十只 LEW.1A 大鼠作为血糖正常对照 (97+/-15 mg%)。骨折后 1、2、3、4 和 6 周处死每组 10 只动物，对标本进行未脱钙处理，用于定量组织形态计量学和定性光学显微镜。在骨组织形态计量学方面，在骨折后的前 4 周内，严重的矿化障碍仅出现在代偿性糖尿病代谢状态较差的大鼠中，与自发性糖尿病大鼠相比，所有基于荧光染料的矿化、并置、形成和矿化时间的参数均显着降低。补偿良好的代谢状态和对照大鼠。这在组织学上得到了证实。自发性糖尿病 BB/OK 大鼠的早期骨折愈合仅在代偿不良的糖尿病代谢状态下延迟，并且骨折后 6 周，测量和动态计算的参数在组织形态学上仍然存在显着缺陷。这项研究表明，严格控制胰岛素治疗，导致糖尿病代谢状态得到良好补偿，将改善 IDDM 骨折愈合受损的早期矿化和细胞分化障碍。
Several clinical series, analyzing fracture healing in patients with insulin-dependent type 1 diabetes (IDDM) demonstrated significant incidence of delayed union, non-union, and pseudarthrosis. The purpose of this study was to examine the detailed histomorphometry and histology of bone formation and remodeling during fracture healing depending on the diabetic metabolic state in spontaneously diabetic BB/O(ttawa)K(arlsburg) rats, a rat strain that represents a close homology to IDDM in man.A standardized fracture model was chosen and based on blood-glucose values at the time of surgery (mg%), postoperative blood-glucose course (mg%) and postoperative insulin requirements (IU/kg), 100 spontaneously diabetic BB/OK rats were divided into groups with well-compensated (n=50, 167 +/- 77 mg%; 244+/-68 mg%; 1.8+/-1.9 IU/kg) or poorly compensated (n=50, 380+/-89 mg%; 415+/-80 mg%; 6.0+/-1.0 IU/kg) metabolic state. Fifty LEW.1A rats served as the normoglycemic controls (97+/-15 mg%). Ten animals from each group were killed 1, 2, 3, 4 and 6 weeks after fracture and specimens were processed undecalcified for quantitative histomorphometry and for qualitative light microscopy.In terms of bone histomorphometry, within the first four weeks after fracture, severe mineralization disorders occurred exclusively in the rats with poorly compensated diabetic metabolic states with a significantly decrease of all fluorochrome-based parameters of mineralization, apposition, formation and timing of mineralization in comparison to the spontaneously diabetic rats with well-compensated metabolic states and to the control rats. This was confirmed histologically.Early fracture healing in the spontaneously diabetic BB/OK rats is delayed exclusively in poorly compensated diabetic metabolic states, and 6 weeks after fracture, histomorphometrically significant deficits in the measured and dynamically calculated parameters remain. This study suggests that strictly controlled insulin treatment resulting in well-compensated diabetic metabolic states will ameliorate the impaired early mineralization and cell differentiation disorders of IDDM fracture healing.