The effect of aging on distraction osteogenesis in the rat
The effect of aging on distraction osteogenesis in the rat
复制标题
DOI：
10.1016/s0736-0266(00)90025-1
复制
发表时间：
2001-05-01
影响因子：
2.8
通讯作者：
Lumpkin, CK
中科院分区：
文献类型：
--
作者：
Aronson, J;Gao, GG;Lumpkin, CK
在两项研究中，使用来自两个不同年龄群体的 Sprague-Dau ley (SD) 大鼠（CAMM：9 个月与 24 个月，Harlan：4 个月与 24 个月），研究了年龄对牵引成骨 (DO) 肢体延长模型中骨形成的影响。将外固定器放置在30只雄性SD大鼠（20只CAMM，10只Harlan）的右侧胫骨上，并进行中骨干截骨术。以 0.2 mm bid 进行分散注意力，持续 20 天 (CAMM) 或 14 天 (Harlan)。实验（DO）和对照（对侧）胫骨被移除，用于高分辨率射线照相和脱钙组织学。使用视频显微镜对放射密度、组织学（基质类型）和细胞增殖的相关区域进行定量，并通过增殖细胞核抗原（PCNA）免疫化学进行鉴定。两项研究均表明，牵引间隙中矿化骨百分比（放射密度）随年龄而下降（CAMM 9 个月对比 24 个月：68% 对比 51%，P < 0.003；Harlan 4 对比 24 个月：95% 对比 36%，P < 0.001），并且 24 个月大大鼠的两个群体之间没有发现显着的集落或牵引时间特异性差异。对 Harlan 大鼠进行组织学检查。与 4 月龄大鼠相比，34 月龄大鼠的 DO 间隙显示出较少的骨内膜新骨（P < 0.01），但骨膜新骨相当。在 4 个月大的大鼠中，PCNA 免疫染色的细胞沿着初级基质前沿（类骨质首次沉积的地方）组织，延伸穿过骨膜和骨内膜表面。在 24 个月大的大鼠中，PCNA + 细胞仅组织在沿着骨膜新骨前沿的区域中，并且不规则地散布在纤维血管非骨化基质内的整个骨内间隙中。这些结果表明，24 个月大的大鼠在骨内膜骨形成方面存在相对缺陷，这可能与细胞增殖无关，而是与细胞组织有关。该模型反映了老年患者的放射学检查结果显示 DO 期间矿化显着延迟的临床情况。我们相信，老年大鼠的 DO 模型提供了独特的体内机会来测试以下假设：(1) 衰老对骨修复的影响，(2) 药物对老年环境中骨修复的影响，以及 (3) 研究 DO 的机制。 (C) 2001 年骨科研究学会。由爱思唯尔科学有限公司出版。保留所有权利。
The effect of age on bone formation in the limb lengthening model of distraction osteogenesis (DO) was investigated in two studies using Sprague-Dau ley (SD) rats from two colonies at various ages (CAMM: 9 vs 24 months, Harlan: 4 vs 24 months). External fixators were placed on the right tibiae of 30 male SD rats (20 CAMM, 10 Harlan) and mid-diaphyseal osteotomies were performed. Distraction was performed at 0.2 mm bid for 20 days (CAMM) or 14 days (Harlan). The experimental (DO) and control (contra-lateral) tibiae were removed For high-resolution radiography and decalcified histology. Videomicroscopy was used to quantitate radiodensity, histology (matrix type) and relative areas of cell proliferation, which was identified by proliferating cell nuclear antigen (PCNA) immunochemistry. Both studies demonstrated an age-related decrease in the percent mineralized bone (radiodensity) in the distraction gap (CAMM 9 vs 24 months: 68% vs 51%, P < 0.003; Harlan 4 vs 24 months: 95% vs 36%, P < 0.001) and no significant colony or distraction rime-specific difference was seen between the two colonies of 24-month-old rats. Histology was performed on the Harlan rats. The DO gaps in the 34-month-old rats demonstrated less endosteal new bone compared to the 4-month-old rats (P < 0.01), but equivalent periosteal new bone. In 4-month-old rats, PCNA-immunostained cells were organized along the primary matrix front (where the first deposition of osteoid occurs) extending across both periosteal and endosteal surfaces. In 24-month-old rats, PCNA + cells were organized in zones along the periosteal new bone fronts only and irregularly scattered throughout the endosteal gap within a fibrovascular non-ossifying matrix. These results indicate that 24-month-old rats have a relative deficit in endosteal bone formation which may not be related to cell proliferation but rather to cell organization. This model reflects the clinical situation where radiographic findings in older patients demonstrate significant delays in mineralization during DO. We believe this model of DO in aged rats presents unique in vivo opportunities to test hypotheses concerning (1) the effects of aging on bone repair, (2) the effects of pharmacological agents on bone repair in a geriatric setting, and (3) to study the mechanisms underlying DO. (C) 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.