BIOSYNTHETIC RESPONSE OF CARTILAGE EXPLANTS TO DYNAMIC COMPRESSION
BIOSYNTHETIC RESPONSE OF CARTILAGE EXPLANTS TO DYNAMIC COMPRESSION
复制标题
DOI：
10.1002/jor.1100070502
复制
发表时间：
1989-09-01
影响因子：
2.8
通讯作者：
SANDY, JD
中科院分区：
文献类型：
--
作者：
SAH, RLY;KIM, YJ;SANDY, JD
在宽范围的振幅、波形和频率下，检查小牛关节软骨外植体对动态压缩的生物合成反应。通过35S-硫酸盐掺入评估糖胺聚糖合成，通过3H-脯氨酸掺入评估氨基酸摄取和蛋白质合成。设计了两个培养室以允许软骨盘的单轴径向无侧限压缩和机械测试：一个室在标准培养箱内使用;另一个室与机械光谱仪一起使用，并允许在压缩期间监测载荷和位移。3 mm直径圆盘的动态刚度测量确定了一个特征频率[0.001 Hz（周期/秒）]，该频率将低频和高频区域分开，其中不同的流动和变形现象占主导地位;例如，在0.0001 - 0.001 Hz时，软骨盘渗出大量液体，而在0.01 - 1 Hz时，软骨盘内的流体层压增加。在较高频率下，仅100%-5%的振荡应变刺激3H-脯氨酸和35S-硫酸根掺入100%-40%。相反，在较低频率下，（a）<5%的压缩没有影响，这与静态压缩的生物合成抑制剂量测定一致（25%的压缩导致放射性标记掺入的20%的抑制），和（B）更高的振幅（在1.25和0.88 - 1.00 mm的圆盘厚度之间循环）刺激3S-硫酸盐掺入20 - 40%，与对单次2 h压缩和释放的响应动力学一致。没有一种压缩方案与可检测到的改变相关（例如，总糖胺聚糖含量的压缩诱导消耗。这项研究提供了一个框架，以确定物理和生物学机制，动态压缩可以调节软骨细胞的生物合成。此外，培养和压缩方法可能允许在体外评价连续被动运动疗法的临床策略，以刺激软骨重塑。
The biosynthetic response of calf articular cartilage explants to dynamic compression was examined over a wide range of amplitudes, waveforms, and frequencies. Glycosaminoglycan synthesis was assessed by35S‐sulfate incorporation, and amino acid uptake and protein synthesis were assessed by3H‐proline incorporation. Two culture chambers were designed to allow uniaxial radially unconfined compression and mechanical testing of cartilage disks: one chamber was used inside a standard incubator; the other was used with a mechanical spectrometer and allowed load and displacement to be monitored during compression. Dynamic stiffness measurements of 3‐mm diameter disks identified a characteristic frequency [0.001 Hz (cycles/sec)] that separated low‐ and high‐frequency regimes in which different flow and deformation phenomena predominated; e.g., at 0.0001–0.001 Hz, significant fluid was exuded from cartilage disks, whereas at 0.01–1 Hz, hydrostratic pressure increased within disks. At the higher frequencies, oscillatory strains of only ∼1–5% stimulated3H‐proline and35S‐sulfate incorporation by ∼20–40%. In contrast, at the lower frequencies (a) compressions of <5% had no effect, consistent with the dosimetry of biosynthetic inhibition by static compression (∼25% compression caused a ∼20% inhibition of radiolabel incorporation), and (b) higher amplitudes (cycling between disk thicknesses of 1.25 and 0.88–1.00 mm) stimulated3S‐sulfate incorporation by ∼20–40%, consistent with the kinetics of response to a single 2‐h compression and release. None of the compression protocols was associated with detectable alterations in (e.g., compression‐induced depletion of) total glycosaminoglycan content. This study provides a framework for identifying both the physical and biological mechanisms by which dynamic compression can modulate chondrocyte biosynthesis. In addition, the culture and compression methodology potentially allows in vitro evaluation of clinical strategies of continuous passive motion therapy to stimulate cartilage remodeling.