BIOCHEMICAL-CHANGES IN ARTICULAR-CARTILAGE AFTER JOINT IMMOBILIZATION BY CASTING OR EXTERNAL FIXATION
BIOCHEMICAL-CHANGES IN ARTICULAR-CARTILAGE AFTER JOINT IMMOBILIZATION BY CASTING OR EXTERNAL FIXATION
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DOI：
10.1002/jor.1100070305
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发表时间：
1989-05-01
影响因子：
2.8
通讯作者：
OEGEMA, TR
中科院分区：
文献类型：
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作者：
BEHRENS, F;KRAFT, EL;OEGEMA, TR
成年犬双膝长腿石膏固定6周，角度为8°~15°。其他人研究的一种模型，或使用外固定器的一种新的、更严格的保持关节僵硬的模型。部分动物在制动后1周内恢复正常。对关节软骨进行组织学和生化检查。固定6周后，与正常膝关节软骨相比，铸型关节和固定器固定关节的水分增加了7%，己糖醛酸分别减少了23%和28%。与刚性外固定器组相比，管型允许的有限运动导致了较小的蛋白多糖合成抑制和固定过程中较少的蛋白多糖丢失。有限活动的保护作用在恢复期表现明显：以己糖醛酸含量为指标，铸型关节软骨在治疗后1周内基本恢复，而外固定器组在治疗后1周内几乎没有恢复。与前人对铸型关节的研究不同，新合成的[35S]硫酸盐标记和从固定器固定的软骨中积累的未标记蛋白多糖都能够与外源透明质酸形成与对照软骨相同程度的复合体。因此，在固定的软骨中，新合成的蛋白多糖不能与透明质酸结合，这并不是蛋白多糖加速丢失的机制。蛋白多糖的加速周转似乎是由分泌的蛋白多糖合成减少和蛋白分解增加共同引起的。临床上，用于固定关节损伤的外固定器应在尽可能短的时间内使用，如果可能，应进行机械修改，以允许高达10度。联合运动。
Knees of mature dogs were immobilized for 6 weeks by long-leg casts allowing 8.degree.-15.degree. of motion, a model studied by others, or with external fixators, a new, more severe model that kept the joints rigid. Some animals were allowed to recover for 1 week after the immobilization period. Articular cartilage was examined histologically and biochemically. After 6 weeks of immobilization, water increased 7% in both casted and fixator-immobilized joints compared with normal knee cartilage, while hexturonic acid was 23 and 28% lower, respectively. The limited motion permitted by the casts resulted in a smaller depression of proteoglycan synthesis and less proteoglycan loss during immobilization than occurred in the rigid external fixator group. The protective effect of limited motion was shown clearly during th recovery period: as measured by hexuronic acid content, cartilage from the casted joints had almost recovered within 1 week, whereas the external fixator group experienced little or no recovery during the week after treatment. In contrast to previous studies by others with casted joint, both newly synthesized [35S]sulfate-labeled and accumulated unlabeled proteoglycans from both casted and fixator-immobilized cartilages were able to form complexes with exogenous hyaluronic acid to the same extent as those from control cartilage. Thus, in immobilized cartilage, failure of the newly synthesized proteoglycan to bind to hyaluronate is not a mechanism of accelerated proteoglycan loss. The accelerated proteoglycan turnover appears to be caused by a combination of decreased synthesis and increased proteolysis of the secreted proteoglycans. Clinically, external fixators used to immobilize joint injuries should be applied for the shortest time possible and if possible should be mechanically modified to allow up to 10.degree. of joint motion.