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神经源性加速退行性关节病变

Neurogenic acceleration of degenerative joint lesions.

作者信息

O'Connor B L, Palmoski M J, Brandt K D

出版信息

J Bone Joint Surg Am. 1985 Apr;67(4):562-72.

PMID:3980502
Abstract

A severe form of degenerative joint lesion (neuropathic arthropathy) is known to complicate a variety of diseases that are associated with sensory abnormalities. We studied the relationship between sensory deficits and the development of degenerative joint lesions in dogs in two complementary experiments. In Experiment 1, dogs that were subjected to unilateral dorsal-root ganglionectomy (fourth lumbar to first sacral vertebra) failed to show biochemical, gross, or histological evidence of degenerative joint lesions in ipsilateral femoral condylar cartilage after sixteen months. In Experiment 2, five of six dogs that were subjected to transection of the anterior cruciate ligament two weeks after deafferentation of the ipsilateral limb showed striking gross or histological lesions, or both, of the femoral condylar cartilage three weeks after ligament transection (five weeks after ganglionectomy). We concluded that the neuromuscular mechanisms that protect normal joints from damage are inadequate to protect unstable joints from becoming rapidly and severely damaged.

摘要

一种严重的退行性关节病变(神经性关节病)已知会使各种与感觉异常相关的疾病复杂化。我们在两个互补实验中研究了犬类感觉缺陷与退行性关节病变发展之间的关系。在实验1中,接受单侧背根神经节切除术(第四腰椎至第一骶椎)的犬在16个月后,同侧股骨髁软骨未出现退行性关节病变的生化、大体或组织学证据。在实验2中,六只犬中有五只在同侧肢体去传入神经两周后进行前交叉韧带横断,在韧带横断三周后(神经节切除术后五周),股骨髁软骨出现明显的大体或组织学病变,或两者皆有。我们得出结论,保护正常关节免受损伤的神经肌肉机制不足以保护不稳定关节免受快速和严重的损伤。

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