The Dysplastic Hip Joint: Its Radiographic and Histologic Development1
The Dysplastic Hip Joint: Its Radiographic and Histologic Development1
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发育不良的髋关节：其放射学和组织学发展1
DOI：
10.1111/j.1740-8261.1973.tb00655.x
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发表时间：
1973
影响因子：
1.7
通讯作者：
W. Riser
中科院分区：
文献类型：
--
作者：
W. Riser
犬髋关节发育不良仍然是一个复杂而重要的问题，无论是狗的幻想和兽医专业。关于病因、遗传性、治疗和控制的理论差别很大。髋关节发育不良的发病机制是本研究的主题。髋关节发育不良是不是很清楚。然而，为了使本报告有意义，一些似乎有效的意见已被接受。“现有证据的平衡表明，先天性髋关节脱位的遗传易感性是真实的，并且涉及多个基因。环境因素也很重要，大概是根据个人的遗传易感性（15）。到目前为止，很少有基因主要影响骨骼。骨的变化仅仅反映了软骨中发生的变化，支持结缔组织和肌肉（2）。髋关节发育不良是生物力学疾病的一个例子，代表了原发性肌肉质量和不成比例的快速骨骼生长之间的差异。髋关节发育不良开始与正常髋关节在出生时（6，12，17）。肌肉的滞后或失败，以与骨骼相同的速度发育和达到功能成熟，导致关节不稳定（3）。当髋臼和股骨头拉开并引发一系列事件时，会诱发异常发育，最终导致髋关节发育不良和退行性关节疾病（16）。有力的证据表明，髋关节发育不良的骨性变化是因为软组织没有足够的强度来维持股骨头和髋臼关节面之间的一致性（3）。本研究遵循前面的推理路线，描述了导致髋关节发育不良的影像学和解剖病理学变化。本质上，这种疾病的发病顺序，因为它自发发生，并记录在本文中是一个实验的性质和正常髋关节的发展的描述作为对照（11）。
Canine hip dysplasia continues to be a complex and important problem to both the dog fancy and the veterinary profession. Theories regarding cause, heritability, treatment and control vary widely. The pathogenesis of hip dysplasia is the subject of this study. Hip dysplasia is not well understood. To make this report meaningful, however, a number of observations that seem valid have been accepted. “The balance of the present evidence shows that a genetic predisposition to congenital dislocation of the hip is real, and that multiple genes are involved. Environmental factors also are important, presumably according to the genetic susceptibility of the individual’’ (15). Few genes so far analyzed affect the osseous skeleton primarily. The changes in bone merely reflect changes that occur in the cartilage, supporting connective tissue and muscles (2). Hip dysplasia is an example of a biomechanical disease representing a disparity between primary muscle mass and disproportionately rapid skeletal growth. Hip dysplasia begins with a normal hip at birth (6, 12, 17). The lag or failure of the muscle to develop and reach functional maturity at the same rate as the skeleton results in joint instability ( 3 ) . Abnormal development is induced when the acetabulum and femoral head pull apart and trigger a series of events that end in hip dysplasia and degenerative joint disease (16). The evidence is strong that the bony changes of hip dysplasia occur because the soft tissues do not have sufficient strength to maintain congruity between the articular surfaces of the femoral head and the acetabulum ( 3 ) . This study follows the preceding line of reasoning and is a description of the radiographic and anatomicopathological changes that bring about hip dysplasia. In essence the pathogenic sequence of this disease as it occurs spontaneously and recorded in this paper is an experiment done by nature and the description of the development of the normal hip serves as the control (11).