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神经肌肉疾病导致胎儿活动受限引起的长骨变化。一项影像学和组织学研究。

Changes in the long bones due to fetal immobility caused by neuromuscular disease. A radiographic and histological study.

作者信息

Rodríguez J I, Garcia-Alix A, Palacios J, Paniagua R

机构信息

Department of Pathology, Hospital La Paz, Madrid, Spain.

出版信息

J Bone Joint Surg Am. 1988 Aug;70(7):1052-60.

PMID:3403574
Abstract

The long bones in eleven newborn infants who had neuromuscular disease were studied and were found to be thin, hypomineralized, and elongated. In most of the bones, there were multiple diaphyseal or metaphyseal fractures, or both. By light microscopy, the outstanding findings were fractures through the growth plate and diaphysis and thinning of the cortices. The etiology of the fractures and the insufficient substance of the bone is the reduction in the intrauterine motion of the fetus, which leads to fragility of the bones and contractures of the joints. The severity of the alterations may have been related to the time of the onset of the abnormalities and to the duration and degree of the intrauterine akinesia.

摘要

对11名患有神经肌肉疾病的新生儿的长骨进行了研究,发现这些长骨细、矿化不足且拉长。在大多数骨骼中,存在多处骨干或干骺端骨折,或两者皆有。通过光学显微镜观察,突出的发现是穿过生长板和骨干的骨折以及皮质变薄。骨折和骨质不足的病因是胎儿宫内活动减少,这导致骨骼脆弱和关节挛缩。改变的严重程度可能与异常开始的时间以及宫内运动不能的持续时间和程度有关。

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J Bone Joint Surg Am. 1988 Aug;70(7):1052-60.
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