Dechant J J, Mooney M P, Cooper G M, Smith T D, Burrows A M, Losken H W, Mathijssen I M, Siegel M I
Department of Anthropology, School of Nursing, University of Pittsburgh, PA 15261, USA.
J Craniofac Genet Dev Biol. 1999 Apr-Jun;19(2):64-74.
It has been suggested that craniosynostosis is caused by abnormally located ossification centers (i.e., bony tubers) in the developing skull prior to suture formation [Mathijssen et al., 1996, 1997]. The present study was designed to test this hypothesis in a rabbit model of human familial, nonsyndromic coronal suture (CS) synostosis. Calvariae were taken from 99 New Zealand White rabbit perinates (55 normal controls, 15 with delayed-onset CS synostosis, and 29 with bilateral or unilateral CS synostosis), ranging in age from 23 to 34 days postconception (synostosis occurs at approximately 23 days in this model). Frontoparietal, interfrontal, and interparietal ossification center distances were obtained using a Wild microscope with camera lucida attachment and a 2-D computer digitization technique. Linear regression analysis was used to compare age-related changes in the perinatal ossification centers among groups. Results revealed that frontoparietal ossification center regression line slopes had similar start points (24-day intercepts) with significantly (P < 0.05) diverging slopes over time. Normal and delayed-onset ossification center distance increased more rapidly than in synostosed perinates. No significant (P > 0.05) differences were noted in regression line slopes among groups for interparietal or interfrontal ossification center distances. Results demonstrated that, in synostosed perinates, frontoparietal ossification center location was similar to normals around the time of synostosis and became displaced later. These findings suggest that ossification center (i.e., bony tuber) displacement seen in infants with craniosynostosis is probably a secondary and compensatory, postsynostotic change and not a primary causal factor of synostosis in this rabbit model.
有人提出，颅缝早闭是由于在缝线形成之前发育中的颅骨内骨化中心（即骨结节）位置异常所致[Mathijssen等人，1996年，1997年]。本研究旨在在人类家族性、非综合征性冠状缝（CS）早闭的兔模型中验证这一假设。从99只新西兰白兔围产期仔兔（55只正常对照，15只迟发性CS早闭，29只双侧或单侧CS早闭）获取颅骨，其受孕后年龄在23至34天之间（在此模型中，早闭约在23天发生）。使用配备明视野显微镜附件的Wild显微镜和二维计算机数字化技术测量额顶、额间和顶间骨化中心距离。采用线性回归分析比较各组围产期骨化中心与年龄相关的变化。结果显示，额顶骨化中心回归线斜率起始点相似（24天截距），但随着时间推移斜率有显著差异（P<0.05）。正常和迟发性骨化中心距离的增加速度比早闭仔兔更快。顶间或额间骨化中心距离的回归线斜率在各组之间未观察到显著差异（P>0.05）。结果表明，在早闭仔兔中，额顶骨化中心位置在早闭时与正常仔兔相似，之后发生移位。这些发现表明，在颅缝早闭婴儿中所见的骨化中心（即骨结节）移位可能是一种继发性和代偿性的早闭后变化，而不是该兔模型中早闭的主要病因。
