Seeman E, Karlsson M K, Duan Y
Department of Medicine, Austin and Repatriation Medical Center, University of Melbourne, Australia.
J Bone Miner Res. 2000 Nov;15(11):2259-65. doi: 10.1359/jbmr.2000.15.11.2259.
Skeletal development is heterogeneous. Throughout growth, bone size is more maturationally advanced than the mineral being accrued within its periosteal envelope; before puberty, appendicular growth is more rapid than axial growth; during puberty, appendicular growth slows and axial growth accelerates. We studied women with differing age of onset of anorexia nervosa to determine whether this temporal heterogeneity in growth predisposed to the development of deficits in bone size and volumetric bone mineral density (vBMD), which varied by site and severity depending on the age at which anorexia nervosa occurred. Bone size and vBMD of the third lumbar vertebra and femoral neck were measured using dual-energy X-ray absorptiometry in 210 women aged 21 years (range, 12-40 years) with anorexia nervosa. Results were expressed as age-specific SDs (mean +/- SEM). Bone width depended on the age of onset of anorexia nervosa; when the onset of anorexia nervosa occurred (1) before 15 years of age, deficits in vertebral body and femoral neck width did not differ (-0.77+/-0.27 SD and -0.55+/-0.17 SD, respectively); (2) between 15 and 19 years of age, deficits in vertebral body width (-0.95+/-0.16 SD) were three times the deficits in femoral neck width (-0.28+/-0.14 SD; p < 0.05 comparing the deficits), (3) after 19 years of age, deficits in the vertebral body width (-0.49+/-0.26 SD; p = 0.05) were half that in women with earlier onset of anorexia nervosa. No deficit in bone width was observed at the femoral neck. Deficits in vBMD at the vertebra and femoral neck were independent of the age of onset of anorexia nervosa but increased as the duration of anorexia nervosa increased, being about 0.5 SD lower at the vertebra than femoral neck. We infer that the maturational development of a region at the time of exposure to disease, and disease duration, determine the site, magnitude, and type of trait deficit in anorexia nervosa. Bone fragility due to reduced bone size and reduced vBMD in adulthood is partly established during growth.
骨骼发育是不均一的。在整个生长过程中,骨骼大小比其骨膜包绕内所积累的矿物质在成熟度上更为超前;青春期前,四肢生长比轴向生长更快;青春期期间,四肢生长减缓而轴向生长加速。我们研究了神经性厌食症发病年龄不同的女性,以确定生长过程中的这种时间异质性是否易导致骨骼大小和骨体积密度(vBMD)的缺陷,这些缺陷因部位和严重程度而异,具体取决于神经性厌食症发生的年龄。使用双能X线吸收法测量了210名年龄在21岁(范围为12 - 40岁)的神经性厌食症女性第三腰椎和股骨颈的骨骼大小及vBMD。结果以年龄特异性标准差(均值±标准误)表示。骨宽度取决于神经性厌食症的发病年龄;当神经性厌食症发病时:(1)在15岁之前,椎体和股骨颈宽度的缺陷无差异(分别为 - 0.77±0.27标准差和 - 0.55±0.17标准差);(2)在15至19岁之间,椎体宽度的缺陷( - 0.95±0.16标准差)是股骨颈宽度缺陷( - 0.28±0.14标准差)的三倍(比较缺陷时p < 0.05);(3)在19岁之后,椎体宽度的缺陷( - 0.49±0.26标准差;p = 0.05)是神经性厌食症发病较早女性的一半。股骨颈未观察到骨宽度缺陷。椎体和股骨颈的vBMD缺陷与神经性厌食症的发病年龄无关,但随着神经性厌食症持续时间的增加而增加,椎体处比股骨颈处低约0.5标准差。我们推断,患病时一个区域的成熟发育以及疾病持续时间决定了神经性厌食症性状缺陷的部位、程度和类型。成年期因骨骼大小减小和vBMD降低导致的骨脆性在生长过程中部分就已形成。