Childhood fractures are associated with decreased bone mass gain during puberty: An early marker of persistent bone fragility?
Childhood fractures are associated with decreased bone mass gain during puberty: An early marker of persistent bone fragility?
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DOI：
10.1359/jbmr.051215
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发表时间：
2006-04-01
影响因子：
6.2
通讯作者：
Rizzoli, R
中科院分区：
文献类型：
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作者：
Ferrari, SL;Chevalley, T;Rizzoli, R
骨折儿童的峰值骨量是否较低仍不确定。在对125名女孩进行8.5年随访的队列中，42名受试者报告了58例骨折。其中，多个部位的BMC增加和青春期成熟时的椎骨尺寸显著降低。因此，儿童骨折可能是低峰值骨量收购和持续的骨骼fragmental.Introduction：骨折在童年可能会导致从快速纵向增长过程中的骨量积累赤字的标志。无论是低骨量持续超过这一时期，但仍然unknowed.Materials和方法：BMC在脊柱，桡骨，髋关节，股骨骨干进行了前瞻性测量超过8.5年，125名女孩使用DXA。使用非参数检验分析了骨折和未骨折女孩之间骨量和大小的差异。结果：125名女童中有42例发生58处骨折（累积发生率46.4%），占前臂和腕部骨折的一半。有骨折和没有骨折的女孩年龄，身高，体重相似。和钙摄入量。在青春期前和青春期早期，骨折组桡骨干的BMC和宽度低于非骨折组（p < 0.05），而aBMD和BMAD在两组中相似。在青春期成熟时（坦纳5期，平均年龄+/- SD，16.4 +/- 0.5岁），桡骨超远端的BMC（UD Rad.），骨折女孩的股骨粗隆、腰椎（LS）和LS投影骨面积均显著降低。在整个青春期，骨折组这些部位的BMC增加也减少（LS，-8.0%，p = 0.015; UD Rad.，-12.0%，p = 0.004;转子，-8.4%，p = 0.05 vs无骨折）。青春期前与青春期成熟之间BMC高度相关（R = 0.54-0.81）。成年女儿与母亲的关系（R = 0.32-0.46）。钙的摄入量与骨折risk.Conclusions：骨折的女孩在达到青春期成熟时，在轴向和approximular骨骼中的骨量增加减少，椎骨的大小减少。结合BMC的跟踪和遗传性证据，这些观察结果表明，儿童骨折可能是低峰值骨量和持续骨脆性的标志。
Whether peak bone mass is low among children with fractures remains uncertain. In a cohort of 125 girls followed over 8.5 years, 42 subjects reported 58 fractures. Among those, BMC gain at multiple sites and vertebral bone size at pubertal maturity were significantly decreased. Hence, childhood fractures may be markers of low peak bone mass acquisition and persistent skeletal fragility.Introduction: Fractures in childhood may result from a deficit in bone mass accrual during rapid longitudinal growth. Whether low bone mass persists beyond this period however remains unknown.Materials and Methods: BMC at the spine, radius, hip, and femur diaphysis was prospectively measured over 8.5 years in 125 girls using DXA. Differences in bone mass and size between girls with and without fractures were analyzed using nonparametric tests. The contribution of genetic factors was evaluated by mother-daughter correlations and that of calcium intake by Cox proportional hazard models.Results: Fifty-eight fractures Occurred in 42 among 125 girls (cumulative incidence, 46.4%), one-half of all fractures affecting the forearm and wrist. Girls with and without fractures had similar age, height, weight. and calcium intake at all time-points. Before and during early puberty, BMC and width of the radius diaphysis was lower in the fracture compared with no-fracture group (p < 0.05), whereas aBMD and BMAD were similar in the two groups. At pubertal maturity (Tanner's stage 5, mean age +/- SD, 16.4 +/- 0.5 years), BMC at the ultradistal radius (UD Rad.), femur trochanter, and lumbar spine (LS), and LS projected bone area were all significantly lower in girls with fractures. Throughout puberty, BMC gain at these sites was also decreased in the fracture group (LS, -8.0%, p = 0.015; UD Rad., -12.0%,p = 0.004; trochanter, -8.4%,p = 0.05 versus no fractures). BMC was highly correlated between prepuberty and pubertal maturity (R = 0.54-0.81.) and between mature daughters and their mothers (R = 0.32-0.46). Calcium intake was not related to fracture risk.Conclusions: Girls with fractures have decreased bone mass gain in the axial and appendicular skeleton and reduced vertebral bone size when reaching pubertal Maturity. Taken together with the evidence of tracking and heritability for BMC, these observations indicate that childhood fractures may be markers for low peak bone mass and persistent bone fragility.