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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Does bone resorption stimulate periosteal expansion? A cross-sectional analysis of β-C-telopeptides of type i collagen (CTX), genetic markers of the RANKL pathway, and periosteal circumference as measured by pQCT
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Does bone resorption stimulate periosteal expansion? A cross-sectional analysis of β-C-telopeptides of type i collagen (CTX), genetic markers of the RANKL pathway, and periosteal circumference as measured by pQCT

机译：骨吸收会刺激骨膜扩张吗？用pQCT测量的i型胶原蛋白（CTX）的β-C端肽（CTX），RANKL通路的遗传标记和骨膜周长的横断面分析

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We hypothesized that bone resorption acts to increase bone strength through stimulation of periosteal expansion. Hence, we examined whether bone resorption, as reflected by serum β-C-telopeptides of type I collagen (CTX), is positively associated with periosteal circumference (PC), in contrast to inverse associations with parameters related to bone remodeling such as cortical bone mineral density (BMDC). CTX and mid-tibial peripheral quantitative computed tomography (pQCT) scans were available in 1130 adolescents (mean age 15.5 years) from the Avon Longitudinal Study of Parents and Children (ALSPAC). Analyses were adjusted for age, gender, time of sampling, tanner stage, lean mass, fat mass, and height. CTX was positively related to PC (β = 0.19 [0.13, 0.24]) (coefficient = SD change per SD increase in CTX, 95% confidence interval)] but inversely associated with BMDC (β = -0.46 [-0.52,-0.40]) and cortical thickness [β = -0.11 (-0.18, -0.03)]. CTX was positively related to bone strength as reflected by the strength-strain index (SSI) (β = 0.09 [0.03, 0.14]). To examine the causal nature of this relationship, we then analyzed whether single-nucleotide polymorphisms (SNPs) within key osteoclast regulatory genes, known to reduce areal/cortical BMD, conversely increase PC. Fifteen such genetic variants within or proximal to genes encoding receptor activator of NF-κB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were identified by literature search. Six of the 15 alleles that were inversely related to BMD were positively related to CTX (p 0.05 cut-off) (n = 2379). Subsequently, we performed a meta-analysis of associations between these SNPs and PC in ALSPAC (n = 3382), Gothenburg Osteoporosis and Obesity Determinants (GOOD) (n = 938), and the Young Finns Study (YFS) (n = 1558). Five of the 15 alleles that were inversely related to BMD were positively related to PC (p 0.05 cut-off). We conclude that despite having lower BMD, individuals with a genetic predisposition to higher bone resorption have greater bone size, suggesting that higher bone resorption is permissive for greater periosteal expansion.
机译：我们假设骨吸收通过刺激骨膜扩张来增加骨强度。因此，我们检查了由I型胶原的血清β-C-端肽（CTX）反映的骨吸收与骨膜周长（PC）是否正相关，而与与骨重塑有关的参数（例如皮质骨）的反向关联却相反矿物质密度（BMDC）。雅芳父母和儿童纵向研究（ALSPAC）的1130名青少年（平均年龄15.5岁）可以进行CTX和胫骨中部外周定量计算机断层扫描（pQCT）扫描。调整分析的年龄，性别，采样时间，鞣制阶段，瘦肉质量，脂肪质量和身高。 CTX与PC呈正相关（β= 0.19 [0.13，0.24]）（系数= CTX每SD增加的SD变化，置信区间为95％），但与BMDC呈负相关（β= -0.46 [-0.52，-0.40] ）和皮层厚度[β= -0.11（-0.18，-0.03）]。 CTX与骨骼强度呈正相关，如强度-应变指数（SSI）所反映（β= 0.09 [0.03，0.14]）。为了检查这种关系的因果性质，我们然后分析了关键破骨细胞调节基因（已知会减少区域/皮质BMD）中的单核苷酸多态性（SNP）是否反过来增加了PC。通过文献检索鉴定了在NF-κB（RANK），RANK配体（RANKL）和骨保护素（OPG）受体激活因子的基因内或附近的15种此类遗传变异。与BMD负相关的15个等位基因中有6个与CTX正相关（p <0.05截止）（n = 2379）。随后，我们对ALSPAC（n = 3382），哥德堡骨质疏松症和肥胖决定因素（GOOD）（n = 938）和年轻芬兰人研究（YFS）（n = 1558）中这些SNP与PC之间的关联进行了荟萃分析。 。与BMD负相关的15个等位基因中有5个与PC正相关（p <0.05截止）。我们得出的结论是，尽管BMD较低，但具有较高骨吸收基因遗传倾向的个体具有较大的骨大小，这表明较高的骨吸收是允许更大的骨膜扩张的原因。

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