Structural basis of growth-related gain and age-related loss of bone strength.
Structural basis of growth-related gain and age-related loss of bone strength.
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DOI：
10.1093/rheumatology/ken177
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发表时间：
2008-07
期刊：
影响因子：
--
通讯作者：
Seeman E
中科院分区：
文献类型：
--
作者：
Seeman E
如果骨骼的强度是唯一的要求，它可以达到散装，但骨骼也必须是轻的。在生长过程中，骨骼建模和重塑通过将骨骼存放在需要的地方来优化强度，并通过将骨骼从不需要的地方移除来最小化质量。骨骼特征的群体差异在青春期之前就建立起来了，个体的骨骼大小和质量的位置在起源的百分位数中跟踪。较大的横截面具有相对较大的骨髓腔，这导致较低的体积骨密度(VBMD)，从而避免了肿块。因此，骨髓腔的挖掘可以最大限度地减少质量，并使皮质径向移动，增加硬度。通过挖掘较小的骨髓腔来组装较小的横截面，留下相对较厚的皮质，产生较高的vBMD，从而避免细长的脆弱性。骨膜和皮质内被膜周围细胞活动的变化形成了相邻横断面的不同形状。增龄与骨膜骨形成减少，每个基本多细胞单位(BMU)形成的骨体积减少，每个BMU持续吸收，以及绝经后高度重塑有关。青壮年的骨丢失有轻微的结构和生物力学后果，因为负的BMU平衡是由骨形成减少、重建缓慢以及骨膜对位继续径向移动变薄的皮质所驱动的。但绝经后，增加的重塑，恶化的负BMU平衡和骨膜位置的下降，加速皮质变薄和孔洞，骨小梁变薄和失去连接。未暴露于表面重塑的间质骨变得更致密矿化，骨细胞较少，胶原交联度较高，并积累微损伤。这些变化产生了导致骨骼脆性的材料和结构异常。
If bone strength was the only requirement of skeleton, it could be achieved with bulk, but bone must also be light. During growth, bone modelling and remodelling optimize strength, by depositing bone where it is needed, and minimize mass, by removing it from where it is not. The population variance in bone traits is established before puberty and the position of an individual's bone size and mass tracks in the percentile of origin. Larger cross-sections have a comparably larger marrow cavity, which results in a lower volumetric BMD (vBMD), thereby avoiding bulk. Excavation of a marrow cavity thus minimizes mass and shifts the cortex radially, increasing rigidity. Smaller cross-sections are assembled by excavating a smaller marrow cavity leaving a relatively thicker cortex producing a higher vBMD, avoiding the fragility of slenderness. Variation in cellular activity around the periosteal and endocortical envelopes fashions the diverse shapes of adjacent cross-sections. Advancing age is associated with a decline in periosteal bone formation, a decline in the volume of bone formed by each basic multicellular unit (BMU), continued resorption by each BMU, and high remodelling after menopause. Bone loss in young adulthood has modest structural and biomechanical consequences because the negative BMU balance is driven by reduced bone formation, remodelling is slow and periosteal apposition continues shifting the thinned cortex radially. But after the menopause, increased remodelling, worsening negative BMU balance and a decline in periosteal apposition accelerate cortical thinning and porosity, trabecular thinning and loss of connectivity. Interstitial bone, unexposed to surface remodelling becomes more densely mineralized, has few osteocytes and greater collagen cross-linking, and accumulates microdamage. These changes produce the material and structural abnormalities responsible for bone fragility.
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影响因子：
4.1
作者：
Duan, YB;Wang, XF;Seeman, E
通讯作者：
Seeman, E
影响因子：
158.5
作者：
GILSANZ, V;ROE, TF;GOODMAN, WG
通讯作者：
GOODMAN, WG
影响因子：
6.2
作者：
Bliziotes, M;Sibonga, JD;Orwoll, E
通讯作者：
Orwoll, E
影响因子：
2.4
作者：
CURREY, JD
通讯作者：
CURREY, JD
影响因子：
4.1
作者：
Ciarelli, TE;Fyhrie, DP;Parfitt, AM
通讯作者：
Parfitt, AM