今年夏天你得到足夠的日照了嗎?據(jù)一項新的研究報告，維生素 D 缺乏可能會加快人骨骼的老化,，而這又會增加發(fā)生骨折的風險,。
這些研究發(fā)現(xiàn)表明，缺乏該“日照維生素”不僅會降低骨密度,，而且還會影響骨骼的質量,。維生素 D 是鈣質吸收及其被骨骼攝取所必不可少的。沒有鈣,，骨骼無法礦質化或進行重建并變得更加強固,。缺乏維生素 D 的人有罹患多種疾病的風險，其中包括骨質疏松,。
來自德國漢堡大學醫(yī)學中心的研究人員對采自 30 名參與者(他們中有一半缺乏維生素 D )的骨骼樣本進行了分析,。他們采用了最先進的技術——其中包括基于同步輻射的微計算機斷層掃描——在最小尺度來描述從納米到微米的骨骼質量,。研究人員能夠在一系列的測試中實時追蹤骨骼開裂的進展并檢測了發(fā)生開裂的阻力。正如所預期的,，他們發(fā)現(xiàn)維生素 D 缺乏的受試者在其骨骼的表面有著較少的礦質化,。但在骨表面以下的骨骼實際上有著更多的礦質化。它還顯示了較老的及較脆的骨骼的結構特點,。
研究人員注意到,，這些礦質化骨島被一個膠原性邊界所包圍，而這會阻止它們被適當?shù)馗慕?。在被切斷了破骨細?mdash;—這些細胞在正常情況下會對骨骼進行改建——的供應時,，這些礦質化骨的孤立部分開始老化，而整體的骨骼礦質化則會因為鈣的缺乏而減少,。
研究人員表示,，在維生素 D 缺乏時會出現(xiàn)老化骨骼區(qū)域、骨骼質量降低并導致骨折風險增高,。闡明人類骨骼結構的復雜性可能會讓人們對防止或治療骨折的更有效的方法有所了解,。一則相關的《焦點》文章對這些結果進行了討論。（生物谷Bioon.com）
生物谷推薦英文摘要：
Science doi: 10.1126/scitranslmed.3006286
Vitamin D Deficiency Induces Early Signs of Aging in Human Bone, Increasing the Risk of Fracture
Bjorn Busse,Hrishikesh A. Bale,Elizabeth A. Zimmermann1,Brian Panganiban,Holly D. Barth
Vitamin D deficiency is a widespread medical condition that plays a major role in human bone health. Fracture susceptibility in the context of low vitamin D has been primarily associated with defective mineralization of collagenous matrix (osteoid). However, bone’s fracture resistance is due to toughening mechanisms at various hierarchical levels ranging from the nano- to the microstructure. Thus, we hypothesize that the increase in fracture risk with vitamin D deficiency may be triggered by numerous pathological changes and may not solely derive from the absence of mineralized bone. We found that the characteristic increase in osteoid-covered surfaces in vitamin D–deficient bone hampers remodeling of the remaining mineralized bone tissue. Using spatially resolved synchrotron bone mineral density distribution analyses and spectroscopic techniques, we observed that the bone tissue within the osteoid frame has a higher mineral content with mature collagen and mineral constituents, which are characteristic of aged tissue. In situ fracture mechanics measurements and synchrotron radiation micro–computed tomography of the crack path indicated that vitamin D deficiency increases both the initiation and propagation of cracks by 22 to 31%. Thus, vitamin D deficiency is not simply associated with diminished bone mass. Our analyses reveal the aged nature of the remaining mineralized bone and its greatly decreased fracture resistance. Through a combination of characterization techniques spanning multiple size scales, our study expands the current clinical understanding of the pathophysiology of vitamin D deficiency and helps explain why well-balanced vitamin D levels are essential to maintain bone’s structural integrity.
