Musculoskeletal Quantitative Imaging Research Group, Department of Radiology & Biomedical Imaging, University of California San Francisco, San Francisco, CA, United States.
Department of Rheumatology and Clinical Immunology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Front Endocrinol (Lausanne). 2021 Mar 16;12:599316. doi: 10.3389/fendo.2021.599316. eCollection 2021.
Diabetic bone disease is characterized by an increased fracture risk which may be partly attributed to deficits in cortical bone quality such as higher cortical porosity. However, the temporal evolution of bone microarchitecture, strength, and particularly of cortical porosity in diabetic bone disease is still unknown. Here, we aimed to prospectively characterize the 5-year changes in bone microarchitecture, strength, and cortical porosity in type 2 diabetic (T2D) postmenopausal women with (DMFx) and without history of fragility fractures (DM) and to compare those to nondiabetic fracture free controls (Co) using high resolution peripheral quantitative computed tomography (HR-pQCT).
Thirty-two women underwent baseline HR-pQCT scanning of the ultradistal tibia and radius and a FU-scan 5 years later. Bone microarchitectural parameters, including cortical porosity, and bone strength estimates µFEA were calculated for each timepoint and annualized. Linear regression models (adjusted for race and change in BMI) were used to compare the annualized percent changes in microarchitectural parameters between groups.
At baseline at the tibia, DMFx subjects exhibited the highest porosity of the three groups (66.3% greater Ct.Po, 71.9% higher Ct.Po.Volume than DM subjects, p < 0.022). Longitudinally, porosity increased significantly over time in all three groups and at similar annual rates, while DMFx exhibited the greatest annual decreases in bone strength indices (compared to DM 4.7× and 6.7× greater decreases in failure load [F] and stiffness [K], p < 0.025; compared to Co 14.1× and 22.2× greater decreases in F and K, p < 0.020).
Our data suggest that despite different baseline levels in cortical porosity, T2D women with and without fractures experienced long-term porosity increases at a rate similar to non-diabetics. However, the annual loss in bone strength was greatest in T2D women with a history of a fragility fractures. This suggests a potentially non-linear course of cortical porosity development in T2D bone disease: major porosity may develop early in the course of disease, followed by a smaller steady annual increase in porosity which in turn can still have a detrimental effect on bone strength-depending on the amount of early cortical pre-damage.
糖尿病性骨病的特征是骨折风险增加，这可能部分归因于皮质骨质量的缺陷，如更高的皮质孔隙率。然而，糖尿病性骨病中骨微结构、强度，特别是皮质孔隙率的时间演变仍然未知。在这里，我们旨在前瞻性地描述 2 型糖尿病（T2D）绝经后女性（DMFx）和无脆性骨折史（DM）的 5 年骨微结构、强度和皮质孔隙率变化，并使用高分辨率外周定量 CT（HR-pQCT）将其与非糖尿病无骨折对照组（Co）进行比较。
32 名女性接受了超远端胫骨和桡骨的基线 HR-pQCT 扫描，并在 5 年后进行了 FU 扫描。计算了每个时间点和年化的骨微结构参数，包括皮质孔隙率和骨强度估计 µFEA。使用线性回归模型（调整种族和 BMI 变化）比较了组间微结构参数的年化百分比变化。
在基线时，DMFx 组的胫骨皮质孔隙率最高（比 DM 组高 66.3%，比 DM 组高 71.9%，p<0.022）。纵向来看，所有三组的孔隙率随着时间的推移都显著增加，且增加速度相似，而 DMFx 组的骨强度指标的年化下降最大（与 DM 组相比，失效负荷[F]和刚度[K]分别下降 4.7 倍和 6.7 倍，p<0.025；与 Co 组相比，F 和 K 分别下降 14.1 倍和 22.2 倍，p<0.020）。
我们的数据表明，尽管皮质孔隙率的基线水平不同，但有和无骨折的 T2D 女性在类似的速率下经历了长期的孔隙率增加。然而，在有脆性骨折史的 T2D 女性中，骨强度的年损失最大。这表明 T2D 骨病中皮质孔隙率的发展可能是非线性的：主要的孔隙率可能在疾病早期发展，随后是较小的稳定的年增长率，而这仍然会对骨强度产生不利影响，具体取决于早期皮质的预损伤量。
