Division of Plastic and Reconstructive Surgery, Department of Surgery, Medical University Vienna, Vienna, Austria.
Department of Plastic, Reconstructive, and Aesthetic Surgery, Medical University of Innsbruck, Innsbruck, Austria.
J Bone Miner Res. 2017 Dec;32(12):2381-2393. doi: 10.1002/jbmr.3211. Epub 2017 Nov 9.
Severe burn injury triggers massive alterations in stress hormone levels with a dose-dependent hypermetabolic status including increased bone resorption. This study evaluated bone microarchitecture measured by noninvasive high-resolution peripheral quantitative computed tomography (HR-pQCT). Changes of serum bone turnover markers (BTM) as well as regulators of bone signaling pathways involved in skeletal health were assessed. Standardized effect sizes as a quantitative measure regarding the impact of serum changes and the prediction of these changes on bone microarchitecture were investigated. In total, 32 male patients with a severe burn injury (median total body surface area [TBSA], 40.5%; median age 40.5 years) and 28 matched male controls (median age 38.3 years) over a period of 24 months were included. In patients who had sustained a thermal injury, trabecular and cortical bone microstructure showed a continuous decline, whereas cortical porosity (Ct.Po) and pore volume increased. Initially, elevated levels of BTM and C-reactive protein (CRP) continuously decreased over time but remained elevated. In contrast, levels of soluble receptor activator of NF-κB ligand (sRANKL) increased over time. Osteocalcin, bone-specific alkaline phosphatase (BALP), intact N-terminal type 1 procollagen propeptide (P1NP), and cross-linked C-telopeptide (CTX) acutely reflected the increase of Ct.Po at the radius (R = 0.41), followed by the reduction of trabecular thickness at the tibia (R = 0.28). In adult male patients, early and sustained changes of markers of bone resorption, formation and regulators of bone signaling pathways, prolonged inflammatory cytokine activities in conjunction with muscle catabolism, and vitamin D insufficiency were observed. These alterations are directly linked to a prolonged deterioration of bone microstructure. The probably increased risk of fragility fractures should be of clinical concern and subject to future interventional studies with bone-protective agents. © 2017 American Society for Bone and Mineral Research.
严重烧伤会引发应激激素水平的剧烈变化,导致代谢亢进状态,包括骨吸收增加。本研究通过非侵入性高分辨率外周定量 CT(HR-pQCT)评估了骨微结构。评估了血清骨转换标志物(BTM)的变化以及参与骨骼健康的骨信号通路调节剂。研究了标准化效应大小,作为评估血清变化影响和这些变化对骨微结构预测的定量指标。共纳入 32 名男性严重烧伤患者(中位总体表面积 [TBSA],40.5%;中位年龄 40.5 岁)和 28 名匹配的男性对照者(中位年龄 38.3 岁),随访时间为 24 个月。在发生热损伤的患者中,小梁和皮质骨微结构呈持续下降趋势,而皮质孔隙率(Ct.Po)和孔体积增加。最初,BTM 和 C 反应蛋白(CRP)水平升高持续下降,但仍处于较高水平。相反,可溶性核因子 κB 配体受体激活剂(sRANKL)水平随时间升高。骨钙素、骨碱性磷酸酶(BALP)、完整 N 端 1 型原胶原脯氨酸肽(P1NP)和交联 C 端肽(CTX)在桡骨(R=0.41)上急性反映 Ct.Po 的增加,随后胫骨(R=0.28)上的小梁厚度减少。在成年男性患者中,观察到骨吸收、形成标志物和骨信号通路调节剂的早期和持续变化、延长的炎症细胞因子活性伴肌肉分解代谢和维生素 D 不足。这些改变与骨微结构的持续恶化直接相关。骨折风险增加可能需要临床关注,并进行未来具有骨保护作用的药物的干预研究。2017 年美国骨骼与矿物质研究协会。