Department of Clinical-Surgical, Diagnostic and Pediatric Sciences, University of Pavia, Pavia, Italy.
Department of Health Sciences, University of Piemonte Orientale, Novara, Italy.
Front Endocrinol (Lausanne). 2022 Jul 7;13:921353. doi: 10.3389/fendo.2022.921353. eCollection 2022.
Obesity is a global health challenge that warrants effective treatments to avoid its multiple comorbidities. Bariatric surgery, a cornerstone treatment to control bodyweight excess and relieve the health-related burdens of obesity, can promote accelerated bone loss and affect skeletal strength, particularly after malabsorptive and mixed surgical procedures, and probably after restrictive surgeries. The increase in bone resorption markers occurs early and persist for up to 12 months or longer after bariatric surgery, while bone formation markers increase but to a lesser extent, suggesting a potential uncoupling process between resorption and formation. The skeletal response to bariatric surgery, as investigated by dual-energy X-ray absorptiometry (DXA), has shown significant loss in bone mineral density (BMD) at the hip with less consistent results for the lumbar spine. Supporting DXA studies, analyses by high-resolution peripheral quantitative computed tomography (HR-pQCT) showed lower cortical density and thickness, higher cortical porosity, and lower trabecular density and number for up to 5 years after bariatric surgery. These alterations translate into an increased risk of fall injury, which contributes to increase the fracture risk in patients who have been subjected to bariatric surgery procedures. As bone deterioration continues for years following bariatric surgery, the fracture risk does not seem to be dependent on acute weight loss but, rather, is a chronic condition with an increasing impact over time. Among the post-bariatric surgery mechanisms that have been claimed to act globally on bone health, there is evidence that micro- and macro-nutrient malabsorptive factors, mechanical unloading and changes in molecules partaking in the crosstalk between adipose tissue, bone and muscle may play a determining role. Given these circumstances, it is conceivable that bone health should be adequately investigated in candidates to bariatric surgery through bone-specific work-up and dedicated postsurgical follow-up. Specific protocols of nutrients supplementation, motor activity, structured rehabilitative programs and, when needed, targeted therapeutic strategies should be deemed as an integral part of post-bariatric surgery clinical support.
肥胖是一个全球性的健康挑战,需要有效的治疗方法来避免其多种合并症。减重手术是控制体重过度和缓解肥胖相关健康负担的基石治疗方法,可以促进骨丢失加速,并影响骨骼强度,特别是在吸收不良和混合手术之后,可能在限制手术后也是如此。骨吸收标志物的增加发生较早,并在减重手术后长达 12 个月或更长时间持续存在,而骨形成标志物增加,但程度较小,表明骨吸收和形成之间可能存在潜在的解偶联过程。双能 X 射线吸收法 (DXA) 研究表明,减重手术后骨密度 (BMD) 显著降低,腰椎的结果不太一致。支持 DXA 研究,高分辨率外周定量计算机断层扫描 (HR-pQCT) 的分析显示,在减重手术后长达 5 年内,皮质骨密度和厚度降低,皮质骨孔隙率增加,小梁骨密度和数量降低。这些改变转化为跌倒损伤的风险增加,这导致接受过减重手术的患者骨折风险增加。由于减重手术后多年来骨恶化持续存在,骨折风险似乎不依赖于急性体重减轻,而是随着时间的推移逐渐增加的慢性疾病。在被认为对骨骼健康有全身性作用的减重手术后机制中,有证据表明,微量和宏量营养素吸收不良因素、机械卸载以及参与脂肪组织、骨骼和肌肉之间串扰的分子变化可能起决定性作用。考虑到这些情况,可以想象通过骨特异性检查和专门的术后随访,在接受减重手术的患者中充分调查骨骼健康状况。营养补充剂、运动活动、结构化康复计划的具体方案,以及在需要时的靶向治疗策略,应被视为减重手术后临床支持的一个组成部分。