Department of Medicine, Western Health, Melbourne Medical School, University of Melbourne, St Albans, Melbourne, VIC, Australia; Australian Institute for Musculoskeletal Science (AIMSS), University of Melbourne and Western Health, St Albans, Melbourne, VIC, Australia.
Connecticut Convergence Institute for Translation in Regenerative Engineering, University of Connecticut Health, Farmington, CT, United States of America; Center on Aging, University of Connecticut Health, Farmington, CT, United States of America.
Bone. 2022 Aug;161:116425. doi: 10.1016/j.bone.2022.116425. Epub 2022 Apr 27.
Two mechanisms implicated in telomere shortening are oxidative stress and inflammation, both of which are linked to bone and muscle loss suggesting a pathological link between telomere attrition and osteosarcopenia. Using older adults aged 60 years and over in the UK Biobank, we examined the association between leukocyte telomere length and osteosarcopenia.
Baseline leukocyte telomere length was measured using a multiplex qPCR technique and expressed as the amount of the telomere amplification product (T) to that of a single-copy gene (S) (T/S ratio). Osteosarcopenia data was from the first imaging visit and defined by WHO criteria (femoral neck bone density T score ≤ -1) for osteopenia/osteoporosis plus either the EWGSOP2 (low appendicular lean mass/height and low grip strength) or SDOC (low grip strength and slow walking pace) criteria for sarcopenia. Binary or multinomial logistic regression models were used to associate telomere length and osteosarcopenia or its components, adjusting for the covariates: age, sex, race, education, Townsend deprivation index, alcohol, smoking, BMI/weight, physical activity levels.
Among 20,400 older adults (mean age: 67.79 ± 4.9 years, 53% men), the prevalence of osteosarcopenia by EWGSOP2 (n = 96, 0.47%) or SDOC (n = 205, 1%) criteria was low at the first imaging visit (mean 8.82 years after baseline). Baseline telomere length was not associated with osteosarcopenia by EWGSOP2 (Relative Risk (RR): 1.00, 95% CI: 0.82-1.23 comparing osteosarcopenia to normal (non-osteopenic, non-osteoporotic, and non-sarcopenic) per Standard Deviation (SD) increase in telomere length) or SDOC (RR: 0.95, 95% CI: 0.83-1.09) criteria. Longer telomere length was associated with a lower risk of slow walking pace (Odds Ratio: 0.92, 95% CI: 0.87-0.99 per SD increase in telomere length, p = 0.021). Telomere length, however, was not associated with low grip strength, low bone density or low appendicular lean mass/height (p > 0.05).
In this population-based study, telomere length was not associated with osteosarcopenia; however, slow walking pace was. Further studies are needed to reexamine this relationship, including a greater number of the oldest-old (≥75 years) where osteosarcopenia is more prevalent.
端粒缩短的两种机制是氧化应激和炎症，这两种机制都与骨和肌肉丧失有关，这表明端粒损耗和肌少骨松症之间存在病理联系。我们使用英国生物银行中年龄在 60 岁及以上的老年人，研究了白细胞端粒长度与肌少骨松症之间的关系。
使用多重 qPCR 技术测量基线白细胞端粒长度，并表示为端粒扩增产物（T）与单拷贝基因（S）的量的比值（T/S 比）。肌少骨松症数据来自第一次影像学检查，根据世卫组织标准（股骨颈骨密度 T 评分≤-1）定义为骨质疏松/骨量减少，同时符合 EWGSOP2（四肢瘦体重/身高低和握力低）或 SDOC（握力低和行走速度慢）标准的肌少症。使用二元或多项逻辑回归模型来关联端粒长度和肌少骨松症或其成分，调整了协变量：年龄、性别、种族、教育程度、汤森剥夺指数、酒精、吸烟、BMI/体重、身体活动水平。
在 20400 名老年人（平均年龄：67.79±4.9 岁，53%为男性）中，第一次影像学检查时肌少骨松症的患病率较低（EWGSOP2 标准的发生率为 0.47%（n=96）或 SDOC 标准的发生率为 1%（n=205））。基线端粒长度与 EWGSOP2（RR：1.00，95%CI：0.82-1.23，与每标准偏差（SD）增加端粒长度相比，正常（非骨质疏松、非骨量减少和非肌少症）相比，RR：0.95，95%CI：0.83-1.09）标准的肌少骨松症无关。较长的端粒长度与较慢的行走速度的风险降低相关（OR：0.92，95%CI：0.87-0.99，每 SD 增加端粒长度，p=0.021）。然而，端粒长度与低握力、低骨密度或四肢瘦体重/身高无关（p>0.05）。
在这项基于人群的研究中，端粒长度与肌少骨松症无关；然而，慢走速度却有关。需要进一步的研究来重新检查这种关系，包括更多的最老年人（≥75 岁），其中肌少骨松症更为普遍。
