Tendon ageing is a complicated process caused by multifaceted pathways and ageing plays a critical role in the occurrence and severity of tendon injury. The role of tendon stem/progenitor cells (TSPCs) in tendon maintenance and regeneration has received increasing attention in recent years. The decreased capacity of TSPCs in seniors contributes to impaired tendon functions and raises questions as to what extent these cells either affect, or cause ageing, and whether these age-related cellular alterations are caused by intrinsic factors or the cellular environment. In this review, recent discoveries concerning the biological characteristics of TSPCs and age-related changes in TSPCs, including the effects of cellular epigenetic alterations and the mechanisms involved in the ageing process, are analyzed. During the ageing process, TSPCs ageing might occur as a natural part of the tendon ageing, but could also result from decreased levels of growth factor, hormone deficits and changes in other related factors. Here, we discuss methods that might induce the rejuvenation of TSPC functions that are impaired during ageing, including moderate exercise, cell extracellular matrix condition, growth factors and hormones; these methods aim to rejuvenate the features of youthfulness with the ultimate goal of improving human health during ageing.

Objective This cross-sectional study was aimed to update the assessment of prevalence, characteristics, and risk factors of the elderly with hip fractures in a non-institutionalized American population. Methods This current study included a total of 31,034 participants from the existing National Health and Nutritional Examination Survey (NHANES) database from 2005 to 2010, and 4,265 participants aged 65 years and older were ultimately identified. Their condition of hip fractures was determined by method of questionnaires according to the orthopedic surgeons’ diagnosis, and related epidemiological and demographic data were further collected. The univariate analysis was used to screen the risk factors of hip fractures in the elderly, and the logistic regression model was established to conduct the multivariate analysis. Results Of the total 4,265 participants with clear information of hip fractures in elderly, 127 individuals with hip fractures were identified according to results of questionnaires, exhibiting a prevalence of 28.49 per 1,000 (95% confidence interval [CI]=21.38–35.60) for males and 31.03 per 1,000 (95% CI=23.72–38.35) for females. The mean age of the elderly with hip fractures was 77.12±5.88 years and tumble (48.0%) was the primary factor. In univariate analysis, age, race, smoking, drinking alcohol, and combined with osteoporosis were regarded as risk factors. Multivariate analysis showed that age (80 years and older), living alone, smoking, combined with diabetes and osteoporosis were the independent risk factors. Conclusion Our nationwide data indicate the prevalence of hip fractures in the elderly is generally on the rise, and the female occupies a higher proportion. Age (especially aged 80 years and older), race (mainly Non-Hispanic white), smoking, drinking alcohol, living alone, combined with diabetes and osteoporosis may be closely linked to the occurrence of hip fractures in the elderly, although these variables still need to be verified in further prospective investigations.

There is accumulating evidence of an increased incidence of tendon disorders in people with diabetes mellitus. Diabetic tendinopathy is an important cause of chronic pain, restricted activity, and even tendon rupture in individuals. Tenocytes and tendon stem/progenitor cells (TSPCs) are the dominant cellular components associated with tendon homeostasis, maintenance, remodeling, and repair. Some previous studies have shown alterations in tenocytes and TSPCs in high glucose or diabetic conditions that might cause structural and functional variations in diabetic tendons and even accelerate the development and progression of diabetic tendinopathy. In this review, the biomechanical properties and histopathological changes in diabetic tendons are described. Then, the cellular and molecular alterations in both tenocytes and TSPCs are summarized, and the underlying mechanisms involved are also analyzed. A better understanding of the underlying cellular and molecular pathogenesis of diabetic tendinopathy would provide new insight for the exploration and development of effective therapeutics.

Aged tendon-derived stem/progenitor cells (TSPCs) lead to age-related tendon disorders and impair tendon healing. However, the underlying molecular mechanisms of TSPC aging remain largely unknown. Here, we investigated the role of connective tissue growth factor (CTGF) in TSPC aging. CTGF protein and mRNA levels were markedly decreased in the aged TSPCs. Moreover, recombinant CTGF attenuates TSPC aging and restores the age-associated reduction of self-renewal and differentiation of TSPCs. In addition, cell cycle distribution of aged TSPCs was arrested in the G1/S phase while recombinant CTGF treatment promoted G1/S transition. Recombinant CTGF also rescued decreased levels of cyclin D1 and CDK4 and reduced p27kip1 expression in aged TSPCs. Our results demonstrated that CTGF plays a vital role in TSPC aging and might be a potential target for molecular therapy of age-related tendon disorders.

No abstract