Abstract
Senile osteoporosis has become a worldwide bone disease with the aging of the world population. It increases the risk of bone fracture and seriously affects human health. Unlike postmenopausal osteoporosis which is linked to menopause in women, senile osteoporosis is due to aging, hence, affecting both men and women. It is commonly found in people with more than their 70s. Evidence has shown that with age increase, bone marrow stromal cells (BMSCs) differentiate into more adipocytes rather than osteoblasts and undergo senescence, which leads to decreased bone formation and contributes to senile osteoporosis. Therefore, it is necessary to uncover the molecular mechanisms underlying the functional changes of BMSCs. It will benefit not only for understanding the senile osteoporosis development, but also for finding new therapies to treat senile osteoporosis. Here, we review the recent advances of the functional alterations of BMSCs and the related mechanisms during senile osteoporosis development. Moreover, the treatment of senile osteoporosis by aiming at BMSCs is introduced.
Highlights
The word “osteoporosis” means “porous bone”, which is a worldwide metabolic bone disorder with high incidence
The functional change of bone marrow stromal cells (BMSCs) has been demonstrated to contribute to senile osteoporosis, showing as BMSCs differentiate into fewer osteoblasts, but more adipocytes and BMSCs become senescent
Recent findings demonstrate that numerous transcriptional factors, signaling pathways, epigenetic regulations and other factors play key roles in regulating the differentiation and senescence of BMSCs, the alteration of which contributes to senile osteoporosis
Summary
The word “osteoporosis” means “porous bone”, which is a worldwide metabolic bone disorder with high incidence. It occurs due to the imbalance between bone formation and bone resorption [2] It has been observed in all races, gender and age groups, but more commonly found in women and older people [3]. It remains hidden until being revealed as a disorder through bone fractures, due to minor strokes [4]. Tahteiorenf,otrhe,ubso,tchaaubsneosremnailledioffsetreeonptioartoiosnisa.nd senescence of BMSCs lead to the reduced number of osteoblasts in old ages, which result in decreased bone formation, cause senile osteoporosis. We focus on the role of altered differentiation of BMSCs and senescence of BMSCs in senile osteoporosis development
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