Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

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.

Impact of 3D cell culture on bone regeneration potential of mesenchymal stromal cells

“…An additional factor playing a role in the lower osteogenic potential of osteoporotic MSCs is that in senile osteoporosis, MSCs undergo cellular senescence resulting in a growth arrest [57].…”

ASPH Regulates Osteogenic Differentiation and Cellular Senescence of BMSCs

“…Osteogenesis and cellular senescence of BMSCs play great roles in bone formation (Qadir et al, 2020). In this study, our data showed ASPH longest isoform promoting the osteogenesis while inhibiting cellular senescence, indicating it potentially results in an elevated capacity of bone formation.…”

Molecular Basis of Bone Aging

“…Several data confirm that aging is characterized by the reduction of bone tissue which is replaced by bone marrow adipose tissue, as a consequence of decreased osteoblastogenesis and a concomitant enhanced adipogenesis from BMSCs [59] (Table 2). It has been shown that the changes in BMSC proliferation and the switch of differentiation toward the adipogenic lineage is one of the main physio-pathological mechanisms of senile osteoporosis [60,61]. BMSCs deriving from elderly subjects present a decline of osteoblastogenesis and a tendency for adipogenic differentiation [62].…”