Molecular and Cellular Mechanisms of Osteoporosis

Abstract

Osteoporosis is a widespread systemic disease characterized by a decrease in bone mass and an imbalance of the microarchitecture of bone tissue. Experimental and clinical studies devoted to investigating the main pathogenetic mechanisms of osteoporosis revealed the important role of estrogen deficiency, inflammation, oxidative stress, cellular senescence, and epigenetic factors in the development of bone resorption due to osteoclastogenesis, and decreased mineralization of bone tissue and bone formation due to reduced function of osteoblasts caused by apoptosis and age-depended differentiation of osteoblast precursors into adipocytes. The current review was conducted to describe the basic mechanisms of the development of osteoporosis at molecular and cellular levels and to elucidate the most promising therapeutic strategies of pathogenetic therapy of osteoporosis based on articles cited in PubMed up to September 2023.

Defining the most potent osteoinductive culture conditions for MC3T3-E1 cells reveals no implication of oxidative stress or energy metabolism

“…In an effort to further explore the cause in the aforementioned results, we evaluated key molecules of oxidative stress and energy metabolism, cellular processes that affect bone health and bone-related diseases such as osteoporosis [16,[49][50][51][52][53][54]. We first examined the gene and/or protein expression levels of Pgc1a and Tfam, as important factors of mitochondrial biogenesis in bone cells [24].…”

The role of magnesium in the pathogenesis of osteoporosis

“…( Figure 1 ) Various factors affect the axis and enhance the formation of OCs to a state of decompensation, resulting in reduced bone mass and damage to the bone tissue microstructure, which leads to the occurrence of OP ( 23 ). In the process of OC differentiation and activation, OBs participate in the regulation of OC differentiation by expressing RANKL and OPG ( 24 ). RANKL binds to RANK and activates OC differentiation through the activation of downstream signaling pathways, while OPG inhibits these effects by inhibiting the RANKL-RANK interaction.…”

Exosomes as a potential therapeutic approach in osteoimmunology

“…The effects of factors of the TNF family, to which RANKL belongs, may partially overlap due to similar binding domains; moreover, macrophages activated by TNF-α and osteoclasts activated by RANKL are differentiated from monocytes. Therefore, osteoclasts are sensitive to TNF-α, whereas RANKL is involved in maintaining dendritic cell survival and immune system functioning ( 10 , 11 ). Prolonged changes in the cytokine profile alter the functioning of many cells outside the immune system, especially osteoclasts ( 12 ).…”