FROM CELLS TO SIMULATIONS: THERAPEUTIC INSIGHTS INTO BONE CADENCE MODULATION IN OSTEOPOROTIC WOMEN

Abstract

It is common hypothesis that postmenopausal osteoporosis starts when there is a low level of estrogen after menopause. Estrogen deficiency interacts with cytokines and upregulates osteoclast formation.It has been indicated that an increase of proinflammatory cytokines IL-1, IL-6, and TNF-a are linked to ovarian dysfunction. RANKL and MCS-F are the other key cytokines that control the growth and activation of osteoclasts by regulating an intricate signaling mechanism. This study describes how oxidative stress contributes to bone loss under estrogen deficiency. The study estimated the oxidative stress pattern, inflammatory measures, hormonal pattern, and circulatory markers in the blood of 300postmenopausal osteoporotic women and 100 healthy normal females. The findings of the current study indicate that in females' postmenopausal osteoporosis depends on higher oxidative stress, Endothelial Dysfunction and lower estrogen levels. The resultant elevated proinflammatory cytokines, MMPs, deteriorated anti-oxidative defence system and a crammed activity of the glutathione reductase enzyme. The in-silico studies indicate that Epigallocatechin-3-gallate and Stigmasterol are possible therapeutic molecules, which influence osteoporosis cell proliferation and bone cadence expression.