Pharmacological and mechanistic aspects of quercetin in osteoporosis

TL;DR

This paper reviews quercetin's potential as a new osteoporosis treatment with fewer side effects.

Contribution

A comprehensive review of quercetin's anti-osteoporotic mechanisms and pharmacological effects.

Findings

Quercetin enhances osteoblast activity and reduces osteoclast activity in osteoporosis.

It acts through multiple pathways like Wnt/β-catenin and BMP/SMAD/RUNX2.

Quercetin shows potential as a safer alternative to current osteoporosis medications.

Abstract

Osteoporosis (OP) is a bone disease associated with increasing age. Currently, the most common medications used to treat OP are anabolic agents, anti-resorptive agents, and medications with other mechanisms of action. However, many of these medications have unfavorable adverse effects or are not intended for long-term use, potentially exerting a severe negative impact on a patient’s life and career and placing a heavy burden on families and society. There is an urgent need to find new drugs that can replace these and have fewer adverse effects. Quercetin (Que) is a common flavonol in nature. Numerous studies have examined the therapeutic applications of Que. However, a comprehensive review of the anti-osteoporotic effects of Que has not yet been conducted. This review aimed to describe the recent studies on the anti-osteoporotic effects of Que, including its biological, pharmacological, pharmacokinetic, and toxicological properties. The outcomes demonstrated that Que could enhance OP by increasing osteoblast differentiation and activity and reducing osteoclast differentiation and activity via the pathways of Wnt/β-catenin, BMP/SMAD/RUNX2, OPG/RANKL/RANK, ERK/JNK, oxidative stress, apoptosis, and transcription factors. Thus, Que is a promising novel drug for the treatment of OP.

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