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Dear Colleagues,

Osteoporosis still represents a pathological condition that remains largely underdiagnosed and undertreated, mainly due to the low frequency of screening and the controversies in BMD testing standards. Testosterone, estrogen, SHBG, and FSH levels interact in determining bone mass accrual, BMD maintenance, and lifetime decrease.

As a general example of this, in recent decades the global rise in obesity and sedentary lifestyles, together with an aging population, lead to the increased incidence and prevalence of type 2 diabetes, a known major cause of disability, socioeconomic costs, and increased risk of all-cause mortality. Fragility fractures are increasingly recognized as an important complication of T2DM. Osteoporosis is often an underdiagnosed T2DM-related complication.

The appropriate early diagnosis of osteoporosis is mandatory in order to start the adequate treatment of these subjects, representing a very important step in clinical practice as it may impact mortality more in women.

This Special Issue aims to update the pathophysiology and preclinical approach to osteoporosis and overall fracture risk, including humans affected by dysmetabolism, systemic disorders, and with or without type 2 diabetes, to move the field forward and suggest how to decrease the fracture rate in specific clinical scenarios.

We welcome both original research and review articles.

Dr. Alberto Falchetti
Guest Editor

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Keywords

osteoporosis
fractures in T2DM
preclinical and instrumental diagnostic tools of bone fragility
pathogenesis of bone fragility
biomarkers predictive of bone mass reduction as well as bone fragility
prevention of fractures
the role of antidiabetic drugs in bone health and fracture rate
the effects of antiosteoporotic drugs

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Published Papers (2 papers)

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Research

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Open AccessArticle

Long Non-Coding RNA Malat1 Increases the Rescuing Effect of Quercetin on TNFα-Impaired Bone Marrow Stem Cell Osteogenesis and Ovariectomy-Induced Osteoporosis

and

Int. J. Mol. Sci. 2023, 24(6), 5965; https://doi.org/10.3390/ijms24065965 (registering DOI) - 22 Mar 2023

Abstract

Osteoporosis, a common systematic bone homeostasis disorder related disease, still urgently needs innovative treatment methods. Several natural small molecules were found to be effective therapeutics in osteoporosis. In the present study, quercetin was screened out from a library of natural small molecular compounds by a dual luciferase reporter system. Quercetin was found to upregulate Wnt/β-catenin while inhibiting NF-κB signaling activities, and thereby rescuing osteoporosis-induced tumor necrosis factor alpha (TNFα) impaired BMSCs osteogenesis. Furthermore, a putative functional lncRNA, Malat1, was shown to be a key mediator in quercetin regulated signaling activities and TNFα-impaired BMSCs osteogenesis, as mentioned above. In an ovariectomy (OVX)-induced osteoporosis mouse model, quercetin administration could significantly rescue OVX-induced bone loss and structure deterioration. Serum levels of Malat1 were also obviously rescued in the OVX model after quercetin treatment. In conclusion, our study demonstrated that quercetin could rescue TNFα-impaired BMSCs osteogenesis in vitro and osteoporosis-induced bone loss in vivo, in a Malat1-dependent manner, suggesting that quercetin may serve as a therapeutic candidate for osteoporosis treatment. Full article

(This article belongs to the Special Issue Osteoporosis 2.0)

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Review

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Open AccessReview

Li-Ting Wang

Li-Ru Chen

and

Kuo-Hu Chen

Int. J. Mol. Sci. 2023, 24(6), 5814; https://doi.org/10.3390/ijms24065814 - 18 Mar 2023

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Abstract

Osteoporosis resulting from an imbalance of bone turnover between resorption and formation is a critical health issue worldwide. Estrogen deficiency following a nature aging process is the leading cause of hormone-related osteoporosis for postmenopausal women, while glucocorticoid-induced osteoporosis remains the most common in drug-induced osteoporosis. Other medications and medical conditions related to secondary osteoporosis include proton pump inhibitors, hypogonadism, selective serotonin receptor inhibitors, chemotherapies, and medroxyprogesterone acetate. This review is a summary of the cellular and molecular mechanisms of bone turnover, the pathophysiology of osteoporosis, and their treatment. Nuclear factor-κβ ligand (RANKL) appears to be the critical uncoupling factor that enhances osteoclastogenesis. In contrast, osteoprotegerin (OPG) is a RANKL antagonist secreted by osteoblast lineage cells. Estrogen promotes apoptosis of osteoclasts and inhibits osteoclastogenesis by stimulating the production of OPG and reducing osteoclast differentiation after suppression of IL-1 and TNF, and subsequent M-CSF, RANKL, and IL-6 release. It can also activate the Wnt signaling pathway to increase osteogenesis, and upregulate BMP signaling to promote mesenchymal stem cell differentiation from pre-osteoblasts to osteoblasts rather than adipocytes. Estrogen deficiency leads to the uncoupling of bone resorption and formation; therefore, resulting in greater bone loss. Excessive glucocorticoids increase PPAR-2 production, upregulate the expression of Dickkopf-1 (DKK1) in osteoblasts, and inhibit the Wnt signaling pathway, thus decreasing osteoblast differentiation. They promote osteoclast survival by enhancing RANKL expression and inhibiting OPG expression. Appropriate estrogen supplement and avoiding excessive glucocorticoid use are deemed the primary treatment for hormone-related and glucocorticoid-induced osteoporosis. Additionally, current pharmacological treatment includes bisphosphonates, teriparatide (PTH), and RANKL inhibitors (such as denosumab). However, many detailed cellular and molecular mechanisms underlying osteoporosis seem complicated and unexplored and warrant further investigation. Full article

(This article belongs to the Special Issue Osteoporosis 2.0)

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