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Osteoporosis 2.0
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Osteoporosis 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 August 2023) | Viewed by 7742

Special Issue Editor

Dr. Alberto Falchetti

E-Mail Website
Guest Editor
Unit of Endocrinology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy
Interests: osteoporosis; metabolic bone diseases; parathyroid diseases; multiple endocrine neoplasia; genetic diseases of bone
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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

Related Special Issue

Published Papers (3 papers)

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Research

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16 pages, 3370 KiB  
Article
Anaphase-Promoting Complex Subunit 1 Associates with Bone Mineral Density in Human Osteoporotic Bone
by Petra Malavašič, Sara Polajžer and Nika Lovšin
Int. J. Mol. Sci. 2023, 24(16), 12895; https://doi.org/10.3390/ijms241612895 - 17 Aug 2023
Viewed by 1079
Abstract
Genome-wide association studies (GWAS) are one of the most common approaches to identify genetic loci that are associated with bone mineral density (BMD). Such novel genetic loci represent new potential targets for the prevention and treatment of fragility fractures. GWAS have identified hundreds [...] Read more.
Genome-wide association studies (GWAS) are one of the most common approaches to identify genetic loci that are associated with bone mineral density (BMD). Such novel genetic loci represent new potential targets for the prevention and treatment of fragility fractures. GWAS have identified hundreds of associations with BMD; however, only a few have been functionally evaluated. A locus significantly associated with femoral neck BMD at the genome-wide level is intronic SNP rs17040773 located in the intronic region of the anaphase-promoting complex subunit 1 (ANAPC1) gene (p = 1.5 × 10−9). Here, we functionally evaluate the role of ANAPC1 in bone remodelling by examining the expression of ANAPC1 in human bone and muscle tissues and during the osteogenic differentiation of human primary mesenchymal stem cells (MSCs). The expression of ANAPC1 was significantly decreased 2.3-fold in bone tissues and 6.2-fold in muscle tissue from osteoporotic patients as compared to the osteoarthritic and control tissues. Next, we show that the expression of ANAPC1 changes during the osteogenic differentiation process of human MSCs. Moreover, the silencing of ANAPC1 in human osteosarcoma (HOS) cells reduced RUNX2 expression, suggesting that ANAPC1 affects osteogenic differentiation through RUNX2. Altogether, our results indicate that ANAPC1 plays a role in bone physiology and in the development of osteoporosis. Full article
(This article belongs to the Special Issue Osteoporosis 2.0)
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14 pages, 5339 KiB  
Article
Long Non-Coding RNA Malat1 Increases the Rescuing Effect of Quercetin on TNFα-Impaired Bone Marrow Stem Cell Osteogenesis and Ovariectomy-Induced Osteoporosis
by Lu Feng, Zhengmeng Yang, Nan Hou, Ming Wang, Xuan Lu, Yucong Li, Haixing Wang, Yaofeng Wang, Shanshan Bai, Xiaoting Zhang, Yuejun Lin, Xu Yan, Sien Lin, Micky D. Tortorella and Gang Li
Int. J. Mol. Sci. 2023, 24(6), 5965; https://doi.org/10.3390/ijms24065965 - 22 Mar 2023
Cited by 5 | Viewed by 1788
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 [...] Read more.
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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25 pages, 1285 KiB  
Review
Hormone-Related and Drug-Induced Osteoporosis: A Cellular and Molecular Overview
by 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
Cited by 23 | Viewed by 4357
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 [...] Read more.
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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