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Osteoporosis: From Molecular Research to Novel Therapies

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: 20 February 2026 | Viewed by 1180

Special Issue Editors


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Guest Editor
Department of Experimental and Clinical Medicine, University of Catania, 95123 Catania, Italy
Interests: osteoporosis; metabolic bone diseases; hypovitaminosis D-related disorders; rare bone diseases; metabolic link between atherosclerosis and bone metabolism
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Guest Editor
UOSD Talassemia, AOU Policlinico “G. Rodolico-San Marco”, 95123 Catania, Italy
Interests: osteoporosis; metabolic bone diseases; hypovitaminosis D-related disorders; rare bone diseases; haemoglobinopathies

Special Issue Information

Dear Colleagues,

The identification of the mechanisms underlying the pathophysiology of, and therapies for, osteoporosis continues to represent an area of significant research, attracting scientists from a variety of different fields. The discovery of the Wnt/beta catenin signal and the OPG/RANK/RANKL system has contributed significantly to the design and development of new drugs and molecules for the treatment of osteoporosis and other metabolic bone diseases.

For this Special Issue, we invite authors to submit research manuscripts and review papers targeting the gamut of methodological and scientific innovation in this field. Papers focused on the discovery of novel drug targets, signaling pathways, and molecular mechanisms of action relevant to osteoporosis are of particular interest. These contributions can include basic science and translational research or be highly focused on research models related to specific conditions, such as drug-induced bone loss or other secondary forms of osteoporosis.

Dr. Agostino Gaudio
Dr. Anastasia Xourafa
Guest Editors

Manuscript Submission Information

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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
  • bone metabolism
  • OPG/RANK/RANKL system
  • Wnt/beta catenin signalling
  • secondary osteoporosis

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Published Papers (1 paper)

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Review

37 pages, 2753 KB  
Review
Osteoporosis After Menopause and After Drug Therapy: The Molecular Mechanism of Bone Loss and Its Treatment
by Kelly I-Rong Lee, Jie-Hong Chen and Kuo-Hu Chen
Int. J. Mol. Sci. 2026, 27(2), 641; https://doi.org/10.3390/ijms27020641 - 8 Jan 2026
Viewed by 739
Abstract
Osteoporosis is a prevalent skeletal disorder characterized by reduced bone mass and microarchitectural deterioration, leading to increased fracture risk, particularly in aging populations. Postmenopausal osteoporosis (PMOP) remains the most common primary form and results from abrupt estrogen deficiency after menopause, which disrupts bone [...] Read more.
Osteoporosis is a prevalent skeletal disorder characterized by reduced bone mass and microarchitectural deterioration, leading to increased fracture risk, particularly in aging populations. Postmenopausal osteoporosis (PMOP) remains the most common primary form and results from abrupt estrogen deficiency after menopause, which disrupts bone remodeling by accelerating the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis, suppressing Wnt/β-catenin signaling, and promoting inflammatory cytokine production. In contrast, drug-induced osteoporosis (DIOP) encompasses a heterogeneous group of secondary bone disorders arising from pharmacologic exposures. Glucocorticoids suppress osteoblastogenesis, enhance osteoclast activity, and increase reactive oxygen species; long-term bisphosphonate therapy may oversuppress bone turnover, resulting in microdamage accumulation; denosumab withdrawal triggers a unique rebound surge in RANKL activity, often leading to rapid bone loss and multiple vertebral fractures. Medications including aromatase inhibitors, SSRIs, proton pump inhibitors, heparin, and antiepileptic drugs impair bone quality through diverse mechanisms. Standard antiresorptive agents remain first-line therapies, while anabolic agents such as teriparatide, abaloparatide, and romosozumab provide enhanced benefits in high-risk or drug-suppressed bone states. Transitional bisphosphonate therapy is essential when discontinuing denosumab, and individualized treatment plans—including drug holidays, lifestyle interventions, and monitoring vulnerable patients—are critical for optimizing outcomes. Emerging approaches such as small interfering RNA (siRNA)-based therapeutics, anti-sclerostin agents, digital monitoring technologies, and regenerative strategies show promise for future precision medicine management. Understanding the distinct and overlapping molecular mechanisms of osteoporosis is essential for improving fracture prevention and long-term skeletal health. Full article
(This article belongs to the Special Issue Osteoporosis: From Molecular Research to Novel Therapies)
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