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Cells
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Molecular Research in Osteoporosis
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Molecular Research in Osteoporosis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 March 2027 | Viewed by 2575

Editors

Dr. Virginia Visconti

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Guest Editor
Department of Biomedicine and Prevention, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy
Interests: genetics; epigenetics; molecular biology; osteoporosis; osteosarcopenia; myotonic dystrophies
Dr. Annalisa Botta

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Guest Editor
Department of Biomedicine and Prevention, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy
Interests: myotonic dystrophies; epigenetics; medical genetics; neuromuscular diseases; biomarkers; molecular diagnosis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Umberto Tarantino

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Guest Editor
Department of Orthopaedics and Traumatology Policlinico Tor Vergata Foundation, University of Rome Tor Vergata, Rome, Italy
Interests: osteoporosis; bone metabolism; fracture healing; osteoarthritis; age related-bone disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Osteoporosis is the most prevalent bone disease, characterized by the micro-architectural deterioration of bone tissue, often associated with decreased muscle mass. Bone and muscle are intimately connected biomechanically and biochemically, together constituting the bone–muscle unit. The presence of low bone and muscle quality, reflecting the concomitant diagnosis of osteoporosis and sarcopenia, is currently referred to as “osteosarcopenia”. The pathogenesis of osteoporosis reflects complex interactions among genetic, hormonal, and environmental factors, which have not yet been fully characterized. These shortcomings, together with the related risk of developing fragility fractures, represent a major social burden which significantly impacts the quality of human life. In this context, it is crucial that we globally characterize the genetic determinants of osteoporosis through genome-wide association studies aimed at identifying genetic loci associated with low bone mineral density and osteoporotic fractures. Moreover, in-depth explorations of epigenetic mechanisms, such as DNA methylation, non-coding RNAs, and histone modification, may better define the signatures of the impaired bone metabolism. This Special Issue will summarize the current knowledge on the molecular mechanisms underlying osteoporosis. To this end, we are pleased to invite submissions of research articles and reviews addressing the characterization of novel genetic and transcriptomic biomarkers of osteoporosis to implement clinical tools against bone–muscle unit decay.

Dr. Virginia Visconti
Dr. Annalisa Botta
Prof. Dr. Umberto Tarantino
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • osteosarcopenia
  • bone–muscle crosstalk
  • genetics, epigenetics
  • transcriptomics
  • biomarkers
  • therapeutic strategy

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Published Papers (3 papers)

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Research

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21 pages, 3515 KB  
Article
Epigenetic Regulation of Galectin-1 and Galectin-3 in Osteoporosis: A Pilot Study in Patients Undergoing Total Joint Arthroplasty
by Marina Russo, Gianluca Conza, Caterina Claudia Lepre, Gabriele Martin, Annalisa Itro, Adriano Braile, Gerardo Grossi, Nicoletta Tangredi, Michele D’Amico, Anca Hermenean, Maria Consiglia Trotta and Giuseppe Toro
Cells 2026, 15(12), 1119; https://doi.org/10.3390/cells15121119 - 21 Jun 2026
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Abstract
Background: Osteoporosis (OP) is a chronic disease characterized by decreased bone mass and altered microarchitecture, leading to bone fragility and fracture risk. To date, although carbohydrate-binding proteins Galectins 1 and 3 (Gal-1/Gal-3) have been implicated in bone metabolism, inflammation and aging, their levels [...] Read more.
Background: Osteoporosis (OP) is a chronic disease characterized by decreased bone mass and altered microarchitecture, leading to bone fragility and fracture risk. To date, although carbohydrate-binding proteins Galectins 1 and 3 (Gal-1/Gal-3) have been implicated in bone metabolism, inflammation and aging, their levels and potential regulation by microRNAs (miRNAs) have not yet been investigated in OP. Methods: In this pilot study, 13 osteoporotic (OP) and 10 non-osteoporotic (NOP) patients, all undergoing hip or knee arthroplasty, were enrolled. Due to the unavailability of DXA measurements, OP classification was based on cortical bone ratio and distal femoral cortical index. Clinical parameters and blood samples were collected preoperatively, while bone biopsies were obtained intraoperatively. ELISA and qRT-PCR were used to quantify Gal-1, Gal-3, miR-22 and miR-21 in bones and sera. Correlations with clinical parameters were assessed. Results: Several OP biopsies exhibited a reduction in Gal-1 levels, whereas miR-22, Gal-3 and miR-21 were increased. Serum analysis revealed similar dysregulation patterns, with increased miR-21 and decreased Gal-1 and miR-22 levels in several OP patients. Conclusions: This pilot study suggests a putative association of Gal-1, Gal-3, and their previously reported related miRNAs with osteoporotic bone status, indicating their potential involvement in OP-related bone metabolism. Full article
(This article belongs to the Special Issue Molecular Research in Osteoporosis)
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Review

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20 pages, 3156 KB  
Review
Vesicular Communication in the Bone–Muscle Unit: Physiological Functions, Aging, and Therapeutic Potential
by Virginia Veronica Visconti, Chiara Greggi, Antonio Matticari, Riccardo Iundusi, Elena Gasbarra, Annalisa Botta and Umberto Tarantino
Cells 2026, 15(15), 1413; https://doi.org/10.3390/cells15151413 - 4 Aug 2026
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Abstract
Extracellular vesicles (EVs) have emerged as fundamental pillars of intercellular communication, acting as primary mediators of the bidirectional biochemical crosstalk within the integrated bone–muscle unit. This review provides a comprehensive synthesis of EV-mediated signaling across the bone–muscle axis, offering a side-by-side mapping of [...] Read more.
Extracellular vesicles (EVs) have emerged as fundamental pillars of intercellular communication, acting as primary mediators of the bidirectional biochemical crosstalk within the integrated bone–muscle unit. This review provides a comprehensive synthesis of EV-mediated signaling across the bone–muscle axis, offering a side-by-side mapping of vesicular biogenesis, cargo composition, and functional roles in both tissues. Under physiological conditions, skeletal muscle- and bone-derived EVs orchestrate tissue homeostasis, adaptations to physical exercise, myogenesis, and bone remodeling by transferring unique molecular cargos of proteins and specific microRNAs. However, aging induces a profound remodeling of the EV secretome toward a senescent profile characterized by harmful vesicular factors. This dysfunctional vesicular signaling impairs both muscle regeneration and osteogenesis, directly contributing to the pathogenesis of interconnected age-related disorders like sarcopenia, osteoporosis, and osteosarcopenia. Concurrently, circulating EVs represent valuable, minimally invasive biomarkers for early diagnosis. On the therapeutic front, this review critically evaluates emerging EV-based approaches, utilizing mesenchymal stem cell-derived, bioengineered, or biomaterial-incorporated EVs, offering promising, low-immunogenic alternatives to cell transplantation to enhance musculoskeletal tissue repair and restore bone–muscle homeostasis. Despite persisting technical challenges regarding large-scale production and standardization, targeting or leveraging EV-mediated communication represents one of the most innovative and revolutionary strategies to counteract age-related musculoskeletal decline. By unifying physiological mechanisms, age-related molecular reprogramming, and therapeutic engineering across both muscle and bone into a single narrative, this review provides a comprehensive framework to guide future research and clinical translation in musculoskeletal health. Full article
(This article belongs to the Special Issue Molecular Research in Osteoporosis)
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23 pages, 406 KB  
Review
Profiling Osteoporosis via Integrated Multi-Omics Technologies
by Adriano Braile, Adriano Bani, Seyedeh Fatemeh Hosseininasab, Nicola del Regno, Nicola Orabona, Antonio Bove and Mariantonia Braile
Cells 2026, 15(5), 472; https://doi.org/10.3390/cells15050472 - 5 Mar 2026
Cited by 2 | Viewed by 1379
Abstract
Background: Osteoporosis is a complex disorder involving bone loss and muscle degeneration. Multi-omics technologies provide novel insights into its molecular mechanisms and may support biomarker discovery, patient stratification, and therapeutic development. Objective: This scoping review aimed to synthesize current evidence on the application [...] Read more.
Background: Osteoporosis is a complex disorder involving bone loss and muscle degeneration. Multi-omics technologies provide novel insights into its molecular mechanisms and may support biomarker discovery, patient stratification, and therapeutic development. Objective: This scoping review aimed to synthesize current evidence on the application of multi-omics approaches in osteoporosis, focusing on molecular insights, methodological diversity, and translational potential. Methods: A literature search of PubMed, Embase, and Scopus retrieved 433 records using the keywords “osteoporosis,” “osteosarcopenia,” and “omics.” After removing duplicates and screening titles, abstracts, and full texts, 30 studies met the inclusion criteria. Data on study populations, biological samples, multi-omics techniques, and integration methods were extracted. Results: Studies employed transcriptomics, proteomics, metabolomics, lipidomics, epigenomics, and metagenomics, often combined in multi-omics analyses with computational modeling. Key pathways included osteoclast differentiation, immune regulation, ferroptosis, and microbiome–metabolite interactions. Multi-omics integration enabled the identification of molecular subtypes, candidate biomarkers, and potential therapeutic targets. Limitations included small or single-center cohorts, heterogeneous designs, and limited validation, restricting generalizability and clinical translation. Conclusions: Multi-omics approaches offer a powerful framework to uncover the molecular mechanisms underlying bone and muscle degeneration and to guide precision diagnostics and interventions. Future studies should prioritize large, multicenter, longitudinal designs integrating multi-omics data with clinical and functional validation to facilitate clinical application. Full article
(This article belongs to the Special Issue Molecular Research in Osteoporosis)
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