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Cells
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Osteoblasts, Osteoclasts and Bone Diseases: Cellular Crosstalk and Therapeutic Opportunities
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Osteoblasts, Osteoclasts and Bone Diseases: Cellular Crosstalk and Therapeutic Opportunities

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 4757

Special Issue Editor

Dr. Thomas Nicholson

E-Mail Website
Guest Editor
Department of Inflammation and Ageing, School of Infection Inflammation and Immunology, University of Birmingham, Birmingham B15 2TT, UK
Interests: musculoskeletal ageing; chronic inflammation; tissue regeneration; multi-omics; therapeutic targets

Special Issue Information

Dear Colleagues,

Bone is a dynamic tissue that is continuously remodelled through the coordinated actions of osteoblasts, osteoclasts, and osteocytes. Disruption of these finely balanced processes underlies a wide spectrum of bone diseases, including osteoporosis, osteoarthritis, Paget’s disease and inflammatory bone loss. Recent research has begun to explore the complex molecular and cellular networks that govern bone homeostasis and has identified key roles for signalling pathways such as RANK/RANKL/OPG, Wnt/β-catenin, mechanical factors and bone–tissue crosstalk. This Special Issue invites contributions exploring the fundamental biology of osteoblasts, osteoclasts and osteocytes, mechanisms driving bone remodelling, and translational research aimed at targeting skeletal pathologies. We welcome original research, reviews, and methodological advances focusing on cell signalling, transcriptional regulation, epigenetics, biomaterials, therapeutic interventions and bone crosstalk. By fostering a deeper understanding of the cellular mechanisms involved in bone health and disease, this Special Issue aims to support the development of innovative treatments and diagnostic tools for skeletal disorders.

Dr. Thomas Nicholson
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 250 words) can be sent to the Editorial Office for assessment.

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. 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

  • osteoblasts
  • osteoclasts
  • bone remodelling
  • osteoporosis
  • skeletal diseases
  • bone homeostasis
  • bone interactions
  • bone crosstalk
  • targeted therapies

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Published Papers (3 papers)

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Research

13 pages, 3686 KB  
Communication
Foretinib Alleviates Osteoblast Senescence and Protects Against Bone Loss in Ovariectomized Mice by Promoting Osteoblast Differentiation
by Jiin Oh, Jueun Lee, Eok-Cheon Kim, Jae-Ryoung Kim, Hyunil Ha, Taesoo Kim, Kyunghee Lee and Daewon Jeong
Cells 2025, 14(24), 1945; https://doi.org/10.3390/cells14241945 - 8 Dec 2025
Viewed by 107
Abstract
Osteoporosis is a major global health challenge, causing millions of fragility fractures each year and imposing an escalating socioeconomic burden worldwide. Despite advances with antiresorptive and anabolic therapies, substantial residual fracture risk persists, and targeting aging biology may yield disease modifying benefits beyond [...] Read more.
Osteoporosis is a major global health challenge, causing millions of fragility fractures each year and imposing an escalating socioeconomic burden worldwide. Despite advances with antiresorptive and anabolic therapies, substantial residual fracture risk persists, and targeting aging biology may yield disease modifying benefits beyond current standards of care. Senescent cells secrete senescence-associated secretory phenotype (SASP) factors, which impair osteoblast differentiation and contribute to bone loss. We investigated foretinib, a quinoline-based multi-tyrosine kinase inhibitor, as a potential anti-aging agent in osteoblast lineage cells. Foretinib inhibited doxorubicin-induced senescence in osteoblast progenitors via the p53/p21 and p16 pathways and reduced the expression of osteogenesis-inhibiting SASP factors, including CCL2, interleukin (IL)-1α, IL-1β, and IL-6. As a result, foretinib restored the impaired osteogenic differentiation of aged osteoblasts to near-normal levels in vitro. In ovariectomized, estrogen-deficient mice, foretinib significantly reduced trabecular and cortical bone loss by enhancing in vivo osteoblast differentiation, as shown by histological analysis and micro-computed tomography of femoral bone. These results suggest that foretinib alleviates osteoblast senescence and enhances osteogenic differentiation, supporting its promise as a therapeutic candidate for postmenopausal osteoporosis. Full article
(This article belongs to the Special Issue Osteoblasts, Osteoclasts and Bone Diseases: Cellular Crosstalk and Therapeutic Opportunities)
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18 pages, 3942 KB  
Article
Cortical Bone Loss and Fragility in a 2-Month Triple Transgenic Mouse Model of Alzheimer’s Disease
by Giuseppina Storlino, Francesca Posa, Teresa Stefania Dell'Endice, Federica Piccolo, Graziana Colaianni, Tommaso Cassano, Maria Grano and Giorgio Mori
Cells 2025, 14(22), 1816; https://doi.org/10.3390/cells14221816 - 19 Nov 2025
Viewed by 571
Abstract
Alzheimer’s disease (AD) and osteoporosis frequently co-occur in the elderly; however, the pathophysiological link between these two diseases remains unclear. This study investigates skeletal alterations in a triple transgenic 3xTg-AD mouse model of AD (3xTg-AD), which harbors mutations in β-amyloid precursor protein (βAPP [...] Read more.
Alzheimer’s disease (AD) and osteoporosis frequently co-occur in the elderly; however, the pathophysiological link between these two diseases remains unclear. This study investigates skeletal alterations in a triple transgenic 3xTg-AD mouse model of AD (3xTg-AD), which harbors mutations in β-amyloid precursor protein (βAPPSwe), presenilin-1 (PS1M146V), and tauP301L, and recapitulates key aspects of AD pathology, including age-dependent β-amyloid plaque accumulation and cognitive decline. To assess early skeletal changes, we analyzed femurs and tibiae of 2-month-old male non-Tg and 3xTg-AD mice (n = 9/group) using micro-CT. Despite the absence of β-amyloid plaques at this stage, 3xTg-AD mice showed significant cortical bone loss, with reduced bone surface, periosteal and endosteal perimeters, total and cortical cross-sectional area, and polar moment of inertia. The 3-point-bending test confirmed compromised mechanical properties, including reduced maximum load-to-fracture and stiffness. Histological analyses highlighted an increased number of Empty Osteocyte Lacunae, reduced TRAP+ osteocytes, and an elevated number of osteoclasts; such evidence indicates impaired osteocyte function and increased bone resorption. These findings indicate that cortical bone loss and compromised mechanical properties occur before detectable neuropathological hallmarks in this AD model. Full article
(This article belongs to the Special Issue Osteoblasts, Osteoclasts and Bone Diseases: Cellular Crosstalk and Therapeutic Opportunities)
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12 pages, 3458 KB  
Article
Adenosine A2a Receptor Stimulation Mitigates Periodontitis and Is Mitoprotective in Gingival Fibroblasts Promoting Cellular Resilience
by A. C. Morandini, S. Dawson, N. Paladines, N. Adams and E. S. Ramos-Junior
Cells 2025, 14(16), 1266; https://doi.org/10.3390/cells14161266 - 16 Aug 2025
Viewed by 3838
Abstract
Adenosine signaling plays protective roles in gingival mitochondrial health and inflammation control, with the ectoenzyme CD73 implicated in periodontitis. Here, we investigated the effects of selective adenosine A2a receptor (A2aR) stimulation using the agonist CGS21680 in a mouse model of ligature-induced periodontitis (LIP) [...] Read more.
Adenosine signaling plays protective roles in gingival mitochondrial health and inflammation control, with the ectoenzyme CD73 implicated in periodontitis. Here, we investigated the effects of selective adenosine A2a receptor (A2aR) stimulation using the agonist CGS21680 in a mouse model of ligature-induced periodontitis (LIP) and in gingival fibroblast mitochondrial function. Mature C57Bl/6 mice underwent LIP and received daily intraperitoneal injections of CGS21680 (0.1 mg/Kg) or saline. After 8 days, gingival tissues and maxillae were analyzed for alveolar bone loss and Il-1β levels. In parallel, murine gingival fibroblasts (mGFs) were treated with Tnf-α (5 ng/mL) ± CGS21680 (10 µM) to assess mitochondrial function, morphology, and quality control. A2aR activation significantly reduced alveolar bone loss and Il-1β expression in vivo. In vitro, CGS21680 suppressed Tnf-α-induced Cxcl10 and Cxcl12 expressions and enhanced Vegf production. Mitochondrial analysis revealed increased mitochondrial complex levels, membrane potential, and mass, alongside reduced reactive oxygen species (ROS), proton leak, and mitochondrial stress. Ultrastructural studies showed elongated, healthier mitochondria and increased pro-fusion markers, indicating enhanced mitochondrial quality control. Overall, A2aR stimulation attenuates periodontal inflammation and confers mitoprotective effects on gingival fibroblasts, supporting its potential as a therapeutic strategy to both mitigate periodontitis progression and preserve tissue bioenergetics supporting cellular resilience. Full article
(This article belongs to the Special Issue Osteoblasts, Osteoclasts and Bone Diseases: Cellular Crosstalk and Therapeutic Opportunities)
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