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Bone Cell Biology
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Bone Cell Biology

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 7313

Special Issue Editors

Dr. Yohei Abe

E-Mail Website
Guest Editor
Department of Cellular and Molecular Medicine, University of California, San Diego, CA 92093, USA
Interests: cellular and molecular medicine; bone; osteoclast; osteoblast; osteocyte; inflammation
Dr. Giulia Lanzolla

E-Mail Website
Guest Editor
1. Department of Clinical and Experimental Medicine, Endocrinology Unit I-II, University of Pisa and University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy
2. Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Interests: Graves’ disease; hyperthyroidism; GD extrathyroidal manifestations; thyroid autoimmunity; thyroid disease; Graves’ orbitopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bone remodeling is directly coordinated by three skeletal cell types: osteoclasts, osteoblasts and osteocytes for the removal of old bone and formation of new bone. As bone remodeling is a complex and delicate process mediated by all skeletal cells, the disfunction of cell–cell communications can lead to an imbalance and related diseases. Therapeutic approaches for bone diseases predominantly relieve symptoms and improve bone structural features, while there has not been an established therapy to realize longer-acting bone mass and density maintenance while decreasing the side effects. The current challenge is to understand the functional interactions between molecular networks underying cell–cell communications integrated by cell signaling, and also how the genomic architecture is changed in health and disease. This journal publishes the outstanding progress and novel understanding relating bone biology. The journal highlights breakthrough discoveries in basic studies related to bone physiology and pathology. Submissions are favored regarding basic studies on bone development and metabolism in its related diseases. In particular, this Special Issue focuses on mechanistic studies showing multi-omics data integration including epigenetics, transcriptomics and/or proteomics.

Dr. Yohei Abe
Dr. Giulia Lanzolla
Guest Editors

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Keywords

  • osteoclast
  • osteoblast
  • osteocyte
  • bone density
  • macrophage
  • RANK
  • transcription factor
  • cell signaling

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Published Papers (5 papers)

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Research

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20 pages, 10682 KiB  
Article
Temporal Profiling of Cellular and Molecular Processes in Osteodifferentiation of Dental Pulp Stem Cells
by Bibiána Baďurová, Kristina Nystøl, Terézia Okajček Michalič, Veronika Kucháriková, Dagmar Statelová, Slavomíra Nováková, Ján Strnádel, Erika Halašová and Henrieta Škovierová
Biology 2025, 14(3), 257; https://doi.org/10.3390/biology14030257 - 4 Mar 2025
Viewed by 563
Abstract
Based on the potential of DPSCs as the most promising candidates for bone tissue engineering, we comprehensively investigated the time-dependent cellular and molecular changes that occur during their osteodifferentiation. To analyze this area in-depth, we used both cellular and molecular approaches. Morphological changes [...] Read more.
Based on the potential of DPSCs as the most promising candidates for bone tissue engineering, we comprehensively investigated the time-dependent cellular and molecular changes that occur during their osteodifferentiation. To analyze this area in-depth, we used both cellular and molecular approaches. Morphological changes were monitored using bright-field microscopy, while the production of mineral deposits was quantified spectrophotometrically. The expression of a key mesenchymal stem cell marker, CD90, was assessed via flow cytometry. Finally, protein-level changes in whole cells were examined by fluorescence microscopy. Our results show successful long-term osteodifferentiation of the patient’s DPSCs within 25 days. In differentiated cells, mineralized extracellular matrix production gradually increased; in contrast, the expression of the specific stem cell marker CD90 significantly decreased. We observed dynamic changes in intracellular and extracellular proteins when collagen1 A1 and osteopontin appeared as earlier markers of osteogenesis, while apolipoprotein A2, bone morphogenetic protein 9, dentin sialophosphoprotein, and matrix metalloproteinase 8 were produced mainly in the late stages of this process. A decrease in actin microfilament expression indicated a reduction in cell proliferation, which could be used as another marker of osteogenic initiation. Our results suggest a coordinated process in vitro in which cells synthesize the necessary proteins and matrix components to regulate the growth of hydroxyapatite crystals and form the bone matrix. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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16 pages, 1748 KiB  
Article
IL-1 Receptor Antagonist Anakinra Inhibits the Effect of IL-1β- Mediated Osteoclast Formation by Periodontal Ligament Fibroblasts
by Elizabeth Steemers, Wael M. I. Talbi, Jolanda M. A. Hogervorst, Ton Schoenmaker and Teun J. de Vries
Biology 2025, 14(3), 250; https://doi.org/10.3390/biology14030250 - 28 Feb 2025
Viewed by 663
Abstract
Rheumatoid arthritis and periodontitis are comorbidities that share mutual pathways. IL-1β is a pro-inflammatory cytokine that plays a crucial role in both diseases. One of the treatment options for rheumatoid arthritis is the use of an IL-1 receptor antagonist (IL-1RA) such as anakinra. [...] Read more.
Rheumatoid arthritis and periodontitis are comorbidities that share mutual pathways. IL-1β is a pro-inflammatory cytokine that plays a crucial role in both diseases. One of the treatment options for rheumatoid arthritis is the use of an IL-1 receptor antagonist (IL-1RA) such as anakinra. Anakinra tempers the disease by decreasing bone resorption and it could possibly stimulate bone formation. Here, we investigate the effect of anakinra in a periodontal disease setting on osteoclastogenesis by co-culturing periodontal ligament fibroblasts (PDLFs) and peripheral blood mononuclear cells (PBMCs) that contain monocytes, a source of osteoclast precursors, as well as by culturing PBMCs alone. The effect of anakinra on PDLF-mediated osteogenesis was studied under mineralization conditions. To mimic a chronic infection such as that prevalent in periodontitis, 10 ng/mL of IL-1β was added either alone or with 10 µg/mL of anakinra. Osteoclastogenesis experiments were performed using co-cultures of PDLF and PBMCs and PBMCs only. Osteoclastogenesis was determined through the formation of multinucleated cells in co-cultures of PDLF and PBMCs, as well as PBMCs alone, at day 21, and gene expression through qPCR at day 14. Osteogenesis was determined by measuring alkaline phosphatase activity (ALP) per cell at day 14. Anakinra is effective in downregulating IL-1β mediated leukocyte clustering and osteoclastogenesis in the co-cultures of both PDLF and PMBCs and PBMCs alone. Gene expression analysis shows that IL-1β increases the expression of the osteoclastogenic marker RANKL and its own expression. This higher expression of IL-1β at the RNA level is reduced by anakinra. Moreover, IL-1β downregulates OPG expression, which is upregulated by anakinra. No effects of anakinra on osteogenesis were seen. Clinically, these findings suggest that anakinra could have a beneficial systemic effect on periodontal breakdown in rheumatoid arthritis patients taking anakinra. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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12 pages, 1707 KiB  
Article
Targeted Overexpression of Claudin 11 in Osteoblasts Increases Trabecular Bone Mass by Stimulating Osteogenesis at the Expense of Adipogenesis in Mice
by Weirong Xing, Sheila Pourteymoor, Anakha Udayakumar, Yian Chen and Subburaman Mohan
Biology 2024, 13(2), 108; https://doi.org/10.3390/biology13020108 - 9 Feb 2024
Viewed by 2085
Abstract
Mice lacking Claudin11 (Cldn11) manifest reduced trabecular bone mass. However, the impact of Cldn11 expression in osteoblasts in vivo remains understudied. Herein, we generated osteoblast-specific transgenic (Tg) mice expressing Cldn11 and characterized their skeletal phenotype. Micro-CT analyses of the distal metaphysis [...] Read more.
Mice lacking Claudin11 (Cldn11) manifest reduced trabecular bone mass. However, the impact of Cldn11 expression in osteoblasts in vivo remains understudied. Herein, we generated osteoblast-specific transgenic (Tg) mice expressing Cldn11 and characterized their skeletal phenotype. Micro-CT analyses of the distal metaphysis of the femur showed a 50% and a 38% increase in trabecular bone mass in Tg male and female mice, respectively, due to a significant increase in trabecular number and a reduction in trabecular separation. Histomorphometry and serum biomarker studies uncovered that increased trabecular bone mass in Cldn11 Tg mice was the consequence of enhanced bone formation. Accordingly, an abundance of bone formation (Alp, Bsp), but not bone resorption (Ctsk), markers were augmented in the femurs of Cldn11 Tg mice. Since the trabecular bone density is known to inversely correlate with the amount of marrow adipose tissue (MAT), we measured the MAT in osmium-tetroxide-labeled bones by micro-CT scanning. We found 86% less MAT in the proximal tibia of the Tg males. Consistently, the expression levels of the adipogenic markers, adiponectin and leptin, were 50% lower in the femurs of the Tg males. Our data are consistent with the possibility that claudin11 exerts anabolic effects in osteoblastic lineage cells that act via promoting the differentiation of marrow stem cells towards osteoblasts at the expense of adipocytes. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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Review

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24 pages, 995 KiB  
Review
The Role of Ferroptosis in Osteoporosis and Advances in Chinese Herbal Interventions
by Pan Li, Tian-Yang Xu, Ao-Xue Yu, Jing-Ling Liang, Ya-Shuang Zhou, Huai-Zhu Sun, Yu-Lin Dai, Jia Liu and Peng Yu
Biology 2025, 14(4), 367; https://doi.org/10.3390/biology14040367 - 2 Apr 2025
Viewed by 594
Abstract
OP, a systemic bone disorder marked by reduced bone mass and heightened fracture risk, poses a significant global health burden, particularly among aging populations. Current treatments, including bisphosphonates and calcium supplementation, are limited by adverse effects and incomplete efficacy. Emerging research highlights ferroptosis—an [...] Read more.
OP, a systemic bone disorder marked by reduced bone mass and heightened fracture risk, poses a significant global health burden, particularly among aging populations. Current treatments, including bisphosphonates and calcium supplementation, are limited by adverse effects and incomplete efficacy. Emerging research highlights ferroptosis—an iron-dependent cell death driven by lipid peroxidation—as a critical contributor to OP pathogenesis, characterized by dysregulated iron metabolism, oxidative stress, and lipid peroxide accumulation, which disrupt bone remodeling by impairing osteoblast function and enhancing osteoclast activity. This review elucidates the mechanistic interplay between ferroptosis and OP subtypes (diabetic osteoporosis (DOP), glucocorticoid-induced (GIOP), and postmenopausal osteoporosis (PMOP)) and evaluates the efficacy of Chinese herbal interventions in mitigating ferroptosis-driven bone loss. Key findings reveal that excess iron exacerbates lipid peroxidation via the Fenton reaction, while glutathione peroxidase 4 (GPX4) inactivation and system Xc- inhibition amplify oxidative damage. In DIOP, hyperglycemia-induced ROS and advanced glycation end products suppress osteogenesis, countered by melatonin and naringenin via nuclear factor -related factor 2 (Nrf2)/GPX4 activation. GIOP involves dexamethasone-mediated GPX4 downregulation, mitigated by exosomes and melatonin through phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling. PMOP driven by estrogen deficiency-induced iron overload is alleviated by aconitine and icariin (ICA) via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription 3 (STAT3) pathways. Chinese herbs, including active compounds (quercetin, gastrodin, ICA, etc.) and formulations (Bugu Shengsui Capsule, Erxian Decoction (EXD), etc.), regulate iron metabolism, enhance antioxidant defenses (Nrf2/heme oxygenase 1(HO-1)), and inhibit lipid peroxidation, effectively restoring bone homeostasis. These findings underscore ferroptosis as a pivotal mechanism in OP progression and highlight the therapeutic promise of Chinese herbs in bridging traditional medicine with modern mechanistic insights. Future research should prioritize elucidating precise molecular targets, optimizing formulations, and validating clinical efficacy to address current therapeutic gaps. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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15 pages, 1306 KiB  
Review
Roles of Toll-like Receptor Signaling in Inflammatory Bone Resorption
by Tsukasa Tominari, Chiho Matsumoto, Yuki Tanaka, Kensuke Shimizu, Masaru Takatoya, Moe Sugasaki, Kento Karouji, Urara Kasuga, Chisato Miyaura, Shinji Miyata, Yoshifumi Itoh, Michiko Hirata and Masaki Inada
Biology 2024, 13(9), 692; https://doi.org/10.3390/biology13090692 - 4 Sep 2024
Cited by 7 | Viewed by 2463
Abstract
Toll-like receptors (TLRs) are pattern recognition receptors expressed in immune cells, including neutrophils, macrophages, and dendritic cells. Microbe-associated molecular patterns, including bacterial components, membranes, nucleic acids, and flagella are recognized by TLRs in inflammatory immune responses. Periodontal disease is an inflammatory disease known [...] Read more.
Toll-like receptors (TLRs) are pattern recognition receptors expressed in immune cells, including neutrophils, macrophages, and dendritic cells. Microbe-associated molecular patterns, including bacterial components, membranes, nucleic acids, and flagella are recognized by TLRs in inflammatory immune responses. Periodontal disease is an inflammatory disease known to cause local infections associated with gingival inflammation, subsequently leading to alveolar bone resorption. Prostaglandin E2 (PGE2) is a key mediator of TLR-induced inflammatory bone resorption. We previously reported that membrane-bound PGE synthase (mPGES-1)-deficient mice failed to induce bone resorption by lipopolysaccharide (LPS), a major pathogenic factor involved in periodontal bone resorption. Further experiments exploring specific pathogen-promoting osteoclast differentiation revealed that various TLR ligands induced osteoclast differentiation in a co-culture model. The ligands for TLR2/1, TLR2/6, TLR3, and TLR5, as well as TLR4, induce osteoclast differentiation associated with the production of PGE2 and the receptor activator of nuclear factor-kappa B ligand (RANKL), an inevitable inducer of osteoclast differentiation in osteoblasts. In vivo, local injection of TLR ligands, including TLR2/1, TLR2/6, and TLR3, resulted in severe alveolar bone resorption. This review summarizes the latest findings on TLR-mediated osteoclast differentiation and bone resorption in inflammatory diseases, such as periodontal diseases. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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