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Life
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Bone Remodeling
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Bone Remodeling

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3350

Special Issue Editor

Dr. Tada-aki Kudo

E-Mail Website
Guest Editor
Division of Oral Physiology, Tohoku University Graduate School of Dentistry, Sendai 980-8575, Japan
Interests: physical stimulations inducing cell differentiation; cell signaling; neural regeneration; bone remodeling; taste sensitivity and preference
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bone is a hard tissue that plays roles in supporting the body, protecting internal organs, and enabling movement. However, even after growth has ended, bone tissue in adults maintains its volume and quality through remodeling. This process involves a cycle in which osteoclasts absorb and remove damaged or aged bone tissue, followed by osteoblasts forming new bone to fill in the gaps. Additionally, the precise molecular regulation of bone remodeling is crucial for maintaining proper bone physiology and microstructure, which, in turn, provides systemic homeostasis. This remodeling is necessary not only to maintain the structural integrity of the skeleton but also to fulfill its metabolic functions as a storehouse of calcium and phosphorus. The remodeling process is regulated by the rich neural innervation of the skeleton, which serves as a source of various growth factors, neurotransmitters, and hormones that modulate bone function. The smooth execution of bone remodeling involves various molecular mechanisms that operate in a coordinated manner under precise spatiotemporal control, and, in recent years, the analysis of these molecular mechanisms has advanced rapidly. This Special Issue, titled “Bone Remodeling”, therefore welcomes contributions in all fields of recent in vivo and in vitro research associated with novel physiological and pathological functions and regulatory mechanisms of bone remodeling, as shown above.

Dr. Tada-aki Kudo
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. Life is an international peer-reviewed open access monthly 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 2600 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

  • bone remodeling
  • osteoblast
  • osteoclast
  • osteocyte
  • osteoporosis

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Published Papers (3 papers)

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Research

21 pages, 3292 KiB  
Article
Frequency-Regulated Repeated Micro-Vibration Promotes Osteoblast Differentiation Through BMP Signaling in MC3T3-E1 Cells
by Ayumu Matsushita, Tada-aki Kudo, Kanako Tominami, Yohei Hayashi, Takuya Noguchi, Takakuni Tanaka, Satoshi Izumi, Keiko Gengyo-Ando, Atsushi Matsuzawa, Guang Hong and Junichi Nakai
Life 2025, 15(4), 588; https://doi.org/10.3390/life15040588 - 3 Apr 2025
Viewed by 578
Abstract
Physical stimulation, which is a key factor affecting the metabolism of osteoblasts and their precursor cells, plays an important role in bone remodeling; however, the role of micro-vibrations in osteoblast differentiation is unclear. In the present study, we determined the effects of frequency-regulated [...] Read more.
Physical stimulation, which is a key factor affecting the metabolism of osteoblasts and their precursor cells, plays an important role in bone remodeling; however, the role of micro-vibrations in osteoblast differentiation is unclear. In the present study, we determined the effects of frequency-regulated repeated micro-vibration (FRMV) on cell proliferation and established a method to induce osteoblast differentiation through FRMV using the mouse pre-osteoblast-like cell line MC3T3-E1, which is widely used in bone metabolism research. The results indicated that FRMV significantly influenced the proliferation of MC3T3-E1 cells in a normal growth medium. FRMV at 42.2 Hz significantly promoted proliferation, whereas FRMV at 92.1 Hz showed no effect on the proliferation rate. Moreover, FRMV at 42.2 Hz significantly increased alkaline phosphatase (ALP) enzyme activity and ALP gene expression in MC3T3-E1 cells. Treatment with LDN193189, a bone morphogenetic protein (BMP) signaling inhibitor, revealed that the FRMV-induced upregulation in ALP enzyme activity and ALP gene expression were significantly suppressed in MC3T3-E1 cells. The results suggest that the FRMV protocol developed in the present study induces osteoblast differentiation through the BMP signaling pathway. Thus, FRMV may contribute to the development of effective bone regeneration technologies. Full article
(This article belongs to the Special Issue Bone Remodeling)
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14 pages, 1869 KiB  
Article
Prevention of Osteoporosis in SAMP6 Mice by Rikkunshi-To: Japanese Kampo Medicine
by Kouichi Yamamoto and Keiko Yamamoto
Life 2025, 15(4), 557; https://doi.org/10.3390/life15040557 - 29 Mar 2025
Viewed by 380
Abstract
Osteoporosis can increase the risk of fracture in elderly patients, and insufficient control affects quality of life. Rikkunshi-To (RKT) has been prescribed for elderly patients to improve gastrointestinal function. We postulated that RKT has preventive potential for the development of osteoporosis. Thus, we [...] Read more.
Osteoporosis can increase the risk of fracture in elderly patients, and insufficient control affects quality of life. Rikkunshi-To (RKT) has been prescribed for elderly patients to improve gastrointestinal function. We postulated that RKT has preventive potential for the development of osteoporosis. Thus, we developed a simple method to evaluate osteoporosis using a continuous series of X-ray images of femurs in mice, and investigated the effects of RKT on the development of osteoporosis in these mice. Male senescence-accelerated mouse strain P6 (SAMP6) mice, a model of senile osteoporosis in humans, were fed diets with or without RKT (1%). We collected X-ray images of the whole body of each mouse weekly and measured the ratio of cortical thickness of the femur (C/F index). The C/F index in SAMP6 mice fed the normal diet was increased between 50 and 80 days old, but it was significantly decreased after 120 days old. On the other hand, the C/F index in SAMP6 mice fed the RKT diet was increased between 50 and 80 days old; however, it remained unchanged throughout the experimental period. We also confirmed that the C/F index in SAMP6 mice fed the RKT diet suddenly decreased on the replacement of the RKT diet with a normal diet, suggesting that we can collect data related to a series of continuous changes in bone mass, and that RKT is useful for the prevention of osteoporosis. Full article
(This article belongs to the Special Issue Bone Remodeling)
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20 pages, 6424 KiB  
Article
Osteogenic CpG Oligodeoxynucleotide, iSN40, Inhibits Osteoclastogenesis in a TLR9-Dependent Manner
by Rena Ikeda, Chihaya Kimura, Yuma Nihashi, Koji Umezawa, Takeshi Shimosato and Tomohide Takaya
Life 2024, 14(12), 1572; https://doi.org/10.3390/life14121572 - 30 Nov 2024
Viewed by 1539
Abstract
A CpG oligodeoxynucleotide (CpG-ODN), iSN40, was originally identified as promoting the mineralization and differentiation of osteoblasts, independent of Toll-like receptor 9 (TLR9). Since CpG ODNs are often recognized by TLR9 and inhibit osteoclastogenesis, this study investigated the TLR9 dependence and anti-osteoclastogenic effect of [...] Read more.
A CpG oligodeoxynucleotide (CpG-ODN), iSN40, was originally identified as promoting the mineralization and differentiation of osteoblasts, independent of Toll-like receptor 9 (TLR9). Since CpG ODNs are often recognized by TLR9 and inhibit osteoclastogenesis, this study investigated the TLR9 dependence and anti-osteoclastogenic effect of iSN40 to validate its potential as an osteoporosis drug. The murine monocyte/macrophage cell line RAW264.7 was treated with the receptor activator of nuclear factor-κB ligand (RANKL) to induce osteoclast differentiation, then the effect of iSN40 on was quantified by tartrate-resistant acid phosphatase (TRAP) staining and real-time RT-PCR. iSN40 completely inhibited RANKL-induced differentiation into TRAP+ multinucleated osteoclasts by suppressing osteoclastogenic genes and inducing anti-/non-osteoclastogenic genes. Treatment with a TLR9 inhibitor, E6446, or a mutation in the CpG motif of iSN40 abolished the intracellular uptake and anti-osteoclastogenic effect of iSN40. These results demonstrate that iSN40 is subcellularly internalized and is recognized by TLR9 via its CpG motif, modulates RANKL-dependent osteoclastogenic gene expression, and ultimately inhibits osteoclastogenesis. Finally, iSN40 was confirmed to inhibit the osteoclastogenesis of RAW264.7 cells cocultured with the murine osteoblast cell line MC3T3-E1, presenting a model of bone remodeling. This study demonstrates that iSN40, which exerts both pro-osteogenic and anti-osteoclastogenic effects, may be a promising nucleic acid drug for osteoporosis. Full article
(This article belongs to the Special Issue Bone Remodeling)
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