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Biomedicines
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Osteoclast and Osteoblast: Current Status and Future Prospects
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Osteoclast and Osteoblast: Current Status and Future Prospects

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 2540

Special Issue Editor

Dr. Satoru Shindo

E-Mail Website
Guest Editor
Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University, 3200 South University Drive, Fort Lauderdale, FL 33328, USA
Interests: osteoimmunology; infectious disease; periodontology; immunology; mechanosensing

Special Issue Information

Dear Colleagues,

Bone remodeling is distinctively modulated by a crosstalk between bone-resorbing cells, osteoclasts, and bone-forming cells, osteoblasts. The dysregulated coupling process of either osteoclasts or osteoblasts causes bone diseases such as osteoporosis or osteopetrosis, depending on whether a deficiency in mature osteoclasts or osteoblasts is experienced. In addition, inflammatory bone diseases, such as rheumatoid arthritis and periodontal disease, lead to the dysfunction of bone coupling due to excess osteoclast formation. Osteoblasts, originating from mesenchymal stem cells, produce a coupling factor or uncoupling factor in order to promote or attenuate osteoclast differentiation, such as M-CSF, RANKL and OPG. Osteoclasts, originating from hematopoietic stem cells, influence osteoblast maturation via Sclerostin, S1P and Semaphorin4D. Understanding the exact molecular mechanism of bone coupling, as well as bone uncoupling, can help to prevent bone diseases caused by bone uncoupling. Furthermore, emerging evidence regarding bone remodeling might apply to the application of novel therapeutic strategies for such diseases. This Special Issue aims to develop our understanding of the complex mechanisms involved in both osteoclast and osteoblast formation in not only homeostatic bone remodeling, but also in pathogenic bone resorption and formation. It also aims to share conceptual or technical innovations that could lead to the realization of novel therapeutic strategies for bone disease.

Dr. Satoru Shindo
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. Biomedicines 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

  • osteoclasts
  • osteoblasts
  • coupling factor
  • uncoupling factor
  • osteoprosis
  • osteopetrosis
  • inflammatory bone resorption
  • bone regeneration

Published Papers (3 papers)

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Research

10 pages, 2553 KiB  
Article
The Effects of Local Treatment of PTH(1-34) and Whitlockite and Hydroxyapatite Graft to the Calvarial Defect in a Rat Osteoporosis Model
by Jiwoon Jeong, Jung Hee Shim and Chan Yeong Heo
Biomedicines 2024, 12(4), 820; https://doi.org/10.3390/biomedicines12040820 - 8 Apr 2024
Viewed by 546
Abstract
With the aging population, there is a rising incidence of senile diseases, notably osteoporosis, marked by fractures, prolonged recovery, and elevated mortality rates, underscoring the urgency for effective treatments. In this study, we applied the method of absorbing parathyroid hormone (PTH), a treatment [...] Read more.
With the aging population, there is a rising incidence of senile diseases, notably osteoporosis, marked by fractures, prolonged recovery, and elevated mortality rates, underscoring the urgency for effective treatments. In this study, we applied the method of absorbing parathyroid hormone (PTH), a treatment for osteoporosis, into graft materials. Two types of graft materials with different properties, whitlockite (WH) and hydroxyapatite (HAP), were used. After forming calvarial defects in osteoporotic rats, WH and HAP grafts were implanted, with PTH applied directly to the graft sites. Micro-CT analysis was employed to assess bone regeneration, while tissue sections were stained to elucidate the regeneration process and bone cell dynamics. The results showed that bone regeneration was higher in the grafts that were actively degraded by osteoclasts in the early stage of regeneration. When PTH was applied, osteoclast activity increased, leading to enhanced bone regeneration. Furthermore, the activation of osteoclasts resulted in the penetration and formation of new bone within the degraded graft, which exhibited higher osseointegration. Therefore, for osteoporotic bone defects, bone grafts that can be easily degraded by osteoclasts are more suitable. Additionally, treatment with PTH can activate osteoclasts around the bone graft in the early stages of regeneration, inducing higher bone regeneration and improving osseointegration. Full article
(This article belongs to the Special Issue Osteoclast and Osteoblast: Current Status and Future Prospects)
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11 pages, 1866 KiB  
Article
Increased Circulating CD14+ Monocytes in Patients with Psoriatic Arthritis Presenting Impaired Apoptosis Activity
by Shang-Hung Lin, Chung-Yuan Hsu and Sung-Chou Li
Biomedicines 2024, 12(4), 775; https://doi.org/10.3390/biomedicines12040775 - 1 Apr 2024
Viewed by 619
Abstract
Psoriatic arthritis (PsA) is a chronic inflammatory arthritis primarily affecting peripheral and axial joints. The osteolytic effect in the damaged joint is mediated by osteoclast activation. We aimed to investigate differential gene expression in peripheral CD14+ monocytes between patients with psoriatic arthritis ( [...] Read more.
Psoriatic arthritis (PsA) is a chronic inflammatory arthritis primarily affecting peripheral and axial joints. The osteolytic effect in the damaged joint is mediated by osteoclast activation. We aimed to investigate differential gene expression in peripheral CD14+ monocytes between patients with psoriatic arthritis (n = 15) and healthy controls (HCs; n = 15). Circulating CD14+ monocytes were isolated from peripheral blood mononuclear cells using CD14+ magnetic beads. Cell apoptosis was measured via Annexin V using flow cytometry. The gene expression profiling was analyzed via microarray (available in the NCBI GEO database; accession number GSE261765), and the candidate genes were validated using PCR. The results showed a higher number of peripheral CD14+ monocytes in patients with PsA than in the HCs. By analyzing the microarray data, identifying the differentially expressed genes, and conducting pathway enrichment analysis, we found that the apoptosis signaling pathway in CD14+ cells was significantly impaired in patients with PsA compared to the HCs. Among the candidate genes in the apoptotic signaling pathway, the relative expression level of cathepsin L was confirmed to be significantly lower in the PsAs than in the HCs. We concluded that the numbers of peripheral CD14+ monocytes increased, and their apoptosis activity was impaired in patients with PsA, which could lead to enhanced macrophage maturation and osteoclast activation. The resistance of apoptotic death in peripheral CD14+ monocytes may contribute to active joint inflammation in PsA. Full article
(This article belongs to the Special Issue Osteoclast and Osteoblast: Current Status and Future Prospects)
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18 pages, 1220 KiB  
Article
Osteoprotegerin Gene as a Biomarker in the Development of Osteoporosis in Postmenopausal Women
by Filip Przerwa, Izabela Uzar, Anna Bogacz, Katarzyna Kotrych, Tadeusz Sulikowski, Marlena Wolek, Adam Kamiński, Paweł Ziętek and Bogusław Czerny
Biomedicines 2023, 11(12), 3218; https://doi.org/10.3390/biomedicines11123218 - 4 Dec 2023
Viewed by 962
Abstract
Osteoporosis is a multifactorial and polygenic disease caused by an imbalance between osteoclastogenesis and osteoblastogenesis, leading to a decrease in bone mineral density and the occurrence of disorders in the microarchitecture and metabolism of bone tissue. In postmenopausal women, there is a significant [...] Read more.
Osteoporosis is a multifactorial and polygenic disease caused by an imbalance between osteoclastogenesis and osteoblastogenesis, leading to a decrease in bone mineral density and the occurrence of disorders in the microarchitecture and metabolism of bone tissue. In postmenopausal women, there is a significant decrease in the production of estrogens, which play a key role in maintaining proper bone mineral density. Estrogens have an inhibitory effect on the development and activity of osteoclasts by reducing the synthesis of pro-resorption cytokines and stimulating the expression of osteoprotegerin (OPG). Osteoprotegerin is a cytokine that prevents bone loss by inhibiting the process of osteoclastogenesis, reducing bone resorption. The aim of our study was to determine the influence of the rs3102735 (−163A>G), rs3134070 (−245T>G), rs207361 (−950T>C), rs7844539 (6890A>C), and rs2073618 (1181G>C) polymorphisms of the OPG gene on the risk of osteoporosis and osteopenia in postmenopausal Polish women. The study included 802 unrelated women (osteoporosis: n = 317, osteopenia: n = 110, controls: n = 375) at postmenopausal age (54.7 ± 8.6 years). Genetic analysis was performed using real-time PCR. BMD values as well as clinical and bone parameters with the tested polymorphisms were analyzed among the study population. Analysis of the PPARG rs1801282 variants did not show any association with the risk of osteoporosis and osteopenia. However, for the OPG rs207361 polymorphism, we observed a statistically significant association with the risk of osteoporosis, suggesting that the OPG rs207361 variant may be one of the genetic markers associated with the pathogenesis of osteoporosis. Full article
(This article belongs to the Special Issue Osteoclast and Osteoblast: Current Status and Future Prospects)
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