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Advances in Bone Growth, Development and Metabolism
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Advances in Bone Growth, Development and Metabolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 3646

Special Issue Editors

Prof. Dr. Anna Charuta

E-Mail Website
Guest Editor
Institute of Health, Faculty of Medical and Health Sciences, Siedlce University of Natural Sciences and Humanities, Konarskiego 2, 08-110 Siedlce, Poland
Interests: anatomy; histology; psychology; human sciences
Dr. Agnieszka Paziewska

E-Mail Website
Guest Editor
Institute of Health Sciences, Faculty of Medical and Health Sciences, Siedlce University of Natural Sciences and Humanities, Konarskiego 2, 08-110 Siedlce, Poland
Interests: cancer pathogenesis; cancer therapy; cancer progression; tumor biomarker

Special Issue Information

Dear Colleagues,

The purpose of this Special Issue is to present the latest research Advances in Bone Growth, Development and Metabolism.

Bone tissue is a living, metabolically active tissue that plays a major role in regulating electrolyte concentrations in the body. Bone tissue is a metabolic depot of ions, mainly calcium, phosphorus and magnesium. Bone tissue and calcium homeostasis in the body depends on the balance of bone resorption and bone formation. Bone tissue undergoes remodeling during an individual's lifetime. Bone modeling continues throughout life with varying degrees of severity. It is dependent on hormones, mainly parathormone and calcitonin. In trabecular bone, the synthesis and resorption of bone tissue occur on the surface of the trabeculae. In the case of compact bone, internal bone remodeling consists of the resorption of bone tissue, followed by the formation of new Haversian systems.

This Special Issue invites researchers to submit original research papers and reviews on all aspects of bone metabolism. Topics of interest include, but are not limited to, the following: (1) anatomy and pathology of the skeletal system, including selected concepts from orthopedics, traumatology and rheumatology; (2) bone grafts, their properties, remodeling of bone grafts; (3) growth and modeling of bone tissue, bone tissue remodeling, biochemical markers of bone tissue remodeling (osteonectin, osteocalcin); (4) distology and histopathology of bone tissue; (5) basic studies of bone metabolism related to cell biology and molecular biology; (6) preclinical studies in metabolic diseases and bone homeostasis; (7) pathophysiology of metabolic bone diseases (osteoporosis); (8) disorders of the immune system in relation to bone tissue; (9) and genetic bone diseases.

Dr. Anna Charuta
Dr. Agnieszka Paziewska
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 metabolism
  • osteoporosis
  • bone mineral density
  • postmenopausal women
  • bone marrow
  • osteoimmunology
  • magnetic resonance imaging
  • bone and bones
  • osteoporosis, postmenopausal* prevention and control
  • femur neck
  • osteomicrobiology
  • neuroskeletal biology
  • genetic background of bone diseases

Published Papers (5 papers)

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Research

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17 pages, 2227 KiB  
Article
Influence of Various Strontium Formulations (Ranelate, Citrate, and Chloride) on Bone Mineral Density, Morphology, and Microarchitecture: A Comparative Study in an Ovariectomized Female Mouse Model of Osteoporosis
by Agnieszka Tomczyk-Warunek, Karolina Turżańska, Agnieszka Posturzyńska, Filip Kowal, Tomasz Blicharski, Inés Torné Pano, Anna Winiarska-Mieczan, Anna Nikodem, Sławomir Dresler, Ireneusz Sowa, Magdalena Wójciak and Piotr Dobrowolski
Int. J. Mol. Sci. 2024, 25(7), 4075; https://doi.org/10.3390/ijms25074075 - 06 Apr 2024
Viewed by 468
Abstract
Osteoporosis stands out as a prevalent skeletal ailment, prompting exploration into potential treatments, including dietary strontium ion supplements. This study assessed the efficacy of supplementation of three strontium forms—strontium citrate (SrC), strontium ranelate (SrR), and strontium chloride (SrCl)—for enhancing bone structure in 50 [...] Read more.
Osteoporosis stands out as a prevalent skeletal ailment, prompting exploration into potential treatments, including dietary strontium ion supplements. This study assessed the efficacy of supplementation of three strontium forms—strontium citrate (SrC), strontium ranelate (SrR), and strontium chloride (SrCl)—for enhancing bone structure in 50 female SWISS mice, aged seven weeks. In total, 40 mice underwent ovariectomy, while 10 underwent sham ovariectomy. Ovariectomized (OVX) mice were randomly assigned to the following groups: OVX (no supplementation), OVX + SrR, OVX + SrC, and OVX + SrCl, at concentrations equivalent to the molar amount of strontium. After 16 weeks, micro-CT examined trabeculae and cortical bones, and whole-bone strontium content was determined. Results confirm strontium administration increased bone tissue mineral density (TMD) and Sr content, with SrC exhibiting the weakest effect. Femur morphometry showed limited Sr impact, especially in the OVX + SrC group. This research highlights strontium’s potential in bone health, emphasizing variations in efficacy among its forms. Full article
(This article belongs to the Special Issue Advances in Bone Growth, Development and Metabolism)
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17 pages, 3116 KiB  
Article
(D-Ala2)GIP Inhibits Inflammatory Bone Resorption by Suppressing TNF-α and RANKL Expression and Directly Impeding Osteoclast Formation
by Angyi Lin, Hideki Kitaura, Fumitoshi Ohori, Takahiro Noguchi, Aseel Marahleh, Jinghan Ma, Jiayi Ren, Mariko Miura, Ziqiu Fan, Kohei Narita and Itaru Mizoguchi
Int. J. Mol. Sci. 2024, 25(5), 2555; https://doi.org/10.3390/ijms25052555 - 22 Feb 2024
Viewed by 706
Abstract
Glucose-insulinotropic polypeptide (GIP) is an incretin hormone that induces insulin secretion and decreases blood glucose levels. In addition, it has been reported to suppress osteoclast formation. Native GIP is rapidly degraded by dipeptidyl peptidase-4 (DPP-4). (D-Ala2)GIP is a newly developed GIP [...] Read more.
Glucose-insulinotropic polypeptide (GIP) is an incretin hormone that induces insulin secretion and decreases blood glucose levels. In addition, it has been reported to suppress osteoclast formation. Native GIP is rapidly degraded by dipeptidyl peptidase-4 (DPP-4). (D-Ala2)GIP is a newly developed GIP analog that demonstrates enhanced resistance to DPP-4. This study aimed to evaluate the influence of (D-Ala2)GIP on osteoclast formation and bone resorption during lipopolysaccharide (LPS)-induced inflammation in vivo and in vitro. In vivo, mice received supracalvarial injections of LPS with or without (D-Ala2)GIP for 5 days. Osteoclast formation and bone resorption were evaluated, and TNF-α and RANKL expression were measured. In vitro, the influence of (D-Ala2)GIP on RANKL- and TNF-α-induced osteoclastogenesis, LPS-triggered TNF-α expression in macrophages, and RANKL expression in osteoblasts were examined. Compared to the LPS-only group, calvariae co-administered LPS and (D-Ala2)GIP led to less osteoclast formation, lower bone resorption, and decreased TNF-α and RANKL expression. (D-Ala2)GIP inhibited osteoclastogenesis induced by RANKL and TNF-α and downregulated TNF-α expression in macrophages and RANKL expression in osteoblasts in vitro. Furthermore, (D-Ala2)GIP suppressed the MAPK signaling pathway. The results suggest that (D-Ala2)GIP dampened LPS-triggered osteoclast formation and bone resorption in vivo by reducing TNF-α and RANKL expression and directly inhibiting osteoclastogenesis. Full article
(This article belongs to the Special Issue Advances in Bone Growth, Development and Metabolism)
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Review

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17 pages, 609 KiB  
Review
Circadian Regulation of Bone Remodeling
by Nobuaki Kikyo
Int. J. Mol. Sci. 2024, 25(9), 4717; https://doi.org/10.3390/ijms25094717 - 26 Apr 2024
Viewed by 237
Abstract
Adult bones are continuously remodeled by the balance between bone resorption by osteoclasts and subsequent bone formation by osteoblasts. Many studies have provided molecular evidence that bone remodeling is under the control of circadian rhythms. Circadian fluctuations have been reported in the serum [...] Read more.
Adult bones are continuously remodeled by the balance between bone resorption by osteoclasts and subsequent bone formation by osteoblasts. Many studies have provided molecular evidence that bone remodeling is under the control of circadian rhythms. Circadian fluctuations have been reported in the serum and urine levels of bone turnover markers, such as digested collagen fragments and bone alkaline phosphatase. Additionally, the expressions of over a quarter of all transcripts in bones show circadian rhythmicity, including the genes encoding master transcription factors for osteoblastogenesis and osteoclastogenesis, osteogenic cytokines, and signaling pathway proteins. Serum levels of calcium, phosphate, parathyroid hormone, and calcitonin also display circadian rhythmicity. Finally, osteoblast- and osteoclast-specific knockout mice targeting the core circadian regulator gene Bmal1 show disrupted bone remodeling, although the results have not always been consistent. Despite these studies, however, establishing a direct link between circadian rhythms and bone remodeling in vivo remains a major challenge. It is nearly impossible to repeatedly collect bone materials from human subjects while following circadian changes. In addition, the differences in circadian gene regulation between diurnal humans and nocturnal mice, the main model organism, remain unclear. Filling the knowledge gap in the circadian regulation of bone remodeling could reveal novel regulatory mechanisms underlying many bone disorders including osteoporosis, genetic diseases, and fracture healing. This is also an important question for the basic understanding of how cell differentiation progresses under the influence of cyclically fluctuating environments. Full article
(This article belongs to the Special Issue Advances in Bone Growth, Development and Metabolism)
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31 pages, 1252 KiB  
Review
Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective
by Basant Elaasser, Nour Arakil and Khalid S. Mohammad
Int. J. Mol. Sci. 2024, 25(5), 2846; https://doi.org/10.3390/ijms25052846 - 29 Feb 2024
Viewed by 910
Abstract
The treatment of patients with advanced cancer poses clinical problems due to the complications that arise as the disease progresses. Bone metastases are a common problem that cancer patients may face, and currently, there are no effective drugs to treat these individuals. Prostate, [...] Read more.
The treatment of patients with advanced cancer poses clinical problems due to the complications that arise as the disease progresses. Bone metastases are a common problem that cancer patients may face, and currently, there are no effective drugs to treat these individuals. Prostate, breast, and lung cancers often spread to the bone, causing significant and disabling health conditions. The bone is a highly active and dynamic tissue and is considered a favorable environment for the growth of cancer. The role of osteoblasts and osteoclasts in the process of bone remodeling and the way in which their interactions change during the progression of metastasis is critical to understanding the pathophysiology of this disease. These interactions create a self-perpetuating loop that stimulates the growth of metastatic cells in the bone. The metabolic reprogramming of both cancer cells and cells in the bone microenvironment has serious implications for the development and progression of metastasis. Insight into the process of bone remodeling and the systemic elements that regulate this process, as well as the cellular changes that occur during the progression of bone metastases, is critical to the discovery of a cure for this disease. It is crucial to explore different therapeutic options that focus specifically on malignancy in the bone microenvironment in order to effectively treat this disease. This review will focus on the bone remodeling process and the effects of metabolic disorders as well as systemic factors like hormones and cytokines on the development of bone metastases. We will also examine the various therapeutic alternatives available today and the upcoming advances in novel treatments. Full article
(This article belongs to the Special Issue Advances in Bone Growth, Development and Metabolism)
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16 pages, 308 KiB  
Review
Exploring the Interplay between Bone Marrow Stem Cells and Obesity
by Fiorenzo Moscatelli, Antonietta Monda, Giovanni Messina, Elisabetta Picciocchi, Marcellino Monda, Marilena Di Padova, Vincenzo Monda, Antonio Mezzogiorno, Anna Dipace, Pierpaolo Limone, Antonietta Messina and Rita Polito
Int. J. Mol. Sci. 2024, 25(5), 2715; https://doi.org/10.3390/ijms25052715 - 27 Feb 2024
Viewed by 723
Abstract
Obesity, a complex disorder with rising global prevalence, is a chronic, inflammatory, and multifactorial disease and it is characterized by excessive adipose tissue accumulation and associated comorbidities. Adipose tissue (AT) is an extremely diverse organ. The composition, structure, and functionality of AT are [...] Read more.
Obesity, a complex disorder with rising global prevalence, is a chronic, inflammatory, and multifactorial disease and it is characterized by excessive adipose tissue accumulation and associated comorbidities. Adipose tissue (AT) is an extremely diverse organ. The composition, structure, and functionality of AT are significantly influenced by characteristics specific to everyone, in addition to the variability connected to various tissue types and its location-related heterogeneity. Recent investigation has shed light on the intricate relationship between bone marrow stem cells and obesity, revealing potential mechanisms that contribute to the development and consequences of this condition. Mesenchymal stem cells within the bone marrow, known for their multipotent differentiation capabilities, play a pivotal role in adipogenesis, the process of fat cell formation. In the context of obesity, alterations in the bone marrow microenvironment may influence the differentiation of mesenchymal stem cells towards adipocytes, impacting overall fat storage and metabolic balance. Moreover, bone marrow’s role as a crucial component of the immune system adds another layer of complexity to the obesity–bone marrow interplay. This narrative review summarizes the current research findings on the connection between bone marrow stem cells and obesity, highlighting the multifaceted roles of bone marrow in adipogenesis and inflammation. Full article
(This article belongs to the Special Issue Advances in Bone Growth, Development and Metabolism)
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