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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: closed (30 April 2023) | Viewed by 12453

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Special Issue Editor

Dr. Agostino Gaudio

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Guest Editor

Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
Interests: osteoporosis; metabolic bone diseases; hypovitaminosis D-related disorders; rare bone diseases; metabolic link between atherosclerosis and bone metabolism

Special Issue Information

Bone metabolism disorders include common clinical conditions such as osteoporosis, osteomalacia and primary hyperparathyroidism as well as rare conditions such as Paget's disease, fibrous dysplasia, tumour-induced osteomalacia, osteogenesis imperfecta and several sclerosing bone diseases.

The identification of mechanisms underlying the pathophysiology of metabolic bone diseases continues to be an area of significant research efforts, attracting scientists from different fields.

Therefore, this Special Issue invites the submission of research and review papers targeting the gamut of methodological and scientific innovation in this field. Of specific interest to this Special Issue are papers focused on the discovery of novel drug targets, signalling pathways involved in the pathogenesis of rare metabolic bone diseases and secondary forms of osteoporosis.

These contributions can be general and broad in their basic science and focused on translational research, or can be highly focused on specific research models related to specific conditions.

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

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Keywords

Bone metabolism
Osteoporosis
Sclerosing bone diseases
Wnt signalling
OPG/RANKL system

Published Papers (4 papers)

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Research

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20 pages, 2189 KiB

Open AccessArticle

The Effect of Sclerostin and Monoclonal Sclerostin Antibody Romosozumab on Osteogenesis and Osteoclastogenesis Mediated by Periodontal Ligament Fibroblasts

by Karina E. Pigeaud, Melanie L. Rietveld, Aster F. Witvliet, Jolanda M. A. Hogervorst, Chen Zhang, Tim Forouzanfar, Nathalie Bravenboer, Ton Schoenmaker and Teun J. de Vries

Int. J. Mol. Sci. 2023, 24(8), 7574; https://doi.org/10.3390/ijms24087574 - 20 Apr 2023

Cited by 1 | Viewed by 1326

Abstract

Sclerostin is a bone formation inhibitor produced by osteocytes. Although sclerostin is mainly expressed in osteocytes, it was also reported in periodontal ligament (PDL) fibroblasts, which are cells that play a role in both osteogenesis and osteoclastogenesis. Here, we assess the role of sclerostin and its clinically used inhibitor, romosozumab, in both processes. For osteogenesis assays, human PDL fibroblasts were cultured under control or mineralizing conditions with increasing concentrations of sclerostin or romosozumab. For analyzing osteogenic capacity and alkaline phosphatase (ALP) activity, alizarin red staining for mineral deposition and qPCR of osteogenic markers were performed. Osteoclast formation was investigated in the presence of sclerostin or romosozumab and, in PDLs, in the presence of fibroblasts co-cultured with peripheral blood mononuclear cells (PBMCs). PDL-PBMC co-cultures stimulated with sclerostin did not affect osteoclast formation. In contrast, the addition of romosozumab slightly reduced the osteoclast formation in PDL-PBMC co-cultures at high concentrations. Neither sclerostin nor romosozumab affected the osteogenic capacity of PDL fibroblasts. qPCR analysis showed that the mineralization medium upregulated the relative expression of osteogenic markers, but this expression was barely affected when romosozumab was added to the cultures. In order to account for the limited effects of sclerostin or romosozumab, we finally compared the expression of SOST and its receptors LRP-4, -5, and -6 to the expression in osteocyte rich-bone. The expression of SOST, LRP-4, and LRP-5 was higher in osteocytes compared to in PDL cells. The limited interaction of sclerostin or romosozumab with PDL fibroblasts may relate to the primary biological function of the periodontal ligament: to primarily resist bone formation and bone degradation to the benefit of an intact ligament that is indented by every chew movement. Full article

(This article belongs to the Special Issue Disorders of Bone Metabolism)

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12 pages, 2929 KiB

Open AccessArticle

Overexpression of Neurogenin 1 Negatively Regulates Osteoclast and Osteoblast Differentiation

by Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, Jeong-Tae Koh and Nacksung Kim

Int. J. Mol. Sci. 2022, 23(12), 6708; https://doi.org/10.3390/ijms23126708 - 16 Jun 2022

Cited by 3 | Viewed by 1822

Abstract

Neurogenin 1 (Ngn1) belongs to the basic helix–loop–helix (bHLH) transcription factor family and plays important roles in specifying neuronal differentiation. The present study aimed to determine whether forced Ngn1 expression contributes to bone homeostasis. Ngn1 inhibited the p300/CREB-binding protein-associated factor (PCAF)-induced acetylation of nuclear factor of activated T cells 1 (NFATc1) and runt-related transcription factor 2 (Runx2) through binding to PCAF, which led to the inhibition of osteoclast and osteoblast differentiation, respectively. In addition, Ngn1 overexpression inhibited the TNF-α- and IL-17A-mediated enhancement of osteoclast differentiation and IL-17A-induced osteoblast differentiation. These findings indicate that Ngn1 can serve as a novel therapeutic agent for treating ankylosing spondylitis with abnormally increased bone formation and resorption. Full article

(This article belongs to the Special Issue Disorders of Bone Metabolism)

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Review

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18 pages, 11833 KiB

Open AccessReview

Osteomalacia Is Not a Single Disease

by Luisella Cianferotti

Int. J. Mol. Sci. 2022, 23(23), 14896; https://doi.org/10.3390/ijms232314896 - 28 Nov 2022

Cited by 7 | Viewed by 6263

Abstract

Among bone-material qualities, mineralization is pivotal in conferring stiffness and toughness to the bone. Osteomalacia, a disease ensuing from inadequate mineralization of the skeleton, is caused by different processes leading to decreased available mineral (calcium and/or phosphate) or enzymatic alterations. Vitamin D deficiency, which remains the major cause of altered mineralization leading to inadequate intestinal calcium and phosphate absorption, may be also associated with other conditions primarily responsible for abnormal mineralization. Given the reality of widespread vitamin D inadequacy, a full biochemical assessment of mineral metabolism is always necessary to rule out or confirm other conditions. Both too-high or too-low serum alkaline phosphatase (ALP) levels are important for diagnosis. Osteomalacic syndrome is reversible, at least in part, by specific treatment. Osteomalacia and bone mineralization themselves constitute largely unexplored fields of research. The true prevalence of the different forms of osteomalacia and the recovery after proper therapy have yet to be determined in the real world. Although non-invasive techniques to assess bone mineralization are not available in clinical practice, the systematic assessment of bone quality could help in refining the diagnosis and guiding the treatment. This review summarizes what is known of osteomalacia recent therapeutic developments and highlights the future issues of research in this field. Full article

(This article belongs to the Special Issue Disorders of Bone Metabolism)

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Other

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7 pages, 1317 KiB

Open AccessCase Report

Spontaneous Bone Marrow Edema: Perfusion Abnormalities and Treatment with Surgical Decompression

by Jake Littman, Holly Gil and Roy Aaron

Int. J. Mol. Sci. 2023, 24(7), 6761; https://doi.org/10.3390/ijms24076761 - 05 Apr 2023

Cited by 1 | Viewed by 2445

Abstract

Bone marrow edema (BME), also termed bone marrow lesions, is a syndrome characterized by bone pain and the appearance of high signal intensity on T2 fat-suppressed and short tau inversion recovery (STIR) MRI sequences. BME can be related to trauma or a variety of non-traumatic diseases, and current treatment modalities include non-steroidal anti-inflammatory drugs (NSAIDS), bisphosphonates, denosumab, extracorporeal shockwave therapy (ESWT), the vasoactive prostacyclin analogue iloprost, and surgical decompression. Spontaneous BME is a subset that has been observed with no apparent causative conditions. It is most likely caused by venous outflow obstruction and intraosseous hypertension. These are mechanistically related to impaired perfusion and ischemia in several models of BME and are related to bone remodeling. The association of perfusion abnormalities and bone pain provides the pathophysiological rationale for surgical decompression. We present a case of spontaneous BME and a second case of spontaneous migratory BME treated with surgical decompression and demonstrate resolution of pain and the high signal intensity on MRI. This report provides an integration of the clinical syndrome, MR imaging characteristics, circulatory pathophysiology, and treatment. It draws upon several studies to suggest that both the bone pain and the MRI characteristics are related to venous stasis, and when circulatory pathologies are relieved by decompression or fenestration, both the bone pain and the MRI signal abnormalities resolve. Full article

(This article belongs to the Special Issue Disorders of Bone Metabolism)

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