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Special Issue "Metabolic Bone Diseases: Pathophysiology and Molecular Biology"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 October 2019.

Special Issue Editors

Guest Editor
Prof. Dr. Andreas K. Nüssler Website E-Mail
Department of Trauma and Reconstructive Surgery, Siegfried Weller Research Institute, Eberhard Karls University Tuebingen, BG Trauma Center Tuebingen, 72076 Tuebingen, Germany
Interests: bone metabolic diseases; bone biology; stem cell; bone tissue; osteogenic differentiation
Guest Editor
Dr. Sabrina Ehnert Website E-Mail
Department of Trauma and Reconstructive Surgery, Siegfried Weller Research Institute, Eberhard Karls University Tuebingen, BG Trauma Center Tuebingen, 72076 Tuebingen, Germany
Interests: bone biology; stem cell; bone tissue; osteogenic differentiation; musculoskeletal

Special Issue Information

Dear Colleagues,

Nowadays dramatic demographic changes towards an aging society along with a quiescent lifestyle results in a raised incidence of metabolic diseases worldwide, such as diabetes mellitus type 2. Many of these diseases affect bone metabolism. Indeed, there are more than 70 diseases and health conditions reported causing so-called metabolic bone diseases—characterized by bone pain, altered posture, and poor bone quality (e.g. osteopenia or osteoporosis), and consequently an increased fracture risk. In the case of a fracture, patient-centered care is a great challenge, including fixing the fracture, handling of the surrounding soft tissue and the patients’ mobilization. Despite all the medical progress, these patients often face delayed/impaired bone healing rich in complications.

All this forces society to tackle the existing gaps in the knowledge of metabolic bone disorders. Most metabolic bone diseases have in common an imbalance in osteoblast and osteoclast function, resulting in poor bone quality. However, the mechanisms leading to metabolic bone diseases are far from being elucidated.

This Special Issue will contain a collection of manuscripts that describe investigations into the different stages of bone metabolic diseases, reflecting our current knowledge and describing several diseases and the underlying molecular mechanisms, molecular diagnostics, and novel molecular treatment/therapeutic options.

Prof. Dr. Andreas K. Nüssler
Dr. Sabrina Ehnert
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 papers will be 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
  • bone microenvironment
  • metabolic bone diseases
  • molecular mechanisms
  • aging
  • diabetic osteopathy
  • hepatic osteodystrophy
  • osteoblast
  • bone density
  • osteoclast

Published Papers (3 papers)

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Research

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Open AccessArticle
Cigarette Smoke Induces the Risk of Metabolic Bone Diseases: Transforming Growth Factor Beta Signaling Impairment via Dysfunctional Primary Cilia Affects Migration, Proliferation, and Differentiation of Human Mesenchymal Stem Cells
Int. J. Mol. Sci. 2019, 20(12), 2915; https://doi.org/10.3390/ijms20122915 - 14 Jun 2019
Abstract
It is well established that smoking has detrimental effects on bone integrity and is a preventable risk factor for metabolic bone disorders. Following orthopedic surgeries, smokers frequently show delayed fracture healing associated with many complications, which results in prolonged hospital stays. One crucial [...] Read more.
It is well established that smoking has detrimental effects on bone integrity and is a preventable risk factor for metabolic bone disorders. Following orthopedic surgeries, smokers frequently show delayed fracture healing associated with many complications, which results in prolonged hospital stays. One crucial factor responsible for fracture repair is the recruitment and differentiation of mesenchymal stem cells (MSCs) at early stages, a mechanism mediated by transforming growth factor β (TGF-β). Although it is known that smokers frequently have decreased TGF-β levels, little is known about the actual signaling occurring in these patients. We investigated the effect of cigarette smoke on TGF-β signaling in MSCs to evaluate which step in the pathway is affected by cigarette smoke extract (CSE). Single-cell-derived human mesenchymal stem cell line (SCP-1 cells) were treated with CSE concentrations associated with smoking up to 20 cigarettes a day. TGF-β signaling was analyzed using an adenovirus-based reporter assay system. Primary cilia structure and downstream TGF-β signaling modulators (Smad2, Smad3, and Smad4) were analyzed by Western blot and immunofluorescence staining. CSE exposure significantly reduced TGF-β signaling. Intriguingly, we observed that protein levels of phospho-Smad2/3 (active forms) as well as nuclear translocation of the phospho-Smad3/4 complex decreased after CSE exposure, phenomena that affected signal propagation. CSE exposure reduced the activation of TGF-β modulators under constitutive activation of TGF-β receptor type I (ALK5), evidencing that CSE affects signaling downstream of the ALK5 receptor but not the binding of the cytokine to the receptor itself. CSE-mediated TGF-β signaling impaired MSC migration, proliferation, and differentiation and ultimately affected endochondral ossification. Thus, we conclude that CSE-mediated disruption of TGF-β signaling in MSCs is partially responsible for delayed fracture healing in smokers. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Pathophysiology and Molecular Biology)
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Review

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Open AccessReview
The Endocrine Function of Osteocalcin Regulated by Bone Resorption: A Lesson from Reduced and Increased Bone Mass Diseases
Int. J. Mol. Sci. 2019, 20(18), 4502; https://doi.org/10.3390/ijms20184502 - 11 Sep 2019
Abstract
Bone is a peculiar tissue subjected to a continuous process of self-renewal essential to assure the integrity of the skeleton and to explicate the endocrine functions. The study of bone diseases characterized by increased or reduced bone mass due to osteoclast alterations has [...] Read more.
Bone is a peculiar tissue subjected to a continuous process of self-renewal essential to assure the integrity of the skeleton and to explicate the endocrine functions. The study of bone diseases characterized by increased or reduced bone mass due to osteoclast alterations has been essential to understand the great role played by osteocalcin in the endocrine functions of the skeleton. The ability of osteoclasts to regulate the decarboxylation of osteocalcin and to control glucose metabolism, male fertility, and cognitive functions was demonstrated by the use of animal models. In this review we described how diseases characterized by defective and increased bone resorption activity, as osteopetrosis and osteoporosis, were essential to understand the involvement of bone tissue in whole body physiology. To translate this knowledge into humans, recently published reports on patients were described, but further studies should be performed to confirm this complex hormonal regulation in humans. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Pathophysiology and Molecular Biology)
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Open AccessReview
Hepatic Osteodystrophy—Molecular Mechanisms Proposed to Favor Its Development
Int. J. Mol. Sci. 2019, 20(10), 2555; https://doi.org/10.3390/ijms20102555 - 24 May 2019
Cited by 1
Abstract
Almost all patients with chronic liver diseases (CLD) show altered bone metabolism. Depending on the etiology, this manifests in a severe osteoporosis in up to 75% of the affected patients. Due to high prevalence, the generic term hepatic osteodystrophy (HOD) evolved, describing altered [...] Read more.
Almost all patients with chronic liver diseases (CLD) show altered bone metabolism. Depending on the etiology, this manifests in a severe osteoporosis in up to 75% of the affected patients. Due to high prevalence, the generic term hepatic osteodystrophy (HOD) evolved, describing altered bone metabolism, decreased bone mineral density, and deterioration of bone structure in patients with CLD. Once developed, HOD is difficult to treat and increases the risk of fragility fractures. Existing fractures affect the quality of life and, more importantly, long-term prognosis of these patients, which presents with increased mortality. Thus, special care is required to support the healing process. However, for early diagnosis (reduce fracture risk) and development of adequate treatment strategies (support healing of existing fractures), it is essential to understand the underlying mechanisms that link disturbed liver function with this bone phenotype. In the present review, we summarize proposed molecular mechanisms favoring the development of HOD and compromising the healing of associated fractures, including alterations in vitamin D metabolism and action, disbalances in transforming growth factor beta (TGF-β) and bone morphogenetic protein (BMP) signaling with histone deacetylases (HDACs) as secondary regulators, as well as alterations in the receptor activator of nuclear factor kappa B ligand (RANKL)–osteoprotegerin (OPG) system mediated by sclerostin. Based on these mechanisms, we give an overview on the limitations of early diagnosis of HOD with established serum markers. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Pathophysiology and Molecular Biology)
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