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Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy
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Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy

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 November 2020) | Viewed by 35093

Special Issue Editor

Dr. Agostino Gaudio

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, 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 Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Identification of the mechanisms underlying the pathophysiology and therapies of metabolic bone diseases continues to be an area of significant research, attracting scientists from a variety of different fields. The discovery of the Wnt signal and the OPG/Rankl system has contributed significantly to the design and development of new drugs and molecules for the treatment of osteoporosis and other metabolic bone diseases.

For this Special Issue, we invite authors to submit manuscript research and review papers targeting the gamut of methodological and scientific innovation in this field. Of specific interest are papers focused on the discovery of novel drug targets, signaling pathways, and mechanisms of action relevant to metabolic bone diseases. These contributions can involve basic science and translational research or be highly focused on research models related to specific conditions like drug-induced bone loss or other secondary forms of osteoporosis or rare metabolic bone diseases.

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.

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
  • Wnt signaling
  • OPG/Rankl system
  • osteoblast
  • osteoclast
  • osteoporosis

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Related Special Issue

Published Papers (6 papers)

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Editorial

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2 pages, 185 KiB  
Editorial
Special Issue: Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy
by Anastasia Xourafa and Agostino Gaudio
Int. J. Mol. Sci. 2023, 24(10), 9065; https://doi.org/10.3390/ijms24109065 - 22 May 2023
Cited by 1 | Viewed by 1321
Abstract
Bone is a vital tissue as it carries out various metabolic functions: support of the body, protection of the internal organs, mineral deposit and hematopoietic functions [...] Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)

Research

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12 pages, 1578 KiB  
Article
Increased Bone Resorption during Lactation in Pycnodysostosis
by Ineke D.C. Jansen, Socrates E. Papapoulos, Nathalie Bravenboer, Teun J. de Vries and Natasha M. Appelman-Dijkstra
Int. J. Mol. Sci. 2021, 22(4), 1810; https://doi.org/10.3390/ijms22041810 - 11 Feb 2021
Cited by 6 | Viewed by 2630
Abstract
Pycnodysostosis, a rare autosomal recessive skeletal dysplasia, is caused by a deficiency of cathepsin K. Patients have impaired bone resorption in the presence of normal or increased numbers of multinucleated, but dysfunctional, osteoclasts. Cathepsin K degrades collagen type I and generates N-telopeptide (NTX) [...] Read more.
Pycnodysostosis, a rare autosomal recessive skeletal dysplasia, is caused by a deficiency of cathepsin K. Patients have impaired bone resorption in the presence of normal or increased numbers of multinucleated, but dysfunctional, osteoclasts. Cathepsin K degrades collagen type I and generates N-telopeptide (NTX) and the C-telopeptide (CTX) that can be quantified. Levels of these telopeptides are increased in lactating women and are associated with increased bone resorption. Nothing is known about the consequences of cathepsin K deficiency in lactating women. Here we present for the first time normalized blood and CTX measurements in a patient with pycnodysostosis, exclusively related to the lactation period. In vitro studies using osteoclasts derived from blood monocytes during lactation and after weaning further show consistent bone resorption before and after lactation. Increased expression of cathepsins L and S in osteoclasts derived from the lactating patient suggests that other proteinases could compensate for the lack of cathepsin K during the lactation period of pycnodysostosis patients. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)
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17 pages, 6647 KiB  
Article
Aesculetin Inhibits Osteoclastic Bone Resorption through Blocking Ruffled Border Formation and Lysosomal Trafficking
by Woojin Na, Eun-Jung Lee, Min-Kyung Kang, Yun-Ho Kim, Dong Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh and Young-Hee Kang
Int. J. Mol. Sci. 2020, 21(22), 8581; https://doi.org/10.3390/ijms21228581 - 13 Nov 2020
Cited by 18 | Viewed by 5263
Abstract
For the optimal resorption of mineralized bone matrix, osteoclasts require the generation of the ruffled border and acidic resorption lacuna through lysosomal trafficking and exocytosis. Coumarin-type aesculetin is a naturally occurring compound with anti-inflammatory and antibacterial effects. However, the direct effects of aesculetin [...] Read more.
For the optimal resorption of mineralized bone matrix, osteoclasts require the generation of the ruffled border and acidic resorption lacuna through lysosomal trafficking and exocytosis. Coumarin-type aesculetin is a naturally occurring compound with anti-inflammatory and antibacterial effects. However, the direct effects of aesculetin on osteoclastogenesis remain to be elucidated. This study found that aesculetin inhibited osteoclast activation and bone resorption through blocking formation and exocytosis of lysosomes. Raw 264.7 cells were differentiated in the presence of 50 ng/mL receptor activator of nuclear factor-κB ligand (RANKL) and treated with 1–10 μM aesculetin. Differentiation, bone resorption, and lysosome biogenesis of osteoclasts were determined by tartrate-resistance acid phosphatase (TRAP) staining, bone resorption assay, Western blotting, immunocytochemical analysis, and LysoTracker staining. Aesculetin inhibited RANKL-induced formation of multinucleated osteoclasts with a reduction of TRAP activity. Micromolar aesculetin deterred the actin ring formation through inhibition of induction of αvβ3 integrin and Cdc42 but not cluster of differentiation 44 (CD44) in RANKL-exposed osteoclasts. Administering aesculetin to RANKL-exposed osteoclasts attenuated the induction of autophagy-related proteins, microtubule-associated protein light chain 3, and small GTPase Rab7, hampering the lysosomal trafficking onto ruffled border crucial for bone resorption. In addition, aesculetin curtailed cellular induction of Pleckstrin homology domain-containing protein family member 1 and lissencephaly-1 involved in lysosome positioning to microtubules involved in the lysosomal transport within mature osteoclasts. These results demonstrate that aesculetin retarded osteoclast differentiation and impaired lysosomal trafficking and exocytosis for the formation of the putative ruffled border. Therefore, aesculetin may be a potential osteoprotective agent targeting RANKL-induced osteoclastic born resorption for medicinal use. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)
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Review

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22 pages, 383 KiB  
Review
Osteoporosis in Men: A Review of an Underestimated Bone Condition
by Giuseppe Rinonapoli, Carmelinda Ruggiero, Luigi Meccariello, Michele Bisaccia, Paolo Ceccarini and Auro Caraffa
Int. J. Mol. Sci. 2021, 22(4), 2105; https://doi.org/10.3390/ijms22042105 - 20 Feb 2021
Cited by 138 | Viewed by 10674
Abstract
Osteoporosis is called the ‘silent disease’ because, although it does not give significant symptoms when it is not complicated, can cause fragility fractures, with serious consequences and death. Furthermore, the consequences of osteoporosis have been calculated to weigh heavily on the costs of [...] Read more.
Osteoporosis is called the ‘silent disease’ because, although it does not give significant symptoms when it is not complicated, can cause fragility fractures, with serious consequences and death. Furthermore, the consequences of osteoporosis have been calculated to weigh heavily on the costs of health systems in all the countries. Osteoporosis is considered a female disease. Actually, the hormonal changes that occur after menopause certainly determine a significant increase in osteoporosis and the risk of fractures in women. However, while there is no doubt that women are more exposed to osteoporosis and fragility fractures, the literature clearly indicates that physicians tend to underestimate the osteoporosis in men. The review of the literature done by the authors shows that osteoporosis and fragility fractures have a high incidence also in men; and, furthermore, the risk of fatal complications in hip fractured men is higher than that for women. The authors report the evidence of the literature on male osteoporosis, dwelling on epidemiology, causes of osteoporosis in men, diagnosis, and treatment. The analysis of the literature shows that male osteoporosis is underscreened, underdiagnosed, and undertreated, both in primary and secondary prevention of fragility fractures. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)
18 pages, 889 KiB  
Review
Mechanisms of Bone Fragility: From Osteogenesis Imperfecta to Secondary Osteoporosis
by Ahmed El-Gazzar and Wolfgang Högler
Int. J. Mol. Sci. 2021, 22(2), 625; https://doi.org/10.3390/ijms22020625 - 10 Jan 2021
Cited by 57 | Viewed by 9046
Abstract
Bone material strength is determined by several factors, such as bone mass, matrix composition, mineralization, architecture and shape. From a clinical perspective, bone fragility is classified as primary (i.e., genetic and rare) or secondary (i.e., acquired and common) osteoporosis. Understanding the mechanism of [...] Read more.
Bone material strength is determined by several factors, such as bone mass, matrix composition, mineralization, architecture and shape. From a clinical perspective, bone fragility is classified as primary (i.e., genetic and rare) or secondary (i.e., acquired and common) osteoporosis. Understanding the mechanism of rare genetic bone fragility disorders not only advances medical knowledge on rare diseases, it may open doors for drug development for more common disorders (i.e., postmenopausal osteoporosis). In this review, we highlight the main disease mechanisms underlying the development of human bone fragility associated with low bone mass known to date. The pathways we focus on are type I collagen processing, WNT-signaling, TGF-ß signaling, the RANKL-RANK system and the osteocyte mechanosensing pathway. We demonstrate how the discovery of most of these pathways has led to targeted, pathway-specific treatments. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)
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18 pages, 1151 KiB  
Review
The Osteoporosis/Microbiota Linkage: The Role of miRNA
by Massimo De Martinis, Lia Ginaldi, Alessandro Allegra, Maria Maddalena Sirufo, Giovanni Pioggia, Alessandro Tonacci and Sebastiano Gangemi
Int. J. Mol. Sci. 2020, 21(23), 8887; https://doi.org/10.3390/ijms21238887 - 24 Nov 2020
Cited by 48 | Viewed by 5438
Abstract
Hundreds of trillions of bacteria are present in the human body in a mutually beneficial symbiotic relationship with the host. A stable dynamic equilibrium exists in healthy individuals between the microbiota, host organism, and environment. Imbalances of the intestinal microbiota contribute to the [...] Read more.
Hundreds of trillions of bacteria are present in the human body in a mutually beneficial symbiotic relationship with the host. A stable dynamic equilibrium exists in healthy individuals between the microbiota, host organism, and environment. Imbalances of the intestinal microbiota contribute to the determinism of various diseases. Recent research suggests that the microbiota is also involved in the regulation of the bone metabolism, and its alteration may induce osteoporosis. Due to modern molecular biotechnology, various mechanisms regulating the relationship between bone and microbiota are emerging. Understanding the role of microbiota imbalances in the development of osteoporosis is essential for the development of potential osteoporosis prevention and treatment strategies through microbiota targeting. A relevant complementary mechanism could be also constituted by the permanent relationships occurring between microbiota and microRNAs (miRNAs). miRNAs are a set of small non-coding RNAs able to regulate gene expression. In this review, we recapitulate the physiological and pathological meanings of the microbiota on osteoporosis onset by governing miRNA production. An improved comprehension of the relations between microbiota and miRNAs could furnish novel markers for the identification and monitoring of osteoporosis, and this appears to be an encouraging method for antagomir-guided tactics as therapeutic agents. Full article
(This article belongs to the Special Issue Metabolic Bone Diseases: Molecular Biology, Pathophysiology and Therapy)
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