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Special Issue "Secondary Osteoporosis in Adults 2.0"

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: 30 April 2022.

Special Issue Editor

Prof. Dr. Iacopo Chiodini
E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Unit for Bone Metabolism Diseases and Diabetes, Istituto Auxologico Italiano, IRCCS, Milan, Italy
Interests: adrenal diseases; parathyroid diseases; osteoporosis; metabolic bone diseases; endocrine hypertension
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Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue "Secondary Osteoporosis in Adults".

It is known that skeletal fragility may represent the effect of several systemic diseases and drugs, leading to “secondary osteoporosis”. The typical characteristic of secondary osteoporosis is an alteration of bone quality that, in turn, increases the risk of fractures even in the presence of normal or slightly reduced bone mineral density.

Very often, fragility fractures are the manifest symptoms of these underlying diseases that otherwise could be completely asymptomatic for many years. The diagnosis of a systemic disease in a patient with an inexplicable form of osteoporosis or fragility fracture may often help to prevent the extra-skeletal consequences of the underlying disease. Moreover, a correct diagnosis reduces the risk of inadequate treatments, and this is particularly important in secondary osteoporosis as far as, by curing the underlying disease, we have a good opportunity for reducing the fracture risk.

In this Special Issue, we will include several reviews covering the most frequent and important forms of secondary osteoporosis due to obesity and diabetes, or to endocrine, gastrointestinal, hematologic, rheumatological, neuro-psychiatric and kidney diseases, and, finally, genetic disorders and drugs. Moreover, we welcome your contributions in the form of original research on all the aspects of secondary osteoporosis.

Dr. Iacopo Chiodini
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 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

  • Osteoporosis
  • Endocrine diseases
  • Gastrointestinal diseases
  • Hematologic diseases
  • Genetic diseases
  • Neuro-psychiatric diseases
  • Kidney diseases
  • Bone-impacting drugs

Published Papers (3 papers)

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Research

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Article
A Neuroprotective Bovine Colostrum Attenuates Apoptosis in Dexamethasone-Treated MC3T3-E1 Osteoblastic Cells
Int. J. Mol. Sci. 2021, 22(19), 10195; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910195 - 22 Sep 2021
Viewed by 210
Abstract
Glucocorticoid-induced osteoporosis (GIO) is one of the most common secondary forms of osteoporosis. GIO is partially due to the apoptosis of osteoblasts and osteocytes. In addition, high doses of dexamethasone (DEX), a synthetic glucocorticoid receptor agonist, induces neurodegeneration by initiating inflammatory processes leading [...] Read more.
Glucocorticoid-induced osteoporosis (GIO) is one of the most common secondary forms of osteoporosis. GIO is partially due to the apoptosis of osteoblasts and osteocytes. In addition, high doses of dexamethasone (DEX), a synthetic glucocorticoid receptor agonist, induces neurodegeneration by initiating inflammatory processes leading to neural apoptosis. Here, a neuroprotective bovine colostrum against glucocorticoid-induced neuronal damage was investigated for its anti-apoptotic activity in glucocorticoid-treated MC3T3-E1 osteoblastic cells. A model of apoptotic osteoblastic cells was developed by exposing MC3T3-E1 cells to DEX (0–700 μM). Colostrum co-treated with DEX was executed at 0.1–5.0 mg/mL. Cell viability was measured for all treatment schedules. Caspase-3 activation was assessed to determine both osteoblast apoptosis under DEX exposure and its potential prevention by colostrum co-treatment. Glutathione reduced (GSH) was measured to determine whether DEX-mediated oxidative stress-driven apoptosis is alleviated by colostrum co-treatment. Western blot was performed to determine the levels of p-ERK1/2, Bcl-XL, Bax, and Hsp70 proteins upon DEX or DEX plus colostrum exposure. Colostrum prevented the decrease in cell viability and the increase in caspase-3 activation and oxidative stress caused by DEX exposure. Cells, upon colostrum co-treated with DEX, exhibited higher levels of p-ERK1/2 and lower levels of Bcl-XL, Bax, and Hsp70. Our data support the notion that colostrum may be able to reduce DEX-induced apoptosis possibly via the activation of the ERK pathway and modulation of the Hsp70 system. We provided preliminary evidence on how bovine colostrum, as a complex and multi-component dairy product, in addition to its neuroprotective action, may affect osteoblastic cell survival undergoing apoptosis. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 2.0)
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Article
Antiepileptic Stiripentol May Influence Bones
Int. J. Mol. Sci. 2021, 22(13), 7162; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22137162 - 02 Jul 2021
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Abstract
Bone structure abnormalities are increasingly observed in patients chronically treated with antiepileptic drugs (AEDs). The majority of the available data concern older conventional AEDs, while the amount of information regarding newer AEDs, including stiripentol, is limited. The aim of the study was to [...] Read more.
Bone structure abnormalities are increasingly observed in patients chronically treated with antiepileptic drugs (AEDs). The majority of the available data concern older conventional AEDs, while the amount of information regarding newer AEDs, including stiripentol, is limited. The aim of the study was to assess the effect of stiripentol on bones. For 24 weeks, male Wistar rats, received 0.9% sodium chloride (control group) or stiripentol (200 mg/kg/day) (STP group). In the 16th week of the study, we detected lower serum PINP levels in the STP group compared to the control group. In the 24th week, a statistically significant lower 1,25-dihydroxyvitamin D3 level, higher inorganic phosphate level and higher neutrophil gelatinase-associated lipocalin (NGAL) levels in serum were found in the STP group compared to the control. Micro X-ray computed tomography of the tibias demonstrated lower bone volume fraction, lower trabecular thickness, higher trabecular pattern factor and a higher structure model index in the stiripentol group. Considering the results of this experiment on rats which suggests that long-term administration of stiripentol may impair the cancellous bone microarchitecture, further prospective human studies seem to be justified. However, monitoring plasma vitamin D, calcium, inorganic phosphate and kidney function in patients on long-term stiripentol therapy may be suggested. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 2.0)
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Review

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Review
Congenital Metabolic Bone Disorders as a Cause of Bone Fragility
Int. J. Mol. Sci. 2021, 22(19), 10281; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910281 - 24 Sep 2021
Viewed by 160
Abstract
Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of [...] Read more.
Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of high-impact trauma. The most common cause of bone fragility is primary osteoporosis in the elderly. However, bone fragility can manifest at any age, within the context of a wide spectrum of congenital rare bone metabolic diseases in which the inherited genetic defect alters correct bone modeling and remodeling at different points and aspects of bone synthesis and/or bone resorption, leading to defective bone tissue highly prone to long bone bowing, stress fractures and pseudofractures, and/or fragility fractures. To date, over 100 different Mendelian-inherited metabolic bone disorders have been identified and included in the OMIM database, associated with germinal heterozygote, compound heterozygote, or homozygote mutations, affecting over 80 different genes involved in the regulation of bone and mineral metabolism. This manuscript reviews clinical bone phenotypes, and the associated bone fragility in rare congenital metabolic bone disorders, following a disease taxonomic classification based on deranged bone metabolic activity. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 2.0)
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