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Secondary Osteoporosis in Adults 3.0
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Secondary Osteoporosis in Adults 3.0

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: closed (31 May 2023) | Viewed by 8520

Special Issue Editors

Dr. Iacopo Chiodini

E-Mail Website
Guest Editor
1. Department of Medical Biotechnology and Translational Medicine, University of Milan, 20122 Milan, Italy
2. Unit of Endocrinology, ASST Ospedale Niguarda, 20162 Milan, Italy
Interests: adrenal diseases; parathyroid diseases; osteoporosis; metabolic bone diseases; endocrine hypertension
Special Issues, Collections and Topics in MDPI journals
Dr. Elisa Cairoli

E-Mail Website
Guest Editor
Unit for Bone Metabolism Diseases and Diabetes, Istituto Auxologico Italiano, IRCCS, 20149 Milan, Italy
Interests: primary and secondary osteoporosis; endocrinopathies; hormone therapy; metabolic bone diseases; calcium-phosphorus metabolism disorders; rare skeletal diseases

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue, “Secondary Osteoporosis in Adults 2.0”.

It is well 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 could otherwise 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 extraskeletal 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 to reduce 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, neuropsychiatric, and kidney diseases, and, finally, genetic disorders and drugs. Moreover, we welcome your contributions in the form of original research on all aspects of secondary osteoporosis.

Dr. Iacopo Chiodini
Dr. Elisa Cairoli
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

  • 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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13 pages, 2157 KiB  
Article
Annexin A2 Improves the Osteogenic Differentiation of Mesenchymal Stem Cells Exposed to High-Glucose Conditions through Lessening the Senescence
by Parin Klabklai, Jitrada Phetfong, Rattanawan Tangporncharoen, Chartchalerm Isarankura-Na-Ayudhya, Tulyapruek Tawonsawatruk and Aungkura Supokawej
Int. J. Mol. Sci. 2022, 23(20), 12521; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012521 - 19 Oct 2022
Cited by 4 | Viewed by 1985
Abstract
Osteoporosis is frequently found in chronic diabetic patients, and it results in an increased risk of bone fractures occurring. The underlying mechanism of osteoporosis in diabetic patients is still largely unknown. Annexin A2 (ANXA2), a family of calcium-binding proteins, has been reported to [...] Read more.
Osteoporosis is frequently found in chronic diabetic patients, and it results in an increased risk of bone fractures occurring. The underlying mechanism of osteoporosis in diabetic patients is still largely unknown. Annexin A2 (ANXA2), a family of calcium-binding proteins, has been reported to be involved in many biological process including bone remodeling. This study aimed to investigate the role of ANXA2 in mesenchymal stem cells (MSCs) during in vitro osteoinduction under high-glucose concentrations. Osteogenic gene expression, calcium deposition, and cellular senescence were determined. The high-glucose conditions reduced the osteogenic differentiation potential of the MSCs along with the lower expression of ANXA2. Moreover, the high-glucose conditions increased the cellular senescence of the MSCs as determined by senescence-associated β-galactosidase staining and the expression of p16, p21, and p53 genes. The addition of recombinant ANXA2 could recover the glucose-induced deterioration of the osteogenic differentiation of the MSCs and ameliorate the glucose-induced cellular senescence of the MSCs. A Western blot analysis revealed an increase in p53 and phosphorylated p53 (Ser 15), which was decreased by recombinant ANXA2 in MSC osteoblastic differentiation under high-glucose conditions. Our study suggested that the alteration of ANXA2 in high-glucose conditions may be one of the plausible factors in the deterioration of bones in diabetic patients by triggering cellular senescence. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 3.0)
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Review

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13 pages, 1075 KiB  
Review
Haemophilia and Fragility Fractures: From Pathogenesis to Multidisciplinary Approach
by Angelo Alito, Federica Bellone, Simona Portaro, Giulia Leonardi, Vittorio Cannavò, Francesca Coppini, Danilo Leonetti, Antonino Catalano, Giovanni Squadrito and Domenico Fenga
Int. J. Mol. Sci. 2023, 24(11), 9395; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24119395 - 28 May 2023
Cited by 3 | Viewed by 1639
Abstract
Haemophilia A (HA) and haemophilia B (HB) are X-linked inherited bleeding disorders caused by the absence or deficiency of coagulation factors VIII (FVIII) and IX (FIX), respectively. Recent advances in the development of effective treatments for haemophilia have led to a significant increase [...] Read more.
Haemophilia A (HA) and haemophilia B (HB) are X-linked inherited bleeding disorders caused by the absence or deficiency of coagulation factors VIII (FVIII) and IX (FIX), respectively. Recent advances in the development of effective treatments for haemophilia have led to a significant increase in life expectancy. As a result, the incidence of some comorbidities, including fragility fractures, has increased in people with haemophilia (PWH). The aim of our research was to perform a review of the literature investigating the pathogenesis and multidisciplinary management of fractures in PWH. The PubMed, Scopus and Cochrane Library databases were searched to identify original research articles, meta-analyses, and scientific reviews on fragility fractures in PWH. The mechanism underlying bone loss in PWH is multifactorial and includes recurrent joint bleeding, reduced physical activity with consequent reduction in mechanical load, nutritional deficiencies (particularly vitamin D), and FVIII and FIX deficiency. Pharmacological treatment of fractures in PWH includes antiresorptive, anabolic and dual action drugs. When conservative management is not possible, surgery is the preferred option, particularly in severe arthropathy, and rehabilitation is a key component in restoring function and maintaining mobility. Appropriate multidisciplinary fracture management and an adapted and tailored rehabilitation pathway are essential to improve the quality of life of PWH and prevent long-term complications. Further clinical trials are needed to improve the management of fractures in PWH. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 3.0)
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25 pages, 1086 KiB  
Review
Obesity and Bone Health: A Complex Relationship
by Ana Piñar-Gutierrez, Cristina García-Fontana, Beatriz García-Fontana and Manuel Muñoz-Torres
Int. J. Mol. Sci. 2022, 23(15), 8303; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158303 - 27 Jul 2022
Cited by 31 | Viewed by 4365
Abstract
Recent scientific evidence has shown an increased risk of fractures in patients with obesity, especially in those with a higher visceral adipose tissue content. This contradicts the old paradigm that obese patients were more protected than those with normal weight. Specifically, in older [...] Read more.
Recent scientific evidence has shown an increased risk of fractures in patients with obesity, especially in those with a higher visceral adipose tissue content. This contradicts the old paradigm that obese patients were more protected than those with normal weight. Specifically, in older subjects in whom there is a redistribution of fat from subcutaneous adipose tissue to visceral adipose tissue and an infiltration of other tissues such as muscle with the consequent sarcopenia, obesity can accentuate the changes characteristic of this age group that predisposes to a greater risk of falls and fractures. Other factors that determine a greater risk in older subjects with obesity are chronic proinflammatory status, altered adipokine secretion, vitamin D deficiency, insulin resistance and reduced mobility. On the other hand, diagnostic tests may be influenced by obesity and its comorbidities as well as by body composition, and risk scales may underestimate the risk of fractures in these patients. Weight loss with physical activity programs and cessation of high-fat diets may reduce the risk. Finally, more research is needed on the efficacy of anti-osteoporotic treatments in obese patients. Full article
(This article belongs to the Special Issue Secondary Osteoporosis in Adults 3.0)
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