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Molecular Research in Primary Osteoporosis
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Molecular Research in Primary Osteoporosis

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: closed (30 January 2024) | Viewed by 4141

Special Issue Editors

Dr. Manuela Dicarlo

E-Mail Website
Guest Editor
Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), University of Bari Aldo Moro, Piazza Giulio Cesare 11, 70124 Bari, Italy
Interests: neurodegenerative diseases; Alzheimer’s disease; depression; anxiety; memory; learning; ageing; neuroinflammation; neurotrophic factors; synaptic plasticity; cell biology; irisin; prefrontal cortex; hippocampus; histology; electron microscopy
Special Issues, Collections and Topics in MDPI journals
Dr. Angela Oranger

E-Mail Website
Co-Guest Editor
Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), Section of Human Anatomy and Histology, University of Bari, 70124 Bari, Italy
Interests: multiple myeloma bone disease; bone remodeling; citokynes and bone mass modulation; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Primary osteoporosis, a frequent disorder of bone remodeling process, is characterized by the decrease in bone mass and mineral density (BMD). Because of the impairment in bone quality and microarchitecture, osteoporotic patients are more exposed to low-energy fractures in long bones and vertebrae than normal population. Primary osteoporosis predominantly affects postmenopausal women (type I osteoporosis) and the elderly population (type II osteoporosis); therefore, this skeletal disorder is often considered as an aging-associated disease. However, an idiopathic juvenile osteoporosis that may occur in children and young adults has also been described.

The high prevalence of primary osteoporosis increased the interest of the research to shed light on its pathogenesis trying to improve its current prevention and treatment methods.

In line with this aim, in this Special Issue, we welcome molecular- or cellular-level original research articles and comprehensive reviews relating to molecular pathophysiology and targeted therapies of this topic. Submissions of clinical studies with biomolecular experiments or pathological research with case sample data are also welcomed.

Dr. Manuela Dicarlo
Dr. Angela Oranger
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

  • idiopathic juvenile osteoporosis
  • postmenopausal osteoporosis
  • senile osteoporosis
  • bone loss
  • bone fragility
  • ageing

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Published Papers (2 papers)

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Research

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18 pages, 3608 KiB  
Article
Lipidomics Profiling of Patients with Low Bone Mineral Density (LBMD)
by Shereen M. Aleidi, Mysoon M. Al-Ansari, Eman A. Alnehmi, Abeer K. Malkawi, Ahmad Alodaib, Mohamed Alshaker, Hicham Benabdelkamel and Anas M. Abdel Rahman
Int. J. Mol. Sci. 2022, 23(19), 12017; https://doi.org/10.3390/ijms231912017 - 10 Oct 2022
Cited by 16 | Viewed by 2484
Abstract
The relationship between lipid metabolism and bone mineral density (BMD) is still not fully elucidated. Despite the presence of investigations using osteoporotic animal models, clinical studies in humans are limited. In this work, untargeted lipidomics profiling using liquid chromatography-mass spectrometry (LC-MS) analysis of [...] Read more.
The relationship between lipid metabolism and bone mineral density (BMD) is still not fully elucidated. Despite the presence of investigations using osteoporotic animal models, clinical studies in humans are limited. In this work, untargeted lipidomics profiling using liquid chromatography-mass spectrometry (LC-MS) analysis of human serum samples was performed to identify the lipidomics profile associated with low bone mineral density (LBMD), with a subsequent examination of potential biomarkers related to OP risk prediction or progression. A total of 69 participants were recruited for this cohort study, including the osteoporotic group (OP, n = 25), osteopenia group (ON, n = 22), and control (Ctrl, n = 22). The LBMD group included OP and ON patients. The lipidomics effect of confounding factors such as age, gender, lipid profile, body mass index (BMD), chronic diseases, and medications was excluded from the dataset. The results showed a clear group separation and clustering between LBMD and Ctrl (Q2 = 0.944, R2 = 0.991), indicating a significant difference in the lipids profile. In addition, 322 putatively identified lipid molecules were dysregulated, with 163 up- and 159 down-regulated in LBMD, compared with the Ctrl. The most significantly dysregulated subclasses were phosphatidylcholines (PC) (n = 81, 25.16% of all dysregulated lipids 322), followed by triacylglycerol (TG) (n = 65, 20.19%), and then phosphatidylethanolamine (PE) (n = 40, 12.42%). In addition, groups of glycerophospholipids, including LPC (7.45%), LPE (5.59%), and PI (2.48%) were also dysregulated as of LBMD. These findings provide insights into the lipidomics alteration involved in bone remodeling and LBMD. and may drive the development of therapeutic targets and nutritional strategies for OP management. Full article
(This article belongs to the Special Issue Molecular Research in Primary Osteoporosis)
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Review

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33 pages, 1346 KiB  
Review
Primary Osteoporosis Induced by Androgen and Estrogen Deficiency: The Molecular and Cellular Perspective on Pathophysiological Mechanisms and Treatments
by Shao-Heng Hsu, Li-Ru Chen and Kuo-Hu Chen
Int. J. Mol. Sci. 2024, 25(22), 12139; https://doi.org/10.3390/ijms252212139 - 12 Nov 2024
Viewed by 758
Abstract
Primary osteoporosis is closely linked to hormone deficiency, which disrupts the balance of bone remodeling. It affects postmenopausal women but also significantly impacts older men. Estrogen can promote the production of osteoprotegerin, a decoy receptor for RANKL, thereby preventing RANKL from activating osteoclasts. [...] Read more.
Primary osteoporosis is closely linked to hormone deficiency, which disrupts the balance of bone remodeling. It affects postmenopausal women but also significantly impacts older men. Estrogen can promote the production of osteoprotegerin, a decoy receptor for RANKL, thereby preventing RANKL from activating osteoclasts. Furthermore, estrogen promotes osteoblast survival and function via activation of the Wnt signaling pathway. Likewise, androgens play a critical role in bone metabolism, primarily through their conversion to estrogen in men. Estrogen deficiency accelerates bone resorption through a rise in pro-inflammatory cytokines (IL-1, IL-6, TNF-α) and RANKL, which promote osteoclastogenesis. In the classic genomic pathway, estrogen binds to estrogen receptors in the cytoplasm, forming a complex that migrates to the nucleus and binds to estrogen response elements on DNA, regulating gene transcription. Androgens can be defined as high-affinity ligands for the androgen receptor; their combination can serve as a ligand-inducible transcription factor. Hormone replacement therapy has shown promise but comes with associated risks and side effects. In contrast, the non-genomic pathway involves rapid signaling cascades initiated at the cell membrane, influencing cellular functions without directly altering gene expression. Therefore, the ligand-independent actions and rapid signaling pathways of estrogen and androgen receptors can be harnessed to develop new drugs that provide bone protection without the side effects of traditional hormone therapies. To manage primary osteoporosis, other pharmacological treatments (bisphosphonates, teriparatide, RANKL inhibitors, sclerostin inhibitors, SERMs, and calcitonin salmon) can ameliorate osteoporosis and improve BMD via actions on different pathways. Non-pharmacological treatments include nutritional support and exercise, as well as the dietary intake of antioxidants and natural products. The current study reviews the processes of bone remodeling, hormone actions, hormone receptor status, and therapeutic targets of primary osteoporosis. However, many detailed cellular and molecular mechanisms underlying primary osteoporosis seem complicated and unexplored and warrant further investigation. Full article
(This article belongs to the Special Issue Molecular Research in Primary Osteoporosis)
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