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Biomedicines
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Molecular and Cellular Mechanisms of Bone and Cartilage Diseases 2.0
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Molecular and Cellular Mechanisms of Bone and Cartilage Diseases 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 7782

Special Issue Editor

Dr. M. Alaa Terkawi

E-Mail Website
Guest Editor
Department of Orthopaedic Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan
Interests: interaction between the skeletal and immune systems in health and diseases; bone and cartilage metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bones and cartilage form the most important parts of the musculoskeletal system that provides mobility and maintains body posture. Musculoskeletal disorders, namely, those affecting bone and cartilage, limit the mobility and productivity of individuals, leading to early retirement from work and a reduced ability of people to participate in society. Osteoarthritis, rheumatoid arthritis, osteoporosis, and low back pain are the major musculoskeletal disorders and represent a significant socioeconomic burden on individuals and medical services worldwide. A better understanding of the pathophysiology of bone and cartilage in these diseases should provide important clues for the discovery of new therapies. The current Special Issue focuses on molecular and cellular mechanisms underlining bone and cartilage pathology and novel therapeutic approaches targeting the above diseases. We welcome research or review articles focusing on the following topics:

  • Molecular and cellular mechanisms underlining bone and cartilage pathology in related diseases;
  • Bone and cartilage metabolism in health and disease;
  • Therapeutic strategies for prevention of bone and cartilage pathology;
  • Novel approaches for bone and cartilage regeneration.

Dr. M. Alaa Terkawi
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • pathophysiology of bone and cartilage
  • therapy
  • osteoarthritis
  • rheumatoid arthritis
  • osteoporosis
  • low back pain

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Related Special Issue

Published Papers (3 papers)

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Research

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14 pages, 1151 KiB  
Article
The Analysis of ECE1 and PPARG Variants in the Development of Osteopenia and Osteoporosis in Postmenopausal Women
by Izabela Uzar, Anna Bogacz, Małgorzata Łuszczyńska, Marlena Wolek, Katarzyna Kotrych, Andrzej Modrzejewski, Bogusław Czerny, Paweł Ziętek and Adam Kamiński
Biomedicines 2024, 12(7), 1440; https://doi.org/10.3390/biomedicines12071440 - 27 Jun 2024
Viewed by 629
Abstract
Osteoporosis is a multifactorial systemic skeletal disease that is characterized by a low bone mineral density (BMD) and the microarchitectural deterioration of bone tissue, leading to bone fragility. The search for new genes that may play an important role in the regulation of [...] Read more.
Osteoporosis is a multifactorial systemic skeletal disease that is characterized by a low bone mineral density (BMD) and the microarchitectural deterioration of bone tissue, leading to bone fragility. The search for new genes that may play an important role in the regulation of bone mass and the development of osteoporosis is ongoing. Recently, it was found that altering the activity of the endothelin-1-converting enzyme encoded by the ECE1 gene may affect bone mineral density (BMD). Another gene involved in the process of osteoblast differentiation and maturation is believed to be PPARG (peroxisome proliferator-activated receptor gamma). This participates in regulating the transformation of stem cells and affects the process of bone formation and resorption. Therefore, we analyzed the association of the ECE1 and PPARG variants with osteopenia and osteoporosis risk in the Polish population. This study included a group (n = 608) of unrelated Polish women (245 individuals with osteoporosis (aged: 57 ± 9), 109 individuals with osteopenia (aged: 53 ± 8) and 254 healthy controls (aged: 54 ± 8)). The real-time PCR technique was used to determine the genetic variants for rs213045 (-338G>T) and rs213046 (-839A>C) of the ECE1 gene and rs1801282 (Pro12Ala, C>G) of the PPARG gene. Analysis of the PPARG rs1801282 variants did not show any association with the risk of osteoporosis and osteopenia. However, in the densitometric results, lower median Z-score values were observed for the T allele compared to the G allele for the rs213045 variant of the ECE1 gene (−1.11 ± 1.07 vs. −0.78 ± 1.21, p = 0.021). Moreover, the TT genotype for the rs213045 variant was more common in women with osteopenia (13.8%, OR = 2.82, p < 0.05) and osteoporosis (7.8%, OR = 1.38, p > 0.05) compared to the control group (5.5%). Additionally, our results suggested that the T allele of rs213045 was more common in women with osteopenia compared to the controls. We further observed that the haplotype containing two major GA alleles of ECE1 (rs213045, rs213046) could reduce the risk of osteopenia in our population. Finally, we found that women with osteoporosis had statistically significantly lower body mass and BMI values compared to the control group. Our results suggest that the ECE1 rs213045 variant may increase the risk of osteopenia. However, the data obtained require confirmation in further studies. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Bone and Cartilage Diseases 2.0)
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Review

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27 pages, 2010 KiB  
Review
Revisiting Resveratrol as an Osteoprotective Agent: Molecular Evidence from In Vivo and In Vitro Studies
by Haryati Ahmad Hairi, Putri Ayu Jayusman and Ahmad Nazrun Shuid
Biomedicines 2023, 11(5), 1453; https://doi.org/10.3390/biomedicines11051453 - 16 May 2023
Cited by 10 | Viewed by 2707
Abstract
Resveratrol (RSV) (3,5,4′-trihydroxystilbene) is a stilbene found in abundance in berry fruits, peanuts, and some medicinal plants. It has a diverse range of pharmacological activities, underlining the significance of illness prevention and health promotion. The purpose of this review was to delve deeper [...] Read more.
Resveratrol (RSV) (3,5,4′-trihydroxystilbene) is a stilbene found in abundance in berry fruits, peanuts, and some medicinal plants. It has a diverse range of pharmacological activities, underlining the significance of illness prevention and health promotion. The purpose of this review was to delve deeper into RSV’s bone-protective properties as well as its molecular mechanisms. Several in vivo studies have found the bone-protective effects of RSV in postmenopausal, senile, and disuse osteoporosis rat models. RSV has been shown to inhibit NF-κB and RANKL-mediated osteoclastogenesis, oxidative stress, and inflammation while increasing osteogenesis and boosting differentiation of mesenchymal stem cells to osteoblasts. Wnt/β-catenin, MAPKs/JNK/ERK, PI3K/AKT, FoxOs, microRNAs, and BMP2 are among the possible kinases and proteins involved in the underlying mechanisms. RSV has also been shown to be the most potent SIRT1 activator to cause stimulatory effects on osteoblasts and inhibitory effects on osteoclasts. RSV may, thus, represent a novel therapeutic strategy for increasing bone growth and reducing bone loss in the elderly and postmenopausal population. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Bone and Cartilage Diseases 2.0)
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29 pages, 1131 KiB  
Review
The Interleukine-17 Cytokine Family: Role in Development and Progression of Spondyloarthritis, Current and Potential Therapeutic Inhibitors
by Anna Davydova, Yuliya Kurochkina, Veronika Goncharova, Mariya Vorobyeva and Maksim Korolev
Biomedicines 2023, 11(5), 1328; https://doi.org/10.3390/biomedicines11051328 - 30 Apr 2023
Cited by 4 | Viewed by 3748
Abstract
Spondyloarthritis (SpA) encompasses a group of chronic inflammatory rheumatic diseases with a predilection for the spinal and sacroiliac joints, which include axial spondyloarthritis, psoriatic arthritis, reactive arthritis, arthritis associated with chronic inflammatory bowel disease, and undifferentiated spondyloarthritis. The prevalence of SpA in the [...] Read more.
Spondyloarthritis (SpA) encompasses a group of chronic inflammatory rheumatic diseases with a predilection for the spinal and sacroiliac joints, which include axial spondyloarthritis, psoriatic arthritis, reactive arthritis, arthritis associated with chronic inflammatory bowel disease, and undifferentiated spondyloarthritis. The prevalence of SpA in the population varies from 0.5 to 2%, most commonly affecting young people. Spondyloarthritis pathogenesis is related to the hyperproduction of proinflammatory cytokines (TNFα, IL-17A, IL-23, etc.). IL-17A plays a key role in the pathogenesis of spondyloarthritis (inflammation maintenance, syndesmophites formation and radiographic progression, enthesites and anterior uveitis development, etc.). Targeted anti-IL17 therapies have established themselves as the most efficient therapies in SpA treatment. The present review summarizes literature data on the role of the IL-17 family in the pathogenesis of SpA and analyzes existing therapeutic strategies for IL-17 suppression with monoclonal antibodies and Janus kinase inhibitors. We also consider alternative targeted strategies, such as the use of other small-molecule inhibitors, therapeutic nucleic acids, or affibodies. We discuss advantages and pitfalls of these approaches and the future prospects of each method. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Bone and Cartilage Diseases 2.0)
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