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New Advances in Osteoarthritis 2.0
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New Advances in Osteoarthritis 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: closed (30 April 2023) | Viewed by 12191

Special Issue Editor

Dr. Gabriela Loots

E-Mail Website
Guest Editor
Department of Molecular and Cell Biology, School of Natural Sciences, University of California, Merced, CA 95340, USA
Interests: bone and cartilage biology; osteoarthritis; post-traumatic osteoarthritis; Wnt signaling; cancer metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Osteoarthritis (OA) is the most common form of joint disease and the leading cause of disability as we age due to stiffness, pain, biomechanical failure, and impaired joint movement. Despite its high prevalence and burden on the healthcare system, no suitable treatments currently exist that can halt disease progression, promote cartilage repair and regeneration, or cure the disease. Furthermore, no specific diagnostic biomarkers have been identified for OA that can identify the disease at its earliest stages. With the substantial progress in molecular biology, genetics, genomics, and animal models of OA, in the last decade, OA has evolved as a disease where systemic inflammation and the immune system significantly modify the disease, classifying it also as an inflammatory disease. Thus, disease-modifying osteoarthritis drugs (DMOADs) are rapidly evolving, and attention is shifting to new targets that include transcription factors, growth factors, and receptors. To help to promote advancements in the field of OA research and disseminate new discoveries and information relevant to OA diagnosis, treatment, and care, we seek manuscripts that present novel basic, pre-clinical, and clinical research in the OA field that includes not only positive but also negative results. The rapid review and fast-tracked publication of your work will help to advance our knowledge and understanding of OA toward improving patient care.

Potential topics include but are not limited to:                   

  • Osteoarthritis                   
  • Post traumatic osteoarthritis                   
  • Joint Inflammation                   
  • Cartilage and chondrocyte function                   
  • Growth factors and other secreted molecules that influence cartilage anabolism and catabolism                   
  • Cartilage–bone interaction                   
  • Cartilage regeneration and repair                   
  • Synovium

Dr. Gabriela Loots
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

  • osteoarthritis
  • post traumatic osteoarthritis
  • joint Inflammation
  • cartilage and chondrocyte function
  • cartilage anabolism and catabolism
  • cartilage–bone interaction
  • cartilage regeneration and repair
  • synovium

Published Papers (6 papers)

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Research

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21 pages, 8254 KiB  
Article
Preparation of Melatonin-Loaded Nanoparticles with Targeting and Sustained Release Function and Their Application in Osteoarthritis
by Haifeng Liang, Yiran Yan, Wei Sun, Xiaogang Ma, Zhiwen Su, Zhongxun Liu, Yan Chen and Bo Yu
Int. J. Mol. Sci. 2023, 24(10), 8740; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24108740 - 14 May 2023
Cited by 2 | Viewed by 1800
Abstract
(1) The vicious cycle of innate immune response and reactive oxygen species (ROS) generation is an important pathological process of osteoarthritis (OA). Melatonin may be a new hope for the treatment of OA because of its antioxidant capacity. However, the mechanism of melatonin [...] Read more.
(1) The vicious cycle of innate immune response and reactive oxygen species (ROS) generation is an important pathological process of osteoarthritis (OA). Melatonin may be a new hope for the treatment of OA because of its antioxidant capacity. However, the mechanism of melatonin in the treatment of OA is still not completely clear, and the physiological characteristics of articular cartilage make melatonin unable to play a long-term role in OA. (2) The effects of melatonin on ROS and the innate immune response system in OA chondrocytes and the therapeutic effect in vivo were evaluated. Then, a melatonin-loaded nano-delivery system (MT@PLGA-COLBP) was prepared and characterized. Finally, the behavior of MT@PLGA-COLPB in cartilage and the therapeutic effect in OA mice were evaluated. (3) Melatonin can inhibit the activation of the innate immune system by inhibiting the TLR2/4-MyD88-NFκB signal pathway and scavenging ROS, thus improving cartilage matrix metabolism and delaying the progression of OA in vivo. MT@PLGA-COLBP can reach the interior of cartilage and complete the accumulation in OA knee joints. At the same time, it can reduce the number of intra-articular injections and improve the utilization rate of melatonin in vivo. (4) This work provides a new idea for the treatment of osteoarthritis, updates the mechanism of melatonin in the treatment of osteoarthritis, and highlights the application prospect of PLGA@MT-COLBP nanoparticles in preventing OA. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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11 pages, 5900 KiB  
Communication
Decreased SIRT1 Activity Is Involved in the Acute Injury Response of Chondrocytes to Ex Vivo Injurious Mechanical Overload
by Sonali Karnik, Hessam Noori-Dokht, Taylor Williams, Amin Joukar, Stephen B. Trippel, Uma Sankar and Diane R. Wagner
Int. J. Mol. Sci. 2023, 24(7), 6521; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24076521 - 30 Mar 2023
Cited by 2 | Viewed by 1412
Abstract
A better understanding of molecular events following cartilage injury is required to develop treatments that prevent or delay the onset of trauma-induced osteoarthritis. In this study, alterations to SIRT1 activity in bovine articular cartilage explants were evaluated in the 24 h following a [...] Read more.
A better understanding of molecular events following cartilage injury is required to develop treatments that prevent or delay the onset of trauma-induced osteoarthritis. In this study, alterations to SIRT1 activity in bovine articular cartilage explants were evaluated in the 24 h following a mechanical overload, and the effect of pharmacological SIRT1 activator SRT1720 on acute chondrocyte injury was assessed. SIRT1 enzymatic activity decreased as early as 5 min following the mechanical overload, and remained suppressed for at least 24 h. The chondrocyte injury response, including apoptosis, oxidative stress, secretion of inflammatory mediators, and alterations in cartilage matrix expression, was prevented with pharmacological activation of SIRT1 in a dose-dependent manner. Overall, the results implicate SIRT1 deactivation as a key molecular event in chondrocyte injury following a mechanical impact overload. As decreased SIRT1 signaling is associated with advanced age, these findings suggest that downregulated SIRT1 activity may be common to both age-related and injury-induced osteoarthritis. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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14 pages, 2218 KiB  
Article
Genome-Wide Association Study and Transcriptome of Japanese Patients with Developmental Dysplasia of the Hip Demonstrates an Association with the Ferroptosis Signaling Pathway
by Yu Mori, Kazuko Ueno, Daisuke Chiba, Ko Hashimoto, Yosuke Kawai, Kazuyoshi Baba, Hidetatsu Tanaka, Takashi Aki, Masanori Ogasawara, Naoto Shibasaki, Katsushi Tokunaga, Toshimi Aizawa and Masao Nagasaki
Int. J. Mol. Sci. 2023, 24(5), 5019; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24055019 - 06 Mar 2023
Cited by 1 | Viewed by 2306
Abstract
This study examined the association between developmental dysplasia of the hip (DDH) and disease-associated loci in a Japanese cohort. A genome-wide association study (GWAS) of 238 Japanese patients with DDH and 2044 healthy individuals was performed. As a replicate, GWAS was also conducted [...] Read more.
This study examined the association between developmental dysplasia of the hip (DDH) and disease-associated loci in a Japanese cohort. A genome-wide association study (GWAS) of 238 Japanese patients with DDH and 2044 healthy individuals was performed. As a replicate, GWAS was also conducted on the UK Biobank data with 3315 cases and matched 74,038 controls. Gene set enrichment analyses (GSEAs) of both the genetics and transcriptome of DDH were performed. Transcriptome analysis of cartilage specimens from DDH-associated osteoarthritis and femoral neck fractures was performed as a control. Most of the lead variants were very low-frequency ones in the UK, and variants in the Japanese GWAS could not be replicated with the UK GWAS. We assigned DDH-related candidate variants to 42 and 81 genes from the Japanese and UK GWASs, respectively, using functional mapping and annotation. GSEA of gene ontology, disease ontology, and canonical pathways identified the most enriched pathway to be the ferroptosis signaling pathway, both in the Japanese gene set as well as the Japanese and UK merged set. Transcriptome GSEA also identified significant downregulation of genes in the ferroptosis signaling pathway. Thus, the ferroptosis signaling pathway may be associated with the pathogenic mechanism of DDH. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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18 pages, 2963 KiB  
Article
Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells
by Gabriella Teti, Eleonora Mazzotti, Valentina Gatta, Francesca Chiarini, Maria Laura Alfieri and Mirella Falconi
Int. J. Mol. Sci. 2023, 24(4), 3109; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24043109 - 04 Feb 2023
Cited by 1 | Viewed by 1558
Abstract
Osteoarthritis (OA) is described as a chronic degenerative disease characterized by the loss of articular cartilage. Senescence is a natural cellular response to stressors. Beneficial in certain conditions, the accumulation of senescent cells has been implicated in the pathophysiology of many diseases associated [...] Read more.
Osteoarthritis (OA) is described as a chronic degenerative disease characterized by the loss of articular cartilage. Senescence is a natural cellular response to stressors. Beneficial in certain conditions, the accumulation of senescent cells has been implicated in the pathophysiology of many diseases associated with aging. Recently, it has been demonstrated that mesenchymal stem/stromal cells isolated from OA patients contain many senescent cells that inhibit cartilage regeneration. However, the link between cellular senescence in MSCs and OA progression is still debated. In this study, we aim to characterize and compare synovial fluid MSCs (sf-MSCs), isolated from OA joints, with healthy sf-MSCs, investigating the senescence hallmarks and how this state could affect cartilage repair. Sf-MSCs were isolated from tibiotarsal joints of healthy and diseased horses with an established diagnosis of OA with an age ranging from 8 to 14 years. Cells were cultured in vitro and characterized for cell proliferation assay, cell cycle analysis, ROS detection assay, ultrastructure analysis, and the expression of senescent markers. To evaluate the influence of senescence on chondrogenic differentiation, OA sf-MSCs were stimulated in vitro for up to 21 days with chondrogenic factors, and the expression of chondrogenic markers was compared with healthy sf-MSCs. Our findings demonstrated the presence of senescent sf-MSCs in OA joints with impaired chondrogenic differentiation abilities, which could have a potential influence on OA progression. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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Review

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27 pages, 3813 KiB  
Review
From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review
by Vladimirs Naumovs, Valērija Groma and Jānis Mednieks
Int. J. Mol. Sci. 2022, 23(24), 16031; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232416031 - 16 Dec 2022
Cited by 3 | Viewed by 2086
Abstract
Nowadays, osteoarthritis (OA), a common, multifactorial musculoskeletal disease, is considered to have a low-grade inflammatory pathogenetic component. Lately, neuropsychiatric sequelae of the disease have gained recognition. However, a link between the peripheral inflammatory process of OA and the development of neuropsychiatric pathology is [...] Read more.
Nowadays, osteoarthritis (OA), a common, multifactorial musculoskeletal disease, is considered to have a low-grade inflammatory pathogenetic component. Lately, neuropsychiatric sequelae of the disease have gained recognition. However, a link between the peripheral inflammatory process of OA and the development of neuropsychiatric pathology is not completely understood. In this review, we provide a narrative that explores the development of neuropsychiatric disease in the presence of chronic peripheral low-grade inflammation with a focus on its signaling to the brain. We describe the development of a pro-inflammatory environment in the OA-affected joint. We discuss inflammation-signaling pathways that link the affected joint to the central nervous system, mainly using primary sensory afferents and blood circulation via circumventricular organs and cerebral endothelium. The review describes molecular and cellular changes in the brain, recognized in the presence of chronic peripheral inflammation. In addition, changes in the volume of gray matter and alterations of connectivity important for the assessment of the efficacy of treatment in OA are discussed in the given review. Finally, the narrative considers the importance of the use of neuropsychiatric diagnostic tools for a disease with an inflammatory component in the clinical setting. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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15 pages, 700 KiB  
Review
Osteoarthritis as an Umbrella Term for Different Subsets of Humans Undergoing Joint Degeneration: The Need to Address the Differences to Develop Effective Conservative Treatments and Prevention Strategies
by David A. Hart
Int. J. Mol. Sci. 2022, 23(23), 15365; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232315365 - 06 Dec 2022
Cited by 9 | Viewed by 2305
Abstract
Osteoarthritis (OA) of joints such as the knee and hip are very prevalent, and the number of individuals affected is expected to continue to rise. Currently, conservative treatments after OA diagnosis consist of a series of increasingly invasive interventions as the degeneration and [...] Read more.
Osteoarthritis (OA) of joints such as the knee and hip are very prevalent, and the number of individuals affected is expected to continue to rise. Currently, conservative treatments after OA diagnosis consist of a series of increasingly invasive interventions as the degeneration and pain increase, leading very often to joint replacement surgery. Most interventions are focused on alleviating pain, and there are no interventions currently available that stop and reverse OA-associated joint damage. For many decades OA was considered a disease of cartilage, but it is now considered a disease of the whole multi-tissue joint. As pain is the usual presenting symptom, for most patients, it is not known when the disease process was initiated and what the basis was for the initiation. The exception is post-traumatic OA which results from an overt injury to the joint that elevates the risk for OA development. This scenario leads to very long wait lists for joint replacement surgery in many jurisdictions. One aspect of why progress has been so slow in addressing the needs of patients is that OA has been used as an umbrella term that does not recognize that joint degeneration may arise from a variety of mechanistic causes that likely need separate analysis to identify interventions unique to each subtype (post-traumatic, metabolic, post-menopausal, growth and maturation associated). A second aspect of the slow pace of progress is that the bulk of research in the area is focused on post-traumatic OA (PTOA) in preclinical models that likely are not clearly relevant to human OA. That is, only ~12% of human OA is due to PTOA, but the bulk of studies investigate PTOA in rodents. Thus, much of the research community is failing the patient population affected by OA. A third aspect is that conservative treatment platforms are not specific to each OA subset, nor are they integrated into a coherent fashion for most patients. This review will discuss the literature relevant to the issues mentioned above and propose some of the directions that will be required going forward to enhance the impact of the research enterprise to affect patient outcomes. Full article
(This article belongs to the Special Issue New Advances in Osteoarthritis 2.0)
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