Inflammation and Oxidative Stress in Articular Cartilage

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1834

Special Issue Editor


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Guest Editor
1. Department of Orthopaedic Surgery, School of Public Health, Johns Hopkins University, Baltimore, MD, USA
2. Department of Molecular Microbiology and Immunology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA
Interests: in vitro models for disease; tissue repair/regeneration; osteoarthritis; nutraceuticals
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Special Issue Information

Dear Colleagues,

Articular cartilage is connective tissue between opposing bones. It functions to bear weight and facilitate joint movement. The only cellular constituents of articular cartilage are chondrocytes that produce the collagenous extracellular matrix. In addition, chondrocytes synthesize an array of biomolecules reported to mediate inflammation and oxidative stress. The aim of this Special Issue of the journal Antioxidants is to review the role of inflammation and oxidative stress in healthy, damaged and diseased joints. There is growing evidence of linkage between these two pathways and their effects on articular cartilage. This Special issue will include in vitro and in vivo studies on animals and man to provide supporting evidence. Joint areas of study include spine, hip, knee, shoulder, elbow, hand, ankle and foot.

Dr. Carmelita G. Frondoza
Guest Editor

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Keywords

  • cartilage
  • chondrocyte
  • joint inflammation
  • arthritis

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Published Papers (2 papers)

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Research

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19 pages, 3310 KB  
Article
The Preparation and Evaluation of Carvacrol-Added Hyaluronic Acid for Early Osteoarthritis Treatment
by Yu-Ping Chen, Jhih-Ni Lin, Chia-Tien Chang, Yu-Ying Lin, Che-Yung Kuan, Yu-Chun Chen and Feng-Huei Lin
Antioxidants 2025, 14(10), 1265; https://doi.org/10.3390/antiox14101265 - 21 Oct 2025
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Abstract
Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage degradation, synovial inflammation, and subchondral bone remodeling, leading to chronic pain and reduced mobility. In early-stage OA, sustained oxidative stress and inflammation drive chondrocyte dysfunction and extracellular matrix (ECM) loss. Hyaluronic acid [...] Read more.
Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage degradation, synovial inflammation, and subchondral bone remodeling, leading to chronic pain and reduced mobility. In early-stage OA, sustained oxidative stress and inflammation drive chondrocyte dysfunction and extracellular matrix (ECM) loss. Hyaluronic acid (HA), a key component of synovial fluid responsible for lubrication and viscoelasticity, is prone to enzymatic and oxidative degradation under inflammatory conditions, limiting its therapeutic effect. To address this, we developed an HA-based system incorporating the natural antioxidant and anti-inflammatory molecule carvacrol. The potential of this formulation was assessed in interleukin-1b-stimulated chondrocytes, which mimic the inflammatory environment of OA. The carvacrol-added HA combination upregulated antioxidant enzyme expression, attenuated pro-inflammatory signaling, and promoted ECM preservation by up regulating cartilage-specific markers and glycosaminoglycan production. In vivo efficacy was further evaluated in a rat model of monosodium iodoacetate-induced OA. HA-Carvacrol treatment alleviated pain-related behaviors and preserved cartilage structure, as confirmed by behavioral assessments and histological analyses. This dual-function formulation integrates the lubricating benefits of HA with the bioactivity of carvacrol, providing preclinical proof-of-concept evidence for its potential in early-stage OA. Full article
(This article belongs to the Special Issue Inflammation and Oxidative Stress in Articular Cartilage)
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Review

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23 pages, 2203 KB  
Review
The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress
by Huiying Zhao and Wei Wu
Antioxidants 2025, 14(10), 1228; https://doi.org/10.3390/antiox14101228 - 13 Oct 2025
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Abstract
Osteoarthritis (OA) is one of the most common joint diseases worldwide, which is characterized by degenerative changes in articular cartilage and secondary osteophyte formation. Numerous factors influence OA, including aging, obesity, joint injury and chronic overloading. Among them, the senescence of chondrocytes is [...] Read more.
Osteoarthritis (OA) is one of the most common joint diseases worldwide, which is characterized by degenerative changes in articular cartilage and secondary osteophyte formation. Numerous factors influence OA, including aging, obesity, joint injury and chronic overloading. Among them, the senescence of chondrocytes is one of the key factors leading to OA. Chondrocyte senescence can trigger inflammatory responses, extracellular matrix (ECM) degradation, mitochondrial dysfunction and oxidative stress (OS), and autophagy. Sirtuin 6 (SIRT6), as a deacetylase related to aging, can regulate chondrocyte senescence and plays a certain part in OA. SIRT6 regulates the number and membrane integrity of mitochondria, alleviates excessive Reactive Oxygen Species (ROS) in mitochondria and reduces inflammation-mediated mitochondrial damage. In addition, SIRT6 can also regulate the activity of antioxidant enzymes, inhibit excessive ROS induced by inflammatory factors, and alleviate OS. However, as aging progresses, the activity of SIRT6 will decrease. Activating the activity of SIRT6 becomes a potential therapeutic target and has a certain alleviating effect on the development of OA. The supplementation of nicotinamide adenine dinucleotide (NAD+) precursors and SIRT6-specific activators can increase SIRT6, alleviate chondrocyte senescence, and reduce OA. This paper aims to focus on mitochondrial dysfunction and OS to explore SIRT6’s effects on OA chondrocytes’ senescence under aging and summarize the potential therapeutic targets for activating SIRT6 to provide assistance for the improvement of OA. Full article
(This article belongs to the Special Issue Inflammation and Oxidative Stress in Articular Cartilage)
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