The Role of Inflammatory and Anti-Inflammatory Cytokines in the Pathogenesis of Osteoarthritis
Open accessAbstract
Osteoarthritis (OA) is the most common chronic disease of human joints. The basis of pathologic changes involves all the tissues forming the joint; already, at an early stage, it has the nature of inflammation with varying degrees of severity. An analysis of the complex relationships indicates that the processes taking place inside the joint are not merely a set that (seemingly) only includes catabolic effects. Apart from them, anti-inflammatory anabolic processes also occur continually. These phenomena are driven by various mediators, of which the key role is attributed to the interactions within the cytokine network. The most important group controlling the disease seems to be inflammatory cytokines, including IL-1 β , TNF α , IL-6, IL-15, IL-17, and IL-18. The second group with antagonistic effect is formed by cytokines known as anti-inflammatory cytokines such as IL-4, IL-10, and IL-13. The role of inflammatory and anti-inflammatory cytokines in the pathogenesis of OA with respect to inter- and intracellular signaling pathways is still under investigation. This paper summarizes the current state of knowledge. The cytokine network in OA is put in the context of cells involved in this degenerative joint disease. The possibilities for further implementation of new therapeutic strategies in OA are also pointed.
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IL-1β induces iNOS expression, generating more nitric oxide and aggravating cartilage disintegration.
“By means of chondrocyte mortality, MMP activation, and proteoglycan synthesis inhibition, IL-1β induces iNOS expression, hence generating more nitric oxide (NO) and aggravating cartilage disintegration [41].”
From Biomarker-Guided Imaging and AI-Augmented Diagnosis of Degenerative Joint Disease (2025) · cites this paper as [41]
Section 2.1 reports that IL-1β affects iNOS, which generates nitric oxide, and separately describes IL-1β-driven cartilage deterioration, MMP production, impaired matrix synthesis, and chondrocyte apoptosis (page not available). It does not say that those effects are the means by which IL-1β induces iNOS, or explicitly attribute cartilage disintegration to the resulting nitric oxide. (LLM, conf=0.84)
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BackgroundInfluentialInflammation in osteoarthritis
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- Authors
- Wojdasiewicz, P., Poniatowski, Ł. A., & Szukiewicz, D.
- Affiliations
- Medical University of Warsaw (PL)
- Corresponding author
- Szukiewicz, Dariusz
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2014
- Volume
- 2014
- Pages
- 1-19
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC4021678
- OpenAlex
- W2164993228
- Cited by
- 1,608
- References
- 6
- Citations by year
- 2026: 85 · 2025: 154 · 2024: 175 · 2023: 157 · 2022: 198 · 2021: 231 · 2020: 188 · 2019: 127 · 2018: 104 · 2017: 85 · 2016: 56 · 2015: 38 · 2014: 7 · 2013: 1 · 2012: 1
- FWCI
- 10.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Keywords
- osteoarthritis, inflammatory cytokines, anti-inflammatory cytokines, cytokine network, joint inflammation, IL-1β, TNF-α, interleukin-6, IL-17, IL-18, IL-10, IL-4, IL-13, signaling pathways, joint degeneration, treatment options
- MeSH terms
- Animals, Anti-Inflammatory Agents, Humans, Immunologic Factors, Inflammation, Joint Diseases, Osteoarthritis, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-4, Interleukin-6, Cytokines, Interleukin-15, Interleukin-17, Interleukin-18, Mice, Interleukin-1beta
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