https://orcid.org/0000-0003-2520-6091
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ABSTRACT
Purpose
This manuscript will summarize the role of pro-inflammatory cytokines and tackle newly discussed ones within the scope of OA pathogenesis as mentioned in the recent literature. This will allow for a better understanding of the mechanisms behind such a complicated disease.
Material and methods
Relevant articles were obtained by searching key terms including “pro-inflammatory cytokines,” “inflammation,” “pathophysiology,” “cartilage damage,” and “OA” in PubMed and Google Scholar databases. The year ranges set for the selection of the articles was between 2015 -2021. Inclusion criteria was based on the relevance and contribution to the field of the study.
Results
Osteoarthritis (OA) has a complex multifactorial pathophysiology which is attributed to molecular and biomechanical changes that disrupt the normal balance of synthesis and degradation of articular cartilage and subchondral bone. Pro-inflammatory cytokines, with their wide range of action and intricate signaling pathways, are the constant subject of new discoveries revolving around this inflammatory disease. The available literature indicates that some of these cytokines such as IL-33, IL-17, IL-6, and IL-22 have a direct relation to cartilage degradation, while others like IL-15, IL-1, IL-7, and IL-34 have an indirect one.
Conclusions
Inflammation has an essential role in the manifestation of osteoarthritis clinical events. Specifically, certain cytokines exhibit pro-inflammatory properties that are markedly activated during the course of the disease and notably alter the homeostasis of the joint environment. However, clinical trials and observational studies remain insufficient to navigate the varying nature of this disease in humans.
Nomenclature
| ADAMTS | = | Adisintegrin and Metalloproteinase with a Thrombospondin Type 1 Motifs |
| Akt | = | Protein Kinase B |
| BMLs | = | Bone Marrow Lesions |
| CD | = | Cluster of Differentiation |
| CiOA | = | Collagenase Induced Osteoarthritis |
| DMM | = | Destabilization of Medial Meniscus |
| ERK | = | Extracellular Signal-Regulated Kinase |
| FLS | = | Fibroblast-like Synoviocytes |
| GAG | = | Glycosaminoglycan |
| GP | = | Glycoprotein |
| IL-1Ra | = | Interleukin-1 Receptor Antagonist |
| IL | = | Interleukin |
| IL1RAcP | = | Interleukin-1 Receptor Accessory Protein |
| ILCs | = | Innate Lymphoid Cells |
| IRAK-1 | = | Interleukin-1 Receptor Associated Kinase |
| Jak | = | Janus Kinase |
| KO | = | Knock-out |
| M-CSF | = | Macrophage Colony-Stimulating Factor |
| MMPs | = | Matrix Metalloproteinases |
| mRNA | = | Messenger Ribonucleic Acid |
| MyD88 | = | Myeloid Differentiation Primary Response 88 |
| NFkB | = | Nuclear Factor kappa B |
| NK | = | Natural Killer |
| NO | = | Nitric Oxide |
| OA | = | Osteoarthritis |
| PI3K | = | Phosphatidylinositol 3-Kinase |
| RA | = | Rheumatic Arthritis |
| SF | = | Synovial Fluid |
| Stat | = | Signal Transducer and Activator of Transcription |
| TH | = | T helper |
| Th17 | = | Interleukin 17-producing T helper cells |
| TLR | = | Toll-like Receptor |
| TNF-alpha | = | Tumor Necrosis Factor alpha |
| TRAF | = | Tumor Necrosis Factor Receptor—Associated Factor |
Authors contribution
Asma Inès Sana Jrad, Maha Trad, and Wafaa Bzeih: contributed equally to the work in Data curation, Methodology, Writing-original draft, Writing-review & editing. Dr. Georges El Hasbani and Dr. Imad Uthman: Supervision, Writing-review, Validation of final review.
Disclosure statement
No potential conflict of interest was reported by the author(s).