Table 1.
Circulating and histological markers of inflammation in human OA.
| Reference | Study Goals | Change of Mediators | Other Results |
|---|---|---|---|
| Circulating mediators of inflammation | |||
| Sohn D.H. et al. [8] | Proteomic analysis of serum/synovial fluid (SF) | Newly identified NF-kB-related proteins, cytokine receptors (IL-12R, IL-18R, IL-20R) and macrophage-derived inflammatory proteins in synovial fluid High levels of IL-6 in SF |
Upregulation of histone deacetylase Upregulated plasma proteins, protease inhibitors, NF-kB subunits and regulators, cytokines (IL-6, MCP-1, VEGF), complement fragments in OA sera |
| Gobezie R. et al. [11] | Synovial protein analysis in OA patients and healthy | ↑ Albumin, fibrinogen, α1-microglobulin/bikunin precursor, α2-macroglobulin, haptoglobin, complement C3 ↓ Cystatin C, aggrecan |
18 Proteins differentially expressed between OA and healthy |
| Krenytska D. et al. [12] | Comparative analysis of plasma cytokines and growth factors in OA, OA + COVID-19 and controls | ↑ IL-1β in OA ↓ TNF-α, NF-kB in OA ↓ VEGF, PDGF, FGF2 in OA No significant changes in IL-6 and HIF-1α |
Maximum values of IL-1β, less pronounced decrease in TNF-α and NF-kB |
| Wang Z.W. et al. [14] | Serum protein analysis in OA patients | ↑ IL-1β, IL-6, TNFα, VEGF in OA patients vs. controls | Increased expression of IL-1β, IL-6, TNFα, VEGF in synoviocytes |
| Stannus O. et al. [19] | Follow-up study of serum cytokines in an elderly cohort | Quartiles of IL-6 and TNF-α are associated with joint space narrowing | Baseline and changes of IL-6 predicts medial and lateral cartilage volume loss |
| Barker T. et al. [20] | Comparative study of serum IL-10 and TNF-α in different OA stages and controls | ↓ IL-10 and IL-10/TNFα in subjects who underwent ACL or TJR surgery No significant changes in TNFα |
IL-10 and IL-10/TNFα significantly differ between Kellgren–Lawrence scores 3 vs. 4 Low IL-10 suggests predisposition for development of severe knee OA |
| Panina S.B. et al. [21] | Comparative study of plasma and SF mediators in post-traumatic OA patients and controls | ↑ plasma leptin, IL-1β and IL-6 | Plasma leptin and SF IL-18 correlate with the Kellgren–Lawrence score in PTOA Significant correlation between plasma and SF leptin, IL-6 and IL-18 |
| Waszczykowski M. et al. [22] | Comparative study of serum and SF cytokines in OA vs. healthy controls | ↑ serum IL-6, IL-18 and IL-20 in OA vs. control group | IL-18 correlates with MMP-3 in OA patients ROC curve of IL-20 suggests diagnostic potential |
| Histological markers of inflammation | |||
| Wang Z.W. et al. [14] | Synovial membrane immunohistochemistry analysis | ↑ IL-1β, IL-6, TNF-α and VEGF synovial membrane expression in moderate/advanced OA compared to mild OA | ↑ serum IL-1β, IL-6, TNFα, VEGF in OA patients vs. controls |
| Qu X.Q. et al. [25] | Comparative genetic and immunohistochemistry study of OA vs. normal cartilage specimens (knee arthroplasty and meniscus surgery) | ↑ IL-6 and MMP-9 expression in OA specimens | ↑ IL-6 and MMP-9 gene expression in OA cartilage |
| Warner S.C. et al. [27] | Immunohistochemistry and explant culture studies of OA patients | ↑ IL-15Rα in OA samples | IL-15 treatment induction of MMP-1 and MMP-3 |
| Scanzello C.R. et al. [28] | Synovial membrane immunohistochemistry in early vs. advanced OA patient cohort | ↑ IL-15Rα in synovial membrane cells from patients with advanced OA | Increased IL-15 in SF, correlating with IL-6 |
| Iannone F. et al. [29] | Comparative immunohistochemistry study of OA vs. healthy subjects | ↑ IL-10 protein and mRNA expression in high-intensity cartilage lesions | No relationship between IL-10R expression and cartilage lesion degree |
| Vuolteenaho et al. [34] | OA patients cohort study of phenotype-explanted cartilage | ↑ IL-6, IL-8, PGE2, Cox-2 expression in cartilage cultures obtained by joint replacement, induced by leptin/IL-1β | Selective inhibition of iNOS suppressed IL-6, IL-8, PGE2 |