الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 185 |  |  |
| | | from | 185 | | |
Abstract
O
steoarthritis is the most prevalent form of arthritis in adults associated with high socioeconomic burden and is a major cause of disability in elderly, it should be considered a syndrome rather than a single disease in which structural changes of hyaline articular cartilage, subchondral bone, ligaments, capsule, synovium, muscles, and periarticular changes are involved. The knee is the most commonly affected joint.
Knee osteoarthritis is classified as either primary or secondary, depending on its cause. Primary knee osteoarthritis is the result of articular cartilage degeneration without any known reason. This is typically thought of as degeneration due to age as well as wear and tear. Secondary knee osteoarthritis is the result of articular cartilage degeneration due to a known reason.
The degradation of the articular cartilage is the central feature of KOA (Sharma, 2021). The local unbalanced biomechanical microenvironment and various biological factors in OA induce cartilage homeostasis dysregulation, resulting in collagen- and proteoglycan-rich extracellular matrix (ECM) degradation, articular surface fibrosis and erosion, cell death, matrix calcification, and vascular invasion.
Pro-inflammatory factors secreted by hypertrophic chondrocytes stimulate synovial cell proliferation and induce T, B lymphocytes and mast cell infiltration in synovial fluid (Primorac et al., 2020). The triggered synovial tissue releases pro-inflammatory mediators to promote the cascade development of KOA (Hsia et al., 2018).
Interleukin-17 (IL-17) is a pleiotropic cytokine that plays a role in inflammatory diseases such as osteoarthritis (OA). IL-17 shares biological activities with IL-1, a cytokine involved in the destruction of cartilage. IL-17 inhibits matrix synthesis by articular chondrocytes in vitro by increasing nitric oxide production (Lubberts et al., 2005; Na et al., 2020).
IL-17 has been shown to induce the release of chemokines by chondrocytes and synovial fibroblasts, contributing to synovial infiltration and cartilage destruction (Yang et al., 2020).
IL-17A, IL-17F, and IL-22 have been associated with osteoclastogenic activation and cartilage destruction in both experimental and human studies (McGonagle et al., 2019).
In our study we correlate IL-17 levels in serum and synovial fluid with disease severity and functional status of the patients based on clinical examination, radiological investigations (using K/L scale) and VAS & WOMAC scoring system.
All our enrolled subjects were subjected to whole blood (5 ml) collection in vacutainer tubes, then allowed to clot for 30 min. at room temperature and then centrifuged for 15 min at 1000 g. The resulting serum was removed and stored at-80°C until use. Serum level of interleukin-17 was measured using Sandwich ELISA technique, according to the instruction of the manufacturer (NOVA, Beijing China).
In Patients with knee effusion Synovial fluid (min 0.5ml) was aspirated under complete aseptic condition and collected in vacutainer tubes, then allowed to stay at room temperature for two hours, then centrifuged for 15 min at 1000g. The resulting supernatant was removed and stored at -80°C until use. Synovial fluid level of interleukin-17 was measured using Sandwich ELISA technique, according to the instruction of the manufacturer (NOVA, Beijing China).
In conclusion, higher IL-17 levels in serum and synovial fluid in primary OA patients were significantly associated with longer disease duration, higher pain scores, worse quality of life, extreme disability, and advanced structural damage. These findings are important because they open a window of possibility for the early use of IL-17 antagonists for the prevention of joint destruction. Further studies with higher numbers of KOA patients are recommended to classify patients according to IL-17 levels and to verify our results.