Background: Osteoarthritis (OA) is a a degenerative joint illness which is marked by the destruction and degeneration of the joint's cartilage. Current medications utilized to treat OA mainly target pain relive but unfortunately can't stop the disease progression. Quercetin has been approved as a potent anti-inflammatory anti-oxidant anti-apoptotic agent. It may have a protective effect on repairing OA-induced cartilage injuries. Objective: To identify the possible impact of quercetin on inflammation in osteoarthritis. Materials and Methods: Thirty- two adult male Sprague- Dawley rats were selected, subdivided into four equal groups: control non-osteoarthritic rats saline- treated group (negative control), control osteoarthritic rats saline- treated group (positive control), osteoarthritic rats quercetin-treated group, and osteoarthritic rats glucosamine sulfate -treated group. The experiment was completed with all rats being subjected to measurement of the following parameters: serum levels of tumor necrosis factor- alpha (TNF-α), matrix metalloproteinase 13 (MMP13), interleukin1- β (IL-1β), and nitric oxide (NO). Results: OA, provoked surgically in rats, produced an incredibly crucial rise in serum MMP13 in control osteoarthritic group compared to control non-osteoarthritic rats. The group of rats that was treated by glucosamine revealed a very considerable decline in MMP-13 relative to the control OA group, while it was still much greater than the control normal group. Quercetin- treated rats produced significant decrease in MMP-13 as compared with osteoarthritic non- treated group, while it was still much greater than the control normal group. OA resulted in a highly significant rise in serum IL-1β in the osteoarthritic control rats compared to control non-arthritic rats. In glucosamine- treated group, IL-1β significantly reduced relative to the control osteoarthritis group, and this difference was highly significant. Additionally, IL-1β levels in the Compared to the osteoarthritis control group, the quercetin-treated group's levels were considerably lower. OA produced a highly significant increase in TNF-α in control osteoarthritic group as compared with control non-osteoarthritic rats. Comparing group that was treated with glucosamine to the control osteoarthritis group, the treated group showed a highly significant drop in TNF-α. Additionally, the quercetin-treated group revealed significantly decreased TNF-α contrasted with control osteoarthritis group. As regard NO; In comparison to control non-osteoarthritic rats, OA resulted in a significantly rise in NO. The NO levels measured in the glucosamine-treated group were noticeably lower than those in the osteoarthritic control group, even though they are still much higher than those of the non-arthritic control group. Additionally, the NO levels in the quercetin-treated group levels were noticeably lower as compared to the osteoarthritis control group. Conclusion: Quercetin has the ability to decrease inflammation and oxidative stress in osteoarthritis, suggesting that it may be used as a disease-modifying medication used to treat osteoarthritis.