## 1 Introduction  
Osteoarthritis (OA) is one of the most common arthropathies and is the leading cause of disability, with a large socioeconomic cost. OA is a condition which can affect any joint in the body. OA generally affects the joints that support most of the weight (such as the knees and feet) and the joints we use the most (e.g., hand joints). In a healthy joint, the cartilage shelters the surface of the bones and supports the bones to move liberally against each other. When a joint develops OA, part of the cartilage tapers and the surface becomes coarser. This means the articulation does not move as easily as it should. When the cartilage becomes worn out or damaged, all the tissues within the articulation become more active than usual as the body attempts to repair the damage. However, the reparation processes do not always operate well, and thus, modifications to the joint structure can occasionally cause or contribute to symptoms such as swelling, pain, and ultimately, disability. One of the leading characteristics of OA is collagen deterioration, as suggested by augmented tissue swelling and the loss of proteoglycans [1]. Both collagen destruction and the loss of proteoglycans unfavorably affect the mechanical properties of cartilage. Chondrocytes respond to tissue injury by increasing collagen and proteoglycan synthesis in an attempt to repair the tissue [2]. If repair fails, the damage will progress to articular cartilage degeneration. It is still not clear exactly what causes osteoarthritis. We do know that it is not simply 'wear and tear' and that the danger of developing OA depends on a number of factors. Furthermore, these degradation processes are thought to be largely elicited through excess production of pro-inflammatory and catabolic mediators. Among them, interleukin-1\(\beta\) (IL-1\(\beta\)) has been demonstrated to be predominantly involved in both disease initiation and progression [3; 4]. Oxidative stress shows a fundamental role in supporting cartilage degradation. In chondrocytes of the joint, the data implicate reactive oxygen species (ROS) as signaling intermediates of IL-1\(\beta\)[5]. It has been proposed that ROS produced internally in the joints may contribute notably to the pathogenesis of OA, as these inorganic oxidants are able to deteriorate cartilage through oxidation of the extra-cellular matrix (ECM) components or post-translational modification (PTM) of metalloproteinases (MMPs) [6; 7]. The existing treatments for postponing OA and rheumatoid arthritis (RA) progression comprise of some disease modifying anti-rheumatic drugs (DMARDs) and biological agents that operate as immunomodulatory drugs in RA [8]. Several also act by inhibiting endothelial cell proliferation and cytokines [9]. Moreover, all of these compounds have potentially grave side effects and there are substantial differences in toxicity among DMARDs [10]. Hyaluronan (HA) is a foremost component of synovial fluid (SF) and is necessary for the proper functioning of joints. Yet, owing to the fact that SF does not have any hyaluronides, it is considered that ROS could also be involved in HA catabolism in the inflamed articulation. A transition metal, e.g., copper or iron, would also be required to show an active function in oxidative HA catabolism. The polymer functions of HA are dimension specific and its fragments represent an information-rich system. The intermediate-sized HA-polymer fragments are inflammatory, immune-stimulatory, and highly angiogenic [11]. Consequently, substances preventing HA from being degraded could have anti-inflammatory and anti-angiogenic properties. Carnosine (CARN), a fundamental endogenous molecule, has several physiological functions: pH buffering, radical scavenging, anti-glycating, heavy metal chelating, and neutralization of toxic aldehydes. CARN is found to have neuroprotective, cataract treating, hepatoprotective, and anti-aging abilities [12]; however, its anti-inflammatory strength in auto-immune systemic inflammatory diseases has been recently investigated.