The review is aimed at the well-known chronic musculosceletal disorders, osteoarthritis (OA) and rheumatoid arthritis (RA), and their increasing incidence during ageing. Especially, collagen type II undergoes age-related non-enzymatic covalent modification (NECM), advanced glycation endproducts (AGE) form, which then accumulate in the articular cartilage. Increased cartilage accumulation of AGE results in cartilage quality alteration and decreases its mechanical damage resistance. This finally contributes to degeneration of collagen fibril network and to initiation and/or progression of joint damage. The molecular events of AGE formation represent reactive oxo-group of the sugar and amino-group of the target molecule condensation (so-called Maillard reaction). This reaction is potentiated by hyperglycemia and oxidative stress. Increased tissue accumulation of AGE is seen not only during the natural process of aging but also during different pathologic conditions (e.g. diabetes, renal insufficiency, some inflammatory and primary degenerative disorders). AGE role in the inflammatory cell response or even in the initiation of the complex autoimmune process in RA has been considered in recent years. Special cell receptor for AGE (RAGE) is important for inflammatory cell activation and the presence ofRAGEon many cell types has already been described. This paper also points at AGE presence in body fluids and tissues, at the usefulness of their detection to follow up the disease activity of various disorders, at the attempts to elucidate pathogenesis of these disorders, and also at the utility of AGE inhibitors, which could be of potential significance slowing the disease progression.

        Key words: osteoarthritis (OA),rheumatoid arthritis (RA), non-enzymatic covalent modification (NECM), Maillard reaction, advanced glycation endproducts (AGE),