Introduction
Arthritis can be differentiated into rheumatoid arthritis (RA) and osteoarthritis (OA). Although the
pathophysiology of RA and OA differs, i.e., RA is a systemic inflammatory disease while OA is a
degenerative joint disease, the common and often debilitating consequences of both diseases are
destruction of articular cartilage leading to bone deformity and loss of joint function, and ultimately,
severe pain.
Articular cartilage is a hydrated (75–80% water by weight) extensive extracellular matrix (ECM)
comprising a small number of chondrocytes ( < 5%), type II collagen and large aggregates of
proteoglycans or aggrecans (20–25%). Chemically an aminomonosaccharide, glucosamine provides
the building blocks for the O-linked and N-linked glycosaminoglycans (GAGs) (Deal and Moskowitz,
1999). Once it is taken up into the chondrocytes of cartilage, glucosamine is incorporated into GAGs.
Proteoglycans, made up of 95 percent polysaccharides and 5 per cent GAGs, are secreted into the ECM
and bind cations and water to form a viscous, elastic matrix that helps to lubricate the joint where
cartilage is found. When this protective cartilaginous layer is compromised due to decreased synthesis or
increased degradation, the loss of cushioning with resultant articular damage occurs.