Joint cartilage is indeed a metabolically active tissue. In this issue of Annals of the Rheumatic Diseases, the results of the study by Anandacoomarasamy et al1 highlight two important issues of joint cartilage and osteoarthritis (OA): cartilage repair and OA progression. Unfortunately, many people equate cartilage repair with procedures that fill cartilage defects rather than replacing degraded molecules with newly synthesised molecules and consider that joint cartilage deterioration in OA is inevitable. In an elegantly designed study in obese subjects, the authors use MRI and delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) to show that weight loss is associated with improvement in medial knee cartilage quality and quantity. In the light of OA mainly developing medially and considering that cartilage quality and OA risk are probably related, their results have significant preventive implications.

In the cartilage matrix, aggrecan is a highly negatively charged proteoglycan that is entrapped in a collagen fibrillar network through carboxylated or sulphated glycosaminoglycans (GAGs). GAGs can bind up to 50 times their weight in water resulting in a swelling pressure that is normally constrained by the tensile strength of the collagen network.1 This interaction is the key mechanism behind the viscoelastic properties of the articular cartilage, which provides joints with the necessary resistance to mechanical loading.2 3

The molecules in the cartilage matrix are continuously and balanced turned over. In joint disease, however, increased degradation versus biosynthesis finally results in the hallmark of OA, namely gradual cartilage loss and overt radiographic changes. The degradation and loss of GAGs is usually considered an early feature in developing OA. However, it is unclear to what extent GAG loss is relative or absolute: less GAG due to dilution by oedema or decreased biosynthesis versus degradation ratio. This may have implications in OA development since OA risk …