Chondrocalcinosis. Clinical impact of intra-articular calcium phosphate crystals

Abstract

Calcium pyrophosphate dihydrate (CPPD) crystals are known to cause acute attacks of pseudogout in joints but crystal deposition has also been reported to be associated with osteoarthritis (OA). Aside from CPPD crystals, basic calcium phosphates (BCPs), consisting of carbonate-substituted hydroxyapatite (HA), tricalcium phosphate and octacalcium phosphate, have been found in synovial fluid, synovium and cartilage of patients with OA. Although CPPD crystals have been found to be associated with OA and are an important factor in joint disease, this has also recently been associated with a genetic defect. However, according to the most recent findings, the association of BCP crystals, such as apatite with OA is much stronger, as their presence significantly correlates with the severity of cartilage degeneration. Identification of BCP crystals in OA joints remains problematic due to a lack of simple and reliable methods of detection. The clinical and pathological relevance of cartilage mineralization in patients with OA is not completely understood. It is well established that mineralization of articular cartilage is often found close to hypertrophic chondrocytes. A significant correlation between the expression of type X collagen, a marker for chondrocyte hypertrophy and cartilage mineralization was observed. In the process of endochondral ossification, the link between hypertrophy and matrix mineralization is particularly well described. Hypertrophic chondrocytes in OA cartilage and at the growth line share certain features, not only hypertrophy but also a capability to mineralize the matrix. Recent data indicate that chondrocyte hypertrophy is a key factor in articular cartilage mineralization strongly linked to OA and does not characterize a specific subset of OA patients, which has important consequences for therapeutic strategies for OA.