Chondrocalcinose

Chondrocalcinose, also known as chondrocalcinosis or calcium pyrophosphate dihydrate (CPPD) deposition disease, refers to the deposition of CPPD crystals in articular cartilage and periarticular tissues. It is often detected on imaging and may be asymptomatic or associated with inflammatory arthritis.

Pathophysiology and risk factors: CPPD crystals form within joint cartilage, leading to inflammation and pain. Risk factors include aging and metabolic disorders such as hyperparathyroidism, hemochromatosis, hypomagnesemia, hypophosphatasia, and hypothyroidism, as well as trauma. In many cases the condition is idiopathic.

Clinical presentation: when symptomatic, chondrocalcinose presents as pseudogout—an acute or subacute inflammatory arthritis. Patients typically experience sudden joint swelling, warmth, pain, and limited motion, most commonly in the knee, but also in the wrist or other large joints. Some individuals have a chronic CPPD arthritis with persistent joint symptoms.

Diagnosis: radiographs may reveal calcification of the menisci or hyaline cartilage (chondrocalcinosis). Definitive diagnosis is obtained from synovial fluid analysis, which shows calcium pyrophosphate crystals that are rhomboid-shaped and weakly positively birefringent under polarized light. It is important to differentiate CPPD from gout, whose crystals are needle-shaped and negatively birefringent. Additional tests may assess coexisting metabolic conditions.

Management and prognosis: treatment of an acute CPPD attack includes NSAIDs, colchicine, or intra-articular corticosteroids. Systemic steroids may be used for severe or refractory cases. Chronic management focuses on pain control and addressing underlying metabolic disorders; there is no disease-modifying therapy specific to CPPD deposition disease. The prognosis varies, and chondrocalcinosis can be an incidental radiographic finding in older adults.