Calcium pyrophosphate deposition disease.

Lancet Rheumatol

Academic Rheumatology, University of Nottingham, Nottingham, UK; NIHR Nottingham Biomedical Research Centre, Nottingham, UK.

Published: November 2024

AI Article Synopsis

  • - Calcium pyrophosphate deposition disease (CPPD) occurs when CPP crystals build up in joints, triggering inflammation and arthritis, particularly in older individuals over 60, and is linked to cartilage deterioration and osteoarthritis.
  • - Common risk factors for CPPD include aging, past joint injuries, and certain metabolic conditions or genetic factors. Diagnosis relies on detecting CPP crystals in joint fluid and imaging techniques like X-rays and ultrasound.
  • - Current treatment focuses on managing inflammation since there’s no cure for dissolving CPP crystals; options include prednisone for acute arthritis, low-dose colchicine, and potential use of biologics for stubborn cases.

Article Abstract

Calcium pyrophosphate deposition (CPPD) disease is a consequence of the immune response to the pathological presence of calcium pyrophosphate (CPP) crystals inside joints, which causes acute or chronic inflammatory arthritis. CPPD is strongly associated with cartilage degradation and osteoarthritis, although the direction of causality is unclear. This clinical presentation is called CPPD with osteoarthritis. Although direct evidence is scarce, CPPD disease might be the most common cause of inflammatory arthritis in older people (aged >60 years). CPPD is caused by elevated extracellular-pyrophosphate concentrations in the cartilage and causes inflammation by activation of the NLRP3 inflammasome. Common risk factors for CPPD disease include ageing and previous joint injury. It is uncommonly associated with metabolic conditions (eg, hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia) and genetic variants (eg, in the ANKH and osteoprotegerin genes). Apart from the detection of CPP crystals in synovial fluid, imaging evidence of CPPD in joints by mainly conventional radiography, and increasingly ultrasonography, has a central role in the diagnosis of CPPD disease. CT is useful in showing calcification in axial joints such as in patients with crowned dens syndrome. To date, no treatment is effective in dissolving CPP crystals, which explains why control of inflammation is currently the main focus of therapeutic strategies. Prednisone might provide the best benefit-risk ratio for the treatment of acute CPP-crystal arthritis, but low-dose colchicine is also effective with a risk of mild diarrhoea. Limited evidence suggests that colchicine, low-dose weekly methotrexate, and hydroxychloroquine might be effective in the prophylaxis of recurrent flares and in the management of persistent CPP-crystal inflammatory arthritis. Additionally, biologics inhibiting IL-1 and IL-6 might have a role in the management of refractory disease.

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Source
http://dx.doi.org/10.1016/S2665-9913(24)00122-XDOI Listing

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