CPPD DEPOSITION DISEASE Calcium Pyrophosphate Dihydrate

Epidemiology Most common in the elderly 10 to 15% of persons 65 to 75 years old and 30 to 60% of those more than 85 years old In most cases this process is asymptomatic

What is CPPD Ca2P2O2.2H2O

Etiology Cause of CPPD deposition is uncertain Because over 80% of patients are more than 60 years old and 70% have preexisting joint damage from other conditions, it is likely that biochemical changes in aging cartilage favor crystal nucleation There is an increased production of inorganic pyrophosphate and decreased levels of pyrophosphatases in cartilage extracts from patients

Pathophysioloy The release of CPPD crystals into the joint space is followed by the phagocytosis of these crystals by neutrophils, which respond by releasing inflammatory substances. In addition, neutrophils release a glycopeptide that is chemotactic for other neutrophils, thus augmenting the inflammatory events

Pathophysioloy A minority of patients with CPPD arthropathy have metabolic abnormalities or hereditary CPPD disease

Conditions associated with CPPD Aging Hyperparathyroidism Hemochromatosis Hypophosphatasia Hypomagnesemia Chronic thophaceous gout Hereditary

. Clinical Manifestations CPPD arthropathy may be asymptomatic, acute, subacute, or chronic or cause acute synovitis superimposed on chronically involved joints

Clinical Manifestations Pseudogout Pseudo-osteoarthritis Pseudo-Rheumatoid Destructive arthropathy Bursitis,tendinitis,enthesitis

Acute Arthritis(Pseudogout) May be precipitated by trauma Knee, wrist, shoulder, ankle, elbow, and hands Symptoms are the same as any acute arthritis Occasionally systemic symptoms:Fever Self limited Patients are asymptomatic between attacks

Imaging Chondrocalcinosis

IS all chondrocaclnosis caused by CPPD Other calcium salts such as calcium hydroxyapatite Ochronosis

Synovial fluid Several thousand cells to 100,000 cells/uL Mean being about 24,000 cells/uL Predominant cell being the PMN

Diagnosis Polarization microscopy usually reveals rod - shape or rhomboid crystals inside fibrin and in PMN

Pseudo-osteoarthritis Pattern of joint involvement Knee,MCP,wrist,elbow,shoulder More likely to be symmetrical Chondrocalcinosis

Pseudo-Rheumatoid RF 10% Involvement of hands CPPD Crystals X-ray

Treatment NSAIDS Colchicin Corticosteroids

CALCIUM HYDROXYAPATITE DEPOSITION DISEASE

Pathogenesis HA is the primary mineral of bone HA may be released from exposed bone and cause the acute synovitis Most patients with HA arthropathy are elderly. Periarticular and articular deposits may coexist and be associated with acute and/or chronic damage to the joint capsule, tendons, bursa, or articular surfaces.

Clinical The most common sites of HA deposition include bursa and tendons in and/or around the knees, shoulders, hips, and fingers Clinical manifestations include: asymptomatic radiographic abnormalities, acute synovitis, bursitis, tendinitis, and chronic destructive arthropathy

Diagnosis Intra- and/or periarticular calcifications crystals are very small, and can only be seen by electron microscopy.

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