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CPPD DEPOSITION DISEASE
Calcium Pyrophosphate Dihydrate
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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
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What is CPPD Ca2P2O2.2H2O
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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
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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
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Pathophysioloy A minority of patients with CPPD arthropathy have metabolic abnormalities or hereditary CPPD disease
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Conditions associated with CPPD
Aging Hyperparathyroidism Hemochromatosis Hypophosphatasia Hypomagnesemia Chronic thophaceous gout Hereditary
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. Clinical Manifestations
CPPD arthropathy may be asymptomatic, acute, subacute, or chronic or cause acute synovitis superimposed on chronically involved joints
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Clinical Manifestations
Pseudogout Pseudo-osteoarthritis Pseudo-Rheumatoid Destructive arthropathy Bursitis,tendinitis,enthesitis
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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
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Imaging Chondrocalcinosis
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IS all chondrocaclnosis caused by CPPD
Other calcium salts such as calcium hydroxyapatite Ochronosis
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Synovial fluid Several thousand cells to 100,000 cells/uL
Mean being about 24,000 cells/uL Predominant cell being the PMN
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Diagnosis Polarization microscopy usually reveals rod - shape or rhomboid crystals inside fibrin and in PMN
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Pseudo-osteoarthritis
Pattern of joint involvement Knee,MCP,wrist,elbow,shoulder More likely to be symmetrical Chondrocalcinosis
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Pseudo-Rheumatoid RF 10% Involvement of hands CPPD Crystals X-ray
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Treatment NSAIDS Colchicin Corticosteroids
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CALCIUM HYDROXYAPATITE DEPOSITION DISEASE
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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.
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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
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Diagnosis Intra- and/or periarticular calcifications
crystals are very small, and can only be seen by electron microscopy.
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