Chondrocalcinosis describes the presence of calcium deposits within the cartilage of joints, most often affecting the knee. The condition is characterized by the accumulation of Calcium Pyrophosphate Dihydrate (CPPD) crystals in the joint’s soft tissues. These deposits can lead to inflammation and joint damage, though they are often found incidentally in people without symptoms. This crystal deposition disease is common in older adults, with prevalence increasing significantly with age.
Understanding Calcium Pyrophosphate Deposition
The underlying pathology of chondrocalcinosis is Calcium Pyrophosphate Deposition (CPPD) disease, a form of crystal-induced arthritis. The crystals settle in both the hyaline cartilage covering the ends of bones and the fibrocartilage found in structures like the knee’s menisci. Advanced age is the most significant risk factor, though the exact reason these crystals begin to form is often unknown.
CPPD crystals are distinct from the monosodium urate crystals that cause gout, though both involve crystal accumulation leading to painful joint attacks. The mechanism of deposition involves changes in the joint environment, possibly related to increased pyrophosphate production by cartilage cells. The condition is sometimes associated with metabolic disorders, such as hyperparathyroidism, hemochromatosis (iron overload), or low magnesium levels.
How Chondrocalcinosis Affects the Knee
Chondrocalcinosis in the knee can manifest in two primary ways: acute attacks or a chronic, persistent form of arthritis. The acute presentation, often called “pseudogout,” involves the sudden onset of pain, swelling, and warmth in the knee joint. This episode can mimic an infection or a gout attack, sometimes accompanied by redness and a low-grade fever.
These acute flare-ups typically affect only one joint, such as the knee, and can last for days or weeks before resolving. Conversely, the chronic form presents as a slowly progressing arthritis, closely resembling osteoarthritis. Patients experience persistent stiffness, aching pain, and a gradual loss of joint function. This chronic arthropathy may involve joints not typically affected by primary osteoarthritis, such as the wrist or elbow.
Confirming the Diagnosis and Treatment Options
Diagnosis
Confirming chondrocalcinosis relies on medical imaging and laboratory analysis of joint fluid. Plain film X-rays are a frequent initial diagnostic tool, as they reveal the characteristic appearance of calcium deposits within the cartilage. The most definitive diagnosis is achieved through joint aspiration (arthrocentesis), where a sample of synovial fluid is withdrawn from the affected knee.
The fluid sample is examined under a polarized light microscope, which allows for the identification of the rhomboid-shaped CPPD crystals. This analysis is vital for ruling out other causes of acute joint inflammation, such as an infection or gout. Finding these specific crystals in the synovial fluid confirms the diagnosis of CPPD disease.
Treatment
Treatment focuses on managing symptoms and reducing inflammation, as no medical intervention can dissolve the crystals once they have formed. Acute attacks are treated with anti-inflammatory medications (NSAIDs) or a short course of colchicine. For localized inflammation, a healthcare provider may inject a corticosteroid directly into the knee joint for rapid relief, often after joint aspiration to remove excess fluid.
Management of chronic symptoms involves strategies similar to those used for osteoarthritis, including physical therapy to maintain joint function and range of motion. Low-dose daily colchicine or NSAIDs can prevent recurrent acute episodes. While no cure exists, a tailored treatment plan can significantly reduce pain and protect the knee joint.