Chondrocalcinosis is a condition characterized by the accumulation of calcium deposits within the cartilage of joints, visible through medical imaging. While often an isolated observation causing no discomfort, this buildup of crystalline material can also cause severe, sudden joint pain and inflammation. Over time, it can lead to joint damage, affecting mobility and quality of life. The clinical presentation varies widely, ranging from being completely asymptomatic to mimicking other forms of inflammatory arthritis.
The Definition of Chondrocalcinosis
Chondrocalcinosis (CC) is a descriptive term used to identify calcification within the joint’s cartilage on an X-ray or other imaging. This finding is the physical sign of Calcium Pyrophosphate Dihydrate (CPPD) deposition disease. The deposits themselves are tiny, rhomboid-shaped crystals of calcium pyrophosphate. CC is the radiographic sign, while CPPD is the underlying disease causing the crystal formation. These CPPD crystals accumulate within the hyaline cartilage, which covers the ends of bones, and the fibrocartilage, such as the menisci in the knee. The knee is the joint most commonly affected, though deposits are frequently found in the wrists, hips, and shoulders.
Underlying Causes and Risk Factors
The formation and deposition of CPPD crystals is primarily associated with increasing age. The prevalence of chondrocalcinosis rises significantly after age 60; nearly half of individuals over 85 show evidence of crystal deposits, though many remain asymptomatic. Changes in the aging joint environment make the cartilage more susceptible to crystal accumulation.
Beyond age, several metabolic and endocrine disorders are linked to CPPD development, particularly in younger individuals. These secondary causes disrupt the body’s normal regulation of calcium and phosphate. For example, hyperparathyroidism, an overactive parathyroid gland, leads to elevated calcium levels in the blood and is strongly associated with CPPD.
Another associated condition is hemochromatosis, a disorder causing excessive iron absorption and overload in the body’s tissues. Deficiencies in certain minerals, such as low blood magnesium (hypomagnesemia) or low thyroid function (hypothyroidism), can also contribute to crystal formation. In rare cases, CPPD has a hereditary component, where a genetic predisposition causes the condition to manifest earlier or more extensively across multiple joints.
Clinical Manifestations and Diagnosis
The clinical presentation of CPPD is highly varied, often complicating the diagnosis. Many people with chondrocalcinosis remain completely asymptomatic, meaning the crystal deposits cause no pain or joint dysfunction. However, the release of these crystals into the joint space can trigger a severe inflammatory response in others.
This acute inflammatory arthritis is commonly referred to as “pseudogout” because it mimics the sudden, intense pain and swelling of a gout attack. A pseudogout flare-up typically affects a single joint, such as the knee or wrist, causing it to become hot, swollen, and painful. The episode often lasts anywhere from a few days to several weeks. Other patients experience a chronic form of arthritis that resembles osteoarthritis, characterized by persistent pain, stiffness, and progressive joint degeneration.
Diagnosis relies on two primary methods to confirm the presence of crystals and rule out other forms of arthritis. The initial step is imaging, where an X-ray confirms chondrocalcinosis by showing the white line of calcification within the cartilage or menisci. The definitive diagnosis is made through joint aspiration, where a physician removes a sample of fluid from the affected joint. This synovial fluid is then analyzed under a polarized light microscope to identify the specific calcium pyrophosphate crystals, which appear as rhomboid-shaped structures.
Managing Acute Flares and Chronic Pain
Since no treatment can dissolve existing CPPD crystals, therapy focuses on managing inflammation and symptoms. The immediate goal during an acute pseudogout flare is rapid pain relief and reduction of swelling. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin or naproxen, are a primary first-line treatment, used at full doses to quickly suppress inflammation.
For localized attacks, a physician may perform joint aspiration to drain inflammatory fluid, followed by an injection of long-acting corticosteroids directly into the affected joint. This intra-articular injection provides potent, targeted anti-inflammatory action with minimal systemic side effects. Oral corticosteroids, such as a short, tapering course of prednisone, are an alternative for patients who cannot tolerate NSAIDs or have multiple affected joints.
Colchicine is an anti-inflammatory medication effective for both treating acute flares and preventing future attacks. For patients experiencing frequent recurrent episodes, a low-dose regimen of colchicine (typically 0.6 milligrams once or twice daily) is recommended as a prophylactic measure. Long-term management involves addressing associated metabolic disorders, such as hyperparathyroidism or hemochromatosis, though treating the underlying cause will not remove existing crystals. Physical therapy and joint protection strategies help slow chronic joint damage and maintain mobility in patients with persistent symptoms.