Hydroxyapatite Deposition Disease (HADD) is characterized by the abnormal accumulation of calcium-containing crystals within the soft tissues, most notably in and around joints. This crystalline material is essentially the same mineral that gives bones and teeth their hardness. The buildup leads to episodes of intense inflammation and pain. Although the condition is often temporary and self-resolving, the sudden onset of discomfort can be debilitating.
Defining Hydroxyapatite Deposition Disease
Hydroxyapatite is a mineral form of calcium phosphate that forms the primary inorganic structure of healthy bone and dental enamel. Hydroxyapatite Deposition Disease occurs when these microscopic crystals incorrectly deposit in soft tissues such as tendons, bursae, and ligaments. The presence of these foreign crystalline clumps triggers a strong inflammatory reaction as the body attempts to break them down and absorb them.
This inflammatory response is the direct cause of the intense pain experienced during a flare-up. HADD is considered one of the crystal-induced arthropathies, but it is distinct from conditions like gout (uric acid crystals) or calcium pyrophosphate dihydrate (CPPD) deposition disease (a different type of calcium crystal).
The progression of HADD is often described in stages, starting with a formative phase where the crystals are deposited, which is frequently asymptomatic. The most painful period, known as the resorptive phase, occurs when the body’s cells begin to attack and break apart the deposits, releasing inflammatory mediators into the surrounding tissue. This process leads to the sudden, severe symptoms that cause people to seek medical help. The condition may then enter a post-calcific stage where the tissue heals and the calcification is resolved.
How HADD Affects Joints and Tissues
The calcific deposits in HADD can occur in various locations, but they most frequently accumulate in the tendons around the shoulder joint. When the rotator cuff tendons are affected, the condition is commonly known as calcific tendinitis, typically involving the supraspinatus tendon. This deposition causes localized tenderness and can severely limit the range of motion.
The pain associated with an acute HADD attack is often sudden and severe. In addition to the shoulder, the deposits may also be found in periarticular tissues around the hips, elbows, wrists, knees, and spine. Symptoms generally involve localized swelling, tenderness, and significant discomfort, especially during movement.
When the crystals are deposited into a bursa (a fluid-filled sac that cushions joints), the condition is referred to as calcific bursitis. The rupture of a calcific deposit into an adjacent bursa can cause an extremely acute inflammatory reaction. Although HADD is usually monoarticular (affecting a single joint at a time), some individuals may experience deposits in multiple locations.
Diagnosing HADD
The diagnosis of HADD begins with a thorough physical examination and a review of the patient’s clinical history, focusing on the abrupt nature and intensity of the pain. Imaging studies are the primary method for confirming the presence of the deposits. Plain film X-rays are usually the first imaging technique used and are highly effective for visualizing the calcium.
On an X-ray, the hydroxyapatite deposits appear as dense, radio-opaque areas within the soft tissues surrounding the joint. The appearance changes depending on the disease stage; during the acute resorptive phase, the calcifications may look ill-defined or “fluffy” as they are being broken down. Ultrasound is a commonly used, radiation-free technique that offers a detailed look at the soft tissues and the exact location of the calcific deposits.
In some complex cases or when the diagnosis is uncertain, cross-sectional imaging like Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) may be used. While CT scans are excellent for confirming the presence of calcium, MRI is more useful for assessing the associated soft tissue inflammation and edema that surrounds the deposits. Blood tests are generally not specific for HADD but can be ordered to rule out other inflammatory conditions.
Treatment and Management Strategies
The initial approach to managing HADD symptoms focuses on pain relief and reducing inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a primary treatment, helping to control both the pain and the body’s inflammatory response to the crystals. Rest and the application of cold therapy to the affected joint can also provide symptomatic relief during a flare-up.
For patients with severe or persistent pain that does not respond adequately to oral medication, a local injection of corticosteroids may be administered. These steroid injections directly reduce the intense inflammation in the affected tendon or bursa, often providing rapid pain relief. This localized treatment can be performed using ultrasound guidance to ensure precise placement of the medication near the inflamed tissue.
A more direct interventional treatment is barbotage, often performed under ultrasound guidance. This technique involves using needles to puncture and mechanically break up the calcific deposit. Saline solution is then injected and aspirated (lavage) to wash out the fragmented calcium material from the tissue. Barbotage is an effective, minimally invasive option that accelerates the resolution of symptoms by physically removing the irritating crystals.
Following the resolution of the acute pain, physical therapy is often initiated to restore full strength and range of motion to the joint, particularly in the shoulder. Surgery to remove the deposits is typically reserved for a small number of chronic cases where conservative and interventional methods have failed to provide lasting relief. The majority of HADD cases are managed successfully with non-surgical treatments that focus on controlling inflammation and facilitating the natural resorption of the crystals.