History and Epidemiology
A typically uniarticular condition, hydroxyapatite (HA) crystal deposition disease (HADD) is marked by the presence of hydroxyapatite crystals in the periarticular soft tissues, especially the tendons1. HA is a mineral found in normal bone, but when it builds up in and around the joints it can cause inflammation, tenderness, and pain.
Hydroxyapatite crystal deposition disease strikes women more frequently than men, and the average age of onset is 45.1 Acute hydroxyapatite crystal deposition disease often occurs in the glenohumeral joint with HA deposits found in or around the supraspinatus tendon in as many as two-thirds of cases. The hip, knee, elbow, wrist, and hand may also be affected by hydroxyapatite crystal deposition disease.2 The HA depot can cause carpal tunnel syndrome.1
Exactly what causes hydroxyapatite crystal deposition disease is not fully understood, but repetitive microtrauma and local ischemia may play a role. It may also occur with other diseases such as end-stage renal failure, collagenosis, or familiar tumorous calcinosis.1
There are typically four stages to hydroxyapatite crystal deposition disease including precalcific, when HA crystals begin to envelop the affected structure; calcific, when HA crystals can be seen as dense, uniform calcifications on X-rays; resorptive, when calcifications start to liquify and seep out of the tendon, causing pain; and postcalcific, when the calcifications disappear.1
Presentation and Diagnosis
Symptoms of hydroxyapatite crystal deposition disease include acute onset of significant joint pain, swelling, tenderness, inflammation, and decreased mobility in the affected joint.3
Approximately half of all patients present with pain, erythema, swelling, and limited motion in the affected joint.3 These symptoms are usually the result of a rupture of a calcific deposit into an adjacent soft tissue space or bursa that triggers inflammation. Not all patients with hydroxyapatite crystal deposition disease will experience symptoms.
Hydroxyapatite Deposition Disease Diagnosis
A diagnosis of hydroxyapatite crystal deposition disease is often made via physical examination and imaging.1,4 Laboratory tests usually come back negative because light microscopy can’t detect crystals unless they form aggregates.4 Plain X-rays can show calcifications in the para-articular tendons, bursae, and capsule. Calcifications are relatively homogeneous, rounded, plurilobulated, amorphous, and located at a joint or a tendon insertion point.
The presence of a typical calcified deposit is sufficient to establish the diagnosis of hydroxyapatite crystal deposition disease. When in doubt, consider computed tomographic (CT) scan and magnetic resonance imaging (MRI).
Hydroxyapatite crystal deposition disease is sometimes mistaken for infectious arthritis, cellulitis, or gout.1 Always rule out infection, tumor, and trauma.4
Other potential differential diagnoses include1,4:
- Bone marrow edema of the lunate
- Lunate and carpal morphology
- Ulnar variance
- Renal osteodystrophy
- Dystrophic calcification
- Collagen vascular disease
- Kienböck’s disease
- Ulnar impaction syndrome
- Intraosseous ganglia
- Lunotriquetral synchondrosis
- Cortical avulsion fractures
- Perilunate osteoarthritis
- Tumoral calcinosis
- Milk-alkali syndrome
- Hypervitaminosis D
Calcium pyrophosphate deposition (CPPD) is most commonly mistaken for hydroxyapatite crystal deposition disease.1
Ultrasound may help detect rotator cuff tears and pathologies in the long head of the biceps.4 Additionally, this imaging can characterize deposit consistency, tendon location, and can guide injections and bursal lavage.
Management (Nonpharmacotherapy and Pharmacotherapy)
Hydroxyapatite deposition disease treatment may involve analgesics, such as NSAIDs, local heat application, physiotherapy, corticosteroids (taken orally or by injection), ultrasound-guided calcific lavage if the calcifications are larger than 1 cm, ultrasound ablation, and surgery to remove calcifications.1,4
Monitoring Side Effects, Adverse Events, Drug-Drug Interactions
Hydroxyapatite deposition disease tends to resolve spontaneously.1 The symptoms of hydroxyapatite crystal deposition disease can resolve within a few weeks.2 Pain and functional impairment may continue if the HA depots are not reabsorbed. Left untreated, HA crystals can cause joint destruction.4
- Goller SS, Hesse N, Dürr HR, Ricke J, Schmitt R. Hydroxyapatite deposition disease of the wrist with intraosseous migration to the lunate bone. Skeletal Radiol. 2021;50(9):1909-1913. doi: 10.1007/s00256-021-03758-z.
- Ruban TN, Albert L. Wrist involvement of calcium hydroxyapatite deposition disease. J Rheumatol. 2015;42(9):1724-1725. doi: 10.3899/jrheum.150178
- Garcia GM, McCord GC, Kumar R. Hydroxyapatite crystal deposition disease. Semin Musculoskelet Radiol. 2003;7(3):187-93. doi: 10.1055/s-2003-43229.
- Ravikanth R, Kamalasekar K, Abraham MJ, Alapati A. Hydroxyapatite crystal deposition disease of the shoulder: A review of cases and literature. Int J Recent Surg Med Sci. 2018;4:43-46.
Denise Mann, MS, is a veteran freelance health writer in New York. Her work has appeared on HealthDay, among other outlets. She was awarded the 2004 and 2011 journalistic Achievement Awards from the American Society for Aesthetic Plastic Surgery. She was also named the 2011 National Newsmaker of the Year by the Community Anti-Drug Coalitions of America. She has also been awarded the Arthritis Foundation’s Northeast Region Prize for Online Journalism, the Excellence in Women’s Health Research Journalism Award, the Gold Award for Best Service Journalism from the Magazine Association of the Southeast, a Bronze Award from The American Society of Healthcare Publication Editors, and an honorable mention in the International Osteoporosis Foundation Journalism Awards. She was part of the writing team awarded a 2008 Sigma Delta Chi award for her part in a WebMD series on autism. Mann has a graduate degree from the Medill School of Journalism at Northwestern University in Evanston, Ill.