Basic calcium phosphate crystal deposition diseases

Last updated: September 10, 2021

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Basic calcium phosphate (BCP) crystal deposition diseases are an uncommon form of crystalline arthropathy. BCP crystals include several different types of calcium phosphate crystals, such as partially carbonate-substituted hydroxyapatite, octacalcium phosphate, and tricalcium phosphate. These crystals are deposited in joints or in periarticular structures, causing BCP-associated arthritis (including Milwaukee shoulder syndrome) and calcific tendinitis. The underlying etiology of articular and periarticular BCP crystal deposition is unknown, but risk factors include female sex, joint trauma, and various metabolic abnormalities. The presentation and management of BCP-associated osteoarthritis are similar to that of age-related osteoarthritis. Milwaukee shoulder syndrome and acute calcific tendinitis manifest with joint pain and swelling, most commonly of the shoulder or other large joints. Diagnosis is based on clinical and radiological findings. Synovial fluid analysis may be helpful in excluding differential diagnoses (e.g., acute gout, pseudogout, septic arthritis) but rarely identifies the small, nonbirefringent BCP crystals. Management is primarily supportive and includes pain relief for acute episodes, physical dissolution of crystals by various methods (e.g., needle aspiration, ultrasound therapy), and surgery in severe cases.

The underlying etiology that results in BCP crystal deposition within joints and periarticular tissue remains poorly understood. The following factors are associated with an increased risk of developing BCP crystal deposition diseases: [1][2][3]

The pathophysiology of BCP crystal deposition diseases is complex and not yet fully understood. BCP crystals appear to cause joint degeneration by inducing both inflammatory and catabolic processes. [1][6]

There are three main subtypes of BCP crystal deposition disease, all of which vary in their clinical presentation and diagnosis.

BCP-associated osteoarthritis (OA) is osteoarthritis associated with the intraarticular deposition of BCP crystals. [6]

  • Epidemiology: BCP-associated OA is widely prevalent. [2][7]
  • Clinical features
    • Similar to clinical features of osteoarthritis
    • The degree of calcification appears to correlate to the severity of OA seen on imaging. [2]
  • Diagnostics

BCP-associated arthropathies typically affect large joints. [1]

Milwaukee shoulder syndrome is a subtype of BCP-associated OA characterized by a noninflammatory osteoclast-mediated destructive arthritis of the shoulder joint and commonly accompanied by non-inflammatory joint effusion and rotator cuff deficits. [2][6][8]

Milwaukee shoulder syndrome is associated with an extensive loss of articular cartilage, destruction of the humeral head, rotator cuff defects, large effusion, and small osteophytes. Conversely, OA is typically associated with prominent osteophytes, an intact rotator cuff, and humeral head sclerosis. [8]

Calcific tendinitis is an inflammatory tendinopathy and periarticular soft tissue inflammation associated with periarticular deposition of BCP crystals. [11]

Periarticular calcium deposits may be asymptomatic and detected incidentally. [1]

The diagnosis of BCP crystal deposition diseases is primarily based on clinical and radiological findings. See “Subtypes and variants” section for specific diagnostic studies. [1]

References: [3][9]

The differential diagnoses listed here are not exhaustive.

General principles

  • The management of BCP crystal deposition diseases is primarily supportive.
  • Treatment for BCP-associated OA is the same as for general OA (see “Treatment of osteoarthritis”).
  • Treatment for other BCP crystal deposition diseases should involve consultation with a rheumatologist.
    • Acute episodes: Treatment is focused on achieving pain relief.
    • Chronic disease: The aim is to physically dissolve the crystals using a variety of modalities.
    • Surgical intervention is a last resort.

Initial management (acute episodes) [1][2]

Subsequent management [1][2]

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  2. Molloy ES, McCarthy GM. Hydroxyapatite deposition disease of the joint. Curr Rheumatol Rep. 2003; 5 (3): p.215-221. doi: 10.1007/s11926-003-0070-0 . | Open in Read by QxMD
  3. Rosenthal AK, Ryan LM. Nonpharmacologic and Pharmacologic Management of CPP Crystal Arthritis and BCP Arthropathy and Periarticular Syndromes. Rheum Dis Clin North Am. 2014; 40 (2): p.343-356. doi: 10.1016/j.rdc.2014.01.010 . | Open in Read by QxMD
  4. McCarthy GM, Dunne A. Calcium crystal deposition diseases — beyond gout. Nat Rev Rheumatol. 2018; 14 (10): p.592-602. doi: 10.1038/s41584-018-0078-5 . | Open in Read by QxMD
  5. Soares I, Mewar D. Milwaukee Shoulder Syndrome - an incidental finding but important cause of acute shoulder arthropathy. Rheumatology Advances in Practice. 2017; 1 (suppl_1). doi: 10.1093/rap/rkx011.005 . | Open in Read by QxMD
  6. Nadarajah CV, Weichert I. Milwaukee Shoulder Syndrome. Case Rep Rheumatol. 2014; 2014 : p.1-4. doi: 10.1155/2014/458708 . | Open in Read by QxMD
  7. Dewachter L, Aerts P, Crevits I, Manelfe RD. Milwaukee shoulder syndrome.. JBR-BTR. 2012; 95 (4): p.243. doi: 10.5334/jbr-btr.629 . | Open in Read by QxMD
  8. Firestein GS. Kelley and Firestein's Textbook of Rheumatology. Elsevier ; 2017
  9. Beckmann NM. Calcium Apatite Deposition Disease: Diagnosis and Treatment. Radiol Res Pract. 2016; 2016 : p.1-16. doi: 10.1155/2016/4801474 . | Open in Read by QxMD
  10. Atzeni F, Sarzi-Puttini P, Bevilacqua M. Calcium Deposition and Associated Chronic Diseases (Atherosclerosis, Diffuse Idiopathic Skeletal Hyperostosis, and Others). Rheum Dis Clin North Am. 2006; 32 (2): p.413-426. doi: 10.1016/j.rdc.2006.02.003 . | Open in Read by QxMD
  11. Hongsmatip P, Cheng KY, Kim C, Lawrence DA, Rivera R, Smitaman E. Calcium hydroxyapatite deposition disease: Imaging features and presentations mimicking other pathologies.. Eur J Radiol. 2019; 120 : p.108653. doi: 10.1016/j.ejrad.2019.108653 . | Open in Read by QxMD

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