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Crystal Arthritis

  • Anastasia Slobodnick
  • Michael Toprover
  • Michael H. PillingerEmail author
Chapter

Abstract

The formation or liberation of crystals, whether of an organic or inorganic composition, can activate the innate immune system to produce both acute and chronic inflammation. Thus, the inflammatory responses to all crystal diseases are similar, though they may vary in degree or kinetics. Crystal diseases differ more dramatically in their epidemiology, the metabolism, biology and chemistry of their crystal formations, their anatomic localizations, and their potentials for deposition and tissue disruption. Here, we review the two most common classes of crystal diseases—gout and crystals that are composed of calcium with various anions. Additionally, we briefly review several other crystals that may be encountered.

Keywords

Gout CPPD Urate Basic calcium phosphate Inflammation Inflammasome 

References

  1. 1.
    Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011;63(10):3136–41.CrossRefGoogle Scholar
  2. 2.
    Hak AE, Curhan GC, Grodstein F, Choi HK. Menopause, postmenopausal hormone use and risk of incident gout. Ann Rheum Dis. 2010;69(7):1305–9.CrossRefGoogle Scholar
  3. 3.
    Kuo CF, See LC, Luo SF, Ko YS, Lin YS, Hwang JS, et al. Gout: an independent risk factor for all-cause and cardiovascular mortality. Rheumatology (Oxford). 2010;49(1):141–6.CrossRefGoogle Scholar
  4. 4.
    Dehghan A, Kottgen A, Yang Q, Hwang SJ, Kao WL, Rivadeneira F, et al. Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study. Lancet (London, England). 2008;372(9654):1953–61.CrossRefGoogle Scholar
  5. 5.
    Moi JH, Sriranganathan MK, Falzon L, Edwards CJ, van der Heijde DM, Buchbinder R. Lifestyle interventions for the treatment of gout: a summary of 2 Cochrane systematic reviews. J Rheumatol Suppl. 2014;92:26–32.CrossRefGoogle Scholar
  6. 6.
    Kuo CF, Grainge MJ, Zhang W, Doherty M. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol. 2015;11(11):649–62.CrossRefGoogle Scholar
  7. 7.
    Emmerson BT. Identification of the causes of persistent hyperuricaemia. Lancet. 1991;337(8755):1461–3.CrossRefGoogle Scholar
  8. 8.
    Desai J, Steiger S, Anders HJ. Molecular pathophysiology of gout. Trends Mol Med. 2017;23(8):756–68.CrossRefGoogle Scholar
  9. 9.
    So AK, Martinon F. Inflammation in gout: mechanisms and therapeutic targets. Nat Rev Rheumatol. 2017;13(11):639–47.CrossRefGoogle Scholar
  10. 10.
    Tramontini N, Huber C, Liu-Bryan R, Terkeltaub RA, Kilgore KS. Central role of complement membrane attack complex in monosodium urate crystal-induced neutrophilic rabbit knee synovitis. Arthritis Rheum. 2004;50(8):2633–9.CrossRefGoogle Scholar
  11. 11.
    Terkeltaub R. What makes gouty inflammation so variable? BMC Med. 2017;15(1):158.CrossRefGoogle Scholar
  12. 12.
    Neogi T, Jansen TL, Dalbeth N, Fransen J, Schumacher HR, Berendsen D, et al. 2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2015;74(10):1789–98.CrossRefGoogle Scholar
  13. 13.
    Shah K, Spear J, Nathanson LA, McCauley J, Edlow JA. Does the presence of crystal arthritis rule out septic arthritis? J Emerg Med. 2007;32(1):23–6.CrossRefGoogle Scholar
  14. 14.
    Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res (Hoboken). 2012;64(10):1431–46.CrossRefGoogle Scholar
  15. 15.
    Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res (Hoboken). 2012;64(10):1447–61.CrossRefGoogle Scholar
  16. 16.
    Choi H, Neogi T, Dalbeth N, Terkeltaubb R. New perspectives in rheumatology: Implications of the Cardiovascular Safety of Febuxostat and Allopurinol in Patients With Gout and Cardiovascular Morbidities Trial and the associated Food and Drug Administration public safety alert. Arthritis Rheumatol. 2018;70(11):1702–1709.CrossRefGoogle Scholar
  17. 17.
    Latourte A, Bardin T, Richette P. Prophylaxis for acute gout flares after initiation of urate-lowering therapy. Rheumatology (Oxford). 2014;53(11):1920–6.CrossRefGoogle Scholar
  18. 18.
    Neame RL, Carr AJ, Muir K, Doherty M. UK community prevalence of knee chondrocalcinosis: evidence that correlation with osteoarthritis is through a shared association with osteophyte. Ann Rheum Dis. 2003;62(6):513–8.CrossRefGoogle Scholar
  19. 19.
    Kleiber Balderrama C, Rosenthal AK, Lans D, Singh JA, Bartels CM. Calcium pyrophosphate deposition disease and associated medical comorbidities: a National Cross-Sectional Study of US Veterans. Arthritis Care Res. 2017;69(9):1400–6.CrossRefGoogle Scholar
  20. 20.
    Williams CJ, Zhang Y, Timms A, Bonavita G, Caeiro F, Broxholme J, et al. Autosomal dominant familial calcium pyrophosphate dihydrate deposition disease is caused by mutation in the transmembrane protein ANKH. Am J Hum Genet. 2002;71(4):985–91.CrossRefGoogle Scholar
  21. 21.
    Rosenthal AK, Ryan LM. Calcium pyrophosphate deposition disease. N Engl J Med. 2016;374(26):2575–84.CrossRefGoogle Scholar
  22. 22.
    Ea HK, Liote F. Calcium pyrophosphate dihydrate and basic calcium phosphate crystal-induced arthropathies: update on pathogenesis, clinical features, and therapy. Curr Rheumatol Rep. 2004;6(3):221–7.CrossRefGoogle Scholar
  23. 23.
    Zhang W, Doherty M, Bardin T, Barskova V, Guerne PA, Jansen TL, et al. European league against rheumatism recommendations for calcium pyrophosphate deposition. Part I: terminology and diagnosis. Ann Rheum Dis. 2011;70(4):563–70.CrossRefGoogle Scholar
  24. 24.
    Grassi W, Okano T, Filippucci E. Use of ultrasound for diagnosis and monitoring of outcomes in crystal arthropathies. Curr Opin Rheumatol. 2015;27(2):147–55.CrossRefGoogle Scholar
  25. 25.
    Andrés M, Sivera F, Pascual E. Therapy for CPPD: options and evidence. Curr Rheumatol Rep. 2018;20(6):31.CrossRefGoogle Scholar
  26. 26.
    Bosworth B. Calcium deposits in the shoulder and subacromial bursitis: a survey of 12,122 shoulders. J Am Med Assoc. 1941;116(22):2477–82.CrossRefGoogle Scholar
  27. 27.
    Clavert P, Sirveaux F. Shoulder calcifying tendinitis. Revue de chirurgie orthopedique et reparatrice de l’appareil moteur 2008;94(8 Suppl):336–55.Google Scholar
  28. 28.
    Stack J, McCarthy G. Basic calcium phosphate crystals and osteoarthritis pathogenesis: novel pathways and potential targets. Curr Opin Rheumatol. 2016;28(2):122–6.CrossRefGoogle Scholar
  29. 29.
    Whyte MP. Hypophosphatasia: enzyme replacement therapy brings new opportunities and new challenges. J Bone Miner Res. 2017;32(4):667–75.CrossRefGoogle Scholar
  30. 30.
    Harvie P, Pollard TC, Carr AJ. Calcific tendinitis: natural history and association with endocrine disorders. J Shoulder Elb Surg. 2007;16(2):169–73.CrossRefGoogle Scholar
  31. 31.
    O’Shea FD, McCarthy GM. Basic calcium phosphate deposition in the joint: a potential therapeutic target in osteoarthritis. Curr Opin Rheumatol. 2004;16(3):273–8.CrossRefGoogle Scholar
  32. 32.
    Ea HK, Liote F. Diagnosis and clinical manifestations of calcium pyrophosphate and basic calcium phosphate crystal deposition diseases. Rheum Dis Clin N Am. 2014;40(2):207–29.CrossRefGoogle Scholar
  33. 33.
    Rosenthal AK. Basic calcium phosphate crystal-associated musculoskeletal syndromes: an update. Curr Opin Rheumatol. 2018;30(2):168–72.CrossRefGoogle Scholar
  34. 34.
    Lorenz EC, Michet CJ, Milliner DS, Lieske JC. Update on oxalate crystal disease. Curr Rheumatol Rep. 2013;15(7):340.CrossRefGoogle Scholar
  35. 35.
    Hoppe B, Beck BB, Milliner DS. The primary hyperoxalurias. Kidney Int. 2009;75(12):1264–71.CrossRefGoogle Scholar
  36. 36.
    Asplin JR. The management of patients with enteric hyperoxaluria. Urolithiasis. 2016;44(1):33–43.CrossRefGoogle Scholar
  37. 37.
    Wise CM, White RE, Agudelo CA. Synovial fluid lipid abnormalities in various disease states: review and classification. Semin Arthritis Rheum. 1987;16(3):222–30.CrossRefGoogle Scholar
  38. 38.
    Reginato AJ, Schumacher HR, Allan DA, Rabinowitz JL. Acute monoarthritis associated with lipid liquid crystals. Ann Rheum Dis. 1985;44(8):537–43.CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2020

Authors and Affiliations

  • Anastasia Slobodnick
    • 1
    • 2
  • Michael Toprover
    • 1
    • 2
  • Michael H. Pillinger
    • 1
    • 2
    Email author
  1. 1.The Crystal Diseases Study Group, Division of Rheumatology, Department of MedicineNew York University School of MedicineNew YorkUSA
  2. 2.Rheumatology Section, Department of MedicineNew York Harbor Health Care System New York Campus, United States Department of Veterans AffairsNew YorkUSA

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