Chondrocalcinosis Treatment & Management

  • Author: Neil J Barkin, MD, FAAOS; Chief Editor: Harris Gellman, MD   more...
 
Updated: Feb 7, 2012
 

Medical Therapy

Treatment depends on the degree of involvement.[24, 25] For patients who demonstrate the most common presentation (ie, arthritic symptoms), treatment should follow the algorithm assigned to patients with osteoarthritis (OA). This includes modified activity, physical therapy, and nonsteroidal anti-inflammatory drugs (NSAIDs). Surgical intervention is indicated when the response to these modalities is unsatisfactory.

For individuals with acute episodes, who usually present with an enhanced level of pain and disability, arthrocentesis in combination with administration of an intra-articular steroid provides reliable prompt relief.

NSAIDs and colchicine may be used to prevent recurrent episodes.

Limited studies have shown favorable results from diminishing the calcium deposits with ethylene diamine tetraacetic acid (EDTA) treatment. EDTA strongly binds to divalent cations (including calcium) and has the potential to eliminate them from the affected area. The role of EDTA in the treatment of chondrocalcinosis will require more extensive investigation because this agent has significant adverse effects.

Pulsed ultrasonography has been show to be an effective treatment for some calcification diseases. Patients often show reduced pain. Ebenbichler et al reported that 47% of patients demonstrated a decrease of at least 50% of the calcification after 6 weeks of treatment. At 9-month follow-up, 65% of patients presented with at least a 50% reduction of calcification, with nearly half showing complete resolution.[26]

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Surgical Therapy

Arthroscopic surgery allows debridement of superficial deposits of the calcium pyrophosphate precipitate. This alone may not materially affect the course of the disease. Surgical treatment of OA with debridement, microfracture chondroplasty, radiofrequency chondroplasty, osteochondral transfers, osteotomy, and, ultimately, partial or total joint replacement completes the armamentarium.

When large space-occupying tophaceous lesions are present, surgical excision is indicated. Although the impact of crystal deposition on the viability and future performance of the articular cartilage and meniscus is not clear, many surgeons believe that the presence of this precipitate renders the tissues more fragile. Not infrequently, meniscal tears or chondral lesions are located directly at the site of the densest accumulation of crystals. Cause and effect have not been determined, yet the impression is created that the deposition is responsible for undermining the integrity of the tissue.

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Intraoperative Details

Changes of OA often are present. These may range from mild to severe.

White crystal precipitate is identified in various locations throughout the joint. This ranges from sparse to extensive.

Tissue disruption in the form of tears (eg, meniscus) to chondral lesions (eg, articular hyaline cartilage) may or may not be present with the crystal deposition.

The white precipitate appears to be both superficially attached and deeply embedded. Often, very little effort is required to sweep the soft tissue with a blunt probe, freeing large quantities of the crystalline material into the joint fluid to be suctioned easily from the joint.

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Postoperative Details

Postoperative management is unchanged from that for the typical patient with OA.

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Follow-up

No specific moderations must be made in the postoperative period.

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Complications

Practitioners who have examined numerous joints arthroscopically often report the impression that chondrocalcinosis increases susceptibility to developing osteoarthritis in those tissues that exhibit the precipitate.

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Outcome and Prognosis

The most interesting issue regarding calcium pyrophosphate deposition (CPPD) disease is its overall impact on the progression of the OA with which it coexists. The literature tends to be ambiguous on this issue. Some studies imply that the presence of CPPD disease accelerates the deterioration of OA, while other studies refute this. A Framingham OA study of 598 knee patients from concluded that the presence of chondrocalcinosis had no demonstrable impact on the natural progression of the disease.[27]

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Future and Controversies

As the etiology of calcium pyrophosphate disease is clarified, more focused metabolic treatment regimens will be used. The goal will be to reduce the inflammation associated with the crystal deposition and to reduce the frequency and intensity of symptoms.

Continuing genetic and molecular insight, such as that provided by studies of the ANKH gene mutation, will allow a detailed understanding of the disease's manifestations and will allow targeted treatments.

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Contributor Information and Disclosures
Author

Neil J Barkin, MD, FAAOS  Consulting Surgeon, Capitol Orthopaedics & Rehabilitation, LLC

Neil J Barkin, MD, FAAOS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Anne Tesar, PA-C  Physician Assistant, Capitol Orthopaedics and Rehabilitation, LLC

Anne Tesar, PA-C is a member of the following medical societies: American Academy of Physician Assistants

Disclosure: Nothing to disclose.

Specialty Editor Board

Jegan Krishnan, MBBS, FRACS, PhD  Professor, Chair, Department of Orthopedic Surgery, Flinders University of South Australia; Senior Clinical Director of Orthopedic Surgery, Repatriation General Hospital; Private Practice, Orthopaedics SA, Flinders Private Hospital

Jegan Krishnan, MBBS, FRACS, PhD, is a member of the following medical societies: Australian Medical Association, Australian Orthopaedic Association, and Royal Australasian College of Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Paul E Di Cesare, MD, FACS  Professor, Department of Orthopedic Sugery, University of California, Davis, School of Medicine

Paul E Di Cesare, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, and Sigma Xi

Disclosure: Stryker Consulting fee Consulting; Smith & Nephew Consulting fee Consulting

Dinesh Patel, MD, FACS  Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital

Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Harris Gellman, MD  Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

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Left images depict femoral and tibial surfaces. Right images depict anterior cruciate ligament.
Upper left image depicts anterior horn medial meniscus. Lower left image depicts undersurface of meniscus. Upper right image depicts medial femoral condyle. Lower right image depicts synovium.
 
 
 
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