eMedicine Specialties > Sports Medicine > Knee

Knee Osteochondritis Dissecans

Author: Brian Jacobs, MD, FACSM, Clinical Assistant Professor, Indiana University School of Medicine; Consulting Staff, Private Practice, Family Medicine of South Bend
Coauthor(s): Janos P Ertl, MD, Clinical Assistant Professor, Department of Orthopedic Surgery, Chief of Orthopedic Trauma, University of California at Davis; Director of Amputee Clinic, Kaiser Hospital; Gyorgy Kovacs, MD, Department of Orthopedic Surgery, Consulting Surgeon, GOC Clinic; Julie A Jacobs, PA-C, Department of Emergency Medicine, EPMG at Lakeland Hospital, Saint Joseph and Niles, Michigan
Contributor Information and Disclosures

Updated: Jul 28, 2006

Introduction

Background

Osteochondritis dissecans (OCD), by definition, is a disorder of one or more ossification centers, characterized by sequential degeneration or aseptic necrosis and recalcification. OCD lesions involve both bone and cartilage. These lesions differ from acute traumatic osteochondral fractures; however, they may manifest in a similar fashion. OCD lesions also must be differentiated from meniscal pathology. OCD causes 50% of loose bodies in the knee. The etiology of these lesions is multifactorial, including trauma, ischemia, abnormal ossification centers, genetic predisposition, or some combination of these factors. Little agreement exists among researchers regarding the etiology of OCD.

In 1558, Ambroïse Paré removed loose bodies from a knee joint. In 1870, Paget described quiet necrosis within the knee. In 1888, König coined the term "osteochondritis dissecans." He proposed this condition was caused by spontaneous necrosis due to trauma.

With the advent of roentgenography, osteochondrotic conditions in other joints, primarily the hip, were recognized. In 1910, Legg, Calvé, and Perthes independently identified a condition of the hip joint in children, which is now known as Legg-Calvé-Perthes disease. In 1921, Waldenström introduced the term coxa plana (ie, disintegration of capital femoral epiphysis.)

Since the introduction of radiography, 50 additional anatomic sites within the body where OCD can occur have been identified.

Frequency

United States

  • The average age at presentation is 10-20 years, but OCD may occur in persons of any age group.
  • The male-to-female ratio is 2-3:1.
  • Bilateral involvement is noted in 30-40% of cases.
  • In 85% of cases, lesions are observed on the medial femoral condyle (MFC) of the knee; 15% of cases are observed on the lateral femoral condyle. Of the MFC lesions, 70% occur in the posterolateral aspect.
  • Of patients with OCD, 21-40% have some history of trauma.

International

In Sweden, prevalence is reported at the following levels:

  • In skeletally immature patients, 150 cases per 250,000 people are reported.
  • In skeletally immature female patients, 18 cases per 100,000 people are reported.
  • In skeletally immature male patients, 29 cases per 100,000 people are reported.

Functional Anatomy

In skeletally immature individuals, the vascularity to epiphyseal bone is very good, supporting both osteogenesis and chondrogenesis. With disruption of the epiphyseal vessels, varying degrees and depth of necrosis occur, resulting in a cessation of growth to both osteocytes and chondrocytes. In turn, this pattern leads to nonspecific changes that produce disordered enchondral ossification, resulting in subchondral avascular necrosis or OCD.

Four stages of OCD have been identified, including revascularization and formation of granulation tissue, osteoclasis of necrotic fragments, intertrabecular osteoid deposition, and remodeling of new bone. With delay in the revascularization stage, an OCD lesion develops. OCD lesions may lead to articular-surface irregularities, which can cause degenerative arthritic changes.

Sport Specific Biomechanics

A proposed cause of OCD is an anatomic variation allowing the lateral aspect of the femoral condyle to abut the tibial spine, leading to repetitive localized epiphyseal microtrauma with osteochondral separation and subsequent OCD. This pattern may lead the patient to walk with the tibia externally rotated to avoid this abutment.

Clinical

History

  • Symptoms are usually vague and poorly localized.
  • A vague ache within the knee, with possible clicking or popping, may be reported.
  • Varying degrees of pain, swelling, and stiffness are reported.
  • Symptoms may be associated with activities (eg, sports, activities of daily living).
  • With complete fragment separation, locking symptoms may occur.
  • Prolonged symptoms lead to progressive degenerative arthritis.
  • Giving way of the knee may occur secondary to quadriceps weakness.

Physical

  • Effusion may be present.
  • Quadriceps atrophy and weakness may be evident.
  • Occasionally, a loose body may be palpable.
  • The patient may lack full knee extension compared with the contralateral knee.
  • Tenderness is noted over the lesion.
  • Evaluate gait for external rotation of the tibia.
  • Perform the Wilson test to check for OCD. The examiner flexes the knee to 90° while internally rotating the tibia. A positive Wilson sign occurs when pain is elicited at 30° of flexion and is relieved with external rotation.

Causes

  • The 2 distinctive subsets of patients are skeletally immature patients and skeletally mature patients.
  • Little agreement exists among researchers regarding the etiology of OCD. Possible etiologies include the following:

    • Trauma
    • Skeletal maturation (accessory centers of ossification)
    • Vascular causes/ischemia
    • Genetic conditions (eg, multiple epiphyseal dysplasia)
    • Metabolic factors
    • Hereditary factors
    • Anatomic variation

More on Knee Osteochondritis Dissecans

Overview: Knee Osteochondritis Dissecans
Differential Diagnoses & Workup: Knee Osteochondritis Dissecans
Treatment & Medication: Knee Osteochondritis Dissecans
Follow-up: Knee Osteochondritis Dissecans
Multimedia: Knee Osteochondritis Dissecans
References

References

  1. Andrews JR, Timmerman LA. Diagnostic and Operative Arthroscopy. Philadelphia, Pa: Harcourt Brace & Company; 1997.

  2. Beaty J. Orthopaedic Knowledge Update 6. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1999:506-507.

  3. Browner BD. Skeletal Trauma: Fractures, Dislocations, Ligamentous Injuries. Philadelphia, Pa: WB Saunders Co; 1998.

  4. Delee JC. Orthopaedic Sports Medicine, Principles and Practice. Vol 2. Philadelphia, Pa: WB Saunders Co; 1994.

  5. Siliski JM. Traumatic Disorders of the Knee. New York, NY: Springer-Verlag; 1994.

Further Reading

Keywords

intra-articular osteochondrosis, OCD, osteochondral fracture, articular osteochondrosis, intra-articular segmental osteonecrosis, ossification disorder, knee injury, loose body formation, knee loose body, disordered enchondral ossification, subchondral avascular necrosis

Contributor Information and Disclosures

Author

Brian Jacobs, MD, FACSM, Clinical Assistant Professor, Indiana University School of Medicine; Consulting Staff, Private Practice, Family Medicine of South Bend
Brian Jacobs, MD, FACSM is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, and American Medical Society for Sports Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Janos P Ertl, MD, Clinical Assistant Professor, Department of Orthopedic Surgery, Chief of Orthopedic Trauma, University of California at Davis; Director of Amputee Clinic, Kaiser Hospital
Janos P Ertl, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, Hungarian Medical Association of America, Orthopaedic Trauma Association, and Sierra Sacramento Valley Medical Society
Disclosure: Nothing to disclose.

Gyorgy Kovacs, MD, Department of Orthopedic Surgery, Consulting Surgeon, GOC Clinic
Disclosure: Nothing to disclose.

Julie A Jacobs, PA-C, Department of Emergency Medicine, EPMG at Lakeland Hospital, Saint Joseph and Niles, Michigan
Julie A Jacobs, PA-C is a member of the following medical societies: American Academy of Physician Assistants
Disclosure: Nothing to disclose.

Medical Editor

Leslie Milne, MD, Department of Emergency Medicine, Assistant Clinical Instructor, Harvard University School of Medicine
Leslie Milne, MD is a member of the following medical societies: American College of Sports Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.

CME Editor

Jon Whitehurst, MD, Consulting Staff, Rockford Orthopedic Associates
Disclosure: Nothing to disclose.

Chief Editor

Wylie D Lowery, Jr, MD, Department of Orthopedic Surgery, Associate Professor, George Washington University
Wylie D Lowery, Jr, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, Medical Society of Virginia, and Phi Beta Kappa
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.