Slipped Femoral Capital Epiphyses

Alternative Names

  • Slipped Capital Femoral Epiphyses
  • SCFE
  • Epiphysiolysis Capitis Femoris
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WHO-ICD-10 version:2010

Diseases of the musculoskeletal system and connective tissue

Osteopathies and chondropathies

OMIM Number

182260

Mode of Inheritance

Autosomal dominant

Description

Slipped capital femoral epiphysis (SCFE) is the most common hip disorder affecting early adolescents with an incidence of 0.2 (Japan) to 10 (United States) per 100,000. In this condition, the ball of the hip joint slips from the femur at the upper growing end (growth plate) of the bone. Most patients with SCFE develop limping and experience pain in the hip. SCFE is classified as stable when the patient can walk, and unstable when the patient is unable to walk even with the aid of crutches. There are two serious complications of SCFE that may occur immediately after the condition develops. One complication is chondrolysis cartilage necrosis, a condition where the articular cartilage of the hip joint is destroyed. The second and most severe complication of SCFE is avascular necrosis which is more common in patients with unstable SCFE. This condition usually occurs when the blood vessels that provide blood to the epiphysis are damaged. Patients also gradually develop arthritis in the hip joint (osteoarthritis). Treatment for SCFE aims to prevent further slippage, achieve closure of the physeal plate, and avoid complications.

The etiology of SCFE is still unknown, but it appears to be a multifactorial disorder with genetic, environmental (particularly mechanical), and hormonal factors in play. Several studies have found an association between Human Leucocyte Antigen (HLA) types A2, A11, B11, B12, B35, DR4, DR52 and SCFE in identical twins as well as unrelated patients.

Molecular Genetics

 It was also suggested that further studies may permit the use of human leukocyte antigens as genetic markers for SCFE.

Epidemiology in the Arab World

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Other Reports

Bahrain

Wong-Chung et al. (2000) determined HLA phenotypes in seven Bahraini patients affected with SCFE to test the association between SCFE and HLA phenotype. All the seven patients studied, except one, were males. They all presented the slip at age 11-13 years. The study also included two brothers with almost identical phenotypes who presented with SCFE at the same age, but 10 years apart. Wong-Chung et al. (2000) found that none of the patients studied have the B12 antigen. While the DR4 antigen was found in only 3 of 7 patients. Neither of the two brothers held the DR4 antigen. The commonest class I and II antigens that are also held by the two brothers were B35, present in 5 of 7 patients (71%) and DR52 in 4 patients (57%), respectively. Wong-Chung et al. (2000) concluded that neither the previously described B12 nor the DR4 antigen can reliably serve as genetic markers for SCFE in this region.

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