Adolescent and Young Adult Hip Dysplasia

David D. Spence, Derek M. Kelly, Marc J. Mihalko and James L. Guyton

Disclosures

Curr Orthop Pract. 2013;24(6):567-575. 

In This Article

Etiology

The etiology of hip dysplasia that presents after infancy is not clearly understood. Although it may be a milder form of infantile DDH that was not detected or the result of only partially treated disease, evidence indicates that it may be a separate disease process altogether.[8] Numerous authors[8–11] have proposed a genetic basis for acetabular dysplasia, with one study linking it to chromosome 13q22, with an autosomal dominant inheritance pattern and another identifying a single genetic locus on chromosome 17q21.[10,11] While the cause of acetabular dysplasia in adolescents is likely multifactorial,[12] studies showing a high rate of bilaterality among patients with adolescent hip dysplasia compared with a high rate of left-sided dislocation among patients with infantile DDH also give credence to the gene argument.[3,9] Lee et al.,[3] in a study of 311 patients, found several statistically significant differences in demographics between the infantile and adolescent forms of hip dysplasia that support the hypothesis that these are two distinct entities: significantly more girls were affected in the infantile group compared with the adolescent group (P<0.0002) in which boys were more frequently affected; the left hip was more frequently involved in the infantile type compared with bilateral involvement in the adolescent type (P<0.0012 and P<0.0077, respectively); and the infantile type was associated with breech presentation at birth more often than the adolescent type (P<0.0012). Although a higher percentage of first-born children were affected in the infantile group compared with the adolescent group, this value was not statistically significant. A significantly higher rate of total hip arthroplasty by the age of 65 was noted in family members of patients with adolescent hip dysplasia than in patients with infantile dysplasia. These authors temporized their findings by stating that it is possible that the adolescent group had an infantile form that was not detected ''precisely because of their demographics (male sex and vertex presentation), which may have lowered the index of suspicion for the disease during infancy.'' Modaressi et al.[13] found four of 150 patients in their study who were treated successfully for hip dysplasia in infancy only to develop significant dysplasia at puberty. They recommended that patients with successful results after treatment for infantile dysplasia be followed to maturity.

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