Acetabular Version Increases After Closure of the Triradiate Cartilage Complex

Although the etiology of primary femoroacetabular impingement (FAI) is considered developmental, the underlying pathogenic mechanisms remain poorly understood. In particular, research identifying etiologic factors associated with pincer FAI is limited. Knowledge of the physiologic growth patterns of the acetabulum during skeletal maturation might allow conclusions on deviations from normal development that could contribute to pincer-related pathomorphologies.

In a population of healthy children, we asked if there were any differences related to skeletal maturation with regard to (1) acetabular version; (2) acetabular depth/width ratio; and (3) femoral head coverage in the same children as assessed by MRIs obtained 1 year apart.

We prospectively compared 129 MRIs in 65 asymptomatic volunteers without a known hip disorder from a mixed primary/high school population (mean age, 12.7 years; range, 7–16 years). All participants underwent two MRI examinations separated by a minimum interval of 1 year. Based on the status of the triradiate cartilage complex (open versus closed [TCC]), all hips were allocated to the following groups: “open-open” = open TCC at both MRIs (n = 45 hips [22 bilateral]); “open-closed” = open TCC at initial and closed TCC at followup MRI (n = 26 hips [13 bilateral]); and “closed-closed” group = closed TCC at both MRIs (n = 58 hips [29 bilateral]). We assessed acetabular version in the axial plane at five different locations (5, 10, 15, 20 mm below the acetabular dome and at the level of the femoral head) as well as three-dimensional (3-D) acetabular depth/width ratio and 3-D femoral head coverage on six radial MRI sequences oriented circumferentially around the femoral neck axis. Using analysis of variance for multigroup comparisons with Bonferroni adjustment for pairwise comparisons, we compared the results between the initial and followup MRI examinations and among the three groups.

Acetabular version was increased in hips of the “open-closed” group at the followup MRI compared with the initial MRI at 5 mm (−6 ± 4.6 [95% confidence interval {CI}, −7.6 to −3.6] versus −1 ± 5.0 [95% CI, −3.3 to 0.7]; p < 0.001), 10 mm (0 ± 4.0 [95% CI, −1.6 to 2.1] versus 7 ± 4.6 [95% CI, 4.4–8.7]; p < 0.001), and 15 mm (8 ± 5.0 [95% CI, 6.1–10.2] versus 15 ± 4.6 [95% CI, 13.3–17.4]; p < 0.001) below the acetabular dome. Acetabular version did not change between the initial and followup MRI in the “open-open” and “closed-closed” groups. Independently of the groups, acetabular version was increased in all hips with a fused TCC compared with hips with an open TCC (mean difference measured at 5 mm below the acetabular dome at initial MRI examination: 2° ± 5.9° [95% CI, 0.2°–3.4°] versus −9° ± 4.4° [95% CI, −9.9° to −7.8°]; p < 0.001; at followup MRI examination: 1° ± 5.7° [95% CI, 0.1°–2.7°] versus −9° ± 3.8° [95% CI, −10° to −7.6°]; p < 0.001). Both acetabular depth/width ratio and femoral head coverage did not differ among the groups or between the initial and followup MRI examinations within each group.

Although acetabular depth/width ratio and femoral head coverage remain relatively constant, acetabular version increases with advancing skeletal maturity. There seems to be a relatively narrow timeframe near physeal closure of the TCC within which acetabular orientation changes to more pronounced anteversion. Further studies with greater numbers and longer followup periods are required to support these findings and determine whether such version changes may contribute to pincer-type pathomorphologies.

Level II, prospective study.