There is still a lack of agreement on the pathogenesis of SCFE.
A review of the literature reveals that reports on the relationship between acetabular morphology and the risk of SCFE tend to be inconsistent [4, 5, 15, 16].
Analysis of 3D models of the hip joint acetabulum in the SCFE group in our study indicated a flattening of the posterosuperior quadrant of the acetabulum in 66.66% of the hips affected by SCFE (18 out of 27 hips). Such flattening in contralateral hips without SCFE was observed only in 9.5% (two out of 21 hips), and in only 6.5% (7 out of 108 hips) in the non-SCFE control group. It is worth mentioning that we observed the flattening of the posterosuperior quadrant of the acetabulum in both acute and chronic SCFE cases. Consistent with Valera M et al. [11], closed-type acetabulum (type I), defined as the invisible posterior acetabular joint surface, was observed only in SCFE hips (11.11% 3 out of 27 hips) in our study. In the contralateral hips without SCFE signs and in the non-SCFE control group, we observed only type II of the posterior wall with visible posterior acetabular joint surface. Many authors report no difference between the acetabular version of SCFE hips and healthy controls; [4, 8, 17, 18] however, many indicate that in SCFE hips, a tendency for acetabular retroversion is observed [5, 16, 19, 20].
Like other authors [9, 20], we observed a lower acetabular version in SCFE and unaffected hips relative to the control group, at the femoral head center. However, these differences were not statistically significant (p > 0.05). We also observed no significant differences in acetabular roofing percentage between SCFE, the unaffected hips, and the control group (p = 0.596 and p = 0.31, respectively). The acetabular version angle was lower, with a tendency toward retroverted orientation at the proximal hip level. At this level in our group, we observed statistical significance relative to the control group for both SCFE (p = 0.004) and unaffected hips (p = 0.009). The lack of statistical significance in the differences regarding the acetabular version at the center of the femoral head is in line with Monazzam et al [5]. It remains unclear whether acetabular retroversion is primarily related to the mechanical etiology of SCFE or whether it is a secondary adaptive reaction of the acetabulum.
Similar to the work of Hesper T et al. [20], in our group, the mean posterior acetabular sector angle in the SCFE hips was lower than in unaffected hips, but slightly higher than in the control group. We observed such a tendency for measurements at the hip joint's middle and upper quarter, but these differences were not statistically significant (p > 0.05).
For the posterior wall analysis, we assessed the posterior wall angle. At the level of the hip center, the values were similar in all groups, with no statistically significant differences. When assessing the PWA values at the upper hip level, where we observed flattening on the 3D acetabular models, we noticed they were higher for all groups, but specifically for SCFE. The mean values of the PWA angle for the SCFE group were significantly higher than in the contralateral hip (p = 0.025) and the control group (p = 0.018). In the superior aspect of the hip, we found that the acetabular orientation was more retroverted in the SCFE group. However, at the same time, we observed an increase in the PASA value in the SCFE hips; therefore, we cannot confirm that a more retroverted acetabular orientation is associated with less posterior acetabular support.
In analysis of axial CT scans, PWA better defines the morphology of the posterior wall than the sector angle. As the PWA angle increases, the mechanical shearing forces at the femoral physis may increase—this requires further research. It is also essential to analyze the spatial relationship between the acetabular posterior wall morphology and the epiphyseal tubercle, a major epiphyseal stabilizer that can provide a rotational pivot point for slippage.