Is Susceptibility to Slipped Capital Femoral Epiphysis Linked to Obesity-Associated Proximal Femoral Morphology?

J Pediatr Orthop · Aug 27 2026 · Recent

Wu J, Zhang D, Canavese F, Li M, Li L

Departments of Pediatric Orthopaedics

Pediatric Orthopaedics

SUMMARY — THE REDUCTIONObesity accelerates skeletal maturation by about a year and raises SCFE risk through body weight effects, not by altering proximal femoral morphology once maturity is accounted for.
Abstract, as published

BACKGROUND: Slipped capital femoral epiphysis (SCFE) is strongly associated with obesity, yet the underlying mechanisms remain unclear. This study evaluated whether alterations in proximal femoral morphology (PFM) associated with obesity contribute to susceptibility to SCFE, after accounting for chronological age and skeletal maturity.

METHODS: Two groups of patients were studied. The first was a group of 42 obese children (6 to 15 y) and 42 age- and sex-matched normal-weight controls. Femoral head diameter, epiphyseal cupping ratio (ECR), Alsberg angle (AA), and posterior sloping angle (PSA) were measured on pelvic radiographs. Skeletal maturity was assessed using the modified Oxford bone score (mOBS). PFM was compared under conditions of chronological age matching and skeletal maturity stratification. The second group was a retrospective cohort of patients diagnosed with SCFE at our institution between 2011 and 2025. Chronological age at onset and skeletal maturity were compared between obese and normal-weight patients.

RESULTS: At 6 to 9 years, obese children matched by chronological age showed a larger femoral head diameter, greater ECR, a smaller AA (63.6±3.7 vs. 66.1±4.1 degrees, P=0.022), and a larger PSA (4.7±3.6 vs. 2.6±4.2 degrees, P=0.049); These differences remained at 10 to 12 years but disappeared by 13 to 15 years. The mOBS was higher in the obese group at 6 to 9 and 10 to 12 years (P=0.032 and P<0.001, respectively) but was similar between groups at 13 to 15 years (P=0.522). After stratification by skeletal maturity, anatomic differences between groups were no longer significant. At equivalent mOBS levels, obese children were about a year younger than normal-weight children (P<0.05). In the SCFE group, obese patients were about a year younger than normal-weight patients, despite similar mOBS scores (19.2±1.4 vs. 19.8±2.0; P=0.199).

CONCLUSION: Obesity accelerates skeletal maturation by about 1 year and is a risk factor for SCFE. However, after adjusting for skeletal maturity, obesity does not alter PFM. Therefore, the increased risk of SCFE in obese children is likely due to high body weight or obesity-related factors, not anatomic characteristics of the proximal femur.

LEVEL OF EVIDENCE: Level III-diagnostic study.

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