F. Boel, M.A. van den Berg, N.S. Riedstra, M.M.A. van Buuren, J. Tang, S.M.A. Bierma-Zeinstra, D. Felson, J.A. Lynch, A.E. Nelson, M. Nevitt, J. Runhaar, R. Agricola
DOI: https://doi.org/10.1016/j.ostima.2024.100201
Different hip morphologies have been shown to be risk factors for hip OA. However, the associations found differ in size and are sometimes even contradictory. Different follow-up times, radiographic hip OA (RHOA) definitions, and quantification of hip morphology might explain these conflicting results. Additionally, previous studies have shown that hip pain in combination with a different hip morphology might alter the association with incident RHOA.
We aimed to investigate whether hips with both hip pain and different morphologies, i.e., acetabular dysplasia, pincer and cam morphology, had a different association with the development of incident RHOA compared to asymptomatic hips with the same morphology.
Individuals from three prospective cohort studies, Cohort Hip and Cohort Knee (CHECK), Johnston County Osteoarthritis Project (JoCoOA) and the Multicenter Osteoarthritis Study (MOST), were included in the current study. Standardized anteroposterior (AP) pelvic or long-limb radiographs were taken at baseline and follow-up (CHECK 8 years, JoCoOA 6 years, MOST 5 years). Incident RHOA was defined at follow-up as KLG ≥ 2 or total hip replacement. The presence of hip pain was self-reported through survey questions and dichotomized. Hip morphology was automatically quantified on the baseline radiographs using an in-house developed, validated pipeline. Acetabular dysplasia was defined by a Wiberg center edge angle (WCEA) ≤ 25°, pincer morphology was defined by a lateral center edge angle (LCEA) ≥ 40°, and cam morphology was defined by an alpha angle ≥ 60°.
Hips free of RHOA (KLG 0) at baseline, with available baseline age, body mass index (BMI), hip morphology measurements, and follow-up KLG were included. When assessing acetabular dysplasia, all hips with pincer morphology were excluded from the dataset, and vice-versa, so that the reference group only consisted of hips with a normal femoral head coverage by the acetabulum. This resulted in the inclusion of 1,768 participants for acetabular dysplasia, 1,526 participants for pincer morphology, and 1,985 participants for cam morphology, see Table 1.
Three generalized mixed-effects logistic regression models with the interaction between hip pain and morphology were employed. These models included three random effect levels (cohort, individual, hip side) and were adjusted for age, biological sex, and body mass index (BMI). Associations were expressed as adjusted odds ratios (aORs) or ratios of aORs with 95% confidence intervals (CIs).
No significant interactions between hip morphology and pain and the development of incident RHOA were found, see Table 2. Additionally, only cam morphology was significantly associated with incident RHOA in asymptomatic hips, aOR 4.7 (95% CI 2.0 – 11.2).
The presence of hip pain was not an effect modifier in the association between acetabular dysplasia, pincer or cam morphology and the development of incident RHOA within 5-8 years. Future research should investigate whether including the duration and severity of symptoms also does not alter this relationship.
