2025 ISAKOS Biennial Congress Paper
Histological Comparison of Symptomatic Cam-Type FAI to End Stage Hip Osteoarthritis Secondary to Cam-Type FAI
Daniel Fedida, BA, Manhasset, New York UNITED STATES
Brian Li, BA, Manhassert, New York UNITED STATES
Haixiang Liang, MD, Manhasset, New York UNITED STATES
Julie Moehringer, High School Diploma, Manhasset, New York UNITED STATES
Daniel A. Grande, PhD, Manhasset, NY UNITED STATES
Srino Bharam, MD, New York, NY UNITED STATES
Feinstein Institutes for Medical Research, Manhasset, New York, UNITED STATES
FDA Status Not Applicable
Summary
Using histologic methods and clinical data, the study reveals that isolated femoroacetabular impingement and hip osteoarthritis secondary to femoroacetabular impingement are distinct degenerative processes on a cellular level.
Abstract
Introduction
Femoroacetabular impingement (FAI) is a condition in which abnormal hip morphology leads to damage of articular cartilage and the labrum. Cam-type FAI (CFAI) is a subtype characterized by a bony growth at the head-neck femoral junction. While the link between FAI and progression to osteoarthritis (OA) is recognized, the histologic differences between isolated CFAI and OA secondary to CFAI are not well understood. The present study compares the histological characteristics of the two conditions and correlates them with clinical metrics.
Methods
Articular cartilage samples were obtained from 15 patients (5 females, 10 males) who underwent either hip arthroscopy for symptomatic isolated CFAI (n=7; aged 18-57) or hip arthroplasty for advanced OA secondary to CFAI (n=8; aged 52-94). Tissue was sampled from cam lesion apices and deidentified. Cartilage samples were fixed and stained with safranin-O using standard technique. The CFAI samples were assessed on a grade from 1 (all red/aggrecan positive) to 4 (all green/aggrecan negative), while OA samples were evaluated using the Kellgren-Lawrence scale from 1 (least severe) to 4 (most severe). Immunohistochemistry (IHC) for collagen type II (COL2) and aggrecan (ACAN) was also performed. The resulting stains were compared to negative controls and between disease groups. Clinical data, including age, sex, BMI, and alpha angle were correlated with safranin-O grades using Pearson’s correlation coefficient and Spearman’s rank correlation coefficient.
Results
Safranin-O staining showed more severe cartilage degeneration in the OA group compared to the CFAI group. This was confirmed by IHC showing decreased ACAN and COL2 patterns in OA compared with CFAI. In the OA group, safranin-O grades correlated positively with alpha angle (r=0.78) and age (r=0.56), confirmed by Spearman’s correlations (alpha angle: rs=0.81, p<0.01; age: rs=0.64, p<0.05). In CFAI, age negatively correlated with cartilage grade (Pearson’s r=-0.56; Spearman’s rs=-0.35, p<0.05).
Discussion
The histologic patterns of safranin-O staining show that CFAI patients tend to have healthier-appearing cartilage than OA patients. This is corroborated by the ACAN and COL2 IHC stains that showed a decreased pattern in the OA group compared with the CFAI group. Analysis of cartilage grade compared to clinical data revealed that the OA group and CFAI group correlated differently with age. Older CFAI patients tend to be associated with lower cartilage grades, meaning increased presence of aggrecan. However, older OA patients tend to be associated with higher cartilage grades, meaning decreased presence of aggrecan. Worsening OA cartilage grades were also associated with a higher alpha angle.
Conclusion
These findings indicate that articular cartilage hyperplasia may be a significant occurrence in CFAI compared to OA which is marked by a typical loss of cartilage. This further suggests that isolated CFAI and OA secondary to CFAI represent distinct degenerative processes at the cellular level.