Bone parameters across different types of hip osteoarthritis and their relationship to osteoporotic fracture risk

Objective The atrophic type of hip osteoarthritis (OA) is characterized by cartilage degradation without the formation of osteophytes. Individuals with atrophic OA have been less well studied, and it is unknown whether this OA type differs from the osteophytic types with regard to bone tissue. The purpose of this study was to examine bone mineral density (BMD), hip structural properties, and fracture risk in individuals with the atrophic type of OA as compared to those with the osteophytic types (normotrophic/hypertrophic) as well as individuals without OA. Methods This study is part of the Rotterdam Study, a large prospective population-based cohort study. We examined 5,006 participants who had been assessed for OA, BMD, and geometric measures at baseline and for incident nonvertebral osteoporotic fractures (mean followup 9.6 years). We estimated the differences in bone characteristics between the OA groups and the controls (no joint space narrowing or osteophytes). Cox proportional hazards regression was used to calculate osteoporotic fracture risk. Results Participants with atrophic OA had systemically lower BMD as compared to those with normotrophic OA and as compared to the controls (6.5% and 9% for total body BMD; 4% and 5% for skull BMD, respectively). Participants with osteophytic OA had approximate to 4% and approximate to 5% higher total body and skull BMD, respectively, a wider femoral neck, and greater bone strength (12% and 5% higher section modulus, respectively) as compared to the controls or to those with atrophic OA. The risk of osteoporotic fractures was almost 50% higher in those with atrophic OA as compared to the controls (hazard risk 1.48, P = 0.008). This difference was not explained by differences in the BMD, number of falls, degree of disability, or use of corticosteroids. Conclusion Individuals with atrophic hip OA have an increased risk of osteoporotic fractures that is not fully explained by systemically lower BMD as compared to controls.