Disparities in Clinical and Experimental Pain Between Non-Hispanic White and Asian American Individuals With Knee Osteoarthritis and the Role of Pain Catastrophizing: Pilot Study in Florida

Background: Although a few studies have delineated the disparities in knee osteoarthritis (KOA) pain between non-Hispanic White and Asian American individuals, a significant research gap persists in elucidating the mechanisms underlying these differences. Objective: This pilot study aims to examine psychological factors, specifically pain catastrophizing and negative affect, as potential explanatory mechanisms for these dissimilarities. Methods: A cross-sectional design was used. Forty community-dwelling participants aged 50-70 years with self-reported KOA pain, including 20 non-Hispanic White and 20 Asian American individuals, were recruited in North Central Florida. Clinical KOA pain intensity was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and the 4 subscales of the Short-Form McGill Pain Questionnaire-2. Quantitative sensory testing was conducted to measure experimental sensitivity to heat- and mechanically induced pain, including heat pain, pressure pain threshold, and punctate mechanical pain, as well as inhibitory pain processes through conditioned pain modulation. Pain catastrophizing was evaluated using the Coping Strategies Questionnaire-Revised Pain Catastrophizing subscale, while negative affect was assessed using the Positive and Negative Affect Schedule. Bayesian mediation analyses were used to examine both direct and indirect effects (mediation) between variables. Results: Asian American individuals exhibited higher pain catastrophizing scores than non-Hispanic White individuals. Pain catastrophizing, at high levels, contributed to WOMAC and Short-Form McGill Pain Questionnaire-2, which measured clinical pain. Race had no direct effects on these pain scores but exerted significant indirect effects via pain catastrophizing (WOMAC pain: 0.96, 95% CI 0.03-2.16; continuous pain: 0.84, 95% CI 0.18-1.70; intermittent pain: 0.78, 95% CI 0.03-1.71; neuropathic pain: 0.43, 95% CI 0.03-0.95; and affective pain: 1.05, 95% CI 0.24-1.99); thus, pain catastrophizing likely fully mediated the relationship between race and these pain measures. While Asian American individuals reported greater experimental pain sensitivity (heat pain, pressure pain threshold, and punctate mechanical pain) than non-Hispanic White individuals, these racial effects were not mediated by pain catastrophizing. Asian American individuals reported higher negative affect scores compared with non-Hispanic White individuals; however, negative affect did not mediate the relationship between race and any pain measures. Conclusions: The results demonstrate the contribution of pain catastrophizing to clinical pain in Asian American individuals with KOA and identify it as a potential mechanism underlying group differences in KOA pain between non-Hispanic White and Asian American individuals. However, caution is warranted due to the exploratory nature of this study and the treatment of Asian American individuals as a monolithic sample. Hence, future replication with larger and more diverse samples is necessary. Additionally, the lack of mediation effects of pain catastrophizing in the relationship between race and experimental pain suggests the need to explore other factors, such as biological, genetic, social, and environmental influences. Moreover, further research is essential to clarify the role of negative affect.