Comparison of Experimental Pain and Functional Impact in Individuals with Single- and Multi-site Osteoarthritis

Abstract

Osteoarthritis (OA) is a painful and disabling disease that can involve a single joint or progress to multiple joints. We have limited understanding whether individuals with multi-site OA exhibit altered pain processing and psychosocial function compared to those with single-site OA. Here, we perform a secondary data analysis to test the hypothesis that individuals with multi-site OA have significantly higher experimental pain and functional impact than individuals with single-site OA or no OA. Individuals between 45 and 85 years of age underwent quantitative sensory testing (QST) and answered clinical questionnaires. Four cohorts were formed: individuals with only CMC pain (n=X), individuals with only knee pain (n=X), individuals with CMC + knee pain (n=X), and pain-free individuals (n=X). ANCOVAS were performed to identify significant differences in experimental pain and psychological variables across cohorts. The CMC + knee pain cohort had significantly higher heat induced pain during temporal summation (forearm at 44°C, p=0.01) in comparison to all other cohorts. This trend was observed across temperatures. The CMC + knee pain cohort also had significantly lower pressure pain thresholds (p≤0.01) compared to the CMC pain cohort but were not different from the knee pain cohort. Lastly, the CMC + knee pain cohort had the highest self-reported pain (p<0.01), disability (p<0.01), and emotional distress (p≤0.03) compared to individuals with only CMC or only knee pain. These results suggest knee OA compounded with CMC OA considerably increases disease impact and poor quality of life in comparison to single-joint OA. The results also support a relationship between the number of painful joints and enhanced widespread sensitivity. This study highlights the importance of measuring pain at sites other than the primary OA location. Enhancing our knowledge of symptoms and function across multiple joints could contribute to more targeted treatment and prevention of OA progression. Grant support from R01AG059809, R01AG067757, and R37AG033906.