Abstract
Background Knee osteoarthritis and poor sleep quality often co-occur and have a reciprocal relationship. Long-term exposure to poor sleep can facilitate pain, and short-lasting experimental sleep disturbances increase pain sensitivity. This study combined experimental knee pain and sleep disturbances to investigate whether short-term sleep disruption increases experimental knee pain intensity and if baseline traits affect this vulnerability. Methods Knee pain was induced using hypertonic saline (7%) injected into the infrapatellar fat pad (IFP) before and after three forced awakenings per night for three nights. Gait was measured using marker-less motion capture. Pain sensitivity was assessed as pressure pain and tolerance thresholds, temporal summation of pain (TSP), and conditioned pain modulation. Questionnaires assessed sleep quality, pain catastrophizing, anxiety, and depression. Results Thirty healthy participants experienced moderate-to-severe knee pain from the hypertonic saline injected into the IFP. Sleep disruption significantly reduced sleep quality. Exploratory analysis revealed that participants with baseline knee pain < 7 (VAS 0-10) experienced increased pain after the sleep disruption (p < 0.05). There were no changes in other measurements. Conclusions This study investigated a potential novel pain model combining experimental knee pain and short-term sleep disturbance but did not find any changes in knee pain intensity, pain sensitivity, psychological factors, or gait characteristics. SIGNIFICANCE STATEMENT: This study introduced an experimental model integrating sleep disruption and knee pain to probe individual pain vulnerability. Results revealed that short-term sleep loss increased knee pain in individuals with lower baseline experimental knee pain intensity, and that a combination of psychophysical factors explained 30%-45% of the substantial variability in knee pain. Temporal summation emerged as a consistent predictor of knee pain, while sleep quality predicted pain after sleep disruption. These findings advance understanding of how sleep modulates individual pain vulnerability.