ABSTRACT Objective High blood pressure (BP) often co‐occurs with osteoarthritis (OA) and may influence pain sensitivity, potentially contributing to pain‐pathology discordance. We hypothesized that higher BP would associate with reduced pain sensitivity and greater OA severity in adults with chronic knee pain. Methods A cross‐sectional analysis of 213 community‐dwelling adults (44–78 years) with chronic knee pain was conducted. Hypertension was defined by diagnosis or antihypertensive use; others were normotensive. Systolic, diastolic, pulse (PP), and mean arterial (MAP) BP were measured. Quantitative sensory testing assessed pressure/thermal pain sensitivity, temporal summation (TS), and conditioned pain modulation (CPM). Radiographic knee OA (rKOA) was graded using the Kellgren‐Lawrence scale. Models adjusted for race, age, BMI, site, and diabetes. Results Blood pressure‐pain associations were moderated by sex and hypertensive status, observed only in normotensive individuals. Among normotensive males, each 10 mmHg increase in BP was associated with reduced pressure pain sensitivity ( β 95% CI: systolic −0.21 −0.42, −0.002; diastolic −0.36 −0.68, −0.05; MAP −0.31 −0.59, −0.03; all p < 0.05) but greater odds of late‐stage rKOA (AOR 95% CI: systolic 1.70 1.07, 2.70; MAP 2.10 1.10, 4.01). Among normotensive females, temporal summation of mechanical pain increased with higher BP ( β 95% CI: systolic 0.14 0.01, 0.27, p = 0.027; PP 0.20 0.02, 0.38, p = 0.026). No significant associations were observed for heat/cold pain sensitivity, TS of heat pain, or CPM. Discussion Elevated BP was associated with hypoalgesia and more severe rKOA severity in normotensive males. In normotensive females, elevated BP showed greater pain facilitation but not rKOA severity. Together, these sex‐specific findings suggest BP as a vascular factor contributing to pain‐pathology mismatch in OA. Significance Statement Associations between arterial blood pressure and pain in older adults with knee pain were found to be sex‐ and hypertension‐dependent, primarily evident in normotensive individuals. Elevated blood pressure was associated with reduced mechanical pain sensitivity but greater radiographic OA in normotensive males; normotensive females showed enhanced pain facilitation without increased OA severity. These findings support arterial pressure as a shared vascular factor in pain–pathology mismatch and highlight the importance of incorporating cardiovascular markers into chronic pain phenotyping and interpretation.
Cruz et al. (Sun,) studied this question.