Introduction: Individuals with osteoarthritis (OA) show increased morbidity and mortality. Telomere length, a measure of cellular aging, predicts increased morbidity and mortality. Telomeres shorten with persisting biological and psychosocial stress. Living with chronic OA pain is stressful. Previous research exploring telomere length in people with OA has produced inconsistent results. Considering pain severity may clarify the relationship between OA and telomeres.

Objectives: We hypothesized that individuals with high OA chronic pain severity would have shorter telomeres than those with no or low chronic pain severity.

Methods: One hundred thirty-six adults, ages 45 to 85 years old, with and without symptomatic knee OA were included in the analysis. Peripheral blood leukocyte telomere length was measured, and demographic, clinical, and functional data were collected. Participants were categorized into 5 pain severity groups based on an additive index of frequency, intensity, time or duration, and total number of pain sites (FITT). Covariates included age, sex, race or ethnicity, study site, and knee pain status.

Results: The no or low chronic pain severity group had significantly longer telomeres compared with the high pain severity group, P50.025. A significant chronic pain severity dose response emerged for telomere length, P50.034. The FITT chronic pain severity index was highly correlated with the clinical and functional OA pain measures. However, individual clinical and functional measures were not associated with telomere length.

Conclusion: Results demonstrate accelerated cellular aging with high knee OA chronic pain severity and provide evidence for the potential utility of the FITT chronic pain severity index in capturing the biological burden of chronic pain.

Background: Determining neuronal topographical information in the cerebral cortex is of fundamental importance for developing neuroprosthetics. Significant progress has been achieved in decoding hand voluntary movement with cortical neuronal activity in nonhuman primates. However, there are few successful reports in scientific literature for decoding lower limb voluntary movement with the cortical neuronal firing. We once reported an experimental system, which consists of a specially designed chair, a visually guided stand and squat task training paradigm and an acute neuron recording setup. With this system, we can record high quality cortical neuron activity to investigate the correlation between these neuronal signals and stand/squat movement.

Methods/Results: In this research, we train two monkeys to perform the visually guided stand and squat task, and record neuronal activity in the vast areas targeted to M1 hind-limb region, at a distance of 1 mm. We find that 76.9% of recorded neurons (1230 out of 1598 neurons) showing task-firing modulation, including 294 (18.4%) during the pre-response window; 310 (19.4%) for standing up; 104 (6.5%) for the holding stand phase; and 205 (12.8%) during the sitting down. The distributions of different type neurons have a high degree of overlap. They are mainly ranged from +7.0 to 13 mm in the Posterior-Anterior dimension, and from +0.5 to 4.0 mm in Dosal-lateral dimension, very close to the midline, and just anterior of the central sulcus.

Conclusions/Significance: The present study examines the neuronal activity related to lower limb voluntary movements in M1 and find topographical information of various neurons tuned to different stages of the stand and squat task. This work may contribute to understanding the fundamental principles of neural control of lower limb movements. Especially, the topographical information suggests us where to implant the chronic microelectrode arrays to harvest the most quantity and highest quality neurons related to lower limb movements, which may accelerate to develop cortically controlled lower limb neuroprosthetics for spinal cord injury subjects.