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Objective: Pain persistence following knee replacement (KR) occurs in ∼20–30% of patients. Although several studies have identified preoperative risk factors for persistent post-KR pain, few have focused on post-KR contributing factors. We sought to determine whether altered nociceptive signaling and other peripheral nociceptive drivers present post-operatively contribute to post-KR pain. Design: We included participants from the Multicenter Osteoarthritis Study who were evaluated ∼12 months after KR. We evaluated the relation of measures of pain sensitivity [pressure pain threshold (PPT), temporal summation (TS), and conditioned pain modulation (CPM)] and the number of painful body sites to post-KR WOMAC knee pain, and of the number of painful sites to altered nociceptive signaling using linear or logistic regression models, as appropriate. Results: 171 participants (mean age 69 years, 62% female) were included. TS was associated with worse WOMAC pain post-KR (β ​= ​0.77 95% CI:0.19–1.35) and reduced odds of achieving patient acceptable symptom state (aOR ​= ​0.54 95%CI:0.34–0.88). Inefficient CPM was also associated with worse WOMAC pain post-KR (β ​= ​1.43 95% CI:0.15–2.71). In contrast, PPT was not associated with these outcomes. The number of painful body sites present post-KR was associated with TS (β ​= ​0.05, 95% CI:0.01, 0.05). Conclusions: Post-KR presence of central sensitization and inefficient descending pain modulation was associated with post-KR pain. We also noted that presence of other painful body sites contributes to altered nociceptive signaling, and this may thus also contribute to the experience of knee pain post-KR. Our findings provide novel insights into central pain mechanisms and other peripheral pain sources contributing to post-KR persistent knee pain.

Chronic pain has become a global health problem contributing to years lived with disability and reduced quality of life. Advances in the clinical management of chronic pain have been limited due to incomplete understanding of the multiple risk factors and molecular mechanisms that contribute to the development of chronic pain. The Acute to Chronic Pain Signatures (A2CPS) Program aims to characterize the predictive nature of biomarkers (brain imaging, high-throughput molecular screening techniques, or “omics,” quantitative sensory testing, patient-reported outcome assessments and functional assessments) to identify individuals who will develop chronic pain following surgical intervention. The A2CPS is a multisite observational study investigating biomarkers and collective biosignatures (a combination of several individual biomarkers) that predict susceptibility or resilience to the development of chronic pain following knee arthroplasty and thoracic surgery. This manuscript provides an overview of data collection methods and procedures designed to standardize data collection across multiple clinical sites and institutions. Pain-related biomarkers are evaluated before surgery and up to 3 months after surgery for use as predictors of patient reported outcomes 6 months after surgery. The dataset from this prospective observational study will be available for researchers internal and external to the A2CPS Consortium to advance understanding of the transition from acute to chronic postsurgical pain.

FCH domain only 1 (FCHO1) is a key molecule involved in clathrin-mediated endocytosis (CME). Here, the authors report homozygous FCHO1 mutations in individuals with variable T and B cell lymphopenia, which are associated with loss-of-function of FCHO1 and impaired formation of clathrin-coated pits in T cells.

Abstract Background The ankle is an important component of the human kinetic chain, and deficits in ankle strength can negatively impact functional tasks such as balance and gait. While peak torque is influenced by joint angle and movement velocity, ankle strength is typically reported for a single angle or movement speed. To better identify deficits and track recovery of ankle strength after injury or surgical intervention, ankle strength across a range of movement velocities and joint angles in healthy adults is needed. Thus, the primary goals of this study were to generate a database of strength values and 3-dimensional strength surface models for plantarflexion (PF) and dorsiflexion (DF) ankle strength in healthy men and women. Secondary goals were to develop a means to estimate ankle strength percentiles as well as examine predictors of maximal ankle strength in healthy adults. Methods Using an isokinetic dynamometer, we tested PF and DF peak torques at five joint angles (−10° [DF], 0° [neutral], 10° [PF], 20° [PF] and 30° [PF]) and six velocities (0°/s, 30°/s, 60°/s, 90°/s, 120°/s and 180°/s) in 53 healthy adults. These data were used to generate 3D plots, or “strength surfaces”, for males and females for each direction; surfaces were fit using a logistic equation. We also tested predictors of ankle strength, including height, weight, sex, and self-reported physical activity levels. Results Torque-velocity and torque-angle relationships at the ankle interact, indicating that these relationships are interdependent and best modeled using 3D surfaces. Sex was the strongest predictor of ankle strength over height, weight, and self-reported physical activity levels. 79 to 97 % of the variance in mean peak torque was explained by joint angle and movement velocity using logistic equations, for men and women and PF and DF directions separately. Conclusions The 3D strength data and surface models provide a more comprehensive dataset of ankle strength in healthy adults than previously reported. These models may allow researchers and clinicians to quantify ankle strength deficits and track recovery in patient populations, using angle- and velocity-specific ankle strength values and/or strength percentiles from healthy adults.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.