Tuhina Neogi1, Laura Frey-Law2, Joachim Scholz3, Jingbo Niu1, Lars Arendt-Nielsen4, Clifford Woolf5, Michael Nevitt6, Laurence Bradley7, David T Felson1. 1. Clinical Epidemiology Research and Training Unit, Boston University School of Medicine, Boston, Massachusetts, USA. 2. Department of Physical Therapy & Rehabilitation Science, University of Iowa, Iowa City, Iowa, USA. 3. Department of Anesthesiology and Pharmacology, Columbia University Medical Center, New York, New York, USA. 4. Department of Health Science and Technology, Center for Sensory-Motor Interaction, Aalborg University, Aalborg, Denmark. 5. F.M. Kirby Center and Program in Neurobiology, Children's Hospital Boston, Boston, Massachusetts, USA. 6. Department of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, California, USA. 7. Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Abstract
OBJECTIVES: It is not clear whether heightened pain sensitivity in knee osteoarthritis (OA) is related to sensitisation induced by nociceptive input from OA pathology ('state') versus other confounding factors. Conversely, some individuals may be predisposed to sensitisation irrespective of OA ('trait'). METHODS: The Multicenter Osteoarthritis Study is a longitudinal cohort of persons with or at risk of knee OA. We obtained knee X-rays, pain questionnaires and comprehensive assessment of factors that can influence pain sensitivity. We examined the relation of sensitisation and sensitivity assessed by mechanical temporal summation (TS) and pressure pain thresholds (PPTs) to knee OA and knee pain severity. To test whether sensitisation and sensitivity is a 'state' induced by OA pathology, we examined the relation of PPT and TS to knee OA duration and severity. RESULTS: In 2126 subjects (mean age 68, mean body mass index (BMI) 31, 61% female), PPT and TS were not associated with radiographic OA (ORs 0.9-1.0 for PPT and TS; p>0.05). However, PPT and TS were associated with pain severity (ORs: 1.7-2.0 for PPT; 1.3-1.6 for TS; p<0.05). Knee OA duration and radiographic severity were not associated with PPT or TS. CONCLUSIONS: PPT and TS were associated with OA-related pain, but not radiographic OA after accounting for pertinent confounders in this large cohort. Lack of association with disease duration suggests at least some sensitisation and pain sensitivity may be a trait rather than state. Understanding the relationship between pathological pain and pain sensitivity/sensitisation offers insight into OA pain risk factors and pain management opportunities. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
OBJECTIVES: It is not clear whether heightened pain sensitivity in knee osteoarthritis (OA) is related to sensitisation induced by nociceptive input from OA pathology ('state') versus other confounding factors. Conversely, some individuals may be predisposed to sensitisation irrespective of OA ('trait'). METHODS: The Multicenter Osteoarthritis Study is a longitudinal cohort of persons with or at risk of knee OA. We obtained knee X-rays, pain questionnaires and comprehensive assessment of factors that can influence pain sensitivity. We examined the relation of sensitisation and sensitivity assessed by mechanical temporal summation (TS) and pressure pain thresholds (PPTs) to knee OA and knee pain severity. To test whether sensitisation and sensitivity is a 'state' induced by OA pathology, we examined the relation of PPT and TS to knee OA duration and severity. RESULTS: In 2126 subjects (mean age 68, mean body mass index (BMI) 31, 61% female), PPT and TS were not associated with radiographic OA (ORs 0.9-1.0 for PPT and TS; p>0.05). However, PPT and TS were associated with pain severity (ORs: 1.7-2.0 for PPT; 1.3-1.6 for TS; p<0.05). Knee OA duration and radiographic severity were not associated with PPT or TS. CONCLUSIONS:PPT and TS were associated with OA-related pain, but not radiographic OA after accounting for pertinent confounders in this large cohort. Lack of association with disease duration suggests at least some sensitisation and pain sensitivity may be a trait rather than state. Understanding the relationship between pathological pain and pain sensitivity/sensitisation offers insight into OA pain risk factors and pain management opportunities. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Authors: Roland Staud; Richard C Cannon; Andre P Mauderli; Michael E Robinson; Donald D Price; Charles J Vierck Journal: Pain Date: 2003-03 Impact factor: 6.961
Authors: Patrick H Finan; Luis F Buenaver; Sara C Bounds; Shahid Hussain; Raymond J Park; Uzma J Haque; Claudia M Campbell; Jennifer A Haythornthwaite; Robert R Edwards; Michael T Smith Journal: Arthritis Rheum Date: 2013-02
Authors: Joshua J Stefanik; David T Felson; Caroline M Apovian; Jingbo Niu; M Margaret Clancy; Michael P LaValley; Tuhina Neogi Journal: Arthritis Care Res (Hoboken) Date: 2018-10 Impact factor: 4.794
Authors: Martin van der Esch; Marike van der Leeden; Leo D Roorda; Willem F Lems; Joost Dekker Journal: Clin Rheumatol Date: 2016-09-17 Impact factor: 2.980
Authors: David T Felson; Jingbo Niu; Emily K Quinn; Tuhina Neogi; Cara L Lewis; Cora E Lewis; Laura Frey Law; Chuck McCulloch; Michael Nevitt; Michael LaValley Journal: Arthritis Rheumatol Date: 2017-02 Impact factor: 10.995