Pain sensitization and osteoarthritis

Editorial Review

Pain sensitization and osteoarthritis

Lars Arendt-Nielsen, Prof., DMSc, PhD

Clinical Experimental Rheumatology 2017; 35 (Suppl. 107): S68-S74

JACO Editorial Reviewer: Scott E Kilmer, DC, FACO, FACC

Published: December 2017
Journal of the Academy of Chiropractic Orthopedists
December 2017, Volume 14, Issue 4

The original article copyright belongs to the original publisher. This review is available from:

© 2017 Kilmer and the Academy of Chiropractic Orthopedists. This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Treating chronic musculoskeletal pain, and chronic joint pain (osteoarthritis (OA) in particular), is challenging as the peripheral and central pain mechanisms are not fully discovered, and safe and as effective analgesic drugs are not available. In general, the preclinical models of OA are limited to provide fundamental understanding of the pain mechanisms involved in patients with chronic joint pain (1). The pain associated with joint discomfort is highly variable, often underestimated by clinicians, and shows only modest association with crude radiological scorings. One reason for the disconnect between the extent of structural damage and pain is neural plastic changes occurring in the peripheral and central nervous system resulting in pain sensitization impacting the patient’s experience of pain. In recent years, a variety of human quantitative and mechanistic pain assessment tools (Quantitative Sensory Testing, QST) have been developed, providing new opportunities for diagnostic phenotyping of OA patients and the associated degree of sensitization. Mechanistic phenotyping has revealed specific subgroups of specifically sensitized OA patients, and been used as a predictive guideline to evaluate which patients are most likely to experience continued chronic pain after an otherwise technically successful knee replacement (chronic postoperative pain). Furthermore, such techniques may be used to profile new or existing drugs together with other e.g. cognitive or behavioral therapies with the potential to manage joint pain.

JACO Editorial Summary:

  • This article was written by Lars Arendt-Nielsen, Prof.,DMSc.,PhD. Dr. Arendt-Nielsen is on the Faculty of Medicine at Aalborg University, School of Medicine in Denmark.
  • The purpose of this paper is to explain pain sensitization in osteoarthritis and show how selected biomarkers are used to help predict those patients that may develop increased pain after total joint arthroplasty (TJA).
  • It is estimated that by 2030 total hip arthroplasty in the US will increase by 200% and total knee arthroplasty will increase by 700%. Additionally, around 20% of total knee arthroplasty patients will have continued pain after surgery and approximately 10% of total hip arthroplasty patients will have continued pain after the surgery.
  • Pain sensitization occurs as a result of “continuous and intense nociceptive input from joints”. Studies have shown this type of nociceptive input occurs with osteoarthritis and is a main driver of peripheral and central sensitization.
  • There are two basic ways to clinically evaluate for pain sensitization. The first is assessment using scores/questionnaires such as VAS, McGill Pain Questionnaire, WOMAC and others. The second method is the use of quantitative mechanistic pain biomarkers. There are two quantitative mechanistic biomarkers used in the study. 1. Temporal Summation. This occurs when neurons in the dorsal horn become more excitable due to repeated nociceptive input. Bedside testing using this method is accomplished by using computer controlled pressure algometry. After repeated stimulation, the patient reports an increase in severity and duration of pain which is not supported by the radiographic findings. 2. Descending Pain Modulation. This type of pain modulation occurs when nociceptive input is received in the brain from a segment remote from the site of pain caused by the osteoarthritis. Clinical testing of descending pain modulation is accomplished with the use of cuff algometry when one cuff delivers a conditioning stimulus and the other delivers a test stimulus. This triggers a “pain inhibits pain phenomenon”. This phenomenon can be diminished in patients with OA and can be used to help identify those patients that may have continued pain after total joint arthroplasty.
  • Using the methods mentioned above to measure for pain sensitization, there is evidence to show that there is a correlation of preoperative hyperalgesia and chronic postoperative pain. Further, joint revision surgery based only on the patient’s report of pain can result in 50% of those patients experiencing chronic/increased pain after the revision.
  • This paper demonstrates how mechanistic phenotyping can be used to aid in predicting which patients would likely develop chronic or increased pain after total joint arthroplasty. Pain sensitization should be evaluated prior to surgery and pain alone should not be used as the sole indicator for total joint arthroplasty.

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