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OP0060 Underinvestigated Mechanisms of Chronic Pain in Knee Osteoarthritis
  1. E. Turovskaya1,2,
  2. L. Alekseeva1,
  3. E. Filatova2
  1. 1laboratory of osteoarthritis, Scientific-Research Institute of Rheumatology RAMS
  2. 2neurological department, I.M.Sechenov First Moscow State Medical University, Moscow, Russian Federation

Abstract

Background In recent studies was shown that chronic pain in knee osteoarthritis (OA) has multicomponent mechanism. Besides degenerative changes of the knee, neuroplastic changes of CNS play a leading role in sustaining pain in chronic status.

Objectives To evaluate the role of CNS in pathogenesis of chronic pain syndrome in knee osteoarthritis (OA).

Methods 62 women (middle age 59±5) OA with chronic knee pain (duration more than 3 months)passed through WOMAC, X-ray and US of the knee. Duration of knee symptoms, and pain intensity were taken into consideration. Neurological examination with detailed analysis of pain sensitivity, as well as qualitative analysis of neuropathic transcripts with the help of neuropathic pain scales (Paindetect and DN4) were performed. We used the prevalence of anxiety and depressive disorders in population with OA, examined the interrelationships between severity of pain and emotional disturbances by Hospital Anxiety and Depression scale.

Results According to the results of DN4 32% (n=20) pt with OA had DN4 score≥4 - neuropatic components of pain compared with 68% (n=42) who had only nociceptive mechanism of pain. Neurologic examination revealed 56%, (n=35) with referred hyperalgesia (not only knee localization (primary hyperalgesia) but also hip and shank localization) and 44%, (n=27) had primary hyperalgesia. No other somatosensory defects were found.

The presence of referred hyperalgesia correlated with higher pain intensity (VAS), poor WOMAC and significantly associated with higher level of depression, poor quality of life.No significant differences between groups were seen in age, body index, duration of knee OA and level of structural changes.

Conclusions Chronic OA is a mixture of pain mechanisms: nociceptive and dysfunctional pain. The presence of signs of NP and referred hyperalgesia, that spreads beyond impacted joint, may be qualified as clinical features of central sensitization.The degree of spreading sensitization is correlated with the level of clinical pain and does not correlate with structural changes.

The central sensitization of pain neurons of spinal chord take place in sustaining chronic pain and demonstrates the important role of these dysfunctional changes of CNS of chronic pain mechanisms in knee osteoarthritis (OA). So rational treatment should also target structures of central nervous system.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.3801

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