Background It is now known that OA pain is a complex interaction between many different pain mechanisms. A subset of adults with chronic, symptomatic knee OA may therefore, have neuropathic mechanisms contributing to their pain experience.
Objectives We evaluate pathogenetic mechanisms involved in the initiation of pain in OA, to measure the prevalence of neuropathic pain and NP(neuropathic) symptoms among adults with this condition and additionally to detect somatosensory deficit
Methods Patients were 39 women aged from 45-65 years with chronic knee pain (the duration of painat least during the last 3 months) and OA severity II-III grade by Kellgren-Lawrence. Two main types of pain: nociceptive and neuropathic pain were revealed with the help of clinical (rheumatologic and neurological) examinations and neuropathic pain scales (Paindetect and DN4). The patients were asked about duration of knee symptoms and knee OA, knee OA severity (WOMAC), and pain intensity. 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. The level of knee destruction was assessed with radiography using the Kellgren-Lawrence grading scale and US examination and rheumatologic examination.
Results Patients were categorized into two groups according to the results of neuropathic questionnaire DN4: patients with DN4 score>4, having a neuropathic pain(NP) features and patients with DN4 score<4, who had no evident neuropathic pain. According to DN4 score patients, who used NP descriptors composed 28%(n=11). No significant differences between groups were seen in age, the character of pain, duration of knee OA, quantity of impacted knee joints, body index, quality of life, radiographic and US severity of knee OA. But the presence of NP features was correlated with higher pain intensity assessed, WOMAC and significantly correlated with higher level of anxiety. In clinical studies, compared to controls, patients with NP features had more diffuse hyperalgesia to mechanical stimuli, no other somatosensory defects were found.
Conclusions The results indicated that people with chronic OA can experience pain due to both nociceptive and neuropathic mechanisms to varying degrees, so OA can be associated with a mixture of pain mechanisms. The likely neuropathic mechanism in OA is central sensitization, that may be the reason for the often observed discreapancy between joint damage (radiological joint changes) and clinical pain intensity. So treatment should also target central nervous system structures.
Disclosure of Interest None Declared