Background/Purpose: Self-reported descriptors of pain in knee osteoarthritis (OA) such as burning and stabbing pain are suggestive of a neuropathic component of pain beyond that of nociceptive pain from structural pathology. However, such descriptors do not necessarily equate to specific pain mechanisms. While there is evidence of proprioceptive and vibration perception abnormalities in knee OA, to date, there have been no studies documenting objective neuropathy involving nociceptive pathways in knee OA. We used the StEP [Scholz, 2009] protocol, which distinguishes neuropathic vs. non-neuropathic pain with feasible bedside evaluations to assess the prevalence of clinical evidence of neuropathy in knee OA.

Methods: The Multicenter Osteoarthritis (MOST) Study is a NIH-funded longitudinal cohort study of persons with or at risk of knee OA. Subjects were evaluated with a peripheral neuropathy screen, and a standardized somatosensory assessment at the knee with von Frey 2g and 26g monofilaments (static allodynia, hypoesthesia), brush (dynamic allodynia), and pinprick (hyperalgesia), each assessed with 4 trials. Abnormal responses were defined as pain (allodynia or hyperalgesia) or no response (hypoesthesia) in ≥3/4 trials. We excluded those with TKR. We evaluated the prevalence of each somatosensory abnormality stratified by # of knees with radiographic knee OA (ROA) and with frequent knee pain (FKP).

Results: There were 1821 participants (mean age 67, mean BMI 30, 62% female, 46% with FKP in either knee, 3.9% with +peripheral neuropathy screen); 722 without ROA (39.6%), 413 with unilateral ROA (22.6%), and 686 with bilateral ROA (37.6%).  The prevalence of allodynia, hyperalgesia, and hypoesthesia was <5% in all groups, regardless of # of knees with ROA or FKP (Figure). For those with unilateral ROA or unilateral FKP, the prevalence of abnormalities were similar in the ipsilateral and contralateral knee.

Conclusion: Using standardized bedside assessment tools for the clinical distinction between neuropathic and nociceptive pain, we observed an overall low prevalence of somatosensory changes that would be consistent with neuropathy. However, these changes did not meet the diagnostic threshold criteria of neuropathic pain, and the presence of abnormalities did not differ by # of knees with ROA or FKP, or by laterality. We cannot rule out subclinical neuropathy that could be detected by nerve conduction study or skin biopsy. Nonetheless, we did not find overt evidence of nerve lesion in those with ROA at a greater frequency than those without ROA, and similar findings for FKP vs. no FKP. Further, the prevalence of abnormalities detected did not approach that reported for “neuropathic-like” pain by self-report on PainDetect. Patient-reported symptoms may not directly reflect underlying mechanisms, highlighting the need for identifying objective means of pain phenotyping to move towards mechanism-based treatments for OA pain.