Background The association between structural abnormalities and knee pain remains controversial. It may be that the association is weaker in those with generalized pain compared to localized pain.
Objectives To determine the effect of pain at other sites on the association between knee structural pathology and knee pain in knee osteoarthritis (OA).
Methods 1099 participants (average age 63 years; range 51 to 81 years) from the population-based Tasmanian Older Adult Cohort study were studied. Presence of pain (yes/no) at the neck, back, hands, shoulders, hips, knees and feet was assessed by questionnaire. T1-weighted or T2-weighted fat saturated MRI of the right knee was performed to measure cartilage defects, bone marrow lesions (BMLs) and effusion. Osteophytes and joint space narrowing (JSN) were assessed by X-ray. Data were analyzed using multi-nominal logistic regression with adjustment for potential confounders including age, sex, body mass index, physical activity, smoking history and pain medication.
Results Knee pain only, knee plus any other site pain, and any other site pain were present in 3%, 44% and 41% of participants respectively. In multivariable analyses, knee pain only was strongly associated with the presence of cartilage defects (OR 16.96, 95% CI 4.03 to 71.32), BMLs (OR 3.27, 95% CI 1.01 to 10.53), effusion (OR 3.52, 95% CI 1.06 to 11.68) and osteophytes (OR 8.22, 95% CI 2.10 to 32.27). There were significant but weaker associations with knee pain plus any other site pain (OR=3.03 to 3.38, all P<0.05). Any other site pain was not found to be associated with any knee structural abnormalities. There was a dose-response relationship between number of knee structural abnormalities, and knee pain only and knee plus any other site pain (both P for trend≤0.002).
Conclusions Knee structural abnormalities are more strongly associated with localized knee pain than generalized pain, suggesting that pain elsewhere may influence the association of knee structural pathology and knee pain. The underlying mechanism may be due to central sensitization implicated in generalized pain which is no longer coupled to peripheral stimuli. Implication of this finding for clinicians and researchers is that pain at other sites needs to be considered while developing an approach to slow OA progression and alleviate symptom by targeting structural abnormalities.
Disclosure of Interest None declared