NGF might induce central sensitisation indirectly by increasing BDNF release from primary afferent neurons.37, 38 Furthermore, synovitis might drive central sensitisation during arthritis.26 Increased paw withdrawal thresholds relapsed more quickly after treatment withdrawal than did weight-bearing asymmetry, suggesting that TrkA inhibition has a more sustained effect on peripheral pain processing than on central sensitisation. This evidence concerns the gene NGF and arthritic joint disease.