Rheumatoid arthritis is a common disease, characterised by persistent synovitis, systemic inflammation and severe pain. A relationship between environmental cold exposure and increased pain in arthritic joints has been suggested (Smedslund and Hagen, 2011), although the underlying mechanisms are unknown. Changes in joint vascularization and the development of pain have been previously hypothesized to be linked in arthritis, with evidence of a correlation provided in osteo-arthritis (Walsh et al., 2010; Ashraf et al., 2011). We have been studying the role of Transient Receptor Potential (TRP) channels in arthritis. We recently found by using a mono-arthritis model induced by a single injection of Complete Freund’s Adjuvant (CFA; 10 ug/joint; 10 ul) in to the knee joint; that the TRP Ankyrin 1 (TRPA1), a suggested cold sensor, mediates CFA-induced secondary mechanical hyperalgesia (Fernandes et al., 2011). We have now investigated the contribution of TRPA1 activation for blood flow changes in the arthritic knee joint of mice exposed for 1h to environmental cold (10oC). We used male CD1 and TRPA1 wild-type (WT) and knockout (KO) mice (10-12 weeks of age). Blood flow was recorded by using full-field laser perfusion imager (FLPI) following cold exposure, 2 weeks after arthritis induction, in anaesthetised mice (mixture of ketamine (75 mg/kg) + medetomidine (1 mg/kg)). Briefly, after anaesthesia, the patellar ligament was carefully dissected off the knee joint to expose the synovial membrane. Changes in blood flow were then recorded for 30 min. Data obtained from the arthritic knee joint (ipsilateral knee; CFA-treated) was compared to the contralateral knee joint (saline-treated; 10 ul/joint). Naive joints were used as controls. Whilst cold exposure caused vasoconstriction in naive mice, a significant vasodilatation was observed in arthritic animals, with both saline- and CFA-treated joints exhibiting increased blood flow (1.5- and 2-fold increase, respectively). This response was not observed in mice treated systemically with the selective TRPA1 antagonist HC-030031 (100 mg/kg; 1h before blood flow recording; n=7). Similarly, vasodilatation was not present in the arthritic knee joints of TRPA1 KO mice (n=9) when compared to their WT controls (n=9). We suggest TRPA1 mediates hemodynamic changes in arthritic joints exposure to lower temperatures. This could be a potential and additional mechanism by which TRPA1 channels modulate arthritis progression and pain sensitivity.