We have developed a model of unilateral adjuvant-arthritis that is reproducible across two mouse strains. DBA/1 and C57BL/6 male mice were injected intra-articularly into a stifle joint with FCA (5 microg in 5 microl) once per week for 4 weeks. Measurements of joint diameter and joint histopathology were used to monitor the course of the arthritis. Inflammatory hyperalgesia was assessed as the pressure causing a limb withdrawal. FCA injection into the mouse stifle joint caused a pronounced increase in joint diameter when compared to the contralateral limb or vehicle controls. There was also a significant decrease in the pressure required to elicit a withdrawal of the injected limb. Histology showed arthritic changes, including synovial hypertrophy and polymorphonuclear neutrophil infiltration. In established chronic inflammation, seven days of treatment with either indomethacin (NSAID) or prednisolone (steroid) caused a significant decrease in joint inflammation and associated hyperalgesia. FCA induces a long-lasting joint inflammation in DBA/1 and C57BL/6 mice, which is restricted to the injected joint and exhibits some of the pathology associated with an arthritic condition. This model will be useful in examining the effect of joint inflammation on nociceptor sensitisation in both normal and transgenic mice.