Rheumatoid arthritis (RA) is chronic disease evident as joint inflammation and progressive joint destruction. Of importance, pain is one of the most egregious symptoms reported by RA patients. Autoantibodies to type II collagen and glucose-6-phosphate isomerise (GPI) are detected in serum of RA patients. Systemic injection of these antibodies to mice rapidly induces arthritis-like symptoms and generates a joint pathology that resembles human RA. While collagen antibody-induced arthritis (CAIA) and K/BxN serum transfer (GPI antibody-mediated) are commonly used the rheumatology field, they have just recently been evaluated as models of arthritis-induced pain. Pain-like behaviors such as mechanical and cold allodynia and reduced locomotor activity are pronounced. Mechanical allodynia is observed not only during the inflammatory phase but outlasts the signs of inflammation by two months. Interestingly, cyclooxygenase and TNF inhibitors only have anti-nociceptive effect during the inflammatory phase, while drugs like gabapentin reduces the hypersensitivity in both phases, indicating that inflammatory and post-inflammatory nociception are maintained through different mechanisms. Microglia and astrocyte activity have been assessed using quantitative PCR and immunohistochemistry and our data indicate that spinal glia is activated in both models. A number of glia-associated factors are upregulated in the spinal cord, and intrathecal injection of pentoxifylline, a general glia inhibitor attenuates the mechanical allodynia, pointing to an important role of spinal glia in arthritis-induced pain. In summary, this presentation will introduce the CAIA and K/BxN models as new experimental models of arthritis-induced pain and discuss the role of spinal glia in long-term hypersensitivity initiated by joint inflammation.