In this chapter, we discuss nociceptive treatment targets for pain in rheumatoid arthritis (RA), including non-steroidal anti-inflammatory drugs (NSAIDs). Sustained nociceptive input, as found in RA, can lead to changes in central pain processing. Nociceptive input is increased following local sensitization of peripheral nerves within the joint. Coupled with inflammation, it is known that major mediators of pain include neuropeptides (e.g. calcitonin gene-related peptide, CGRP) and neurotrophins such as nerve growth factor (NGF), each of which can also sensitize peripheral nerves. Immune cells within the central nervous system (CNS) directly contribute to developing central sensitization through the generation of cytokines such as IL-1. Interest has therefore grown in analgesics for RA pain that may target the CNS, including opiates and centrally acting analgesics. In this chapter, we discuss the scientific basis of pain in RA, followed by treatments currently widely used in clinical practice, including NSAIDs, opioids, and centrally acting analgesics.