The use of the boron neutron capture reaction is a potential means of treating the symptoms of rheumatoid arthritis and related diseases. For this approach, termed boron neutron capture synovectomy (BNCS), the goal is cellular ablation within the inflamed synovium, the membrane lining the inner surface of the joint capsule of articulating joints. To be effective in destroying the synovial membrane, clinical results using beta-particle emitters suggest that radiation doses must be very large (approximately 100 Gy in a single delivery), substantially higher than those used in BNCT of tumors where cessation of reproductive capability in malignant cells is the clinical goal. Generating large radiation doses requires that very high boron concentrations be present in the target tissue at the time of irradiation. While it is unlikely that systemic administration of the boron compound can result in the needed synovial boron concentrations, extremely high boron levels can be readily achieved via intra-articular delivery, that is, by injection of the compound directly into the joint fluid. This delivery approach results in very high synovial boron levels in vivo, which means that radiation treatment times can be very short. Neutron beams based on accelerators, reactors, and isotope sources have been designed at many institutions around the world, and in some cases, these beams have been built and experimentally characterized. With existing neutron sources, human joint irradiations could be performed in a matter of minutes. The efficacy of BNCS in causing synovial necrosis has been clearly demonstrated in an animal model of arthritis. In addition, trends in the reduction of the symptoms of arthritis and histological evidence of selective cell kill suggest that positive clinical results may be possible with substantially lower macroscopic tissue doses than those found to be effective in beta-particle synovectomy. This may be possible by taking advantage of the short pathlengths of the 10B(n,α) reaction products and by confining the boron compound to specific cell types important to maintaining the pathological inflammatory reaction.