Neurotransmitter Glutamate is a Novel Neurogenic Initiator in Arthritic Inflammation by K. Westlund High; P0516.1202

Over 90% of the population will suffer from arthritis during their lifetime but present treatment regimens cannot completely abrogate chronic episodes of inflammation, pain, or disability. This costs an estimated 60 billion dollars/year in total costs of medicines, disability and lost wages (Arthritis Foundation, 2002). It is firmly accepted that neurogenic factors play a role in peripheral inflammation. There are 18 published case reports of stroke and nerve injury victims demonstrating a sparing of arthritic inflammation and subsequent disease progression on the patient’s paralyzed side [1]. One case described partial reversal of previous arthritic damage in the paralyzed joint when followed for three years. One case report showed elevated IL-1 levels on both paralyzed and normal sides, but the active arthritic side also had elevated substance P levels and the paralyzed, non-arthritic side did not. To better understand the underlying initiators and arthritic chronicity, studies have been performed to test the hypothesis that neurotransmitter excitatory amino acids (EAA), such as glutamate (GLU), released into the spinal cord and the joint by sensory nerve fiber endings, play a critical role in initiation and persistence of arthritis. Further, GLU contributes directly to inflammatory cascades and the "vicious cycle of inflammation and pain" of arthritis.