Simplified overview of the pathogenesis of SpA in patients with bowel lesions as the triggers

A simplified overview of how bowel lesions might trigger SpA. The series of events starts with gut commensal dysbiosis. In dysbiosis, there is a change in the composition or diversity of the gut microbiome or an increase in the pathogenic species. These changes lead to activation of several types of bowel innate lymphoid cells (such as ILC3), which can release IL-17 and IL-22. Those immune cells traffic from the bowel to the peripheral joints via homing receptors where they can initiate events that induce arthritis. Those that travel to the bone marrow can initiate events that can induce inflammation, which can result in structural damage such as erosions, replacement of bone marrow by granulation tissue, and, finally, new bone formation. The ultimate pathology in the spine can be bamboo spine, but this is an unusual outcome. Genes, mechanical stress, TNF, and IL-17 all contribute to the process.