Immunopathology of trauma: relationship between physical damage to the musculoskeletal system and the development of rheumatic diseases

Introduction. A physical injury triggers a cascade of pathological processes, including the activation of the immune system and the development of local inflammation. Hereditary predisposition, pronounced structural changes, biomechanical disorders, and comorbid pathology can determine the disorders in the regulation of the post-traumatic inflammatory process, leading to its chronicity and the development of degenerative manifestations (fibrosis, neoangiogenesis, heterotopic ossification).

Objective of the review: to summarize current concepts of the impact of physical trauma on the immune system and the role of post-traumatic inflammation in the development and progression of autoimmune and immune-mediated inflammatory rheumatic diseases, including post-traumatic osteoarthritis.

The central role in the development of post-traumatic inflammation is played by the formation of the damage-associated molecular pattern (DAMP), the activation of Toll-like receptors on macrophages, the hyperproduction of IL-1β, the cascade activation of the synthesis of TNF-α, IL-6, IL-17, CXCL1, CXCL2, CXCL8, and CCL20. A characteristic immune-mediated complication of injuries is the Koebner phenomenon – the appearance of pre-existing skin elements (such as psoriatic plaques) in the area of tissue damage. A similar mechanism (“deep Koebner phenomenon”) can be realized in the development of psoriatic arthritis following joint injury. There is evidence suggesting the role of trauma as a trigger for autoimmune and immune-inflammatory rheumatic diseases, such as rheumatoid arthritis and axial spondyloarthritis.

Conclusion. The most common rheumatic disease that can be considered a complication of injuries is post-traumatic osteoarthritis (PTOA). In its pathogenesis, the leading position is occupied by chronic low-intensity inflammation, which occurs as a result of the activation of macrophage-lineage cells and IL-1β synthesis. To date, there are no specific treatments targeting the underlying causes of PTOA. Nevertheless, it is reasonable to suggest that methods used for idiopathic osteoarthritis, particularly the combination of Symptomatic Slow Acting Drugs for OsteoArthritis (SYSADOA) could also help those with PTOA.