title: Microtrauma: no longer to be ignored in spondyloarthritis?
abstract: OBJECTIVE
  Novel clinical and animal model data support that biomechanical factors play a role in the onset and progression of spondyloarthritis. Bringing together these insights with the progress made in our understanding of the immunopathogenesis and genetic susceptibility of spondyloarthritis may provide new opportunities for better management.
  
  
  RESULTS
  Tail suspension prevents arthritis in a tumor necrosis factor overexpression model. A similar approach also reduces new bone formation after acute arthritis in mice. Physical labor is associated with disease severity, including structural disease progression. Sentinel immune cells in the enthesis provide a link between local damage and the development of inflammation. Loss of stability likely triggers tissue remodeling, including the formation of syndesmophytes. Improving muscle strength and control while avoiding excessive strain or overuse should be considered in the approach toward patients. New regulators of tissue turnover and remodeling are emerging including microRNAs.
  
  
  CONCLUSIONS
  Local damage may provide a trigger for spondyloarthritis. For structural disease progression loss of stability may be an important factor. Control of inflammation will prevent stability issues and improve the long-term prognosis of disease. Physical therapy will continue to provide benefit for patients in the short and in long-term management of disease.
authors.affiliation: Laboratory of Tissue Homeostasis and Disease, Department of Development and Regeneration, Skeletal Biology and Engineering Research Center, KU Leuven and Division of Rheumatology, UZ Leuven.
authors.forename: Margot
authors.initials: M
authors.lastname: Van Mechelen
authors.forename: Rik J
authors.initials: RJ
authors.lastname: Lories
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000209:etiology; D001696:Biomechanical Phenomena; D018450:Disease Progression; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000150:complications; D025241:Spondylarthritis / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014947:Wounds and Injuries / Q000150:complications*
chemical_list: D014409:Tumor Necrosis Factor-alpha