TY - JOUR T1 - An Added Perspective on the 2009 SPARTAN and IGAS Report: An Innate Axial Myofascial Hypertonicity JF - The Journal of Rheumatology JO - J Rheumatol SP - 2092 LP - 2094 DO - 10.3899/jrheum.110330 VL - 38 IS - 10 AU - ALFONSE T. MASI Y1 - 2011/10/01 UR - http://www.jrheum.org/content/38/10/2092.abstract N2 - The 2009 Joint Meeting of the Spondyloarthritis Research and Therapy Network (SPARTAN) and International Genetics of Ankylosing Spondylitis (IGAS) members was recently reported1. These comments offer a novel hypothesis to complement the progress reviewed in that report. Based upon the characteristic clinical and epidemiological features of ankylosing spondylitis (AS), a structural biomechanical contribution in causation is proposed, namely, an innate axial (spinal) myofascial hypertonicity2,3. Such a macro-diathesis would encompass biomechanical models already proposed at micro levels of tissue attachments (entheses) and related sites4,5,6. This commentary can only briefly outline biomechanical and clinical reasons for the proposed novel hypothesis in AS, as described2,3,7. The hypothesis also incorporates myofascial physiology7,8 and tensegrity9,10 mechanisms in the musculoskeletal system.Consensus clinical features of AS1,10,11,12,13 suggest that biomechanical influences may be operating at the level of both the body structure and tissue. Excessive physical force (L, fortis, strong) transmissions can be detrimental to both structures and enthesis sites2,5,7. The magnitudes of imposed (input) or internal (reactive) forces are influenced by the stiffness of a body or its component tissue attachments5,7. Force transmissions become amplified at sites of greater stiffness or resistance and concentrate at transition boundaries (entheses)5,7. Further, in mobile systems like the spine, with flexible links, the fusing (or stiffening) of component parts increases the stress concentrations in remaining connections7. Such physical principles are consistent with the progression of structural lesions in AS1,11, … Address correspondence to Dr. Masi; E-mail: amasi{at}uic.edu ER -