An added perspective on the 2009 SPARTAN and IGAS report: An innate axial myofascial hypertonicity

The Journal of Rheumatology (Impact Factor: 3.19). 10/2011; 38(10):2092-4. DOI: 10.3899/jrheum.110330
Source: PubMed
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    • "These abnormalities often result from chronic mechanical overloading, with or without evidence of inflammation [3]. The novel hypothesis of a potential intrinsic myofascial mechanism is consistent with current enthesopathy concepts [1-3]. Recently, a murine model of spondyloarthritis (SpA) demonstrated that biomechanical stress and strain correlated with entheseal inflammation and new bone formation [4]. "
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    ABSTRACT: Ankylosing spondylitis and axial spondyloarthropathy have characteristic age- and sex-specific onset patterns, typical entheseal lesions, and marked heritability, but the integrative mechanisms causing the pathophysiological and structural alterations remain largely undefined. Myofascial tissues are integrated in the body into webs and networks which permit transmission of passive and active tensional forces that provide stabilizing support and help to control movements. Axial myofascial hypertonicity was hypothesized as a potential excessive polymorphic trait which could contribute to chronic biomechanical overloading and exaggerated stresses at entheseal sites. Such a mechanism may help to integrate many of the characteristic host, pathological, and structural features of ankylosing spondylitis and axial spondyloarthritis. Biomechanical stress and strain were recently documented to correlate with peripheral entheseal inflammation and new bone formation in a murine model of spondyloarthritis. Ankylosing spondylitis has traditionally been classified by the modified New York criteria, which require the presence of definite radiographic sacroiliac joint lesions. New classification criteria for axial spondyloarthritis now include patients who do not fulfill the modified New York criteria. The male-to-female sex ratios clearly differed between the two patient categories - 2:1 or 3:1 in ankylosing spondylitis and 1:1 in non-radiographic axial spondyloarthritis - and this suggests a spectral concept of disease and, among females, milder structural alterations. Magnetic resonance imaging of active and chronic lesions in ankylosing spondylitis and axial spondyloarthritis reveals complex patterns, usually interpreted as inflammatory reactions, but shows similarities to acute degenerative disc disease, which attributed to edema formation following mechanical stresses and micro-damage. A basic question is whether mechanically induced microinjury and immunologically mediated inflammatory mechanisms operate in both ankylosing spondylitis and degenerative disc disease but differ in relative degrees. The hypothesized biomechanical properties raised in this commentary require documentation of their association with the onset risk and course of ankylosing spondylitis and axial spondyloarthritis. If particular subsets of ankylosing spondylitis and axial spondyloarthritis patients are confirmed to have altered axial myofascial properties, their biological basis and underlying biomechanical mechanisms promise to become clarified. Understanding how biomechanical and physical properties can affect symptomatic and structural manifestations of these disorders could also improve their management.
    Arthritis Research & Therapy 04/2014; 16(2):107. DOI:10.1186/ar4532 · 3.75 Impact Factor
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    • "However, the hypothesis has not yet been directly confirmed, due to lack of reported quantitative measurements and research on such mechanisms. Accordingly, the aims of this paper are to (1) expand upon our perspectives on the structural biomechanical concept of AS, (2) integrate mechanobiological pathways with current inflammatory concepts, (3) provide a further rationale for encouraging such research, and (4) indicate innovative techniques which may offer promise in future investigations to test the structural biomechanical hypothesis in AS [10] "
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    ABSTRACT: Ankylosing spondylitis (AS) is not fully explained by inflammatory processes. Clinical, epidemiological, genetic, and course of disease features indicate additional host-related risk processes and predispositions. Collectively, the pattern of predisposition to onset in adolescent and young adult ages, male preponderance, and widely varied severity of AS is unique among rheumatic diseases. However, this pattern could reflect biomechanical and structural differences between the sexes, naturally occurring musculoskeletal changes over life cycles, and a population polymorphism. During juvenile development, the body is more flexible and weaker than during adolescent maturation and young adulthood, when strengthening and stiffening considerably increase. During middle and later ages, the musculoskeletal system again weakens. The novel concept of an innate axial myofascial hypertonicity reflects basic mechanobiological principles in human function, tissue reactivity, and pathology. However, these processes have been little studied and require critical testing. The proposed physical mechanisms likely interact with recognized immunobiological pathways. The structural biomechanical processes and tissue reactions might possibly precede initiation of other AS-related pathways. Research in the combined structural mechanobiology and immunobiology processes promises to improve understanding of the initiation and perpetuation of AS than prevailing concepts. The combined processes might better explain characteristic enthesopathic and inflammatory processes in AS.
    12/2011; 2011(4):205904. DOI:10.1155/2011/205904
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    ABSTRACT: To quantify resting lumbar erector myofascial stiffness in younger ankylosing spondylitis (AS) patients and age-comparable normal control (CN) subjects, using a hand-held mechanical impulse - based myotonometric device. A case-control study of 24 AS patients and 24 age-comparable normal CN subjects. Stiffness (N/m) of the erector spinae myofascia at lumbar (L3-L4) level was quantified using the myotonometer. Surface electromyography (sEMG) was monitored (< 5μV), consistent with resting status. Measurements were made in prone position on left and right sides, at initial and 10 minute resting interval. University Physical Therapy Department PARTICIPANTS: Male (n=19), female (n=5) AS patients and male (n=19), female (n=5) healthy volunteers without low back pain, all ages 18 to 46 years. Not Applicable MAIN OUTCOME MEASURES: Lumbar myofascial stiffness RESULTS: - At initial measurements, median stiffness (N/m) of averaged right- and left-sided values was greater (p=0.021) in 24 AS than 24 CN subjects, 268.9 vs. 238.9, respectively. Repeated measurements after a 10 minute prone resting period were also greater (p=0.007) in AS than CN subjects (281.0 vs. 241.4). The 48 averaged right- and left-sided values from baseline and 10 minute measurements were compared in each subject group. The AS patients more frequently (p=0.012) had stiffness values greater than 250 N/m, 35 (72.9%), vs 22 (45.8%) CN subjects. - Lumbar myofascial stiffness was greater in 24 AS patients than CN subjects. A hypothesized biomechanical concept of increased resting lumbar myofascial stiffness in AS may be supported by this preliminary controlled study. Copyright © 2015 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.
    Archives of physical medicine and rehabilitation 08/2015; 96(11). DOI:10.1016/j.apmr.2015.07.014 · 2.57 Impact Factor