Masi Alfonse T
Arthritis Res Ther. 2014;16(2):107. doi: 10.1186/ar4532. Epub 2014 Apr 8.
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.
强直性脊柱炎和轴向型脊柱关节炎具有特定的年龄和性别发病模式、典型的附着点病变以及显著的遗传度，但导致病理生理和结构改变的综合机制仍 largely 未明确。肌筋膜组织在体内整合形成网状结构，允许传递被动和主动张力，提供稳定支撑并有助于控制运动。轴向肌筋膜高张力被假设为一种潜在的过度多态性特征，可能导致慢性生物力学过载以及附着点部位的过度应力。这样一种机制可能有助于整合强直性脊柱炎和轴向型脊柱关节炎的许多特征性宿主、病理和结构特征。最近在脊柱关节炎的小鼠模型中证实，生物力学应力和应变与外周附着点炎症及新骨形成相关。强直性脊柱炎传统上依据改良纽约标准进行分类，该标准要求存在明确的骶髂关节放射学病变。轴向型脊柱关节炎的新分类标准现纳入了不符合改良纽约标准的患者。这两类患者的男女比例明显不同——强直性脊柱炎中为 2:1 或 3:1，非放射学轴向型脊柱关节炎中为 1:1——这提示了疾病的谱系概念，且在女性中结构改变较轻。强直性脊柱炎和轴向型脊柱关节炎活动期及慢性期病变的磁共振成像显示出复杂模式，通常被解释为炎症反应，但与急性退行性椎间盘疾病相似，后者归因于机械应力和微损伤后形成的水肿。一个基本问题是，机械性诱导的微损伤和免疫介导的炎症机制在强直性脊柱炎和退行性椎间盘疾病中是否都起作用，但相对程度有所不同。本评论中提出的假设生物力学特性需要证明它们与强直性脊柱炎和轴向型脊柱关节炎的发病风险及病程相关。如果强直性脊柱炎和轴向型脊柱关节炎患者的特定亚组被证实具有改变的轴向肌筋膜特性，其生物学基础和潜在生物力学机制有望得到阐明。了解生物力学和物理特性如何影响这些疾病的症状和结构表现也有助于改善其治疗。
