Integrative Structural Biomechanical Concepts of Ankylosing Spondylitis

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.

The sacroiliac joint: an overview of its anatomy, function and potential clinical implications

“…It is possible that AS is not fully explained by inflammatory processes alone (Masi et al. ). Clinical, epidemiological and genetic factors as well as the natural history of disease indicate that additional host‐related risk processes and predispositions are present in the etiology of AS.…”

How to Stop the Structural Progression in Ankylosing Spondylitis

“…Помимо симптоматического эффекта они обладают антипролиферативным. Среди механизмов последнего указывают модулирующее действие циклооксигеназы 2 (ЦОГ-2) на функцию остеобластов и остеокластов, активацию неоангиогенеза под воздействием ЦОГ-2, в связи с чем ингибирование ЦОГ-2 с помощью НПВП может компенсировать эти процессы [32][33][34]. Способность НПВП тормозить рентгенологическое прогрессирование при АС была доказана в нескольких исследованиях [27,35,36], хотя лишь одно из них было крупным рандомизированным клиническим исследованием [35].…”

An Added Perspective on the 2009 SPARTAN and IGAS Report: An Innate Axial Myofascial Hypertonicity: Figure 1.

“…Osteoproliferative lesions could be contributed by injury-related pathways, possibly from continuing consequences of excessive stress mechanisms 2,3,4,5,6 . A critical question is if axial myofascial hypertonicity in AS might precede the onset of pain (not stiffness) and inflammatory indicators?…”

“…Those MRI findings are mainly attributed to altered biomechanical/degenerative origins or excessive tissue stresses, rather than being inflammatory. Possible effects of excessive stresses or other biomechanical mechanisms 2,3,4,5,6 should be considered in the early MRI changes of AS that progress to osteoproliferative lesions.…”