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Masi AT, Nair K, Andonian BJ, et al. Integrative structural biomechanical concepts of ankylosing spondylitis. Arthritis. 2011;2011:205904doi: 10.1155/2011/205904.
Masi, A. T., Nair, K., Andonian, B. J., Prus, K. M., Kelly, J., Sanchez, J. R., & Henderson, J. (2011). Integrative structural biomechanical concepts of ankylosing spondylitis. Arthritis, 2011205904. https://doi.org/10.1155/2011/205904
Masi, Alfonse T, et al. "Integrative structural biomechanical concepts of ankylosing spondylitis." Arthritis vol. 2011 (2011): 205904. doi: https://doi.org/10.1155/2011/205904
Masi AT, Nair K, Andonian BJ, Prus KM, Kelly J, Sanchez JR, Henderson J. Integrative structural biomechanical concepts of ankylosing spondylitis. Arthritis. 2011;2011:205904. doi: 10.1155/2011/205904. Epub 2011 Dec 18. PMID: 22216409; PMCID: PMC3246302.
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Arthritis. 2011;2011:205904. doi: 10.1155/2011/205904. Epub 2011 Dec 18.

Integrative structural biomechanical concepts of ankylosing spondylitis.

Arthritis

Alfonse T Masi, Kalyani Nair, Brian J Andonian, Kristina M Prus, Joseph Kelly, Jose R Sanchez, Jacqueline Henderson

Affiliations

  1. Department of Medicine, University of Illinois College of Medicine, Peoria, IL 61656, USA.

PMID: 22216409 PMCID: PMC3246302 DOI: 10.1155/2011/205904

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.

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