Ankylosing Spondylitis

  • Yan Wang
  • Quanbo Ji


Ankylosing spondylitis (AS) represents a common, highly heritable prototype of an interrelated group of chronic inflammatory rheumatic diseases now referred to as spondyloarthritis (SpA), which characteristically affects the axial skeleton in the spine and bilateral sacroiliac joints, resulting in structural and functional impairments, such as inflammatory back pain, asymmetrical peripheral oligoarthritis (predominantly of lower limbs), enthesitis, and specific organ involvement including psoriasis, acute anterior uveitis (AAU), inflammatory bowel disease (IBD), and the so-called extra-articular manifestations (EAM) [1–4]. The past decade yields major advances in the recognition of AS as an entity, the understanding of genetic and pathophysiological mechanisms, and the management due to the new clinical and imaging techniques or therapies [3]. Proteomic and genomic findings while in an early stage have potential both as diagnostic/prognostic tools to investigate the pathogenesis of AS [5]. The strongest known contributing factor is the main histocompatibility complex (MHC) class I molecule human leukocyte antigen-B27 (HLA-B27); several other genes and genetic regions still remain to be identified [4, 6]. The blockers of tumor necrosis factor (TNF), a major therapeutic advance, have allowed patients refractory to conventional treatment [3]. However, whether the available nonsteroidal anti-inflammatory drugs and the treatment with physiotherapy or the other biological treatments is as yet unclear [7]. In addition, the development of defining better strategies and techniques for early diagnosis, therapeutic modulation, and induction of drug-free remission remains one of the major challenges in AS for clinical practice for the next decade.


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Copyright information

© Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  • Yan Wang
    • 1
  • Quanbo Ji
    • 1
  1. 1.Department of orthopaedicsChinese PLA General HospitalBeijingChina

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