By Barend J. van Royen, Ben A. C. Dijkmans
The 1st and merely interdisciplinary consultant devoted to the topic, this reference leads readers in the course of the pathogenic, genetic, medical, and biomechanical elements of ankylosing spondylitis (AS) and addresses concerns with regards to results overview, clinical remedy, surgical problems, sickness administration, and genetics.
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The 1st and merely interdisciplinary consultant devoted to the topic, this reference leads readers throughout the pathogenic, genetic, scientific, and biomechanical features of ankylosing spondylitis (AS) and addresses concerns regarding results evaluate, clinical remedy, surgical problems, disorder administration, and genetics.
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Additional info for Ankylosing Spondylitis: Diagnosis and Management
40. Leden I. Did Bechterew describe the disease which is named after him? A question raised due to the centennial of his primary report. Scand J Rheumatol 1994; 23:42–45. 41. Bechterew W. Von der Verwachsung oder Steiﬁgkeit der Wirbelsa¨ule. Deutsche Zeitschrift fu¨r Nervenheilkunde 1897; 11:327–337. 42. Bechterew W. Neue Beobachtungen mit patologisch-anatomische Undersuchungen u¨ber Steiﬁgkeit der Wirbelsa¨ule. Deutsche Zeitschrift fu¨r Nervenheilkunde 1899; 15:45–57. ¨ ber ankylosirende Entzu¨ndung der Wirbelsa¨ule und der grossen Erxtre43.
Whether these unusual properties of B27 have any relevance to human disease remains unproven. A further level of complexity is that there are different hypotheses as to how homodimers may cause disease. One hypothesis suggests that B27-homodimers induce disease as a consequence of intracellular accumulation. However, it has also 28 Timms et al. been proposed that they may act by some extracellular mechanism such as aberrant presentation of peptides or recognition by immune cells [either natural killer (NK) cells or cytotoxic T-lymphocytes] (66).
It is unlikely that individuals with different B27 subtypes would have different genetic or environmental factors inﬂuencing their susceptibility to AS. BÃ2706 differs from the disease-associated subtype BÃ2704 by two amino acid substitutions at residues 114 and 116 (Table 2). In a study in the Thai population, BÃ2704 was more frequent in AS patients (91%) as compared to healthy controls (47%), however, Epidemiology, Pathogenesis, and Genetics of AS 31 BÃ2706 was seen in 47% of controls but not observed in AS patients (35).