Immunohistologic analysis of zygapophyseal joints in patients with ankylosing spondylitis

  • Heiner Appel
  • Maren Kuhne
  • Simone Spiekermann
  • Harald Ebhardt
  • Zarko Grozdanovic
  • Dorothee Köhler
  • Marc Dreimann
  • Axel Hempfing
  • Martin Rudwaleit
  • Harald Stein
  • Peter Metz-Stavenhagen
  • Joachim Sieper
  • Christoph Loddenkemper

Abstract

OBJECTIVE: Zygapophyseal joints of the spine are often affected in ankylosing spondylitis (AS). In this study, we undertook a systematic immunohistologic evaluation of the immunopathology of the zygapophyseal joints in patients with advanced AS.

METHODS: We obtained zygapophyseal joints from 16 AS patients undergoing polysegmental correction of kyphosis and from 10 non-AS controls (at autopsy). Immunohistologic analysis of the bone marrow was performed by analyzing the number of infiltrating T cells (CD3, CD4, CD8), B cells (CD20), osteoclasts (CD68), bone marrow macrophages (CD68), and microvessel density (CD34) per high-power field.

RESULTS: Zygapophyseal joints from 6 of 16 AS patients, but from none of the controls, exhibited 2 or more CD3+ T cell aggregates, signifying persistent inflammation. Interstitial CD4+ and CD8+ T cells were significantly more frequent in AS patients compared with non-AS controls (P = 0.002 and P = 0.049, respectively). While there was no clear difference between the number of CD20+ B cells in AS patients overall compared with controls, there was a significant difference when persistently inflamed joints from patients with AS were compared with joints without active inflammation from patients with AS or joints from controls (both P = 0.03). Microvessel density in bone marrow from AS patients with active inflammation was significantly higher than that in bone marrow from controls.

CONCLUSION: This immunohistologic study of bone marrow from zygapophyseal joints demonstrates persistent inflammation in the spine of patients with AS, including those with longstanding disease. The findings of increased numbers of T cells and B cells and neoangiogenesis suggest that these features play a role in the pathogenesis of AS.

Bibliographical data

Original languageEnglish
ISSN0004-3591
DOIs
Publication statusPublished - 01.09.2006
PubMed 16947385