EULAR 2016 | Daily Highlights
WHICH CELLS CORRESPOND TO THE TYPICAL SIGNALS FOR FATTY AND INFLAMMATORY LESIONS SEEN IN MAGNETIC RESONANCE IMAGING IN ANKYLOSING SPONDYLITIS ? – A PROSPECTIVE STUDY USING BIOPSY MATERIAL OBTAINED DURING SPINAL SURGERYAbstract: OP0086
Authors: X. Baraliakos1,*, H. Boehm2, A. Samir2, G. Schett3, J. Braun1
Co Authors: 1Rheumazentrum Ruhrgebiet, Herne, 2Clinic for spinal surgery, Bad Berka, 3Medizinische Klinik 3, Universitätsklinikum Erlangen, Erlangen, Germany
The occurrence of bone marrow edema (BME) and fat metaplasia detected by magnetic resonance imaging (MRI) were shown to be significantly associated with syndesmophyte formation in patients with ankylosing spondylitis (AS). The cell type responsible for the fat signal seen in MRI has not been defined to date.
To histologically analyze the cells seen in fatty lesions (FL) as detected by MRI in spinal biopsies of AS patients and compare them with controls.
Spinal biopsies from vertebral edges of patients with AS and controls who underwent surgery for spinal deformity or spinal stenosis were prospectively collected. All patients had spinal STIR- and T1-weighted MRIs available exactly from the area of biopsy, and all biopsies were taken from areas that had a fat signal on MRI. The biopsies were analysed blinded to patients’ diagnosis. Histomorphological analyses were performed to detect normal bone marrow, fat cells, inflammatory cells and fibroblasts. Histologic results were compared with MRI findings.
Biopsies mostly obtained from the lower thoracic and the lumbar spine of 13 AS patients (mean age 56.3 years, mean disease duration 26 years) and 6 controls (mean age 53.4 years) were available. Similar proportions of AS patients, (12/16, 75%) and non-AS patients (4/6, 67%) had vital bone marrow. Fat cells were found in all 13 biopsies obtained from AS patients from the area of the fat signal vs. only 2 non-AS patients (33%), while inflammatory cells were found in 9 AS patients (56.3%), all of which also had BME on MRI, vs. 3 non-AS patients (50%). Fibroblasts were seen in 3 AS (18.9%) and 2 non-AS patients (33%).
The underlying cell types of FL and BME as detected by MRI in these long standing AS patients were fatty and inflammatory cells. The main difference between AS and non-AS patients was the proportion of biopsies containing fat cells. This suggests that fat cells are responsible for the MRI signal, at least in patients with longstanding ankylosing spondylitis.
Disclosure of Interest
The exact sequence of events leading to bone proliferation and the development of syndesmophytes in the spine of patients with ankylosing spondylitis (AS) is not known. There are some clues from MRI studies, indicating that the risk is for the development of a syndesmophyte is increased 3-fold at a spinal site with bone marrow edema (BME) on STIR sequences (thought to represent inflammation), followed by lesions with a “fatty signal” on T1 sequences (thought to represent fatty metaplasia). But is BME really associated with inflammation and do “fatty lesions” really represent fat? Histomorphological analyses in axial spondyloarthritis are very rare and the current study intended to close this gap. Spinal biopsies were taken from patients with planed spinal surgery because of AS-induced deformity or degenerative disease at sites with “fatty lesions” or Modic II/III lesions on MRI. The following results could be demonstrated: A) The main difference between patients with AS and patients with degenerative spinal disease seems to be the presence of fat cells in AS. B) Fibrotic tissue was only seen in a minority of biopsies. C) The histomorphological correlate of “fatty lesions” is indeed fat and BME is really caused by an inflammatory infiltrate. The latter was not only demonstrated in AS (69%) but also in Modic lesions (50%). Whether BME is caused by different immune cell types in AS versus degenerative disease was, however, not investigated.
PD Dr. Adrian Ciurea
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