Receptor activator of nuclear factor kappa B ligand-mediated osteoclastogenesis is elevated in ankylosing spondylitis.
OBJECTIVE
Ankylosing spondylitis (AS) is an inflammatory arthritis involving the axial skeleton. Decreased bone mineral density has also been reported in AS patients. This study sought to determine whether osteoclastogenesis and osteoclast activity are increased in AS.


METHODS
Twenty patients with AS were evaluated using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and other clinical parameters. Mononuclear cells were separated out from peripheral blood samples taken from AS patients and normal healthy controls and cultured with monocyte colony stimulating factor and receptor activator of the nuclear factor kappa B ligand (RANKL). Multi-nucleated, tartrate-resistant acid phosphatase stain-positive osteoclasts were counted after 9 days, and the areas of calcium absorption on calcium-coated plates were determined.


RESULTS
Osteoclastogenesis was significantly greater in AS patients than in normal controls (number of osteoclasts/1106 mononuclear cells, median, 518.0 vs. 362.5, p=0.036). No differences were observed between AS patients and controls in terms of calcium absorption areas or the serum concentrations of tumor necrosis factor and RANKL. Osteoclastogenesis was greater in AS patients with sacroiliac joint ankylosis than in those without. Osteoclastogenesis and the calcium absorption area were not found to be correlated with BASDAI nor with other clinical parameters including age, erythrocyte sedimentation rate, and C-reactive protein levels.


CONCLUSIONS
Osteoclastogenesis is elevated in AS patients, especially in those with sacroiliac joint ankylosis. Increased osteoclastogenesis may be related to osteopenia in AS patients.
Im
C H
CH
Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine; Seoul, Korea.
Kang
E H
EH
Ki
J Y
JY
Shin
D W
DW
Choi
H J
HJ
Chang
E J
EJ
Lee
E Y
EY
Lee
Y J
YJ
Lee
E B
EB
Kim
H H
HH
Song
Y W
YW
D000135:Acid Phosphatase / Q000378:metabolism; D000328:Adult; D001862:Bone Resorption / Q000473:pathology / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002469:Cell Separation; D002478:Cells, Cultured; D004338:Drug Combinations; D005260:Female; D006304:Health Status; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D008297:Male; D010010:Osteoclasts / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D053245:RANK Ligand / Q000494:pharmacology; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000494:pharmacology / Q000502:physiology*; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000071681:Tartrate-Resistant Acid Phosphatase; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult
D004338:Drug Combinations; D007527:Isoenzymes; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D014409:Tumor Necrosis Factor-alpha; D016173:Macrophage Colony-Stimulating Factor; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D002118:Calcium