Can structural damage be prevented in ankylosing spondylitis?
OBJECTIVE
Current treatment of ankylosing spondylitis such as non-steroidal anti-inflammatory drugs and tumor necrosis factor (TNF)-blockers have shown a good efficacy on sign and symptoms. However, it is less clear whether and how structural damage, determined mainly by new bone formation, can be prevented. Recent progress of the research addressing this question is presented here.


RESULTS
Although treatment with non-steroidal anti-inflammatory drugs over a 2-year period seem to retard growth of syndesmophytes this is not the case in patients treated with TNF-blockers over the same time. First data have been raised on whether new bone formation is coupled to (previous) inflammation or whether these two processes are uncoupled, which are not yet finally conclusive. A better understanding of the interaction between inflammation and new bone formation on the molecular level indicate that inflammatory molecules such as TNFalpha inhibit osteoblasts and that a TNF-blockade induces new bone formation. Thus, TNF-blockers can only be expected to prevent new bone formation if this is coupled to inflammation and if inflammation is treated early enough. Studies on bone biomarkers in ankylosing spondylitis patients support the view that suppression of inflammation induces new bone formation.


CONCLUSIONS
Future research has to clarify whether structural damage can best be prevented by early and effective treatment of inflammation or whether new bone formation has to be targeted additionally.
Medical Department I, Rheumatology, Charité, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin, Germany. Joachim.sieper@charite.de
Joachim
J
Sieper
D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D018450:Disease Progression; D006801:Humans; D010000:Osteitis / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D010006:Osteoblasts / Q000187:drug effects / Q000276:immunology; D010012:Osteogenesis / Q000187:drug effects* / Q000276:immunology; D013131:Spine / Q000187:drug effects* / Q000473:pathology* / Q000503:physiopathology; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000473:pathology* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology
D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D014409:Tumor Necrosis Factor-alpha