Insights into the pathology and treatment of spondyloarthritis: from the bench to the clinic.
OBJECTIVE
The spondyloarthritides are a set of chronic inflammatory diseases that consists of 5 interrelated subsets (ankylosing spondylitis [AS], psoriatic arthritis [PsA], reactive arthritis, arthritis associated with inflammatory bowel disease, and undifferentiated spondyloarthropathy). The aim of this review was to evaluate the classification, genetic susceptibility, pathology, and response to treatment of spondyloarthritis (SpA).


METHODS
Searches were conducted of the PubMed database for articles focusing on the classification, pathology, and treatment of SpA.


RESULTS
The 5 subsets of SpA share many clinical, immunohistochemical, and genetic features, including the common presence of human leukocyte antigen-B27 and the absence of rheumatoid factor. Evidence suggests that the pathology of SpA is mediated by immune cells. In particular, tumor necrosis factor-alpha appears to be an important driver of inflammation and damage in SpA. A number of different SpA classification criteria have been developed, including the Modified New York Criteria for AS, the European Spondyloarthropathy Study Group criteria, the Amor criteria, as well as criteria for PsA, notably the Moll and Wright criteria and the Classification of Psoriatic Arthritis criteria. Suboptimal efficacy and adverse effects often limit the use of conventional pharmacologic treatments for SpA, including nonsteroidal antiinflammatory drugs and disease-modifying antirheumatic drugs, such as methotrexate and sulfasalazine. Recent evidence has demonstrated that targeted biologic response modifiers, such as TNF-alpha antagonists, are well tolerated and efficacious treatments for SpA.


CONCLUSIONS
Significant advances have occurred in our understanding of the pathophysiology, diagnosis, and classification of the spondyloarthritides and effective treatments are available.
Davis
John C
JC
University of California San Francisco, San Francisco, CA, USA.
Mease
Philip J
PJ
D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D000068800:Etanercept; D005260:Female; D020022:Genetic Predisposition to Disease; D015796:HLA-B27 Antigen; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D025242:Spondylarthropathies / Q000145:classification / Q000235:genetics / Q000473:pathology* / Q000628:therapy*; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D015796:HLA-B27 Antigen; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept