Novel Biomarkers May Identify Axial Spondyloarthritis in Patients With IBD

A colon affected by ulcerative colitis with massive pseudopolyps.
A colon affected by ulcerative colitis with massive pseudopolyps.
Sclerostin and antisclerostin-IgG may be novel biomarkers to assess the presence of axial joint involvement in patients with IBD.

In patients with inflammatory bowel disease (IBD), the development of antisclerostin-immunoglobulin G (IgG) and the subsequent decrease of sclerostin serum levels may serve as useful biomarkers in the diagnosis of early spondyloarthritis (SpA), according to a study published in The Journal of Rheumatology.1

While the pathogenesis has yet to be explained, arthritis frequently develops before, simultaneously with, or after the diagnosis of overt IBD. Currently, there are no available serum biomarkers demonstrating the presence of joint inflammation in these patients.1-3 Recently, sclerostin, an antagonist of the Wnt/β-catenin pathway, and antisclerostin-IgG have been suggested as potential markers of articular disease activity in patients with ankylosing spondylitis.1,4,5 Researchers compared sclerostin and antisclerostin-IgG serum levels in 125 patients with IBD, 85 of whom had axial or peripheral SpA, with healthy control patients.1

The investigators found significantly lower levels of sclerostin and higher levels of antisclerostin-IgG in patients with IBD-associated SpA with axial involvement compared with patients with only peripheral arthritis, IBD, and control patients. Sclerostin and antisclerostin-IgG serum levels were found to be inversely correlated and were associated with the duration of articular symptoms. Both biomarkers were good indicators for predicting the presence of axial IBD-associated SpA.

However, further studies in a larger group of patients are needed to confirm the role of sclerostin and antisclerostin-IgG as biomarkers of IBD-associated SpA and their role in the pathogenesis of axial SpA in patients with IBD.

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The authors concluded that, “We demonstrated that in patients with IBD, [sclerostin] and [antisclerostin-IgG] might represent novel biomarkers to assess the presence of axial joint involvement. Moreover, the development of [antisclerostin-IgG] and the subsequent decrease of [sclerostin] serum levels could play a role in the pathogenesis of SpA/IBD.”1         


  1. Luchetti MM, Ciccia F, Avellini C, et al. Sclerostin and antisclerostin antibody serum levels predict the presence of axial spondyloarthritis in patients with inflammatory bowel disease [published online February 1, 2018].  J Rheumatol. doi:10.3899/jrheum.170833
  2. Rodríguez-Reyna TS, Martínez-Reyes C, Yamamoto-Furusho JK. Rheumatic manifestations of inflammatory bowel disease.  World J Gastroenterol. 2009;15:5517-5524.
  3. de Vos M. Joint involvement in inflammatory bowel disease. Aliment Pharmacol Ther. 2004;20(4):36-42.
  4. Appel H, Ruiz-Heiland G, Listing J, et al. Altered skeletal expression of sclerostin and its link to radiographic progression in ankylosing spondylitis.  Arthritis Rheumatol. 2009;60:3257-3262.
  5. Tsui FW, Tsui HW, Las Heras F, Pritzker KP, Inman RD. Serum levels of novel noggin and sclerostin-immune complexes are elevated in ankylosing spondylitis.  Ann Rheum Dis. 2014;73:1873-1879.