The Role of Interleukin 10 Promoter Polymorphisms in the Susceptibility of Distal Interphalangeal Osteoarthritis

NAGHMEH RIYAZI, FINA A.S. KURREEMAN, TOM W.J. HUIZINGA, FRIEDO W. DEKKER, GERRIE STOEKEN-RIJSBERGEN, and MARGREET KLOPPENBURG

ABSTRACT.

Objective. The interleukin (IL)-10 single nucleotide promoter polymorphism (SNP) –2849A is associated with decreased IL-10 production as measured by lipopolysaccharide (LPS) stimulated whole blood cultures. A low innate production of IL-10 using the same assay is associated with an increased risk of familial osteoarthritis (OA). We investigated the association of 7 novel SNP located downstream of the IL-10 transcription start site: –2849,–2763, –1330, –1082, –819, and –592, constituting the 4 ancient haplotypes, with distal interphalangeal (DIP) OA.

Methods. The study population comprised consecutive patients with and without radiological DIP OA (Kellgren-Lawrence score of ≥ 2 in one joint) aged 40–70 years from a cohort of subjects with different types of arthritis in an early stage referred to an Early Arthritis Clinic (EAC). DNA typing for IL-10 SNP as well as radiographs of the hands were performed at clinic enrolment. Patients with rheumatoid arthritis, systemic lupus erythematosus, spondyloarthropathies, and psoriatic arthritis were excluded.

Results. The distribution of DIP OA and IL-10 SNP were comparable to representative samples of the Dutch population. In the cohort of 172 subjects, 57 had DIP OA (33%) and 115 (67%) had no DIP OA. No significant association was found between DIP OA and IL-10 SNP and the 4 common haplotypes IL10.1, IL10.2, IL10.3, and IL10.4.

Conclusion. Our data suggest that IL-10 SNP, including –2849, which is associated with differential production, do not play a major role in the susceptibility of DIP OA. (J Rheumatol 2005;32:1571-5)

Key Indexing Terms:

OSTEOARTHRITIS
HAND
PROMOTER POLYMORPHISMS
CYTOKINES
INTERLEUKIN 10

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From the Departments of Rheumatology and Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.

N. Riyazi, MD; F.A.S. Kurreeman; T.W.J. Huizinga, MD, PhD, Department of Rheumatology; F.W. Dekker, PhD, Department of Clinical Epidemiology; G. Rijsbergen, Department of Rheumatology; M. Kloppenburg, MD, PhD, Departments of Rheumatology and Clinical Epidemiology.

Address reprint requests to Dr. M. Kloppenburg, Leiden University Medical Center, Department of Rheumatology, C4-R, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail: G.Kloppenburg@lumc.nl

Accepted for publication April 11, 2005.

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