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Accelerated Alveolar Bone Loss in Mice Lacking Interleukin-10

¹ Department of Periodontics, School of Dentistry, Loma Linda University, Loma Linda, CA, USA;
² Department of Preventive Dental Science, Periodontics Division, College of Dentistry, King Saud University, Riyadh, Saudi Arabia;
³ Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA, USA;
⁴ Division of Microbiology and Molecular Genetics, School of Medicine, Loma Linda University, Loma Linda, CA, USA; and
⁵ Section of Periodontology, College of Dentistry, The Ohio State University, 305 West 12th Avenue, PO Box 182357, Columbus, OH 43218-2357, USA;

Correspondence: ^* corresponding author, tatakis.1{at}osu.edu

Interleukin-10 regulates pro-inflammatory cytokines, including those implicated in alveolar bone resorption. We hypothesized that lack of interleukin-10 leads to increased alveolar bone resorption. Male interleukin-10(–/–) mice, on 129/SvEv and C57BL/6J background, were compared with age-, sex-, and strain-matched interleukin-10(+/+) controls for alveolar bone loss. Immunoblotting was used for analysis of serum reactivity against bacteria associated with colitis and periodontitis. Interleukin-10(–/–) mice had significantly greater alveolar bone loss than interleukin-10(+/+) mice (p = 0.006). The 30–40% greater alveolar bone loss in interleukin-10(–/–) mice was evident in both strains, with C57BL/6J interleukin-10(–/–) mice exhibiting the most bone loss. Immunoblotting revealed distinct interleukin-10(–/–) serum reactivity against Bacteroides vulgatus, B. fragilis, Prevotella intermedia, and, to a lesser extent, against B. forsythus. The results of the present study suggest that lack of interleukin-10 leads to accelerated alveolar bone loss.

Key Words: alveolar bone loss • antibodies • disease models • interleukin-10 • mice • knockout

Journal of Dental Research, Vol. 82, No. 8, 632-635 (2003)
DOI: 10.1177/154405910308200812


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