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Publication : Accelerated alveolar bone loss in mice lacking interleukin-10: late onset.

First Author  Al-Rasheed A Year  2004
Journal  J Periodontal Res Volume  39
Issue  3 Pages  194-8
PubMed ID  15102048 Mgi Jnum  J:102009
Mgi Id  MGI:3606391 Doi  10.1111/j.1600-0765.2004.00724.x
Citation  Al-Rasheed A, et al. (2004) Accelerated alveolar bone loss in mice lacking interleukin-10: late onset. J Periodontal Res 39(3):194-8
abstractText  OBJECTIVE AND BACKGROUND: Interleukin-10 (IL-10) is an anti-inflammatory cytokine regulating immune responses. We have previously reported that IL-10(-/-) mice experience accelerated alveolar bone loss. The purpose of the present study was to examine the timing of the manifestation of accelerated alveolar bone loss in IL-10(-/-) mice. MATERIALS AND METHODS: Twenty-four IL-10(-/-) and 21 IL-10(+/+) age-matched male 129/SvEv mice were used. Sacrifice times occurred at 1, 3 and 9.5 months of age. Alveolar bone loss was determined morphometrically on defleshed jaws. Enzyme-linked immunosorbent assay (ELISA) was used for determination of serum concentration of type I collagen C-telopeptide, a systemic marker of bone resorption. RESULTS: Alveolar bone loss for the entire IL-10(-/-) group was significantly different than for the IL-10(+/+) group (p = 0.025). There was no significant difference in alveolar bone loss between IL-10(-/-) and IL-10(+/+) mice at 1 and 3 months of age. At 9.5 months of age, IL-10(-/-) mice exhibited 39% greater alveolar bone loss than IL-10(+/+) mice (p = 0.018). For IL-10(-/-) mice, alveolar bone loss significantly increased with age. Serum C-telopeptide levels significantly decreased with age in both groups. IL-10(-/-) mice had consistently higher C-telopeptide levels than IL-10(+/+) mice and the difference between the two groups reached statistical significance (p = 0.011) for the 9.5-month-old mice. CONCLUSIONS: These results suggest that the accelerated alveolar bone loss observed in IL-10(-/-) mice is a late-onset condition and that lack of IL-10 may have an effect on bone homeostasis.
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