B lymphocyte RANKL enhances periodontal disease in type 2 diabetes
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Periodontitis (PD) and type 2 diabetes (T2D) are inflammatory diseases, which have B lymphocyte dysfunction in subjects with both conditions. B lymphocytes, when activated, release receptor activator of nuclear factor kappa-B ligand (RANKL), which is a key element for osteoclastogenesis and periodontal related bone loss. Previous studies have looked at PD or T2D but not together within the context of inflammation. To further understand the impact of T2D potentiated periodontal complications, purified B lymphocytes from mice spleen were plated on dentin plates under both stimulated and unstimulated conditions alone and as co-cultures with T lymphocytes to determine the effect on dentin pit formation, a measure of bone loss. Pit area analysis showed that stimulated B lymphocytes from obese mice had significantly higher pit areas when compared to all lean conditions (B/T unstimulated and stimulated). Because obese B lymphocytes had the largest pit areas, this correlated with the highest osteoclastic activity. This supports the hypothesis that T2D contributes to periodontal disease bone loss specifically through B lymphocyte RANKL function. These results suggest that B lymphocytes may be a therapeutic drug target that can provide new clinical treatments to control T2D potentiated periodontal complications.