Abstract
Bisphosphonate-related osteonecrosis of the jaws (BRONJ) is an adverse effect of bisphosphonate therapy, with highest incidence reported in the oncologic patients receiving intravenous bisphosphonates (BP). Our group previously established that Zolendronate, a potent intravenous BP, caused BRONJ-like disease in mice by suppressing the adaptive regulatory T cell (Tregs) and activating the inflammatory T helper producing interleukin 17 cells (Th17), thereby decreasing the ratio of Treg/Th17. C-telopeptide (CTX), an indicator of bone turnover, is currently used by some clinicians to predict treatment response in BRONJ patients. Here, we determined whether the altered immune homeostasis elicited by bisphosphonate therapy, specifically a suppressed Treg/Th17 renders cancer patients susceptible to BRONJ.
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