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Use of geranylgeraniol to rescue osteoblasts and periodontal ligament fibroblasts from zoledronate‐induced apoptosis (663.16)
Author(s) -
Williams Calli,
Johnson Brooke,
Svrcina Haley,
Kawsky Ben,
Jones Dan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.663.16
Subject(s) - geranylgeraniol , apoptosis , bisphosphonate , periodontal fiber , osteonecrosis of the jaw , medicine , cancer research , pharmacology , chemistry , osteoporosis , farnesol , dentistry , biochemistry
Bisphosphonate treatments can produce an unwanted side effect of bisphosphonate‐related osteonecrosis of the jaw (BRONJ). One of the most potent bisphosphonates, zolendronate (ZOL), is used to treat postmenopausal osteoporosis, Paget’s disease, and cancer metastasis to bone. Individuals affected with BRONJ are unable to heal from dental procedures, leading to painful oral lesions. The goal of the work presented here was to investigate the ability of GGOH to rescue both murine MC3T3E1 osteoblasts and human periodontal ligament fibroblasts from ZOL‐induced apoptosis. Apoptosis was measured using the APOPercentage® assay. In osteoblasts, 72 hours of 50 micromolar ZOL treatment induced apoptosis by 12.5‐fold but simultaneous exposure to 10 micromolar GGOH decreased apoptosis by 64% (p<0.05). In a separate set of experiments, a booster of GGOH was administered 24 hours after the initiation of treatment, dramatically reducing ZOL‐induced apoptosis by 98% (p<0.0001). In periodontal ligament fibroblasts, ZOL treatment induced apoptosis 10‐fold and GGOH reduced apoptosis by 82% (p<0.05). The booster of GGOH reduced ZOL‐induced apoptosis by 99%. Collectively the data demonstrates the ability of GGOH to potentially rescue both hard and soft tissues of the oral cavity from ZOL‐induced apoptosis with a supplemental dosage of GGOH 24 hours following initiation of treatment essentially eliminating apoptosis. Grant Funding Source : Supported by grants from the Indiana Academy of Science and the Hodson Summer Research Institute