Yan Dong, Gurumurthy Aruna, Wright Maggie, Pfeiler T Wayne, Loboa Elizabeth G, Everett Eric T
Dental Research, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Bone. 2007 Dec;41(6):1036-44. doi: 10.1016/j.bone.2007.07.018. Epub 2007 Aug 8.
Excessive fluoride (F) can lead to abnormal bone biology. Numerous studies have focused on the anabolic action of F yet little is known regarding any action on osteoclastogenesis. Little is known regarding the influence of an individual's genetic background on the responses of bone cells to F. Four-week old C57BL/6J (B6) and C3H/HeJ (C3H) female mice were treated with NaF in the drinking water (0 ppm, 50 ppm and 100 ppm F ion) for 3 weeks. Bone marrow cells were harvested for osteoclastogenesis and hematopoietic colony-forming cell assays. Sera were analyzed for biochemical and bone markers. Femurs, tibiae, and lumbar vertebrae were subjected to microCT analysis. Tibiae and femurs were subjected to histology and biomechanical testing, respectively. The results demonstrated new actions of F on osteoclastogenesis and hematopoietic cell differentiation. Strain-specific responses were observed. The anabolic action of F was favored in B6 mice exhibiting dose-dependent increases in serum ALP activity (p<0.001); in proximal tibia trabecular and vertebral BMD (tibia at 50&100 ppm, p=0.001; vertebrae at 50 and 100 ppm, p=0.023&0.019, respectively); and decrease in intact PTH and sRANKL (p=0.045 and p<0.001, respectively). F treatment in B6 mice also resulted in increased numbers of CFU-GEMM colonies (p=0.025). Strain-specific accumulations in bone [F] were observed. For C3H mice, dose-dependent increases were observed in osteoclast potential (p<0.001), in situ trabecular osteoclast number (p=0.007), hematopoietic colony forming units (CFU-GEMM: p<0.001, CFU-GM: p=0.006, CFU-M: p<0.001), and serum markers for osteoclastogenesis (intact PTH: p=0.004, RANKL: p=0.022, TRAP5b: p<0.001). A concordant decrease in serum OPG (p=0.005) was also observed. Fluoride treatment had no significant effects on bone morphology, BMD, and serum PYD cross-links in C3H suggesting a lack of significant bone resorption. Mechanical properties were also unaltered in C3H. In conclusion, short term F treatment at physiological levels has strain-specific effects in mice. The expected anabolic effects were observed in B6 and novel actions hallmarked by enhanced osteoclastogenesis shifts in hematopoietic cell differentiation in the C3H strain.
过量的氟(F)会导致骨骼生物学异常。众多研究聚焦于氟的合成代谢作用,但对于其对破骨细胞生成的作用却知之甚少。关于个体遗传背景对骨细胞对氟反应的影响也所知甚少。将四周龄的C57BL/6J(B6)和C3H/HeJ(C3H)雌性小鼠用饮用水中的氟化钠(0 ppm、50 ppm和100 ppm氟离子)处理3周。采集骨髓细胞进行破骨细胞生成和造血集落形成细胞分析。分析血清中的生化和骨标志物。对股骨、胫骨和腰椎进行显微CT分析。分别对胫骨和股骨进行组织学和生物力学测试。结果表明氟对破骨细胞生成和造血细胞分化有新的作用。观察到了品系特异性反应。氟的合成代谢作用在B6小鼠中更明显,表现为血清碱性磷酸酶(ALP)活性呈剂量依赖性增加(p<0.001);胫骨近端小梁和椎体骨密度增加(50 ppm和100 ppm时的胫骨,p=0.001;50 ppm和100 ppm时的椎体,分别为p=0.023和p=0.019);完整甲状旁腺激素(PTH)和可溶性核因子κB受体活化因子配体(sRANKL)降低(分别为p=0.045和p<0.001)。B6小鼠接受氟处理还导致粒-红-巨噬-巨核系集落形成单位(CFU-GEMM)集落数量增加(p=0.025)。观察到骨中氟含量的品系特异性积累。对于C3H小鼠,观察到破骨细胞潜能呈剂量依赖性增加(p<0.001)、原位小梁破骨细胞数量增加(p=0.007)、造血集落形成单位(CFU-GEMM:p<0.001,CFU-GM:p=0.006,CFU-M:p<0.001)以及破骨细胞生成的血清标志物增加(完整PTH:p=0.004,RANKL:p=0.022,抗酒石酸酸性磷酸酶5b(TRAP5b):p<0.001)。还观察到血清骨保护素(OPG)一致降低(p=0.005)。氟处理对C3H小鼠的骨形态、骨密度和血清吡啶交联物无显著影响,表明缺乏明显的骨吸收。C3H小鼠的力学性能也未改变。总之,生理水平的短期氟处理在小鼠中具有品系特异性作用。在B6小鼠中观察到了预期的合成代谢作用,而在C3H品系中则表现为以破骨细胞生成增强和造血细胞分化改变为特征的新作用。