Kleerekoper M
Center for Osteoporosis Research, Southfield, MI 48076-3956, USA.
Crit Rev Clin Lab Sci. 1996;33(2):139-61. doi: 10.3109/10408369609083059.
Fluoride has the potential to increase skeletal mass to a greater extent than any other pharmacologic agent, yet it has proven difficult to translate this into therapeutic benefit for patients with low bone mass in diseases such as osteoporosis. This apparent paradox can be explained in part by toxic actions of the ion on skeletal mineralization, impairment of the normal processes of bone resorption, and fluoride-induced decreases in strength per unit of bone (mass or volume). In part, the paradox can be explained by the late stage of osteoporosis in most patients enrolled in controlled clinical trials of fluoride, with alterations in skeletal microarchitecture beyond which restoration of mechanical integrity is not likely. Exposure of calcified tissues to environmental fluoride (water supply, dentifrices) also offers paradoxes. The anticaries effects are well documented as are the deleterious skeletal effects of endemic fluorosis when environmental exposure is too high. More controversial is the effect of seemingly nontoxic levels of exposure on the prevalence of osteoporotic fractures of the hip. This review attempts to provide a balanced overview of the conflicting literature concerning therapeutic and environmental effects of fluoride on the skeleton.
氟化物增加骨量的潜力比任何其他药物都要大,但事实证明,在骨质疏松症等疾病中,将其转化为对低骨量患者的治疗益处却很困难。这种明显的矛盾部分可以通过离子对骨骼矿化的毒性作用、正常骨吸收过程的受损以及氟化物导致的单位骨量(质量或体积)强度降低来解释。部分矛盾可以解释为,参与氟化物对照临床试验的大多数患者处于骨质疏松症晚期,骨骼微结构发生改变,恢复机械完整性不太可能。钙化组织暴露于环境氟化物(供水、牙膏)也存在矛盾之处。防龋效果有充分记录,而当环境暴露过高时,地方性氟中毒对骨骼的有害影响也同样如此。关于看似无毒水平的暴露对髋部骨质疏松性骨折患病率的影响则更具争议性。本综述试图对有关氟化物对骨骼的治疗和环境影响的相互矛盾的文献进行全面概述。