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.