Fluoride Action Network


A 52-year-old man presented with severe neck immobility and radiographic osteosclerosis. Elevated fluoride levels in serum, urine, and iliac crest bone revealed skeletal fluorosis. Nearly a decade of detailed follow-up documented considerable correction of the disorder after removal of the putative source of fluoride (toothpaste).

INTRODUCTION: Skeletal fluorosis, a crippling bone disorder, is rare in the United States, but affects millions worldwide. There are no data regarding its reversibility.

MATERIALS AND METHODS: A white man presented in 1996 with neck immobility and worsening joint pains of 7-year duration. Radiographs revealed axial osteosclerosis. Bone markers were distinctly elevated. DXA of lumbar spine (LS), femoral neck (FN), and distal one-third radius showed Z scores of +14.3, +6.6, and -0.6, respectively. Transiliac crest biopsy revealed cancellous volume 4.5 times the reference mean, cortical width 3.2 times the reference mean, osteoid thickness 25 times the reference mean, and wide and diffuse tetracycline uptake documenting osteomalacia. Fluoride (F) was elevated in serum (0.34 and 0.29 mg/liter [reference range: <0.20]), urine (26 mg/liter [reference range: 0.2-1.1 mg/liter]), and iliac crest (1.8% [reference range: <0.1%]). Tap and bottled water were negative for F. Surreptitious ingestion of toothpaste was the most plausible F source.

RESULTS: Monitoring for a decade showed that within 3 months of removal of F toothpaste, urine F dropped from 26 to 16 mg/liter (reference range: 0.2-1.1 mg/liter), to 3.9 at 14 months, and was normal (1.2 mg/liter) after 9 years. Serum F normalized within 8 months. Markers corrected by 14 months. Serum creatinine increased gradually from 1.0 (1997) to 1.3 mg/dl (2006; reference range: 0.5-1.4 mg/dl). Radiographs, after 9 years, showed decreased sclerosis of trabeculae and some decrease of sacrospinous ligament ossification. DXA, after 9 years, revealed 23.6% and 15.1% reduction in LS and FN BMD with Z scores of +9.3 and +4.8, respectively. Iliac crest, after 8.5 years, had normal osteoid surface and thickness with distinct double labels. Bone F, after 8.5 years, was 1.15% (reference range, <0.1), which was a 36% reduction (still 10 times the reference value). All arthralgias resolved within 2 years, and he never fractured, but new-onset nephrolithiasis occurred within 9 months and became a chronic problem.

CONCLUSIONS:  With removal of F exposure, skeletal fluorosis is reversible, but likely impacts for decades. Patients should be monitored for impending nephrolithiasis.


Our patient emphasizes the importance of considering fluoride as an explanation for osteosclerosis, and in diagnosing skeletal fluorosis especially in those who are at high risk from environmental or occupational exposure. Skeletal fluorosis, whether from current or remote exposure, is readily detected using axial DXA and diagnosed using urinary fluoride measurements. Eliminating the source of fluoride toxicity leads to a reversible disorder, albeit one that will likely linger and perhaps impact the patient for decades. Patients should be monitored for hypercalciuria and treated for impending nephrolithiasis. Prophylactic therapy for this complication, including hydration, limiting calcium intake, and use of thiazide diuretics could be beneficial. With removal of fluoride, patients can achieve a fairly rapid amelioration of clinical symptomatology, and forestall the development of more severe skeletal morbidity.