Osteomalacia is now rarely observed in hemodialyzed patients since the prevention of aluminum intoxication and vitamin D deficiency. However, this disorder is still present and may be responsible for bone fractures. Fluoride overload is responsible for mineralization defects. We therefore prospectively measured the bone fluoride content in all dialysis osteomalacic bone biopsies referred to our laboratory from 1988 to 1995. Undecalcified transiliac bone biopsies were embedded in methacrylate. Sections were stained with toluidine blue and Aluminon. Bone fluoride content was measured using a specific electrode and expressed as % of bone ash. Bone biopsies were classified into 3 groups: hyperparathyroidism (HPT) with or without marrow fibrosis defined as BFR > 0.015 um3/um2/d, osteomalacia (OM) defined as low BFR and O. Th > 12.5 11m, and adynamic bone disease (ABD) defined as low BFR and O.Th <12.5 11m. Among the 273 transiliac bone biopsies received during this period, 228 biopsies (83%) showed mild or severe HPT indices, 34 biopsies (12.4%) showed ABD and 11 displayed osteomalacia (3.8%). In this latter group, O.Th was dramatically increased (22.6 ± 8 j1IIl) and no tetracycline double labelled surfaces was observed in any patient. Moderate marrow fibrosis was seen in four biopsies. Six out of the 11 biopsies with osteomalacia had positive aluminum stained surfaces (40 ± 25 %), whereas 5 were devoided of any aluminum deposits. Values of bone fluoride content are <0.1% in normal subjects and >1% in patients with fluorosis. Bone fluoride content was high in the osteomalacic group (1.I±Q.3 %) compared to the 25 randomly selected HPT (0.33± 0.1%. p<O.01) and 25 randomly selected ABD group (18 with aluminum and 7 without aluminum) (0.21± 0.03%, p<O.OI). In this ABD group, fluoride content was low regardless of aluminum intoxication. Auoride content was >0.5% in 7/11 patients. These data show that mineralisation defects observed in hemodialyzed patients are frequently associated with high bone fluoride content. Fluoride may be considered as a potential etiological factor of osteomalacic osteodystrophy.