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Bone mineral structure after six years fluoride treatment investigated by backscattered electron imaging (BSEI) and small angle x-ray scattering (SAXS): a case reportAbstract
NaF, a bone formation stimulating agent, is used for the treatment of osteoporosis. Controversy exists concerning the quality of the newly formed bone and the antifracture effectiveness. We report about a 70 years old woman, who had received 50 mg NaF/d for about 6 years. Calcium or Vit D supplements had not been prescribed. She presented a history of pain in her logs with recurrent character. Spontaneous fractures of the metatarsal bones II and III of the left foot had occurred 6 month before the first clinical visit in our institution. Besides mild anemia and leukocytosis the routine laboratory tests were normal. Ionized Ca was decreased, 25-OH-Vit D3 was slightly elevated. Radiographs of the skeleton and bone scintigraphy showed degenerative osteoathritis. DXA revealed: L2-L4 1.12; neck 0.65; Ward’s triangle 0.51; trochanteric region 0.53 g/cm 2 (all within 1 S.D. of normal range). Due to clinical suspicion of skeletal fluorosis with lower log syndrome, a transiliacal bone biopsy was taken. Histomorphometry revealed a bulky trabecular architecture, high osteoblastic activity and an increased amount of osteoid The Goldner- and calcium salt-stainings displayed abnormal patchy areas. Undecalcified plastic embedded 100 ~Jm thick ground sections were examined by BSEI and SAXS(1). BSEI of trabecular and compact bone showed irregularly shaped and pathologically mineralized bone areas, known as mottled bone. SAXS in these areas revealed abnormally large mineral crystals (in all dimensions larger than 50 nm), which from their size can only be extrafibrillarly located. These findings correspond well to observations in fluorosis(1). The severe deterioration of the collagen/mineral compound and the nearly complete lack of normal “old” bone suggest biomechanical incompetence and explain the pathological fractures. In this patient after 6 years treatment with 50 m 9 NaF/d skeletal fluorosis caused pain, disturbed gait and atraumatic fractures. Interestingly, laboratory findings, skeletal radiographs and bone densitometry, gave no indication for abnormalities of bone metabolism or mineralization. Without bone biopsy we would have failed the correct diagnosis. Careful clinical follow up , therefore, is undispensible whenever NaF is used for the treatment of osteoporosis. Invasive investigation of the skeleton (bone biopsy, histomorphometry, BSEI plus SAXS) is the only diagnostic tool, when skeletal fluorosis is suspected.