Delayed epidural pseudoaneurysm following cervical laminectomy and instrumentation in a patient with canal stenosis secondary to skeletal fluorosis: A case report.

RATIONALE: The typical intraoperative presentation of vertebral artery injury (VAI) usually involves profuse bleeding and requires immediate treatment. However, an occult VAI may occur intraoperatively and result in delayed life-threatening epidural pseudoaneurysm several days postoperatively. PATIENT CONCERNS: A 21-year-old man with compressive cervical myelopathy resulting from canal stenosis of skeletal fluorosis underwent decompression of C1 to C7 and instrumentation from C2 to C7. No impressive bleeding event occurred during the operation. On postoperative day 40, progressive quadriplegia developed. DIAGNOSES: Pseudoaneurysm of the VA was established by angiography. INTERVENTIONS: After occlusion of the right VA, the patient underwent hematoma clearing. OUTCOMES: Fortunately, the patient experienced significant recovery of neurologic function after the second surgery. LESSONS: From this case, we realize even in the absence of obvious signs of VAI during a cervical operation, postoperative evaluation should be mandatory for suspected bleeding events occurring at VAI-prone sites during surgery. Moreover, the bone morphological abnormality of skeletal fluorosis was determined to be the most important risk contributing to VAI in this case. The safety limits of bone removal should be determined preoperatively to avoid the effects of bone morphological abnormalities.

[CHRONIC FLUORIDE INTOXICATION AS A RISK FACTOR FOR THE DEVELOPMENT OF ATHEROSCLEROSIS].

In workers employed in the aluminum industry, the main harmful production factor is exposure to fluoride salts, which can cause chronic fluoride intoxication. For the assessment of the impact of chronic fluoride intoxication on the development of atherosclerosis, we conducted a comprehensive survey of 87 aluminum-metal makers with chronic fluoride intoxication and 43 aluminum-metal makers without occupational diseases, mean age--52.1 ± 0.4 years. There were considered the presence and severity of atherosclerosis of brachiocephalic arteries, and the arteries of the lower extremities in the studied group, there was evaluated the effect of other risk factors for atherosclerosis (smoking, presence of hypertension, diabetes, dyslipidemia). With the use of Doppler ultrasound of the arteries it was revealed that in metallurgists with chronic fluoride intoxication atherosclerosis was detected in 73.6% versus 55.8% in persons of the comparison group. The performed analysis of the prevalence of main risk factors for atherosclerosis showed that in metal makers with chronic fluoride intoxication in combination with atherosclerosis hypertension is more common (in 54.7%) than in metallurgists with chronic fluoride intoxication without atherosclerosis--only 26.1%. According to the frequency of occurrence of smoking, diabetes mellitus, hypercholesterolemia, and hypertriglyceridemia, there were no significant differences between the metallurgists with chronic fluoride intoxication, with and without atherosclerosis, and the control group, the increase in LDL cholesterol occurs significantly more often in metal-makers with chronic fluoride intoxication in combination with atherosclerosis if compared to workers without occupational diseases. Thus, chronic fluoride intoxication acts as a risk factor in the development of atherosclerosis: atherosclerosis in metal-makers with chronic fluoride intoxication occurs more frequently than in workers who do not have professional pathology. Hypertension and elevated levels of LDL cholesterol were established to increase the relative risk of developing atherosclerosis in metallurgists with chronic fluoride intoxication. At that there are no significant differences in the prevalence of common risk factors for atherosclerosis (smoking, diabetes, hypercholesterolemia, hypertriglyceridemia).

Association of lifetime exposure to fluoride and cognitive functions in Chinese children: a pilot study.

BACKGROUND: A systematic review and meta-analysis of published studies on developmental fluoride neurotoxicity support the hypothesis that exposure to elevated concentrations of fluoride in water is neurotoxic during development. METHODS: We carried out a pilot study of 51 first-grade children in southern Sichuan, China, using the fluoride concentration in morning urine after an exposure-free night; fluoride in well-water source; and dental fluorosis status as indices of past fluoride exposure. We administered a battery of age-appropriate, relatively culture-independent tests that reflect different functional domains: the Wide Range Assessment of Memory and Learning (WRAML), Wechsler Intelligence Scale for Children-Revised (WISC-IV) digit span and block design; finger tapping and grooved pegboard. Confounder-adjusted associations between exposure indicators and test scores were assessed using multiple regression models. RESULTS: Dental fluorosis score was the exposure indicator that had the strongest association with the outcome deficits, and the WISC-IV digit span subtest appeared to be the most sensitive outcome, where moderate and severe fluorosis was associated with a digit span total score difference of -4.28 (95% CI -8.22, -0.33) and backward score with -2.13 (95% CI -4.24, -0.02). CONCLUSIONS: This pilot study in a community with stable lifetime fluoride exposures supports the notion that fluoride in drinking water may produce developmental neurotoxicity, and that the dose-dependence underlying this relationship needs to be characterized in detail.

High fluoride and low calcium levels in drinking water is associated with low bone mass, reduced bone quality and fragility fractures in sheep.

UNLABELLED: Chronic environmental fluoride exposure under calcium stress causes fragility fractures due to osteoporosis and bone quality deterioration, at least in sheep. Proof of skeletal fluorosis, presenting without increased bone density, calls for a review of fracture incidence in areas with fluoridated groundwater, including an analysis of patients with low bone mass. INTRODUCTION: Understanding the skeletal effects of environmental fluoride exposure especially under calcium stress remains an unmet need of critical importance. Therefore, we studied the skeletal phenotype of sheep chronically exposed to highly fluoridated water in the Kalahari Desert, where livestock is known to present with fragility fractures. METHODS: Dorper ewes from two flocks in Namibia were studied. Chemical analyses of water, blood and urine were executed for both cohorts. Skeletal phenotyping comprised micro-computer tomography (µCT), histological, histomorphometric, biomechanical, quantitative backscattered electron imaging (qBEI) and energy-dispersive X-ray (EDX) analysis. Analysis was performed in direct comparison with undecalcified human iliac crest bone biopsies of patients with fluoride-induced osteopathy. RESULTS: The fluoride content of water, blood and urine was significantly elevated in the Kalahari group compared to the control. Surprisingly, a significant decrease in both cortical and trabecular bones was found in sheep chronically exposed to fluoride. Furthermore, osteoid parameters and the degree and heterogeneity of mineralization were increased. The latter findings are reminiscent of those found in osteoporotic patients with treatment-induced fluorosis. Mechanical testing revealed a significant decrease in the bending strength, concurrent with the clinical observation of fragility fractures in sheep within an area of environmental fluoride exposure. CONCLUSIONS: Our data suggest that fluoride exposure with concomitant calcium deficit (i) may aggravate bone loss via reductions in mineralized trabecular and cortical bone mass and (ii) can cause fragility fractures and (iii) that the prevalence of skeletal fluorosis especially due to groundwater exposure should be reviewed in many areas of the world as low bone mass alone does not exclude fluorosis.

Effects of fluorosis on QT dispersion, heart rate variability and echocardiographic parameters in children.

OBJECTIVE: Chronic fluoride poisoning is called fluorosis. The aim of the study was to investigate effects of fluorosis on cardiovascular system in children by measuring QT dispersion (QTd), corrected QT dispersion (QTcd), heart rate variability (HRV) and echocardiography findings. METHODS: Thirty-five children with dental fluorosis and 26 children as control group were included in this cross-sectional study. Dean index was used for the clinical diagnosis. The fluoride levels of subjects measured by ion electrode method in spot urine higher than 0.6 ppm were included in the study. Serum electrolytes and thyroid function tests were analyzed. Electrocardiography (ECG), echocardiography and 24-hour ambulatory Holter monitorizations were applied, and all the data were analyzed for measuring HRV, and calculation of QTd and QTcd intervals. Corrected QT (QTc) intervals were determined with the Bazzett formula. Difference between the longest and shortest intervals was considered as dispersion. Statistical analysis was performed Kruskal-Wallis test and Pearson correlation test. RESULTS: Low free thyroxine hormone (FT4) (Control Group, Group 2 1.11 (0.85-1.64) ng/dL, 0.96 (0.85-1.11) ng/dL, p<0.05), calcium (Control Group, Group 1, 2, 9.80 (9.30-10.70) mg/dL, 9.60 (8.90-10.70) mg/dL, 9.50 (8.90-10.10) mg/dL, p<0.05) and high serum sodium levels (Control Group, Group 2 139 (136-142) mEq/L, 141 (138-148) mEq/L, p<0.01), increased QT (Control Group, Group 2 329.8 (300.0-363.5) msec, 351.8 (318.0-372.0) msec, p<0.05) and QTc intervals (Control Group, Group I2 390.6 (309.0-418.5) msec, 366.8 (318.2-468.5) msec, p<0.05) were found in subjects with fluorosis. No significant difference was found with respect to echocardiography and HRV variables. CONCLUSION: Endemic fluorosis is a risk factor for decrease in calcium and FT4 levels, increase in sodium levels and QT prolongation. These findings might be related with some cardiovascular system dysfunctions such as arrhythmias or syncope. Subjects with fluorosis should be monitored in terms of long QT and QTc intervals.

A case of distal renal tubular acidosis, Southeast Asian ovalocytosis and possible fluorosis.

A 39-year old man had periodic paralysis due to hypokalaemia. Investigations led to the diagnosis of distal renal tubular acidosis (dRTA) and Southeast Asian ovalocytosis (SAO). Both can originate in mutations of the anion-exchanger 1 gene (AE1), which codes for band 3, the bicarbonate/chloride exchanger in both the red cell membrane and the basolateral membrane of the collecting tubule alpha-intercalated cell. The finding of diffuse osteosclerosis led to the suspicion of coexisting fluorosis.

[Skeletal fluorosis: a case report]. / Fluorose osseuse: à propos d'un cas.

The authors report a case of skeletal fluorosis described in a 60 years old man living in south-west Tunisian. The main clinical sign is a severe functional legs disability. Radiographic examination has shown a diffused osteocondensation, with cervical spine degenerative discopathy, a pelvis bilateral osteoarthritis and an interosseous membrane ossification of forearms and legs. The skeletal fluorosis diagnosis has been confirmed by high serum and urinary fluoride levels.

Fluorosis as a probable cause of chronic lameness in free ranging eastern grey kangaroos (Macropus giganteus).

A population of eastern grey kangaroos (Macropus giganteus) inhabiting heathland and farmland surrounding an aluminum smelter at Portland, Victoria, Australia, exhibited clinical signs of lameness. An investigation was undertaken to determine the cause of this lameness. Hematology, necropsy, histopathology, fecal egg count, total worm count, reproductive status, and the population age range were examined and failed to reveal any additional underlying disease state. The specific problem of lameness was addressed with bone histopathology, radiography, quantitative ultrasonography, microradiography, and multielement analysis of bone ash samples. The significant lesions observed were: osteophytosis of the distal tibia and fibula, tarsal bones, metatarsus IV, and proximal coccygeal vertebrae; osteopenia of the femur, tibia, and metatarsus IV; incisor enamel hypoplasia; stained, uneven, and abnormal teeth wear; abnormal bone matrix mineralization and mottling; increased bone density; and elevated bone fluoride levels. Microradiography of affected kangaroos exhibited "black osteons," which are a known manifestation of fluorosis. Collectively, these lesions were consistent with a diagnosis of fluorosis.

[Osteofluorosis caused by excess use of toothpaste]. / Ostéose fluorée due à une consommation excessive de dentifrice fluoré.

BACKGROUND: Osteofluorosis is caused by chronic fluoride intoxication. Fluoride is used in toothpaste for the prevention of dental caries, and dental fluorosis has often been reported among children and attributed to ingestion of fluoride toothpaste. We report a case of chronic fluoride intoxication caused by excess use of toothpaste in an adult. CASE: A 45-year-old woman consulted a rheumatologist for painful swelling of the fingers, phalangeal rather than articular. She also had brown staining on her teeth. Radiography of the hands showed periosteal apposition on the phalanges. Further work-up ruled out tumoral or thyroid causes. Laboratory tests showed elevated fluoride levels in the blood (50.9 micromol/L, normal<1.5 micromol/L) and in the urine (721 micromol/L, normal<46 micromol/L). On questioning, we found only one cause for chronic fluoride intoxication: excess and unusual use of toothpaste. The patient brushed her teeth 18 times a day and swallowed the toothpaste, because she liked the taste. She consumed a tube of toothpaste every 2 days, thereby swallowing 68.5 mg of fluoride every day. Suspecting fluorosis from toothpaste, we asked the patient to use a toothpaste without fluoride. Sixteen weeks later, the pain had ceased, and laboratory tests showed massively reduced but still elevated fluoride levels in the blood (6.9 micromol/L) and urine (92.7 micromol/L). CONCLUSION: In this rare case of fluoride intoxication, misuse of a normally innocuous product caused osteofluorosis.

Severe bone deformities in young children from vitamin D deficiency and fluorosis in Bihar-India.

A case-control study was undertaken to understand the etiopathology of the bone deformities among young children in a fluoride-affected village of the Bihar State. Two villages were selected: one village with high fluoride in drinking water (7.9 +/- 4.15 ppm), and the other village with normal levels of fluoride (0.6 +/- 0.31 ppm) as the control village. The source of drinking water was bore wells in both the villages. Two hundred and forty subjects from 54 households (HHs) of the high-fluoride village (HFV) and 1443 subjects from 197 HHs of the control village were selected for the study. Dental mottling (DM) was observed in 50% and skeletal deformities of various forms were observed in 20% of the total population of HFV, whereas, in the control village, DM was 6% and skeletal deformities were absent. The prevalence of both, DM and skeletal deformities was high in the younger age group of 1.5 to 14 years. Genu valgum, genu varum, bowing of tibia, saber shin, and widening of the lower ends of long bones at the wrist were the typical skeletal deformities observed among affected children in the HFV. X-rays of the children with deformities revealed varying degrees of bending of bones and enlargement of epiphyseal ends of metaphyses with fraying of bone and ligamental calcification. A survey indicated significantly low calcium and high phosphorus intake among the population of the HFV as compared to that of the control village, possibly resulting from low intake of milk and high intake of potatoes, respectively. The mean urinary fluoride level was significantly higher in the children of the HPV, both with and without deformities, as compared to that of the control village. The mean serum 25 OHD3 (25 Hydroxy Vitamin D) and calcium levels were significantly lower and alkaline phosphatase activity was significantly higher among the children with deformities as compared to those without deformities from the HFV and the control village. Serum intact parathyroid hormone (IPTH) levels were high in children both with and without deformities in the HFV as compared to those in the control village. No significant differences were observed in the concentration of serum and urinary creatinine, and Cu, and Mg levels between the HFV and the control village. It can be concluded that some of the children from the HFV manifested severe bone deformities (rickets), which were confirmed by the existence of low serum calcium and vitamin D levels.

Fluorosis-induced hyperparathyroidism mimicking a giant-cell tumour of the femur.

We report the case of a young woman who, over a period of five years was diagnosed and treated for a giant-cell tumour of bone, osteomalacia and fluorosis. A review of the literature revealed a correlation between these three diagnoses, the primary pathology being fluorosis and the remaining symptoms being secondary manifestations. It is important to be aware of this association, especially in regions with endemic skeletal fluorosis.

Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature.

STUDY DESIGN: Two cases of ossification of the transverse atlantal ligament (OTAL) are reported, and the literature is reviewed. OBJECTIVE: To report two cases of OTAL, which share fluorosis as a possible etiologic link. SUMMARY OF BACKGROUND DATA: OTAL, a rare phenomenon, may cause upper cervical canal stenosis and spastic quadriparesis. However, the incidence, etiology, and the best therapeutic options are currently unclear. METHODS: Two cases are reported. Included are pertinent history, physical examination, radiographic evaluation, nonsurgical interventions, and outcomes. The available literature is also reviewed. RESULTS: On systemic examination, these two cases were found to have ossification of many ligaments and interosseous membranes, i.e., the atlantal transverse ligament, posterior longitudinal ligament, and interosseous membranes of ribs, forearm, and leg. These findings were coupled with a history of high fluoride intake and dental fluorosis; the diagnosis of fluorosis was made. After 2 weeks of treatment with halo ring traction, and protection and stabilization with a hard cervical collar, the clinical symptoms significantly improved. CONCLUSION: The incidence of OTAL may be not as rare as has been thought. Although the complete etiology of OTAL is not known, fluorosis may be one of the etiologic factors related to OTAL, as well as the ossification of other ligaments and interosseous membranes. Nonsurgical treatment may be safe and effective.