[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.

SAPHO syndrome or psoriatic arthritis? A familial case study.

OBJECTIVE: To discuss the relationships between SAPHO (synovitis, acne, pustulosis, hyperostosis and osteitis) syndrome and the group of spondylarthropathies. METHODS: Few reports of familial SAPHO have been published. We describe three children, two sisters and one brother, whose clinical and radiological presentation was in accordance with SAPHO syndrome. RESULTS: Two children developed psoriasis, and one child palmoplantar pustulosis. Both sacroiliac and sternoclavicular joints were involved in these three cases. Some features in our observations are also common to psoriatic arthritis. No association was found with HLA antigens, but a history of trauma preceding the onset of symptoms was present in all three children. CONCLUSIONS: We can consider that SAPHO is nosologically related to spondylarthropathies. Psoriatic arthritis could be the missing link between SAPHO and spondylarthropathies. It is likely that both genetic and environmental factors are involved.

Phosphate excretion in reflex sympathetic dystrophy syndrome before and after a single infusion of pamidronate.

To clarify the relations between reflex sympathetic dystrophy syndrome and moderate phosphate diabetes, we prospectively determined urinary phosphate excretion parameters (clearance, renal tubular reabsorption of phosphate and threshold of tubular reabsorption of phosphate) in 37 patients with reflex sympathetic dystrophy syndrome before and after treatment with 60 mg of pamidronate (n = 23) and in 35 age- and sex-matched controls. Urinary phosphate excretion parameters were identical in cases and in controls. Fourteen of the 23 cases treated by pamidronate were improved after one to two months. Pamidronate had no effect on phosphate excretion. Four cases versus only one control had phosphate diabetes (X2 = 0.18). Three of the four cases with phosphate diabetes failed to respond to pamidronate therapy but improved under phosphate and 1,25-diOH vitamin D3 therapy.

An X-ray absorptiometry study of reflex sympathetic dystrophy syndrome.

X-ray absorptiometry (Lunar DPX) was performed before and after treatment to determine bone mineral content and density, as well as fat-free mass and body fat, in 28 males and 11 females with a mean age of 37 years who met Doury's criteria for reflex sympathetic dystrophy syndrome. Mean disease duration was eight months. Before treatment, as compared to the unaffected limb, bone mineral content was decreased by 8.8%, bone mineral density by 9.6%, and fat-free mass by 6.2%, whereas body fat was increased by 6%. These differences were largest in those patients with the longest disease durations. The severity of bone loss was not correlated with the outcome, the severity of roentgenographic lesions, or whether the patient was evaluated at the warm or cold stage of the disease process. Study parameters were unchanged after three months both in patients who were and were not improved. After nine to 12 months, increases in bone and fat-free mass were seen in those patients whose clinical manifestations had subsided.