Skeletal fluorosis: an uncommon cause, yet a rescue treatment? Osteoporos Int 2024 Oct;35(10):1859-1863
Date
06/07/2024Pubmed ID
38847810DOI
10.1007/s00198-024-07137-xScopus ID
2-s2.0-85195307155 (requires institutional sign-in at Scopus site) 3 CitationsAbstract
PURPOSE: Skeletal fluorosis (SF) results from chronic exposure to fluoride (F-) causing excessive aberrantly mineralized brittle bone tissue, fractures, and exostoses. There is no established treatment other than avoiding the source of F-. Still, excess F- can persist in bone for decades after exposure ceases.
CASE PRESENTATION: A 50-year-old woman presented with multiple, recurrent, low AQ2 trauma fractures yet high radiologic bone mineral density. Serum F- was elevated, and osteomalacia was documented by non-decalcified transiliac biopsy. She reported intermittently "huffing" a keyboard cleaner containing F- (difluoroethane) for years. Following cessation of her F- exposure, we evaluated the administration of the parathyroid hormone analog, abaloparatide, hoping to increase bone remodeling and diminish her skeletal F- burden.
CONCLUSION: Due to the prolonged half-life of F- in bone, SF can cause fracturing long after F- exposure stops. Anabolic therapy approved for osteoporosis, such as abaloparatide, may induce mineralized bone turnover to replace the poorly mineralized osteomalacic bone characteristic of SF and thereby diminish fracture risk. Following abaloparatide treatment for our patient, there was a decrease in bone density as well as a reduction in F- levels.
Author List
Shariff JRR, Swe KM, Binkley N, Whyte MP, Pabich SKAuthor
Julia Rose Shariff MD Assistant Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Bone DensityBone Density Conservation Agents
Bone Diseases
Bone Remodeling
Female
Fluoride Poisoning
Fluorides
Fractures, Multiple
Humans
Middle Aged
Osteomalacia
Osteoporotic Fractures
Parathyroid Hormone-Related Protein
