Skeletal fluorosis: an uncommon cause, yet a rescue treatment?

• Published in: Osteoporosis international Vol. 35; no. 10; pp. 1859 - 1863
• Main Authors: Shariff, Julia Rose R., Swe, Khine Mon, Binkley, Neil, Whyte, Michael P., Pabich, Samatha K.
• Format: Journal Article
• Language: English
• Published: London Springer London 01.10.2024; Springer Nature B.V
• Subjects: Biopsy; Bone density; Bone Density - drug effects; Bone Density - physiology; Bone Density Conservation Agents - adverse effects; Bone Density Conservation Agents - therapeutic use; Bone diseases; Bone Diseases - chemically induced; Bone mineral density; Bone remodeling; Bone Remodeling - drug effects; Bone Remodeling - physiology; Bone turnover; Case Report; Chronic exposure; Endocrinology; Female; Fluoride Poisoning - physiopathology; Fluorides - adverse effects; Fluorides - therapeutic use; Fluorosis; Fractures; Fractures, Multiple - chemically induced; Humans; Long bone; Medicine; Medicine & Public Health; Middle Aged; Orthopedics; Osteomalacia; Osteomalacia - chemically induced; Osteoporosis; Osteoporotic Fractures - chemically induced; Osteoporotic Fractures - etiology; Osteoporotic Fractures - prevention & control; Parathyroid hormone; Parathyroid Hormone-Related Protein; Rheumatology; Abaloparatide; Fluoride; Fractures; Osteosclerosis; Fluorocarbon; Skeletal fluorosis; Osteomalacia
• DOI: 10.1007/s00198-024-07137-x
• ISSN: 0937-941X; 1433-2965

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.