Evan Austin1,2, Eugene Koo1,2, Jared Jagdeo1,2,3. 1. Department of Dermatology, University of California at Davis, Sacramento, California. 2. Dermatology Service, Sacramento VA Medical Center, Mather, California. 3. Department of Dermatology, State University of New York, Downstate Medical Center, Brooklyn, New York.
Abstract
BACKGROUND: Keloids and hypertrophic scars are conditions of pathologic scarring characterized by fibroblast hyperproliferation and excess collagen deposition. These conditions significantly impact patients by causing psychosocial, functional, and aesthetic distress. Current treatment modalities have limitations. Clinical evidence indicates that botulinum toxin A (BoNT-A) may prevent and treat keloids and hypertrophic scars. OBJECTIVE: To examine investigated cellular pathways involved in BoNT-A therapeutic modulation of keloids and hypertrophic scars. METHODS: The authors searched PubMed, Embase, and Web of Science for basic science articles related to botulinum toxin therapy, scarring, fibroblasts, keloids, and hypertrophic scars. RESULTS: Eleven basic science articles involving keloids and hypertrophic scars were reviewed. DISCUSSION: BoNT-A may reduce skin fibrosis by decreasing fibroblast proliferation, modulating the activity of transforming growth factor-β, and reducing transcription and expression of profibrotic cytokines in keloid-derived and hypertrophic scar-derived dermal fibroblasts. BoNT-A may modulate collagen deposition, but there is a paucity of evidence regarding specific mechanisms of action. CONCLUSION: Overall, BoNT-A has the potential to prevent or treat pathologic scars in patients with a known personal or family history of keloids and hypertrophic scars, which may improve patient psychosocial distress and reduce clinic visits and health care costs. Variability in keloid and hypertrophic scar response to BoNT-A may be due to interexperiment differences in dosing, tissue donors, and assay sensitivity.
BACKGROUND: Keloids and hypertrophic scars are conditions of pathologic scarring characterized by fibroblast hyperproliferation and excess collagen deposition. These conditions significantly impact patients by causing psychosocial, functional, and aesthetic distress. Current treatment modalities have limitations. Clinical evidence indicates that botulinum toxin A (BoNT-A) may prevent and treat keloids and hypertrophic scars. OBJECTIVE: To examine investigated cellular pathways involved in BoNT-A therapeutic modulation of keloids and hypertrophic scars. METHODS: The authors searched PubMed, Embase, and Web of Science for basic science articles related to botulinum toxin therapy, scarring, fibroblasts, keloids, and hypertrophic scars. RESULTS: Eleven basic science articles involving keloids and hypertrophic scars were reviewed. DISCUSSION: BoNT-A may reduce skin fibrosis by decreasing fibroblast proliferation, modulating the activity of transforming growth factor-β, and reducing transcription and expression of profibrotic cytokines in keloid-derived and hypertrophic scar-derived dermal fibroblasts. BoNT-A may modulate collagen deposition, but there is a paucity of evidence regarding specific mechanisms of action. CONCLUSION: Overall, BoNT-A has the potential to prevent or treat pathologic scars in patients with a known personal or family history of keloids and hypertrophic scars, which may improve patientpsychosocial distress and reduce clinic visits and health care costs. Variability in keloid and hypertrophic scar response to BoNT-A may be due to interexperiment differences in dosing, tissue donors, and assay sensitivity.