Objectives: The objective of this work is to present the mechanisms of action and therapeutic effects of botulinum toxin type A in various dermatological pathologies involving different inflammatory and immunological processes. By analyzing its mechanisms, this study aims to assess its relevance and potential applications in treating dermatological conditions. The focus is on evaluating its efficacy beyond its well-known role in neuromuscular inhibition, exploring novel therapeutic pathways that address inflammation, immune modulation, and vascular dysfunction.
Introduction: Botulinum toxin type A is primarily recognized for its inhibitory action on the neuromuscular junction, reducing muscle contraction and dynamic wrinkles. However, over the past decade, multiple studies have highlighted its therapeutic potential in treating pathological scars, inflammatory dermatoses, and facial conditions such as eczema, psoriasis, hidradenitis suppurativa, acne, rosacea, and seborrhea. It has also proved effective in the management of androgenetic alopecia, post-herpetic neuralgia and Raynaud's phenomenon ulcers, suggesting a wider field of clinical application in dermatology
Materials / method: A systematic review of the literature was conducted using the MEDLINE (PubMed) database from January 1, 2019, to November 1, 2024. The search identified 885 articles linking dermatology with botulinum toxin type A. After applying strict inclusion and exclusion criteria, 222 articles were selected for analysis. Studies focusing exclusively on hyperhidrosis were excluded, given the well-established role of the toxin in this indication. The selected studies were analyzed to explore the toxin's mechanisms of action and therapeutic outcomes across dermatological applications.
Results: Botulinum toxin type A acts on both neuronal and non-neuronal cells, including keratinocytes, fibroblasts, sebocytes, endothelial cells, and innate and adaptive immune cells. Its mechanisms involve the inhibition of neurotransmitter and TGFB1 release, both of which play key roles in cellular signaling. Additionally, it reduces free radical production, suppresses monocyte chemotaxis, and inhibits mast cell degranulation, collectively contributing to its anti-inflammatory and immunomodulatory effects.
Conclusion: Beyond its primary role in neuromuscular synapse inhibition, botulinum toxin type A operates through multiple biological mechanisms, affecting vascular, inflammatory, and immune pathways. These additional properties open new opportunities for clinical applications in dermatology, extending beyond aesthetic indications. Its ability to modulate inflammation, immune cell activity, and vascular responses positions it as a versatile and promising therapeutic tool. Further clinical studies will solidify its place as an integral part of dermatological treatment strategies.
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