Mechanism and clinical use of botulinum neurotoxin in head and facial region

Abstract

Food-borne botulism, derived from the Latin term "botulus," which means "sausage," was first described in the 18 th century. The term was used to define a fatal condition characterized by muscular paralysis resulting in respiratory arrest upon the consumption of raw sausages [1]. Botulinum neurotoxins (BoNTs), which cause botulism, are zinc-dependent metalloproteases produced by an anaerobic, spore-forming, Gram-positive bacterium, Clostridium botulinum, and are classified into seven serotypes (BoNT/A-G) based on their antigenic properties. Apart from the seven distinct BoNTs, an additional serotype has been reported; however, further validation is required for confirmation [2,3].Naturally produced BoNTs are non-covalently associated with one or several non-toxic neurotoxin-associated proteins (NAPs) and form high molecular weight (up to ~900kDa) progenitor toxin complexes (PTCs) at an acidic pH. The PTCs dissociate into BoNTs and NAPs at neutral or alkaline pH. NAPs play a vital role in protecting fragile BoNTs from the harsh environment of the gastrointestinal tract and in facilitating the passage of BoNTs through the intestinal epithelial barrier. BoNT is released from PTCs after absorption from the intestinal epithelial barrier. Free BoNTs are transported to neuromuscular junctions (NMJs) via general circulation, subsequently inhibiting acetylcholine exocytosis and resulting in flaccid paralysis [4]. BoNTs are potent toxins and are currently being extensively researched, not only for their lethality but also for their potential use in therapeutic interventions owing to their safety, efficacy, and long duration of action. BoNT/A and BoNT/B are widely used in clinical practice [5].In the early 19 th century, the first toxin of BoNT (BoNT/A) was identified. Immediately after its discovery, it was widely used for developing biological weapons, given its effects on the nervous system, and it was studied extensively during the Second World War. The therapeutic use of BoNT in the medical field began in the late 19 th century [6,7]. Human use of BoNT was first attempted to treat strabismus (crossed eyes) in 1977 by Scott [6]. Since then, many medical practitioners have used BoNT to treat eyelid twitching and muscle spasms [8]. BoNT/A has also been used to treat neurological J Prosthodont Res. 2023; **(**):

Incobotulinum Toxin-A in Professional Musicians with Focal Task-Specific Dystonia: A Double Blind, Placebo Controlled, Cross-Over Study

“…BoNT injections have revolutionized the treatment of many forms of focal dystonia, and level A evidence supports its use in blepharospasm, cervical dystonia, spasmodic dysphonia, and other forms of dystonia [ 9 ]. BoNT injected into muscles selectively blocks synaptic vesicle fusion by interfering with SNAP-25 function (for BoNT type A, the most used form) [ 10 ]. Injections are exceptionally well tolerated for these indications, with the most common side effect of transient minor weakness in the muscles injected.…”

The link between prosthodontics and sleep dentistry

“…In this journal, Uchida et al reported that a night denture was effective in inhibiting the increase in mobility of abutment tooth in patients with sleep bruxism who wear removable partial dentures [6]. In their review, Raman et al described the mechanism and clinical use of botulinum neurotoxin in the head and facial region [7]. In relation to sleep bruxism, although botulinum toxin type A (BonT-A) is effective in reducing masseter and temporal muscle hyperactivity and relieving pain, they noted serious adverse effects and suggested safety precautions.…”