Surgical Correction of the Face with the Square Jaw and Weak Chin: Angle-to-Chin Bone Transfer

Baek, Rong Min; Han, Sang-Baek; Baek, Sora

doi:10.1097/00006534-200107000-00036

Cited by 15 publications

(1 citation statement)

References 9 publications

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“…It is an asymptomatic condition, but patients experience dissatisfaction owing to its unaesthetic appearance. Routine management involves surgical reduction of the masseter muscles, which may lead to several complications, such as restriction of mouth opening and nerve paralysis post-surgery [123,124]. Ideal management involves BoNT injections, which weaken the muscles, thereby reducing their bulky appearance [125].…”

Section: Masseteric Hypertrophy (Bulky Jaws)mentioning

confidence: 99%

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

et al. 2023

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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; **(**):

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Section: Masseteric Hypertrophy (Bulky Jaws)mentioning

confidence: 99%