# Biphasic Injection for Masseter Muscle Reduction with Botulinum Toxin
###### Abstract
Concerning surgical interventions, to achieve a slim and smooth lower facial contour, extraoral or intraoral approaches to perform osteotomy of the mandible along with surgical resection of the masseter have traditionally been recommended [4; 15]. [PERSON], in 1947 [4], tried to solve this condition performing masseteric resection through extra oral approach. In 1951, [PERSON] [15] proposed an intraoral approach for the same purpose, associated with a resection of genital angle. Moreover, radiofrequency was recommended to achieve volumetric reduction of the masseter muscle [16]. However, the drawbacks to these invasive interventions entail many risks such as facial nerve injury, infection, asymmetric resection, hematoma, uneven contour lines, persistent swelling, condyle fracture, postoperative pain, bleeding, scarring, and delayed healing time [4; 5; 6; 7; 8; 9; 10; 11; 12; 13; 14; 15; 16]. Although facial plastic surgery provides success in lower face reshaping, many patients prefer effective, minimally invasive alternative techniques [1; 2; 3; 4; 5; 6; 7; 8; 9; 10; 11; 12; 13; 14; 15; 16; 17]. As demonstrated by the American Society for Aesthetic Plastic Surgery statistical analysis, the demand for nonsurgical aesthetic procedures has increased during the last couple of decades. Even as the quantity of plastic surgery procedures doubled from 1995 to 2015, the amount of non-surgical cosmetic interventions increased by 12-fold [18; 19; 20; 21; 22; 23; 24; 25; 26; 27]. This data demonstrates that among an increasing number of patients seeking for aesthetic improvements, non-surgical interventions are preferred over surgical procedures. As preferences for minimally invasive procedures are growing in cosmetic facial reshaping and according to the favorable safety profile along with no down-time, treatment with botulinum neurotoxin type A (BoNTA) has recently become a first-choice treatment for masseter hypertrophy instead of conventional surgery in lower face contouring. Since it was first introduced in 1976 for strabismus treatment, BoNTA has been widely used to treat facial spasms in rehabilitation hubs [28]. In 1989, the U.S. Food and Drug Administration (FDA) approved the use of botulinum toxin for the treatment of facial spasmodic disorders [29; 30]. While the toxin was being applied for the aforementioneddisorders, [PERSON] suggested in 1987 that BoNTA could be used for cosmetic purposes to remove or ease facial wrinkles [30]. Aesthetic Plastic Surgery Statistics released in 2020 revealed that BoNTA are is still the first procedure performed in the top five nonsurgical approaches with an overall number of 2.643.366, 54.3% more than the year before [31; 32]. These data undoubtedly confirm the increasing use of BoNTA, although are underestimated because they consider only the aesthetic use of BoNTA [33; 34; 35]. Currently, this drug is not used only to reduce wrinkles contractility and restore muscle tone but for the treatment of facial muscle hypertrophy, square-angled mandibula, migraine, headaches, hyperhidrosis, overactive bladder, blepharospasm, hemifacial spasm, oromandibular dystonia, cervical dystonia, focal limb dystonia, laryngeal dystonia, tics, essential tremor, bruxism management, and temporomandibular joint disorders [4; 5; 6; 7; 33; 34; 35; 36]. Even if BoNTA injection cannot reduce the genesis of sleep bruxism, it can be considered as an elective management in reducing the intensity of masticatory muscles during bruxism [13]. Along with occlusal splints, BoNTA injection could result in protecting the masticatory system structures from the excessive force of sleep bruxism [13; 14]. [PERSON] et al. demonstrate the effect of BoNTA on jaw motor activity during sleep by a decrease of contractive intensity in the injected muscles [14]. Nowadays, BoNTA injection into masseter muscle is extensively used as an off-label non-invasive approach for MMH [37; 38; 39]. BoNTA acts selectively on the peripheral cholinergic motor nerve ending plate and inhibits acetylcholine release at neuromuscular junction [39].