Abstract
The purpose of this study was to compare the efficacy of botulinum toxin (BoNT) in masseter muscle reduction depending on the amount of chin deviation. Exploring distinctive effects of BoNT relative to the characteristics of facial asymmetry will aid in planning and predicting treatment outcomes. Sixteen adult volunteers were classified into two groups according to the degree of menton deviation observed in posteroanterior cephalograms. Eight had a menton deviation of 3 mm or more and the other eight had less than 3 mm. A total of 25 Units of BoNT was injected into the unilateral masseter muscle of the prominent side for each participant. Changes in the volume and bulkiest height of the lower face on each side were measured with a 3D laser scan at four time points: before and 4, 8, and 12 weeks after the injection. Two-way mixed ANOVA was employed for analyses. The volume and bulkiest height of the injected side decreased over time in both types of asymmetry, with significant differences at each time point. The reductions in the volume and bulkiest height were significantly greater in subjects without chin deviation. The reductions in the volume and bulkiest height of the lower face using BoNT are more effective for subjects without chin deviation.
Highlights
There has been growing demand for the correction of facial asymmetry as patient expectations have increased [1]
Disharmony of lower facial width is a type of facial asymmetry whose mainstay corrective surgical procedures include orthognathic surgery, resection of the corresponding portion of the mandible, and resection of the masseter muscle [1,2]
The botulinum neurotoxin (BoNT) is produced by Clostridium botulinum and consists of a heavy chain and a light chain linked together by a single disulphide bond [4]
Summary
There has been growing demand for the correction of facial asymmetry as patient expectations have increased [1]. Patients tend to prefer less invasive options, such as botulinum neurotoxin (BoNT) injection into masseter muscle to reduce its volume [3]. The BoNT is produced by Clostridium botulinum and consists of a heavy chain and a light chain linked together by a single disulphide bond [4]. It is synthesised as a relatively inactive single-chain polypeptide approximately 150 kDa, and is activated when proteolytically cleaved into the 100-kDa heavy chain and the 50-kDa light chain [5]. The BoNT permanently binds to the motor end plate at the neuromuscular junction which prevents the release of acetylcholine from the pre-synaptic vesicles causing a pre-synaptic blockade [3]
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