Abstract
BackgroundThe objective of this study was to evaluate the influence of masticatory muscle injection of botulinum toxin type A (BTX-A) on the growth of the mandibular bone in vivo.MethodsEleven Sprague-Dawley rats were used, and BTX-A (n = 6) or saline (n = 5) was injected at 13 days of age. All injections were given to the right masseter muscle, and the BTX-A dose was 0.5 units. All of the rats were euthanized at 60 days of age. The skulls of the rats were separated and fixed with 10% formalin for micro-computed tomography (micro-CT) analysis.ResultsThe anthropometric analysis found that the ramus heights and bigonial widths of the BTX-A-injected group were significantly smaller than those of the saline-injected group (P < 0.05), and the mandibular plane angle of the BTX-A-injected group was significantly greater than in the saline-injected group (P < 0.001). In the BTX-A-injected group, the ramus heights II and III and the mandibular plane angles I and II showed significant differences between the injected and non-injected sides (P < 0.05). The BTX-A-injected side of the mandible in the masseter group showed significantly lower mandibular bone growth compared with the non-injected side.ConclusionBTX-A injection into the masseter muscle influences mandibular bone growth.
Highlights
The objective of this study was to evaluate the influence of masticatory muscle injection of botulinum toxin type A (BTX-A) on the growth of the mandibular bone in vivo
Our results showed the effects of BTX-A injection on the low growth of the mandible
In this study, we evaluated the paralytic effects of BTXA on the mandibular bone growth in vivo
Summary
The objective of this study was to evaluate the influence of masticatory muscle injection of botulinum toxin type A (BTX-A) on the growth of the mandibular bone in vivo. Botulinum toxin type A (BTX-A) is a bacterial neurotoxin produced by the gram-positive bacterium Clostridium botulinum [1]. BTX-A inhibits the release of neurotransmitter in cholinergic nerve terminals and degrades the synaptosomal-associated protein of 25 kDa (SNAP-25) required for acetylcholine fusion and release [2]. It blocks the release of acetylcholine in the presynaptic membranes of neuromuscular junctions and induces reversible muscle weakness and paralysis [3].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
