IADR Abstract Archives
Masseteric Atrophy Evoked by Botulinum Toxin Early Impairs Mandibular Microstructure
Objectives: Masseter muscle injection with Botulinum Toxin Type A (BoNTA) generates muscle paralysis 1d after the intervention. In the mandibular condyle, a significant impairment in bone microstructure at the BoNTA-side has been demonstrated after 14d, with a significant increase in the expression of a molecular marker of bone resorption in just 2d. Microstructure studies in early stages of BoNTA-induced muscle paralysis (2d and 7d) are not reported. Our aim is to compare the bone microstructure parameters of the mouse mandibular condyle 2d and 7d after a BoNTA injection in masseter muscle.
Methods: The unilateral masseter hypofunction was induced by a single injection of BoNTA (0.2U/10 µl) in the right masseter and saline solution in the left masseter of adult male BALB/c mice. After 2d (T1) or 7d (T2), masseter muscles were processed for qPCR detection of atrophy molecular markers (Atrogin1, Murf1) or fibers diameter. Mandibles were scanned by micro-tomography (microCT, voxel size 8.43 µm). The microstructure parameters trabecular thickness (Tb.Th) and bone volume fraction (BV/TV), comparing the BoNTA-side with the control-side, were addressed using BoneJ.
Results: A reduction in muscle mass and fibers diameter was observed in the BoNTA-injected side at T1 and T2. A significant increase (p<0.05) in the expression level of both Atrogin1 and Murf1 was also detected in BoNTA-injected muscles at T1 and T2. There was a tendency to decrease in Tb.Th. and BV/TV on the BoNTA side at T2; changes were not statistically significant, but the reduction in the BoNTA vs control-side was observed in all the animals addressed. No tendency of changes in bone parameters was observed at T1.
Conclusions: We here demonstrated that BoNTA injection in masseter muscle early evokes muscle atrophy. Our data suggest that masseteric atrophy leads to an impairment in mandibular condyle microstructure of the ipsilateral side as early as 7d after the intervention.
Methods: The unilateral masseter hypofunction was induced by a single injection of BoNTA (0.2U/10 µl) in the right masseter and saline solution in the left masseter of adult male BALB/c mice. After 2d (T1) or 7d (T2), masseter muscles were processed for qPCR detection of atrophy molecular markers (Atrogin1, Murf1) or fibers diameter. Mandibles were scanned by micro-tomography (microCT, voxel size 8.43 µm). The microstructure parameters trabecular thickness (Tb.Th) and bone volume fraction (BV/TV), comparing the BoNTA-side with the control-side, were addressed using BoneJ.
Results: A reduction in muscle mass and fibers diameter was observed in the BoNTA-injected side at T1 and T2. A significant increase (p<0.05) in the expression level of both Atrogin1 and Murf1 was also detected in BoNTA-injected muscles at T1 and T2. There was a tendency to decrease in Tb.Th. and BV/TV on the BoNTA side at T2; changes were not statistically significant, but the reduction in the BoNTA vs control-side was observed in all the animals addressed. No tendency of changes in bone parameters was observed at T1.
Conclusions: We here demonstrated that BoNTA injection in masseter muscle early evokes muscle atrophy. Our data suggest that masseteric atrophy leads to an impairment in mandibular condyle microstructure of the ipsilateral side as early as 7d after the intervention.