Changes in Masticatory Muscle Activity Following Interceptive Orthodontic Treatment in Children with Class II Malocclusion: A Multicenter Controlled Longitudinal Surface Electromyographic Study

Résumé fourni par la source

Background/Objectives: Class II malocclusion in growing patients may be associated with altered mandibular posture, occlusal instability, and adaptive changes in masticatory muscle function. This prospective, controlled, non-randomized longitudinal study evaluated changes in masseter and anterior temporalis muscle activity during Andresen functional appliance therapy and compared them with untreated Class I and Class II controls. Methods: Seventy children with skeletal and dental Class II malocclusion were treated with a customized Andresen appliance; 50 untreated Class II children and 30 untreated children with physiological Class I occlusion served as comparison groups. All participants were in mixed dentition and at cervical stage CS3 at baseline. Standardized bilateral sEMG recordings were obtained at T0, T1 (6 months), and T2 (12 months). Longitudinal sEMG outcomes were analyzed using mixed-design repeated-measures ANOVA, with time as the within-subject factor and group as the between-subject factor; prespecified T0-to-T2 contrasts were accompanied by Cohen’s d effect sizes. Results: In the treated Class II cohort, IMPACT increased from 108.64 ± 3.40 at T0 to 111.58 ± 3.13 at T1 and 113.82 ± 3.27 at T2 (within-group time effect p < 0.001). ATTIV changed from −0.88 ± 0.42 at T0 to +0.96 ± 0.55 at T1 and +1.65 ± 0.78 at T2 (p < 0.001). In contrast, neither the untreated Class II nor the physiological Class I group showed statistically significant within-group time effects for IMPACT (p = 0.96 and p = 0.58, respectively) or ATTIV (p = 0.78 and p = 0.93, respectively). Significant T0-to-T2 differences between treated and untreated Class II groups were observed for ATTIV (p < 0.001; d = +5.28) and IMPACT (p < 0.001; d = +2.00). Conclusions: Andresen therapy was associated with statistically supported longitudinal differences in masticatory muscle recruitment compared with untreated Class II controls. The observed pattern may reflect treatment-associated neuromuscular adaptation; however, causal attribution remains limited by the non-randomized design, and the sEMG changes should be interpreted as modifications in muscle recruitment rather than as evidence of physiological normalization or clinical improvement.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.