Open bite can be defined as an absence of occlusion, most frequently located in the anterior region of dental arches and its etiology is multifactorial. We present a clinical case of an 8 years and 10 months child presenting an anterior open bite (AOB) with transverse maxillary deficiency caused by tongue thrust during mixed dentition. The malocclusion was corrected by means of a McNamara expander with a palatal crib jointly with the association of speech therapy for tongue repositioning, and otolaryngology to treat adenoid hypertrophy due to its correlation with AOB. The multidisciplinary approach was effective in correcting the malocclusion with stable results after 2 years post-treatment.

Background: Periodontal disease is a chronic inflammatory condition characterized by progressive destruction of the supporting tissues of the teeth. MicroRNAs (miRNAs) have emerged as key post-transcriptional regulators of immune and inflammatory responses; however, their coordinated expression patterns in periodontal disease remain incompletely understood. Objective: This study aimed to evaluate the expression of miR-141-3p, miR-146a-5p, and miR-148b-3p in periodontal disease and to explore their potential co-regulation in relation to periodontal inflammation. Methods: Gingival samples were collected from individuals with periodontal disease and periodontally healthy controls. miRNA expression levels were quantified by real-time quantitative PCR using TaqMan assays and normalized to miR-191-5p. Relative expression was calculated using the ΔΔCt method. Statistical analyses included group comparisons and correlation analyses to assess relationships among miRNA expression levels. Results: miR-146a-5p expression was significantly reduced in periodontal disease compared with healthy controls (p < 0.05), while miR-141-3p showed a consistent downward trend without reaching statistical significance. No significant differences were observed for miR-148b-3p expression between groups. Notably, strong positive correlations were identified among the three miRNAs, indicating coordinated expression patterns independent of disease stage or grade. Conclusions: The findings demonstrate altered expression of miR-146a-5p and coordinated regulation of miR-141-3p, miR-146a-5p, and miR-148b-3p in periodontal disease. These results support the concept that miRNAs act within regulatory networks rather than as isolated markers and contribute to a more nuanced understanding of miRNA-mediated regulation in periodontal inflammation.