Objective: : To examine the effect of mouth breathing on chewing efficiency by evaluating masticatory variables. Materials and Methods: : Ten adult nasal breathers with normal occlusion and no temporomandibular dysfunction were selected. Subjects were instructed to bite the chewing gum on the habitual side. While breathing through the mouth and nose, the glucide elution from the chewing gum, number of chewing strokes, duration of chewing, and electromyography (EMG) activity of the masseter muscle were evaluated as variables of masticatory efficiency. Results: : The durations required for the chewing of 30, 60, 90, 120, 180, and 250 strokes were significantly ( P < .05) longer while breathing through the mouth. There was no significant difference in the glucide elution rate (%) for each chewing stroke between nose and mouth breathings. The glucide elution rates for 1- and 3-minute chewing were significantly ( P < .05) lower while breathing through the mouth. However, there was no significant difference in the glucide elution rate for 5-minute chewing between nose and mouth breathings. While chewing for 1, 3, and 5 minutes, the chewing stroke and EMG activity of the masseter muscle were significantly ( P < .05) lower during mouth breathing. Conclusions: : It takes a longer amount of time to complete chewing to obtain higher masticatory efficiency when breathing through the mouth. Therefore, mouth breathing will decrease the masticatory efficiency if the duration of chewing is restricted in everyday life.

The differentiation and function of osteocytes are controlled by surrounding cells and mechanical stress; however, the detailed mechanisms are unknown. Recent findings suggest that IL-33 is highly expressed in periodontal tissues in orthodontic tooth movement. The present study aimed to elucidate the effect of IL-33 on the expression of regulatory factors for bone remodeling and their molecular mechanisms in the osteocyte-like cell line MLO-Y4. MLO-Y4 cells were treated with IL-33, and the activation of intracellular signaling molecules and transcriptional factors was determined using Western blot analysis and chromatin immunoprecipitation assay. IL-33 treatment enhanced the expression of IL-6 in MLO-Y4 cells, which was suppressed by the knockdown of the IL-33 receptor ST2L. Additionally, IL-33 treatment induced activation of NF-κB, JNK/AP-1, and p38 MAPK signaling pathways in MLO-Y4 cells. Moreover, pretreatment with specific inhibitors of NF-κB, p38 MAPK, and JNK/AP-1 attenuated the IL-33-induced expression of IL-6. Furthermore, chromatin immunoprecipitation indicated that IL-33 increased c-Jun recruitment to the IL-6 promoter. Overall, these results suggest that IL-33 induces IL-6 expression and regulates osteocyte function via activation of the NF-κB, JNK/AP-1, and p38 MAPK pathways through interaction with ST2L receptors on the plasma membrane.