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Abstract We aimed to examine the effects of sex, age, choice of surgical orthodontic treatment, and skeletal pattern on psychological assessment scores of orthodontic patients before edgewise treatment. They completed the State-Trait Anxiety Inventory (STAI), Beck Depression Inventory (BDI)-II, and the psychological domain of the World Health Organization Quality of Life 26 (Psych-QOL) for assessment of anxiety, depression, and body image, respectively. No significant effects on psychological assessment scores due to sex or age differences were found. Surgical orthodontic treatment patients and patients with skeletal Class III had significantly higher STAI-Trait and/or BDI-II scores and lower Psych-QOL score. Based on the linear mixed-effects model, the choice of surgical orthodontic treatment had a significant effect on the STAI-Trait, BDI-II, and Psych-QOL scores. No significant interaction effect was found between the choice of surgical orthodontic treatment and the skeletal pattern by ANB angle. Patients with skeletal Class I or III who chose surgical orthodontic treatment had higher STAI-Trait and/or BDI-II scores and/or lower body image score, respectively. These results suggest that patients who chose surgical orthodontic treatment, particularly those with skeletal Class I and III, may be more prone to experience anxiety and depression and have body image dissatisfaction.

The rapid aging of the population makes the detection and prevention of frailty increasingly important. Oral frailty has been proposed as a novel frailty phenotype and is defined as a decrease in oral function coexisting with a decline in cognitive and physical functions. Oral frailty has received particular attention in relation to Alzheimer's disease (AD). However, the pathomechanisms of oral frailty related to AD remain unknown. It is assumed that the mesencephalic trigeminal nucleus (Vmes), which controls mastication, is affected by AD pathology, and as a result, masticatory function may be impaired. To investigate this possibility, we included male 3 × Tg-AD mice and their non-transgenic counterpart (NonTg) of 3–4 months of age in the present study. Immunohistochemistry revealed amyloid-β deposition and excessive tau phosphorylation in the Vmes of 3 × Tg-AD mice. Furthermore, vesicular glutamate transporter 1-immunopositive axon varicosities, which are derived from Vmes neurons, were significantly reduced in the trigeminal motor nucleus of 3 × Tg-AD mice. To investigate whether the AD pathology observed in the Vmes affects masticatory function, we analyzed electromyography of the masseter muscle during feeding. The 3 × Tg-AD mice showed a significant delay in masticatory rhythm compared to NonTg mice. Furthermore, we developed a system to simultaneously record bite force and electromyography of masseter, and devised a new method to estimate bite force during food chewing in mice. Since the muscle activity of the masseter showed a high correlation with bite force, it could be accurately estimated from the muscle activity. The estimated bite force of 3 × Tg-AD mice eating sunflower seeds was predominantly smaller than that of NonTg mice. However, there was no difference in masseter weight or muscle fiber cross-sectional area between the two groups, suggesting that the decreased bite force and delayed mastication rhythm observed in 3 × Tg-AD mice were not due to abnormality of the masseter. In conclusion, the decreased masticatory function observed in 3 × Tg-AD mice was most likely caused by AD pathology in the Vmes. Thus, novel quantitative analyses of masticatory function using the mouse model of AD enabled a comprehensive understanding of oral frailty pathogenesis.