Purpose: Producing tongue pressure (TP) by pushing the tongue against the palate consists of lifting the tongue muscles and elevating the floor of the mouth via suprahyoid muscle contraction. Though studies have shown that tongue-pressure resistance training (TPRT) increases tongue function, none have focused on suprahyoid muscle function enhancements. Our study aimed to verify whether TPRT improves both tongue function and hyoid movement during swallowing. Materials and methods: Eighteen patients (mean age: 76.8±6.2 years) with presbyphagia presenting with symptoms such as coughing and choking were enrolled. All patients performed daily living activities independently. None of the participants had diseases causing dysphagia or previous oral or pharyngeal surgery. Participants were instructed to push their tongues against the palate as hard as possible with their mouths closed for 10 seconds, and then resting for 10 seconds. A set consisted of five consecutive exercise and resting periods; two sets per day were performed for a month. TP and the oral diadochokinetic rate (ODKR), measured by repetitions of the syllables /ta/ and /ka/, assessed tongue function. The extent of anterior and superior hyoid movement and parameters related to swallowing, including the penetration aspiration scale (PAS) and the normalized residue ratio scale (NRRS) in the valleculae (NRRSv) and piriform sinus (NRRSp), were evaluated based on videofluoroscopic data. Results: The anterior (P=0.031) and superior hyoid movement (P=0.012), TP (P=0.002), ODKR/ta/ (P=0.034), ODKR/ka/ (P=0.009), and the width of the upper esophageal sphincter (P=0.001) were larger at follow-up than at baseline. NRRSp (P=0.022), PAS (P=0.016), and pharyngeal transit times (P=0.004) were smaller at follow-up than at baseline. Conclusion: TPRT improved tongue strength, dexterity, both anterior and superior hyoid elevation, and swallowing functions. Therefore, TPRT could improve tongue function and suprahyoid muscle function simultaneously and contribute to prevention of sarcopenic dysphagia.

Previous studies have reported a relationship between masseter muscle thickness and tooth loss or limb muscle thickness. However, it is not yet known whether masseter muscle thickness is related to appendicular skeletal muscle mass, and grip strength. The purpose of this study was to determine which of the two variables—tooth loss or appendicular skeletal muscle mass index—is more strongly related to masseter muscle thickness, and to identify a suitable indicator of decreasing masseter muscle thickness in healthy elderly individuals. Grip strength, walking speed, body weight, skeletal muscle mass index, tooth loss, and masseter muscle thickness at rest and during contraction were determined in 97 community-dwelling elderly individuals aged ≥65 years (men: 44, women: 53). Masseter muscle thickness was chosen as the dependent variable, while age, skeletal muscle mass index, body weight, grip strength, and tooth loss were chosen as the independent variables. Multiple regression analysis was conducted using the stepwise regression method. In men, grip strength was the only independent predictor of masseter muscle thickness at rest. Tooth loss and grip strength were independent predictor of masseter muscle thickness during contraction. In women, tooth loss was the independent predictor of masseter muscle thickness both at rest and during contraction, while grip strength and body weight were the independent predictor of masseter muscle thickness at rest only. We confirmed that in healthy elderly individuals, tooth loss has a stronger relationship with masseter muscle thickness than aging and skeletal muscle mass index do. Masseter muscle thickness in both elderly men and women is also associated with grip strength, suggesting that grip strength can be used as an indicator of masseter muscle thickness in this population.

Skeletal muscles have a high metabolic capacity, which play key roles in glucose metabolism. Although periodontal disease increases the risk of metabolic syndrome, the relationship between periodontal bacterial infection and skeletal muscle metabolic dysfunction is unclear. We found that anti‐ Porphyromonas gingivalis ( Pg ) antibody titers positively correlated with intramuscular adipose tissue content (IMAC), fasting blood glucose, and HOMA‐IR in metabolic syndrome patients. In C57BL/6J mice fed a high‐fat diet, recipients of oral Pg (HFPg) had impaired glucose tolerance, insulin resistance, and higher IMAC compared to recipients of saline (HFco). The soleus muscle in HFPg mice exhibited fat infiltration and lower glucose uptake with higher Tnfa expression and lower insulin signaling than in HFco mice. Gene set enrichment analysis showed that TNFα signaling via NFκB gene set was enriched in the soleus muscle of HFPg mice. Moreover, TNF‐α also decreased glucose uptake in C2C12 myoblast cells in vitro. Based on 16S rRNA sequencing, Pg administration altered the gut microbiome, particularly by decreasing the abundance of genus Turicibacter . Microbial network of the gut microbiome was dramatically changed by Pg administration. Our findings suggest that infection with Pg is a risk factor for metabolic syndrome and skeletal muscle metabolic dysfunction via gut microbiome alteration.