Association between Toothbrushing and Cancer Risk.

Background: Most cancers are lifestyle-related and are thus preventable. Lifestyle habits can be improved by individual efforts; for example, because oral health is suggested to play a preventive role in cancer risk, toothbrushing is considered a critical and fundamental measure for controlling oral health. This study aimed to investigate the association between toothbrushing and cancer risk. Methods: Cross-sectional data from the Japan COVID-19 and Society Internet Survey, a large-scale (n = 32,000) online survey conducted in 2022, were used. From September 12 to October 19, 2022, questionnaires were distributed to candidates selected by simple random sampling from a Japanese Internet research company's panelists to represent the Japanese population. The association between toothbrushing and cancer risk according to cancer prevalence was then analyzed. Results: Among all 32,000 participants, 2,495 (7.8%) who had any cancer previously were analyzed. Multivariable logistic regression analysis revealed a significant association between toothbrushing habit and cancer risk. Conclusion: The findings of this study suggest that daily toothbrushing is essential for maintaining oral health and preventing cancer.

Role of peripheral myelin protein 22 in chronic exercise-induced interactions of muscle and bone in mice.

Exercise is important for the prevention and treatment of sarcopenia and osteoporosis. Although the interactions between skeletal muscles and bone have recently been reported, the myokines linking muscle to bone during exercise remain unknown. We previously revealed that chronic exercise using treadmill running blunts ovariectomy-induced osteopenia in mice. We herein performed an RNA sequence analysis of the gastrocnemius and soleus muscles of male mice with or without chronic exercise to identify the myokines responsible for the effects of chronic exercise on the muscle/bone relationship. We extracted peripheral myelin protein 22 (PMP22) as a humoral factor that was putatively induced by chronic exercise in the soleus and gastrocnemius muscles of mice from the RNA sequence analysis. Chronic exercise significantly enhanced the expression of PMP22 in the gastrocnemius and soleus muscles of female mice. PMP22 suppressed macrophage-colony stimulating factor and receptor activator factor κB ligand-induced increases in the expression of osteoclast-related genes and osteoclast formation from mouse bone marrow cells. Moreover, PMP22 significantly inhibited osteoblast differentiation, alkaline phosphatase activity, and mineralization in mouse osteoblast cultures; however, the overexpression of PMP22 did not affect muscle phenotypes in mouse muscle C2C12 cells. A simple regression analysis revealed that PMP22 mRNA levels in the gastrocnemius and soleus muscles were positively related to cortical bone mineral density at the femurs of mice with or without chronic exercise. In conclusion, we identified PMP22 as a novel myokine induced by chronic exercise in mice. We first showed that PMP22 suppresses osteoclast formation and the osteoblast phenotype in vitro.

Renal failure suppresses muscle irisin expression, and irisin blunts cortical bone loss in mice.

BACKGROUND: Chronic renal failure induces bone mineral disorders and sarcopenia. Skeletal muscle affects other tissues, including bone, by releasing myokines. However, the effects of chronic renal failure on the interactions between muscle and bone remain unclear. METHODS: We investigated the effects of renal failure on bone, muscle, and myokines linking muscle to bone using a mouse 5/6 nephrectomy (Nx) model. Muscle mass and bone mineral density (BMD) were analysed by quantitative computed tomography 8 weeks after Nx. RESULTS: Nephrectomy significantly reduced muscle mass in the whole body (12.1% reduction, P < 0.05), grip strength (10.1% reduction, P < 0.05), and cortical BMD at the femurs of mice (9.5% reduction, P < 0.01) 8 weeks after surgery, but did not affect trabecular BMD at the femurs. Among the myokines linking muscle to bone, Nx reduced the expression of irisin, a proteolytic product of fibronectin type III domain-containing 5 (Fndc5), in the gastrocnemius muscles of mice (38% reduction, P < 0.01). Nx increased myostatin mRNA levels in the gastrocnemius muscles of mice (54% increase, P < 0.01). In simple regression analyses, cortical BMD, but not trabecular BMD, at the femurs was positively related to Fndc5 mRNA levels in the gastrocnemius muscles of mice (r = 0.651, P < 0.05). The weekly administration of recombinant irisin to mice ameliorated the decrease in cortical BMD, but not muscle mass or grip strength, induced by Nx (6.2% reduction in mice with Nx vs. 3.3% reduction in mice with Nx and irisin treatment, P < 0.05). CONCLUSIONS: The present results demonstrated that renal failure decreases the expression of irisin in the gastrocnemius muscles of mice. Irisin may contribute to cortical bone loss induced by renal failure in mice as a myokine linking muscle to bone.

Role of irisin in effects of chronic exercise on muscle and bone in ovariectomized mice.

INTRODUCTION: Exercise is beneficial for the prevention and treatment of osteoporosis. Skeletal muscle affects other tissues via myokines, the release of which is regulated by acute exercise. However, the effects of chronic exercise on myokines linking muscle to bone have not been fully elucidated. Therefore, we investigated the effects of chronic exercise on bone and myokines using ovariectomized (OVX) mice. MATERIALS AND METHODS: Treadmill exercise with moderate intensity was performed for 8 weeks after OVX or sham surgery. We measured bone mineral density (BMD) at the femurs and tibias of mice by quantitative computed tomography and myokine mRNA levels in the gastrocnemius and soleus muscles. RESULTS: Treadmill exercise ameliorated decreases in trabecular and cortical BMD in the femurs of OVX mice. Irisin is a proteolytic product of fibronectin type III domain-containing 5 (Fndc5). Among the myokines examined, treadmill exercise increased irisin protein and Fndc5 mRNA levels in the gastrocnemius and soleus muscles of sham and OVX mice. Treadmill exercise increased peroxisome proliferator-activated receptor γ coactivator-1α mRNA levels in the gastrocnemius muscles of mice. Fndc5 mRNA levels in the gastrocnemius muscles positively correlated with trabecular BMD, but not with cortical BMD, at the femurs and tibias of mice in simple regression analyses. CONCLUSIONS: We demonstrated that chronic exercise elevated irisin expression in the gastrocnemius and soleus muscles of estrogen-deficient mice. Irisin might be related to increases in trabecular BMD in mice; however, further studies are needed to clarify the involvement of irisin in the effects of chronic exercise on muscle/bone interactions.

Myonectin inhibits the differentiation of osteoblasts and osteoclasts in mouse cells.

Myonectin is a myokine, which is involved in the pathophysiology of diabetes and obesity, and various myokines are involved in the interactions between skeletal muscle and bone. However, roles of myonectin in bone have still remained unknown. We therefore examined the effects of myonectin on mouse osteoblast and osteoclast differentiation in vitro. Myonectin significantly suppressed the mRNA levels of osteogenic genes and alkaline phosphatase (ALP) activity in mouse osteoblasts. As for osteoclasts, myonectin significantly suppressed osteoclast formation as well as the mRNA levels of osteoclast-related genes enhanced by receptor activator nuclear factor κB ligand (RANKL) from mouse monocytic RAW264.7 cells. Moreover, myonectin significantly suppressed osteoclast formation from mouse bone marrow cells in the presence of macrophage-colony stimulating factor and RANKL. On the other hand, myonectin significantly suppressed RANKL-induced oxygen consumption rate and peroxisome proliferator-activated receptor γ coactivator-1ß mRNA levels in RAW264.7 cells, although myonectin did not affect these mitochondrial biogenesis parameters in mouse osteoblasts. In conclusion, the present study demonstrated that myonectin suppresses the differentiation and ALP activity in mouse osteoblasts. Moreover, myonectin suppressed osteoclast differentiation from mouse bone marrow and RAW264.7 cells partly through an inhibition of mitochondrial biogenesis.