Efficacy of hard gummy candy chewing in improving masticatory function in Japanese children aged 6-12 years: a clinical trial.

OBJECTIVES: Japanese children have been shown to exhibit decreased masticatory function; however, limited evidence is available regarding the efficacy of certain food items in improving this issue. Therefore, this study examined the effects of chewing hard gummy candy on the masticatory function of Japanese children aged 6-12 years. METHODS: The study included 26 participants (10 boys and 16 girls; mean age ± standard error = 9.3 ± 0.3 years) who were asked to chew hard gummy candy twice daily for 4 weeks at home. The lip-closing force, occlusal force, and masticatory performance of the participants were recorded before commencement (T1), 4 weeks after commencement (T2), and 4 weeks after completion (T3) of the training. Statistical analyses were performed using the Wilcoxon rank-sum test or the Wilcoxon signed-rank test with Bonferroni correction. RESULTS: No correlation was observed between masticatory function and sex at T1. The lip-closing and right occlusal forces increased significantly after 4 weeks of exercise, and the effects persisted for another 4 weeks after completion. The masticatory performance also improved after training, although these effects did not persist and deteriorated substantially 4 weeks after completion of the training. CONCLUSIONS: Habitual mastication training using hard gummy candy markedly enhances masticatory function (e.g., lip-closing force, occlusal force, and masticatory performance) in Japanese children.

Extracellular poly(ADP-ribose) is a neurotrophic signal that upregulates glial cell line-derived neurotrophic factor (GDNF) levels in vitro and in vivo.

Synthesis of poly(ADP-ribose) (PAR) is catalyzed by PAR polymerase-1 (PARP-1) in neurons. PARP1 plays a role in various types of brain damage in neurodegenerative disorders. In neurons, overactivation of PARP-1 during oxidative stress induces robust PAR formation, which depletes nicotinamide adenine dinucleotide levels and leads to cell death. However, the role of the newly-formed PAR in neurodegenerative disorders remains elusive. We hypothesized that the effects of PAR could occur in the extracellular space after it is leaked from damaged neurons. Here we report that extracellular PAR (EC-PAR) functions as a neuroprotective molecule by inducing the synthesis of glial cell line-derived neurotrophic factor (GDNF) in astrocytes during neuronal cell death, both in vitro and in vivo. In primary rat astrocytes, exogenous treatment with EC-PAR produced GDNF but not other neurotrophic factors. The effect was concentration-dependent and did not affect cell viability in rat C6 astrocytoma cells. Topical injection of EC-PAR into rat striatum upregulated GDNF levels in activated astrocytes and improved pathogenic rotation behavior in a unilateral 6-hydroxydopamine model of Parkinson disease in rats. These findings indicate that EC-PAR acts as a neurotrophic enhancer by upregulating GDNF levels. This effect protects the remaining neurons following oxidative stress-induced brain damage, such as that seen with Parkinson disease.