Effective oral care is a critical requirement to maintain high quality of life. Most oral diseases are caused by plaque (oral biofilm), which is also correlated with systemic diseases. A common method to remove biofilm is brushing teeth with a toothpaste. However, 3.5 billion people in the world have oral diseases, meaning that more efficient methods of removing biofilms are needed. We have developed a toothbrush applying bioelectric effect (BE) utilizing an electric force for biofilm removal. It demonstrated significantly higher biofilm removal efficiency than non-BE manual toothbrushes. Tests were performed in saline and toothpaste conditions using various pressure. Results showed that the BE toothbrush had a significantly higher biofilm removal efficiency in saline (0.5 N: 215.43 ± 89.92 %, 2.5 N: 116.77 ± 47.02 %) and in a toothpaste slurry (0.5 N: 104.96 ± 98.93 %, 2.5 N: 96.23 ± 35.16 %) than non-BE manual toothbrushes. Results also showed that BE toothbrushes were less dependent on toothpaste. This study suggests that the application of BE can be a new solution to plaque problems in oral care.

Alzheimer's Disease (AD) presents a significant challenge in the wake of its multifaceted nature, characterized by cognitive decline, memory impairment, and neuroinflammation. Despite extensive research, effective pharmacological interventions remain elusive, prompting exploration into non-pharmacological approaches. Microcurrent therapy (MC), utilizing imperceptible currents, has emerged as a potent clinical protocol. While previous studies have focused on its therapeutic effects, this study investigates its impact on neuronal damage and neuroinflammation in an AD mouse model, specifically addressing potential side effects. Utilizing 5xFAD transgenic mice, we examined the effects of MC therapy on neuronal integrity and inflammation. Our findings suggest that MC therapy attenuates memory impairment and reduces neurodegeneration, as evidenced by improved performance in memory tests and preservation of neuronal structure. Additionally, MC therapy significantly decreases amyloid-beta (Aβ) plaque deposition and inhibits apoptosis, indicating its potential to mitigate AD pathology. Our study discovered that MC therapy effectively reduces glial activation by inhibiting the TLR4-MyD88-NFκB pathway, consequently leading to decreased levels of inflammatory factors TNF-α, IL-1β, and IL-6, thus implicating TLR4 in neurodegenerative disease-related neuroinflammation. Furthermore, while our study did not observe significant adverse effects, further clinical trial into potential side effects and neuroinflammatory responses associated with MC therapy is warranted.