This study concerns the use of low-energy pulsed ultrasound as nondestructive photodynamic antimicrobial therapy for controlling dental plaque. We examined the antibacterial and bactericidal effects of low-energy pulsed ultrasound on mutans streptococci and its inhibitory effects on bacterial cell adhesion of Streptococcus mutans. The results indicated weak antibacterial and bactericidal effects. However, ultrasonic stimulation for less than 20 min markedly decreased bacterial cell adhesion. To analyze the mechanism underlying the inhibitory effect, we examined cell surface protein antigen C (PAc) and glucosyltransferase I (GTF-I) expression in S. mutans. The levels of PAc gene and protein expression were markedly decreased by ultrasonic stimulation for 20 min. However, no change in GTF-I expression was observed. The expression of stress response heat shock proteins GroEL and DnaK was also examined. GroEL and DnaK levels were significantly decreased by ultrasonic stimulation, and the expression of the PAc protein was also diminished upon the addition of GroEL or DnaK inhibitors without ultrasonic stimulation. These observations suggest that the expression of the PAc protein in S. mutans may be dependent on heat shock proteins. Thus, low-energy pulsed ultrasound decreases bacterial adhesion by the inhibitory effect on the PAc protein and heat shock protein expression and may be useful as photodynamic antimicrobial chemotherapy in controlling dental plaque.

Previously, CD47 gene expression has been shown to increase during mandible development using a micro array technique. To determine the function of CD47 in osteoblasts, CD47 was silenced using siRNA in vitro. The TGF-β1 and phosphorylated-Smad2 levels and transcription factor genes related to bone metabolism increased dose-dependently with CD47 silencing. Furthermore, we determined the distribution of CD47 in mouse embryonic E13 and E15 in vivo. The CD47-positive cells were localized in Meckel's cartilage and antenatal mandibular bone. These results suggest that TGF-β1 signaling and mandible development might be regulated by CD47.