Sulforaphene (SFE) is a common nutritional supplement with antibacterial, anti-cancer, and anti-inflammatory effects. However, the effects of SFE on the cariogenicity of Streptococcus mutans and dental caries have not been reported. The objectives of this study were to investigate the caries-controlling potential of SFE. The effects of SFE on S. mutans were investigated using the broth microdilution method, crystal violet staining, SEM observation, acid tolerance assays, lactic acid quantification, and polysaccharide measurements. A rat caries model was established to evaluate the caries-controlling effects and biocompatibility of SFE in vivo. SFE inhibited S. mutans growth and biofilm formation. Furthermore, SFE restrained the cariogenic properties of S. mutans, including its acid production, acid tolerance, and extracellular polysaccharide production, without affecting the bacterial viability at sub-inhibitory levels. In the rat caries model, SFE significantly arrested the onset and development of dental caries. Moreover, no visible hemolytic phenomenon or cytotoxicity was detected in the SFE groups. After four weeks of SFE treatment, all rats remained in apparent good health with no significant differences in weight gain; their hemogram and biochemical parameters were normal; no pathological changes were observed in the oral mucosa, liver, or kidneys. In conclusion, SFE was safe and inhibited the development of caries effectively.

Aim: Periodontitis, a highly prevalent chronic inflammatory disease, progressively destroys tooth-supporting tissues, ultimately leading to tooth loss, and significantly increases systemic risks such as cardiovascular disease and diabetic complications. Current mechanical therapies effectively control clinical symptoms but fail to eradicate pathogenic microenvironments or restore periodontal homeostasis. Mitochondrial dysfunction is a critical driver of periodontitis progression; however, the regulatory mechanisms of mitochondria-related genes remain poorly defined. Materials and Methods: This study integrated bulk transcriptome sequencing (bulk RNA-seq) and single-cell RNA-seq (scRNA-seq) analyses to identify mitochondrial dysfunction-associated immune cell alterations in periodontitis. Key mitochondria-related genes inducing disease progression were pinpointed through non-negative matrix factorization (NMF) and weighted gene coexpression network analysis (WGCNA). By integrating ten machine learning algorithms with experimental validation using real-time quantitative polymerase chain reaction (qPCR) and immunofluorescence, peroxiredoxin 4 (PRDX4) was identified as the most crucial hub gene governing mitochondrial homeostasis in periodontitis. Results: Patient stratification based on PRDX4 expression revealed upregulated B cell-related pathways. Pseudotime analysis demonstrated a synchronized upregulation of PRDX4 and B cell signature genes during late-stage disease progression. scRNA-seq and immunofluorescence confirmed PRDX4 upregulation in B cells, particularly in plasma cells and memory B cells, and indicated its involvement in B cell differentiation. Experiments in a mouse model further validated the conserved functional role of PRDX4 in regulating B cells during periodontitis. Finally, we screened traditional Chinese medicinal compounds and identified aloe as a potential PRDX4 inhibitor. Conclusion: These findings establish PRDX4 as a key regulatory node linking mitochondrial dysfunction to periodontitis pathogenesis, providing insights into mitochondria-related genes and potential therapeutic strategies.

Mitochondrial dysfunction contributes to Porphyromonas gingivalis (P. gingivalis)-impaired endothelial function. Given the critical role of the mitochondrial permeability transition pore (mPTP) in mitochondrial homeostasis, this study explored how P. gingivalis promotes dynamin-related protein 1 (Drp1)–dependent mPTP overactivation, leading to mitochondrial damage and endothelial dysfunction. Mitochondrial and endothelial functions were evaluated in P. gingivalis–infected human aortic endothelial cells (HAECs) and C57BL/6 mice. Western blotting, immunofluorescence, and co-immunoprecipitation were used to assess the mitochondrial dynamics and mPTP-related protein interactions. Aortic vasodilation and endothelial integrity were examined following treatment with the Drp1 inhibitor Mdivi-1 or mPTP inhibitor cyclosporin A (CsA). P. gingivalis infection induced significant mitochondrial fragmentation, excessive mPTP opening, and impaired endothelium-dependent vasorelaxation. These changes were associated with enhanced p-Drp1 and its translocation to mitochondria. Mechanistically, P. gingivalis promoted voltage-dependent anion channel 1 (VDAC1) oligomerization in the out membrane of mitochondrial via p-Drp1 activation, which in turn disrupted the VDAC1–hexokinase 2 (HK2) interaction, facilitating mPTP opening. Inhibition of Drp1 and mPTP opening significantly alleviated mitochondrial dysfunction and restored endothelial function both in vitro and in vivo. P. gingivalis impairs endothelial function via Drp1–VDAC1–HK2–mediated mPTP overactivation, highlighting a potential therapeutic target against vascular injury in periodontal infection.

Journal of Clinical Pediatric Dentistry (JOCPD) is an international, peer-reviewed, open access journal, which is currently indexed in SCIE, etc., aming to provide clinically relevant information to enable the practicing dentist to have access to the state of the art in pediatric dentistry.