This work explores the significance of toothbrushing in maintaining optimal oral health, delving into its benefits, proper techniques, and types of toothbrushes. The primary cause of caries, periodontal diseases, and halitosis is oral biofilm development. One of the most fundamental practices in maintaining oral health is toothbrushing. Studies have confirmed that mechanical procedures for controlling plaque and toothbrushing, in particular, significantly decrease plaque accumulation. The significance of teeth brushing in preventing dental caries has been well-acknowledged for a considerable period. Dentists recommend brushing twice daily for at least two min to ensure thorough cleaning. Unfortunately, precise guidelines from dental associations are often missing. Authors mention that two min of brushing are insufficient for significant plaque removal; plaque removal increases with augmented brushing time, with maximum removal at 180 s. Multiple studies have documented that engaging in the practice of brushing one’s teeth twice a day has a preventive impact. Various toothbrush designs, including both manual and electric options, have been created to improve the elimination of dental biofilm and reduce the accumulation and persistence of bacteria. In conclusion, toothbrushing is a simple yet incredibly important practice for maintaining oral health. The benefits extend beyond just a bright smile, encompassing caries, gum disease, halitosis prevention, and the preservation of tooth enamel. Adhering to proper toothbrushing techniques, selecting the right toothbrush, and understanding the connection between oral health and overall well-being can lead to a healthier life. To foster favorable toothbrushing behaviors among the population, dental practitioners and public health experts must know the factors that influence toothbrushing habits.

From a psychoneuroimmunology standpoint, stress and cigarette smoking are plausible modulators of periodontal inflammation through neuroendocrine–immune pathways and cytokine networks. Interleukin-18 (IL-1 family), interleukin-21 (common γ-chain cytokine), and interleukin-15 (tissue-resident lymphocyte activation/homeostasis) are mechanistically relevant candidates to characterize in relation to these exposures. We aimed to quantify serum IL-15, IL-18, and IL-21 and examine their associations with stress, smoking, and periodontal status in Mexican adults. Methods: Cross-sectional study (n = 65; 18–60 years; 70.8% female). Smoking status (23.1% smokers) and periodontal status were recorded; due to low periodontitis frequency (n = 3), periodontal status was analyzed as healthy (23.1%) versus periodontal disease (76.9%; gingivitis + periodontitis). Stress was assessed using the 18-item Symptomatic Stress Questionnaire and dichotomized as no/low stress (0–10; 52.3%) versus pathological stress (11–54; 47.7%). Systolic and diastolic blood pressure were recorded. IL-15, IL-18, and IL-21 were measured in serum by immunoassay. Analyses used medians (IQR), Mann–Whitney U tests with rank-biserial effect sizes, and exploratory Benjamini–Hochberg false discovery rate (FDR) adjustment across the nine primary cytokine-by-contrast tests; correlations with age and diastolic blood pressure were exploratory. Results: Cytokine distributions were right-skewed, particularly for IL-21. Across smoking, stress, and periodontal-status contrasts, no comparison met q < 0.05 after FDR adjustment. Effect-size patterns were heterogeneous rather than uniformly monotonic across exposures (e.g., IL-18 showed higher central tendency in healthy vs. periodontal disease; IL-21 showed higher central tendency in no/low stress vs. pathological stress), indicating substantial inter-individual variability in circulating cytokines within this cohort. Conclusions: In this exploratory cross-sectional sample, serum IL-15, IL-18, and IL-21 did not show robust, multiplicity-resistant differences by smoking, stress, or periodontal status. The findings provide a transparent description of distributional properties and hypothesis-generating patterns that motivate larger, longitudinal studies with repeated cytokine sampling, standardized periodontal assessment, and improved control of key confounders to clarify the relevance of these cytokines to periodontal inflammation under behavioral exposures.

Background/Objectives: Early childhood caries (ECC) remains a major public health concern, with Streptococcus mutans as a primary etiological agent. Current treatments rely on broad-spectrum antimicrobials, which can disrupt the oral microbiome and promote resistance. This study applied a structure-based in silico pipeline to identify molecule modulators of Toll-like receptor 2 (TLR2), a key host receptor implicated in ECC, and to explore their binding potential against major S. mutans proteins. Methods: ECC-related genes were collected from public databases and analyzed by functional enrichment and protein–protein interaction (PPI) network analysis. Hub genes were ranked using centrality algorithms. Virtual screening on TLR2 (DrugCLIP) was followed by molecular docking of selected compounds against the TLR1/TLR2 heterodimer and 50 S. mutans proteins, complemented by in silico absorption, distribution, metabolism, excretion, and toxicity (ADMET) profiling. Results: Fifty-four ECC-related genes and nine hub genes were identified, with TLR2 and cathelicidin antimicrobial peptide (CAMP) as central nodes. Virtual screening yielded five lead compounds fulfilling drug-likeness and toxicity criteria. Docking to TLR1/TLR2 showed favorable binding energies, with Z7684613096 showing the most consistent binding. V026-2549 displayed the highest number of strong interactions with S. mutans targets, including dTDP-glucose 4,6-dehydratase (rmlB), NADP-dependent glyceraldehyde-3-phosphate dehydrogenase (gapN), glucosyltransferase C (gtfC), and 5-methyltetrahydropteroyltriglutamate-homocysteine methyltransferase (metE). Conclusions: Five candidate compounds with promising dual activity against TLR1/TLR2 and S. mutans proteins were prioritized for experimental validation, including TLR2 functional assays and in vitro anti-biofilm studies.