Linking oral microbiota to clinic air during ultrasonic scaling: Quantitative sequencing and CFD modeling reveal pathogenic aerosol emissions, infection risk, and control strategies.

Microbial aerosols from dental procedures pose a recognized yet unquantified airborne infection risk. During ultrasonic scaling, we performed multi-site sampling (saliva, air, surfaces) and combined metagenomics with quantitative 16S rRNA and ITS amplicon sequencing to profile viral, bacterial, and fungal communities. Using size-resolved aerosol sampling and absolute quantification, we determined the emission strength and size distribution of pathogenic bacterial aerosols (PBA), which were key inputs for computational fluid dynamics (CFD) simulations performed at ventilation velocities of 0.1, 0.2, and 0.4 m/s, corresponding to air exchange per hour (ACH) of 2.4, 4.7, and 9.4 h-1, respectively. We first linked patient oral microbiota to clinic aerosols, identifying a shared core of 51 viral, 55 bacterial, and 23 fungal families, of which three bacterial families (Streptococcaceae, Pasteurellaceae, Nocardiaceae) were pathogenic. The emission strength of PBA was ∼3.06 × 103 copies/min, with 66.7% concentrated in the 2.1∼4.7 μm fraction, a size associated with higher deposition in the lower respiratory tract. CFD simulations, fed with real pathogen concentrations and aerodynamic size spectra, revealed that increasing ACH from 0.1 to 0.4 m/s reduced PBA suspension (-26.4%) and surface deposition (-12.7%) during scaling, lowering the inhalation infection risk (IIR) at the dentist's position by 80.8% and keeping overall IIR below 25%. After scaling, lower velocity favours particle removal, supporting a dynamic ventilation strategy (high during treatment, low afterwards). This integrated framework provides a direct scientific basis for infection control in dental operatories.