Precise control of digital dental unit to reduce aerosol and splatter production: new challenges for future epidemics.

BACKGROUND: During dental procedures, critical parameters, such as cooling condition, speed of the rotary dental turbine (handpiece), and distance and angle from pollution sources, were evaluated for transmission risk of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), simulated by spiking in a plasmid encoding a modified viral spike protein, HexaPro (S6P), in droplets and aerosols. METHODS: To simulate routine operation in dental clinics, dental procedures were conducted on a dental manikin within a digital dental unit, incorporating different dental handpiece speeds and cooling conditions. The tooth model was immersed in Coomassie brilliant blue dye and was pre-coated with 100 µL water spiked-in with S6P-encoding plasmid. Furthermore, the manikin was surrounded by filter papers and Petri dishes positioned at different distances and angles. Subsequently, the filter papers and Petri dishes were collected to evaluate the aerosol splash points and the viral load of S6P-encoding plasmid in aerosols and splatters generated during the dental procedure. RESULTS: Aerosol splashing generated a localized pollution area extended up to 60 cm, with heightened contamination risks concentrated within a 30 cm radius. Significant differences in aerosol splash points and viral load by different turbine handpiece speeds under any cooling condition (P < 0.05) were detected. The highest level of aerosol splash points and viral load were observed when the handpiece speed was set at 40,000 rpm. Conversely, the lowest level of aerosol splash point and viral load were found at a handpiece speed of 10,000 rpm. Moreover, the aerosol splash points with higher viral load were more prominent in the positions of the operator and assistant compared to other positions. Additionally, the position of the operator exhibited the highest viral load among all positions. CONCLUSIONS: To minimize the spread of aerosol and virus in clinics, dentists are supposed to adopt the minimal viable speed of a dental handpiece with limited cooling water during dental procedures. In addition, comprehensive personal protective equipment is necessary for both dental providers and dental assistants.

Effect of Helicobacter pylori infection on chronic periodontitis by the change of microecology and inflammation.

Helicobacter pylori (H. pylori), a pathogen inducing peptic disease, is recently found to be binding to the progress of periodontitis. Most previous studies are case-controlled, and they investigate the risk of H. pylori infection in disease the development of while few studies evaluate the correlation between H. pylori and periodontal pathogens. Therefore, we investigated the correlation between H. pylori infection with periodontal parameters, periodontal pathogens and inflammation. The results indicated that patients with H. pylori showed significantly higher probing depth and attachment loss than those without (p < 0.05). Among 28 subgingival plaque samples from 14 patients, the frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum and Treponema denticola were significantly higher with H. pylori infection than those without H. pylori infection (p < 0.05). However, the frequency of Aggregatibacter actinomycetemcomitans was lower (p < 0.05). Furthermore, after human acute monocytic leukemia cell line (THP-1) was stimulated with cagA-positive standard strains (cagA+ H. pylori 26695), the expression of periodontitis-related molecules Wnt5a, interleukin 8 (IL-8), interleukin 6 (IL-6) and interferon gamma (IFN-γ) significantly increased (p < 0.05). Conversely, the expression of tumor necrosis factor alpha (TNF-α) was almost stable. Meanwhile, cagA+ H. pylori promoted significantly higher expression of IL-8 and Wnt5a than isogenic cagA mutants strains (cagA- H. pylori 26695) did. Taken together, our data suggested that H. pylori might promote the growth of some periodontal pathogens and aggravate the progress of chronic periodontitis.