The effect of long-term aspirin intake on the outcome of non-surgical periodontal therapy in smokers: a double-blind, randomized pilot study.

OBJECTIVE: The objective of this parallel, double-blind, randomized pilot study was to determine the effect of a daily dose of 325 mg of aspirin (ASA) on the clinical outcomes of scaling and root planing in a selected group of adult smokers. BACKGROUND: The response to periodontal therapy is inferior among smokers compared to non-smokers. Long-term intake of ASA has been shown to exert a positive impact on reducing both the prevalence and severity of periodontitis, among high-risk groups of subjects such as heavy smokers and diabetics. It is reasonable to assume that systemic administration of ASA in conjunction with reduction of the bacterial load by scaling and root planing may improve and prolong the benefits of periodontal therapy. To date, only few prospective interventional clinical studies have specifically addressed the periodontal needs of smokers. METHODS: The study includes 24 smokers. The following clinical parameters were measured preoperatively and at 3, 6, 9 and 12 mo postoperatively: (i) gingival index; (ii) plaque index; (iii) probing depth; (iii) probing attachment level; (iv) gingival recession; and (v) bleeding scores. Study subjects received scaling and root planing over several visits and were randomly assigned into two equal groups; a control group (C), which received a placebo and a test group (T), which took a daily dose of 325 mg ASA. No additional therapy was provided over the 1 year observation period. RESULTS: There were more statistically significant differences (p < 0.05; one- tailed) between pretest and posttest scores in the T group than in the C group. Mean percent increase in sites with probing depth 1-3 mm (T: 8.78; C: 7.21); mean percent reduction in sites with probing depth 4-6 mm (T: -7.25; C: -5.09 not statistically significant, NS); mean percent reduction in sites with probing depth ≥ 7 mm (T: -1.42; C: -02.09); mean percent reduction in sites with probing attachment level 3-4 mm (T: -3.63; C: 0.48 NS); mean percent reduction in sites with bleeding on probing (T: -12.37; C: -2.59 NS) (p < 0.05, NS). CONCLUSIONS: Daily intake of 325 mg of ASA following scaling and root planing improved treatment outcomes in smokers, without an increase in gingival bleeding tendency. ASA promoted a higher incidence of shallow pockets and more gain in attachment level.

SARS-CoV-2 infection of the oral cavity and saliva.

Despite signs of infection-including taste loss, dry mouth and mucosal lesions such as ulcerations, enanthema and macules-the involvement of the oral cavity in coronavirus disease 2019 (COVID-19) is poorly understood. To address this, we generated and analyzed two single-cell RNA sequencing datasets of the human minor salivary glands and gingiva (9 samples, 13,824 cells), identifying 50 cell clusters. Using integrated cell normalization and annotation, we classified 34 unique cell subpopulations between glands and gingiva. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral entry factors such as ACE2 and TMPRSS members were broadly enriched in epithelial cells of the glands and oral mucosae. Using orthogonal RNA and protein expression assessments, we confirmed SARS-CoV-2 infection in the glands and mucosae. Saliva from SARS-CoV-2-infected individuals harbored epithelial cells exhibiting ACE2 and TMPRSS expression and sustained SARS-CoV-2 infection. Acellular and cellular salivary fractions from asymptomatic individuals were found to transmit SARS-CoV-2 ex vivo. Matched nasopharyngeal and saliva samples displayed distinct viral shedding dynamics, and salivary viral burden correlated with COVID-19 symptoms, including taste loss. Upon recovery, this asymptomatic cohort exhibited sustained salivary IgG antibodies against SARS-CoV-2. Collectively, these data show that the oral cavity is an important site for SARS-CoV-2 infection and implicate saliva as a potential route of SARS-CoV-2 transmission.

Integrated Single-Cell Atlases Reveal an Oral SARS-CoV-2 Infection and Transmission Axis.

Despite signs of infection, the involvement of the oral cavity in COVID-19 is poorly understood. To address this, single-cell RNA sequencing data-sets were integrated from human minor salivary glands and gingiva to identify 11 epithelial, 7 mesenchymal, and 15 immune cell clusters. Analysis of SARS-CoV-2 viral entry factor expression showed enrichment in epithelia including the ducts and acini of the salivary glands and the suprabasal cells of the mucosae. COVID-19 autopsy tissues confirmed in vivo SARS-CoV-2 infection in the salivary glands and mucosa. Saliva from SARS-CoV-2-infected individuals harbored epithelial cells exhibiting ACE2 expression and SARS-CoV-2 RNA. Matched nasopharyngeal and saliva samples found distinct viral shedding dynamics and viral burden in saliva correlated with COVID-19 symptoms including taste loss. Upon recovery, this cohort exhibited salivary antibodies against SARS-CoV-2 proteins. Collectively, the oral cavity represents a robust site for COVID-19 infection and implicates saliva in viral transmission.

Assessment of the Effect of CO2 Laser Irradiation on the Reduction of Bacteria Seeded on Commercially Available Sandblasted Acid-Etched Titanium Dental Implants: An In Vitro Study.

PURPOSE: To evaluate the capability of carbon dioxide (CO2) laser in reducing Escherichia coli on sandblasted acid-etched (SAE) titanium dental implants. MATERIALS AND METHODS: SAE dental implants were contaminated with E coli, incubated in a sterile bacterial culture medium for 24 hours, and then exposed to CO2 laser (10,600-nm wavelength) in superpulsed waves (SPW) at 1.5, 1.7, and 2 W at 100-Hz frequency and continuous wave (CW) at 1.5, 2, and 2.5 W. The presence of bacteria trapped in the implant surfaces after contamination and decontamination was verified using spectrophotometry. Scanning electron microscopy (SEM) was used to evaluate the topography of laser irradiation. After implant surface contamination was verified, implants were exposed to CO2 laser irradiation, and bacterial growth was measured with spectrophotometry. RESULTS: The control implants showed the highest bacterial growth (100% growth). Implants exposed to laser showed progressive increase in the percentage of decontamination (DC%) corresponding to the higher wattage in the SPW and CW groups. The DC% were 20.4%, 49.6%, and 51.7% in the SPW group at 100 Hz, at 1.5, 1.7, and 2 W of power, respectively. In the CW group, the DC% were 34.3%, 69.9%, and 85.5% at 1.7, 2, and 2.5 W, respectively. Kruskal-Wallis statistical analysis showed a significant difference between the groups (P < .05). In the pulsed mode (100-Hz) group, statistical analysis showed that the DC% of 1.5 W was significantly lower than the 2 W power. In the CW group, statistical analysis showed that the DC% at 1.7 W was significantly lower (P < .05) than with the other treatments. SEM assessment showed craterlike wear damages and accretions to the implant surfaces that increased progressively as the laser wattage increased. CONCLUSION: CO2 laser irradiation failed to completely decontaminate the implant surfaces. SEM analysis demonstrated damage to the top of the dental implant threads at all settings studied. Thus, CO2 laser irradiation may not be the optimal method to decontaminate implants.