Background There is no conclusive evidence regarding a causal relationship between periodontitis and atherosclerosis. In this study, we examined the microbiome in the oral cavity and atheromatous plaques from atherosclerosis patients with or without periodontitis to investigate the role of oral bacteria in the formation of atheromatous plaques. We chose four patients with and without periodontitis, who had undergone carotid endarterectomy. Bacterial samples were extracted from saliva on the tongue surface, from periodontal pocket (during the oral examination), and from the atheromatous plaques. We investigated the general and oral conditions from each patient and performed next-generation sequencing analysis for all bacterial samples. Results There were no significant differences between both groups concerning general conditions. However, the microbiome patterns of the gingival pocket showed differences depending on the absence or presence of periodontitis, while those of the saliva were relatively similar. The microbiome pattern of the atheromatous plaques was entirely different from that in saliva present on the tongue surface and gingival pocket, and oral bacteria were seldom detected. However, the microbiome pattern in atheromatous plaques was different in the presence or absence of periodontitis. Conclusion These results indicated that oral bacteria did not affect the formation of atheromatous plaques directly. However, the metabolic products of microbiome or the host inflammatory response might indirectly influence the composition of atheromatous plaques.
Key Clinical MessageOral bacteria cause infective endocarditis (IE), so severe periodontitis is thought to be high risk for IE. We suggest the identification of high‐risk patients by an IgG antibody titer test against periodontal bacteria might become common screening test.
Purpose:We recently reported frequent detection of antibiotic-resistant bacteria on the oral mucosa during the period of hematopoietic cell transplantation (HCT), and suggested an association between oral mucositis and antibiotic-resistant bacterial infection. Methicillin-resistant Staphylococcus spp. were frequently detected, and the oral cavity may be a reservoir of the gene mediating methicillin resistance, mecA. Here, we examined the frequency of mecA carriers in patients undergoing HCT.
Methods:Fifty-nine patients (M: 37, F: 22, 47.3 ± 11.0 y) receiving HCT were enrolled in this study. Buccal swab samples were obtained 4 times from day -7 to day +20 (once/week), and mecA was detected by PCR. Fifty-two subjects without systematic disease, who completed dental treatment, especially periodontal treatment (M:21, F:31, 55.4 ± 14.2 y) were also enrolled as controls, and checked for mecA on the oral mucosa.
Results:Seventy-six percent (45/59) of HCT patients carried mecA at least once in the study period (day -7 to +20), while no control subjects had mecA. The frequency of mecA carriers was 19.2% from day -7 to -1, while it was significantly increased on 4 days +7 to +13 and +14 to +20, with frequencies of 60.9% and 63.2%, respectively (P < 0.01, ANOVA).
Conclusions:mecA was detected in oral mucosa of patients undergoing HCT. The high detection frequency of staphylococci resistant to penicillin and beta-lactams in our recent report was supported.
Key Clinical Message
Taste alteration is one of the complications of severe diabetes. It is important in diabetes treatment to assess taste alteration and perform dietary counseling, therapeutic exercise, and oral care. In this case, multidisciplinary clinical approach by medical staff was successful for a severely diabetic patient with dysgeusia.
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