Introduction: There is a known connection between periodontitis and atherosclerosis and the presence of periopathogens in blood vessels. However, changes of the oral microflora related to the aging process and its possible effects on atherosclerosis, have yet to be analyzed. The aim of this study was to assess temporal changes in the frequency of periodontal bacteria in the subgingival plaque and in atherosclerotic blood vessels of patients with atherosclerosis. Methodology:The study included 100 patients with atherosclerosis and periodontitis, divided into two groups, below and over 60 years of age. Clinical examinations were performedand subgingival plaque specimens were collected as well as biopsy specimens from the following arteries: coronary (34), carotid (29), abdominal (10), femoral (10), mammary (13) and iliac (4). Subgingival and artery specimens were subjected to PCR detection of 5 major periodontal pathogens: Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythensis (Tf) and Treponema denticola (Td). Results:Tf was the most and Td the least frequent bacteria in both age groups and in both types of samples. The frequencies of bacteria in subgingival versus atherosclerotic samples were: Tf (76%:53%), Pi (71%:31%), Pg (60%:38%), Aa (39%:14%) and Td (21%:6%). Only Aa and Pi showed a significant difference of prevalence between younger and older patients. The most colonized artery was a. coronaria, followed by a. carotis, a. abdominalis, a. mammaria, and a. femoralis. Conclusions: Patient’s age and the distance of a given blood vessel from the oral cavity influenced microbiological findings in the atherotic plaque.

The aim of this cross-sectional observational study was to compare the prevalence of different oral Candida spp. in patients with Type 2 Diabetes and chronic periodontitis in two oral sites: dorsal surface of the tongue and subgingival area. In order to determine subgingival areas as potential reservoirs of yeasts, this study aimed to find differences in the yeasts’ detection between the dorsum of the tongue, as the oral site most commonly inhabited with microorganisms, and subgingival samples. Additionally, potential predictors for the yeasts prevalence were determined. Subjects (N = 146) were divided into four groups: group A- healthy individuals without periodontitis, group B- healthy individuals with chronic periodontitis, group C- Type 2 Diabetes patients with good glycoregulation and Chronic periodontitis and group D- Type 2 Diabetes patients with poor glycoregulation and Chronic periodontitis. Samples were obtained from the tongue by swabbing. Subgingival plaque samples were taken by paper points and periodontal curette. Isolation and identification of different Candida spp. was done using ChromAgar medium. In addition, germ-tube production and carbohydrate assimilation tests were performed. The prevalence of Candida spp. was higher in diabetics with poor glycoregulation. The most frequently isolated species was Candida albicans followed by Candida glabrata and Candida tropicalis. In 15.6% of cases, Candida spp. was present in the subgingival area while absent on the tongue. Multivariate regression model showed that HbA1c was Candida spp. predictor for both locations. Our results confirmed that there are Candida spp. carriers among subjects with clinically healthy oral mucosa. Also, this study identified subgingival areas as potential reservoirs of these pathogenic species. Glycoregulation has been recognized as a positive predictor factor of Candida spp.

For decades, cancer risk has been explained mainly by local factors. However, emerging evidence shows that the oral microbiome acts as a systemic modifier of oncogenesis well beyond the head and neck. This review synthesizes clinical and mechanistic data linking dysbiotic oral communities, especially Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, to malignancies across gastrointestinal, respiratory, hepatobiliary, pancreatic, breast, and urogenital systems. We summarize organ-specific associations from saliva, tissue, and stool studies, noting the recurrent enrichment of oral taxa in tumor and peri-tumoral niches of oral, esophageal, gastric, colorectal, lung, pancreatic, liver, bladder, cervical, and breast cancers. Convergent mechanisms include the following: (i) persistent inflammation (lypopolysacharide, gingipains, cytolysins, and collagenases); (ii) direct genotoxicity (acetaldehyde, nitrosation, and CDT); (iii) immune evasion/suppression (TLR/NLR signaling, MDSC recruitment, TAN/TAM polarization, and TIGIT/CEACAM1 checkpoints); and (iv) epigenetic/signaling rewiring (NF-κB, MAPK/ERK, PI3K/AKT, JAK/STAT, WNT/β-catenin, Notch, COX-2, and CpG hypermethylation). Plausible dissemination along an oral–gut–systemic axis, hematogenous, lymphatic, microaspiration, and direct mucosal transfer enables distal effects. While causality is not yet definitive, cumulative data support oral dysbiosis as a clinically relevant cofactor, motivating biomarker-based risk stratification, saliva/stool assays for early detection, and microbiome-targeted interventions (periodontal care, antimicrobials, probiotics, and microbiota modulation) alongside conventional cancer control.

The purpose of this study was to detect Candida spp. on the tongue and in the subgingival sites in healthy and type 2 diabetes (T2D) patients with chronic periodontitis (CP), and to compare the accuracy of sampling methods. This study included 131 patients divided into four groups: healthy control (group A), nondiabetics + CP (Group B), diabetics with good metabolic control + CP (group C) and diabetics with poor glycoregulation + CP (Group D). Cotton swab samples from tongue and subgingival samples were obtained from each patient with help of sterile paper points and a sterile curette. Swab cultures were made on Sabouraud dextrose agar. The number of CFUs was counted. The sampling methods for subgingival plaque were compared by Receiving Operator Curve (ROC). The presence of Candida spp. on the tongue was statistically significant among groups (group D vs. others three groups: χ²: p < 0.005 for each group). Positive findings of subgingival Candida spp. did not differ among the groups. There were no significant differences in the quantification ofCandida spp., neither on the tongue, nor in the subgingival samples. 17.2% of diabetic patients revealed the presence ofCandida spp. in the subgingival samples, with negative finding on tongue. There was a significant difference in the sampling methods for subgingival plaque (p = 0.000). Candida spp. is more prevalent on the tongue of diabetics. The sampling of subgingival plaque by a sterile curette is more accurate than with paper points. Subgingival plaque may represent a reservoir of commensals. It is necessary to standardize the sampling of subgingival plaque.

Oral microbiome disruptions in periodontitis are related to the chronic inflammatory reactions that could in turn lead to the development of multiple oral diseases. The objective of the study was to assess the frequencies of Streptococcus mitis, Prevotella melaninogenica, and Prevotella intermedia in oral benign lesions, oral potentially malignant disorders (OPMDs), and oral squamous cell carcinomas (OSCCs) and investigate the impact of these bacteria on the expression patterns of the selected (potential) target genes (PI3CA/AKT2/mTOR, DUSP16/MAPK14, and COX2). After sample collection (25 benign lesions, 30 OPMDs, and 35 OSCCs) and DNA/RNA extraction, quantitative real-time polymerase chain reaction (qPCR) was performed to detect bacterial presence and assess relative gene expression levels in different lesion groups. Prevotella melaninogenica was the most prevalent of the three analyzed bacteria, with the frequency being 60% in benign lesions, 87% in OPMDs (p = 0.024), and 77% in OSCC. The OPMD tissues in which Prevotella melaninogenica was present exhibited a higher expression level of AKT2 (p = 0.042). Significantly lower expression of DUSP16 was observed in OSCC tissues containing Streptococcus mitis (p = 0.011). The obtained results indicate a substantial contribution of P. melaninogenica and Str. mitis in the pathogenesis of oral mucosal lesions, possibly via AKT2 upregulation and DUSP16 downregulation.