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.

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.

Atherosclerotic coronary artery disease (ACAD) is a major cause of global morbidity and mortality, characterized as an inflammatory process due to damage to blood vessel walls by risk factors like aging, hyperlipidemia, hypertension, smoking, and diabetes. Infectious agents, including Chlamydia pneumoniae (Cpn), Cytomegalovirus (CMV), and Helicobacter pylori (HP), have been implicated in ACAD’s pathophysiology. A study with 56 subjects undergoing coronary artery bypass grafting (CABG) aimed to detect Cpn, CMV, and HP DNA in unaffected artery segments and explore associations with disease progression and inflammation markers. The study found infectious agents’ DNA in 21.4% of samples, HP in eight samples, and CMV and Cpn in four samples each. Significant correlations were observed between HP and overweight or obese subjects, as well as between the presence of infectious agents and inflammation marker values. An association between HP and renal function was also noted. The findings reaffirm previous discoveries of infectious agents in non-clinically affected arteries used as CABG grafts. Correlations identified between the presence of HP, CMV, and Cpn DNA in grafts and several biomarkers of inflammation and obesity emphasize the potential role of these infectious agents in ACAD pathogenesis.

Background/Aim: The objective of the study was to compare cytological diagnoses using transepithelial cytology (oral brush biopsy) with histopathological diagnoses obtained by incisional biopsy in patients with benign lesions, oral potentially malignant disorders and oral squamous cell carcinoma. Material and Methods: The study included 57 patients. Brush biopsy was performed after local anaesthesia administration using the cervical brush. It was immediately followed by an incisional biopsy. Modified Bethesda System was used for cytological analysis and correlated with histopathological diagnoses according to intraepithelial neoplasia. Results: Good agreement was shown between cytological and histopathological diagnosis (kappa = 0.791). The sensitivity of the study was 92.85%, specificity 100%, positive predictive value (PPV) was 100% and negative predictive value (NPV) 93.54%. Conclusions: Oral brush biopsy, which allows the collection of epithelial cells of all layers can provide fast, precise and efficient cytological results which are in good agreement with the 'gold standard' - incisional biopsy followed by histopathology.

Background: Oral squamous cell carcinoma (OSCC) has increasingly been associated with oral microbiota and chronic periodontal inflammation. While major periodontal pathogens have been extensively studied, the role of Capnocytophaga gingivalis (C. gingivalis) in oral carcinogenesis remains unclear. This study investigated the prevalence and quantified the presence of C. gingivalis in benign oral lesions, oral potentially malignant disorders (OPMDs), and OSCCs, as well as its association with carcinogenesis-related gene expression. Methods: Ninety patients with periodontitis were included: 30 with benign lesions, 30 with OPMDs, and 30 with OSCCs. C. gingivalis quantification was performed using qPCR, while relative expression of VEGF, Cyclin D1, PIK3CA, DUSP16, mTOR, and MAPK14 was analyzed by RT-qPCR. Results: C. gingivalis was detected in 2 benign lesions, 11 OPMDs, and 18 OSCC samples (p < 0.001). Overall bacterial burden was significantly higher in OPMD and OSCC groups compared to benign lesions (p = 0.001). Expression of PIK3CA and MAPK14 was significantly increased in the OPMD and OSCC groups. In OSCC samples, C. gingivalis abundance positively correlated with VEGF and Cyclin D1 expression. Conclusions: C. gingivalis showed progressively increased prevalence and abundance across examined lesions and was associated with altered expression of genes involved in carcinogenesis, supporting its potential role in OSCC progression.