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Oral microbiota are among the most diverse in the human body. More than 700 species have been identified in the mouth, and new sequencing methods are allowing us to discover even more species. The anatomy of the oral cavity is different from that of other body sites. The oral cavity has mucosal surfaces (the tongue, the buccal mucosa, the gingiva, and the palate), hard tissues (the teeth), and exocrine gland tissue (major and minor salivary glands), all of which present unique features for microbiota composition. The connection between oral microbiota and diseases of the human body has been under intensive research in the past years. Furthermore, oral microbiota have been associated with cancer development. Patients suffering from periodontitis, a common advanced gingival disease caused by bacterial dysbiosis, have a 2–5 times higher risk of acquiring any cancer compared to healthy individuals. Some oral taxa, especially <i>Porphyromonas gingivalis</i> and <i>Fusobacterium nucleatum</i>, have been shown to have carcinogenic potential by several different mechanisms. They can inhibit apoptosis, activate cell proliferation, promote cellular invasion, induce chronic inflammation, and directly produce carcinogens. These microbiota changes can already be seen with potentially malignant lesions of the oral cavity. The causal relationship between microbiota and cancer is complex. It is difficult to accurately study the impact of specific bacteria on carcinoma development in humans. This review focuses on the elucidating the interactions between oral cavity bacterial microbiota and cancer. We gather literature on the current knowledge of the bacterial contribution to cancer development and the mechanisms behind it.

BackgroundHuman papillomavirus (HPV) infections have been linked to a subset of oral and oropharyngeal cancers. However, little is known on the natural history of oral HPV infections. We designed the prospective Finnish HPV Family Study to assess the dynamics of HPV infections in parents and their infants. This study reports HPV genotype distribution and virus persistence in oral mucosa of the mothers.Materials and MethodsTotally, 324 pregnant women were enrolled at the 3rd trimester of pregnancy and followed-up for 6 years. Oral scrapings taken with a brush were collected and HPV-genotyping was performed with nested PCR and Multimetrix® test (Progen, Heidelberg, Germany). The predictors of persistent oral HPV species 7/9 infections were analyzed using generalized estimating equation models.ResultsThe point prevalence of oral HPV varied from 15% to 24% during the 6-year follow-up. Altogether, 18 HPV genotypes were identified either as single or multiple-type oral infections. HPV16 was the most prevalent type at 9.7%–18.4%, followed by HPV18, HPV6, and multiple infections. Altogether, 74 women had persistent oral HPV infection determined as at least two consecutive samples positive with the same HPV genotype. HPV16 and HPV6 were the two most frequent types to persist (76% and 9%) for a mean of 18.6 and 20.2 months, respectively, followed by multiple infections (8%) for 18.3 months. An increased risk for persistent oral HPV infection with species 7/9 was associated with being seropositive for low-risk (LR)-HPV-types at baseline, whereas the use of oral contraceptives and a second pregnancy during follow-up were protective. Clinical oral lesions were detected in 17% of these women, one-third of whom had persistent oral HPV-infections.ConclusionHPV16 and HPV6 were the most common genotypes in oral HPV-infections and were also most likely to persist. Use of oral contraceptives and a second pregnancy protected against oral HPV persistence.

Persistent high-risk human papillomavirus (HR-HPV) infection is the key event in the progression of HPV lesions, and more data are urgently needed on asymptomatic oral HPV infections in men. Asymptomatic fathers-to-be (n = 131, mean age 28.9 years) were enrolled in the cohort, sampled by serial oral scrapings at baseline and at 2-month, 6-month, 12-month, 24-month, 36-month, and 7-year follow-up visits to accomplish persistent and cleared HPV infections. HPV genotyping was performed using nested PCR and Multimetrix® assay. Covariates of persistent and cleared oral HPV infections were analysed using generalised estimating equation (GEE) and Poisson regression. Altogether, 17 HPV genotypes were detected in male oral mucosa point prevalence, varying from 15.1 % to 31.1 %. Genotype-specific HPV persistence was detected in 18/129 men the mean persistence time ranging from 6.0 to 30.7 months. History of genital warts decreased (p = 0.0001; OR = 0.41, 95 % CI 0.33-0.51) and smoking increased (p = 0.033, OR = 1.92, 95 % CI 1.05-3.50) the risk of persistent species 7/9 HPV infections. Of the 74 HPV-positive men, 71.6 % cleared their infection actuarial and crude clearance times, varying between 1.4 and 79.6 months. No independent predictors were identified for species 7/9 clearance. At the last follow-up-visit, 50.1 % of the fathers had oral mucosal changes, correlating only with smoking (p = 0.046). To conclude, most of the persisting oral infections in males were caused by HPV16. Smoking increased while previous genital warts decreased oral HR-HPV persistence. No predictors of HR-HPV clearance were disclosed.