Dysbiosis in the oral environment may play a role in the etiopathogenesis of oral squamous cell carcinoma (OSCC). This review aims to summarize the current knowledge about the association of oral microbiota with OSCC and to describe possible etiopathogenetic mechanisms involved in processes of OSCC development and progression. Association studies included in this review were designed as case–control/case studies, analyzing the bacteriome, mycobiome, and virome from saliva, oral rinses, oral mucosal swabs, or oral mucosal tissue samples (deep and superficial) and comparing the results in healthy individuals to those with OSCC and/or with premalignant lesions. Changes in relative abundances of specific bacteria (e.g., Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus sp.) and fungi (especially Candida sp.) were associated with OSCC. Viruses can also play a role; while the results of studies investigating the role of human papillomavirus in OSCC development are controversial, Epstein–Barr virus was positively correlated with OSCC. The oral microbiota has been linked to tumorigenesis through a variety of mechanisms, including the stimulation of cell proliferation, tumor invasiveness, angiogenesis, inhibition of cell apoptosis, induction of chronic inflammation, or production of oncometabolites. We also advocate for the necessity of performing a complex analysis of the microbiome in further studies and of standardizing the sampling procedures by establishing guidelines to support future meta-analyses.

Recurrent aphthous stomatitis (RAS) is the most common disease of the oral mucosa, and it has been recently associated with bacterial and fungal dysbiosis. To study this link further, we investigated microbial shifts during RAS manifestation at an ulcer site, in its surroundings, and at an unaffected site, compared with healed mucosa in RAS patients and healthy controls. We sampled microbes from five distinct sites in the oral cavity. The one site with the most pronounced differences in microbial alpha and beta diversity between RAS patients and healthy controls was the lower labial mucosa. Detailed analysis of this particular oral site revealed strict association of the genus Selenomonas with healed mucosa of RAS patients, whereas the class Clostridia and genera Lachnoanaerobaculum, Cardiobacterium, Leptotrichia, and Fusobacterium were associated with the presence of an active ulcer. Furthermore, active ulcers were dominated by Malassezia, which were negatively correlated with Streptococcus and Haemophilus and positively correlated with Porphyromonas species. In addition, RAS patients showed increased serum levels of IgG against Mogibacterium timidum compared with healthy controls. Our study demonstrates that the composition of bacteria and fungi colonizing healthy oral mucosa is changed in active RAS ulcers, and that this alteration persists to some extent even after the ulcer is healed.

Background: This pilot study aimed to investigate how fixed orthodontic appliances simultaneously applied on the upper and lower arches affect the oral environment in the medium term. Methods: The oral status of 30 orthodontic patients was evaluated using the number of decay-missing-filled teeth (DMFT), plaque (PI), and gingival indices (GI) before bonding of fixed orthodontic appliances (T0) and during the therapy (T1). Besides, the gingival crevicular fluid (GCF) and a dental plaque were collected. Samples were analyzed for selected Candida sp. and for 10 selected oral bacteria using mass spectroscopy and multiplex polymerase chain reaction, respectively. Results: In 60% of patients, deterioration of the oral status (demonstrated by the increase in PI) was recorded (p < 0.05). Moreover, the changes in PI correlated with those of GI (p < 0.001). At the T1 time point, the mean representation of Actinomyces sp. in the total prokaryotic DNA in GCF and dental plaque of individual patients increased compared to T0 (p < 0.05). The probability of finding any of the 7 selected periodontal bacteria combined with Candida sp. was 10 times higher in patients in whom PI deteriorated between T0 and T1 (p < 0.01). Conclusions: Changes in the oral microbial diversity and an increase in PI were observed in the medium term after bonding of orthodontic appliance. Our study highlights the importance of a complex approach in this type of research as the association between clinical characteristics and combined microbial parameters is higher than when evaluated separately.

Objective: Dental caries is one of the most frequent multifactorial diseases. Among the numerous factors influencing the risk of caries, genetics plays a substantial role, with heritability ranging from 40 to 60%. Gene variants affecting taste preference and glucose transport were recently associated with caries risk. The aim of this study was to analyze two common polymorphisms in the sweet taste receptor (TAS1R2) and glucose transporter (GLUT2) genes in children with dental caries and healthy controls in the Czech population. Methods: A total of 637 unrelated Caucasian children, aged 11-13 years, were included in this case-control study. One hundred and fifty-five subjects were caries-free (with decayed/missing/filled teeth, DMFT = 0) and 482 children were caries-affected (DMFT ≥ 1). The TAS1R2 (Ile191Val, rs35874116) and GLUT2 (Thr110Ile, rs5400) genotypes were determined using the 5′ nuclease TaqMan® assay for allelic discrimination. Results: Compared with subjects with the common Thr allele, carriers of the Ile allele of GLUT2 had significantly more frequently dental caries (p < 0.05, OR = 1.639, 95% CI: 1.089-2.466). Similarly, children with the Val allele for the TAS1R2 Ile191Val polymorphism were more frequently affected by caries than children who carried the Ile allele (p < 0.05, OR = 1.413, 95% CI: 1.014-1.969). In contrast, no significant associations between GLUT2 and/or TAS1R2 polymorphisms and fillings were found, but allele frequencies of the TAS1R2 variant were marginally significantly different between children with DMFT = 0 and DMFT ≥1 (p = 0.053, OR = 1.339, 95% CI: 0.996-1.799). However, no significant interaction between both genes and risk of dental caries was found. Conclusions: In conclusion, GLUT2 and TASR1 polymorphisms may influence the risk of caries in the Czech population.

Interleukin-17 contributes to the pathogenesis of type 1 diabetes mellitus (T1DM) and chronic periodontitis (CP). We analyzedIL-17A−197A/G andIL-17F+7488C/T polymorphisms in T1DM and CP and determined their associations with IL-17 production and occurrence of periopathogens. Totally 154 controls, 125 T1DM, and 244 CP patients were genotyped using 5′ nucleaseTaqMan®assays. Bacterial colonization was investigated by a DNA-microarray kit. Production of IL-17 afterin vitrostimulation of mononuclear cells by mitogens and bacteria was examined by the Luminex system. Although no differences in the allele/genotype frequencies between patients with CP and T1DM + CP were found, theIL-17A−197 A allele increased the risk of T1DM (P<0.05). Levels of HbA1c were significantly elevated in carriers of the A allele in T1DM patients (P<0.05). Production of IL-17 by mononuclear cells of CP patients (unstimulated/stimulated byPorphyromonas gingivalis) was associated withIL-17AA allele (P<0.05).IL-17Apolymorphism increased the number ofTannerella forsythiaandTreponema denticolain patients with CP and T1DM + CP, respectively (P<0.05).IL-17Agene variability may influence control of T1DM and the “red complex” bacteria occurrence in patients with CP and T1DM + CP. Our findings demonstrated the functional relevance of theIL-17Apolymorphism with higher IL-17 secretion in individuals with A allele.