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Association of oral dysbiosis with oral cancer development (Review)

Giusy La Rosa, Giuseppe Gattuso, Eugenio Pedull� and 3 more

Oncology Letters · 2020 · Review

doi:10.3892/ol.2020.11441

Abstract

Oral squamous cell carcinoma (OSCC) is the leading cause of mortality for oral cancer. Numerous risk factors mainly related to unhealthy habits and responsible for chronic inflammation and infections have been recognized as predisposing factors for oral carcinogenesis. Recently, even microbiota alterations have been associated with the development of human cancers. In particular, some specific bacterial strains have been recognized and strongly associated with oral cancer development (Capnocytophaga gingivalis, Fusobacterium spp., Streptococcus spp., Peptostreptococcus spp., Porphyromonas gingivalis and Prevotella spp.). Several hypotheses have been proposed to explain how the oral microbiota could be involved in cancer pathogenesis by mainly paying attention to chronic inflammation, microbial synthesis of cancerogenic substances, and alteration of epithelial barrier integrity. Based on knowledge of the carcinogenic effects of dysbiosis, it was recently suggested that probiotics may have anti-tumoral activity. Nevertheless, few data exist with regard to probiotic effects on oral cancer. On this basis, the association between the development of oral cancer and oral dysbiosis is discussed focusing attention on the potential benefits of probiotics administration in cancer prevention.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 26, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

1Oral squamous cell carcinoma (OSCC) is the leading cause of death among all oral cancers. This tumor originates from the oral mucosa and accounted for over 350,000 new diagnoses and more than 175,000 recorded deaths worldwide in 2018. It was widely demonstrated that the development of tumors, including that of OSCC, is sustained by several risk factors and predisposing conditions such as fibers, chemicals, pesticides and heavy metals able to induce pro-oncogenic genetic and epigenetic alterations. Other factors, including oral injuries, inflammatory diseases, infections, and bacterial dysbiosis are now recognized as risk factors for cancer development.

2Regarding OSCC, it was demonstrated that its development is strictly influenced by host-related and lifestyle factors mainly represented by smoking, alcohol abuse, tobacco and tobacco-derivate chewing and oral virus infections (HPV). In addition, it was demonstrated that the combination of smoke, alcohol drinking and poor oral hygiene increase the risk of oral cancer onset due to chronic inflammation and infection which constitute the principal factors involved in cancer pathogenesis, influencing the resident microbiota that are involved in the homeostasis of the oral environment. Importantly, a precise distinction must be made between microbiota and microbiome: the former is comprised of all the bacteria species hosted within the oral cavity, while with the latter term is used to define the collective genomes of microorganisms inhabiting the oral mucosa.

3Oral microbiota changes are able to modulate the connection between oral bacteria and humans causing diseases. Oral microbiota seems to influence OSCC through the carcinogenetic modulation of cell metabolism (such as modifying the concentration of nutrients and vitamins), thereby promoting the production of different cytokines known to be involved in several pathological conditions.

4Over 600 bacterial species constitute the oral microbiota. However, the majority of these species are uncultivated. The availability of new sequencing technology allowed the identification of bacterial communities that harbor the oral cavity and that are involved in human health (Table I).

5Researchers have investigated the possible association between microbes and the alteration of physiological conditions. In this context, it was demonstrated that gut microbiota predisposes individuals for the development of different diseases including celiac disease, neurological disorders and blood pressure alterations. All these pathological conditions are involved in the development of severe health conditions mainly represented by neurovascular disorders, chronic degenerative diseases, and cancer. Among all cancers, oral cancer is particularly related with oral and gut microbiota composition as widely demonstrated. Among the different bacteria strongly associated with OSCC, Fusobacterium nucleatum, Porphyromonas gingivalis, and Prevotella intermedia are considered the most represented bacteria types. Moreover, other bacterial genera, such as Actinomyces, Clostridium, Enterobacteriaceae, Fusobacterium, Haemophilus, Porphyromonas, Prevotella, Streptococcus spp. and Veillonella are associated with pre-cancerous lesions and oral cancer. According to other studies, a high bacterial load of Prevotella melaninogenica, Streptococcus mitis and Capnocytophaga gingivalis are identifiable in saliva samples of OSCC patients (Table II).

6Although the association between some species and oral cancer was already established, the complexity of the relationship occurring between cancer and oral microbiota remains unexplained and cannot be limited to the evaluation of a single pathogen. Moreover, there are no concordant analytical protocols for the analysis of oral microbiota and microbiome. Therefore, it is difficult to establish oral cavity-associated microbial patterns in cancer patients and healthy subjects. Consequently, there is a lack of novel microbial biomarkers for the early identification of oral carcinoma.

7Previous findings demonstrated that a strong association between oral microbiota and oral cancer exists. Starting from this supposition, a number of studies focused on the prevention of neoplastic transformation and retardation of cancer progression by modulating the carcinogenic or protective microbiome. In this context, probiotics administration was recently considered a good cancer preventive strategy due to the immunological effects. The beneficial effects of lactic ferments and probiotics were identified in the 19th century by Dr Ilya Metchnikoff. Nevertheless, only in recent years have these products been widely used for the treatment of several diseases. Numerous studies have shown the potential positive effects of probiotics on cancer through several mechanisms that include immune modulation, the prevention of pathogen infections, inflammatory modulation, reduced cancer formation and metastatic process. To the best of our knowledge, few data have been generated about the effects of probiotics in oral cancer development. Of note, the results of a previous study demonstrated that the administration of Lactobacillus rhamnosus GG (LGG) was able to increase the effects of geniposide, an anticancer molecule tested on human oral squamous carcinoma cells (HSC-3), demonstrating the beneficial role of LGG as potential adjuvant of geniposide treatment.

8The aim of this review was to describe the scientific evidence collected during the years pertaining to oral microbiota and neoplastic transformation with special attention for OSCC. Finally, a brief overview on the anti-tumoral effect of probiotics and their applications in oral cancer was reported.

Impact of oral health dysregulation on oral cancer development

9Observational studies have shown a link among oral cancer and infrequent tooth brushing, infrequent dental visits and loss of or missing teeth. These findings, however, pertain only to non-smokers and non-drinkers. Another study revealed that periodontal illnesses are correlated with an increased risk for oral tumors. Furthermore, research performed on 51 tongue cancer patients and 54 normal controls cases revealed that chronic periodontal inflammation is a cancer risk factor. In addition, periodontitis patients showed an increased risk for OSCC compared to healthy controls. Another observational study conducted on a wide cohort of individuals in the USA investigated the use of dental care and oral cancer risk. The analysis of covariates and dental care appointments demonstrated that individuals with a dental appointment during the past 12 months had a lower (62%) oral cancer risk compared with subjects that had not used dental care procedures in the past year.

10According to these results, the research group of Börnigen et al analyzed the role of oral microbiome and its composition by analyzing the biological samples of 121 oral cancer patients and 242 healthy controls matched for age and sex. The multivariate analyses highlighted significant variations of the oral microbiome in subjects with poor dental hygiene, in smokers, and oral cancer patients. In particular, although the microbiome alterations in cancer patients were significant, the alterations were more evident after tooth loss. Therefore, findings of that study showed that both oral microbiome alterations and tooth loss constitute important risk factors for oral cancer development due to the molecular and microenvironmental changes occurring in the oral cavity after these events.

Possible mechanisms of carcinogenesis induced by dysbiosis

11The association between gut microbiota and gastric cancer is well known. However, the association between oral cancer and oral dysbiosis is not fully understood. Different mechanisms of action to elucidate the oral microbiota influence on cancer pathogenesis, including bacterial stimulation of chronic inflammation have been reported. This process causes the production of inflammatory mediators that can cause or facilitate mutagenesis, uncontrolled cell proliferation, angiogenesis and cell degeneration responsible for neurodegenerative disorders and cancer. In addition, bacteria are able to modulate cell proliferation through activation of the nuclear factor κB (NF-κB) and the inhibition of cell apoptosis promoting or inhibiting the development of several cancer types.

12Moreover, Pang et al specified that the integration of virus oncogenes into host genomes or the alteration of epithelial barrier integrity could promote genome instability and favor irreversible cellular damage. In this context, it is noteworthy that the complex interaction among microbiota, epithelial barriers, and inflammation could assume a key role in the carcinogenic process.

13Finally, it was recently demonstrated that microbiota and oral mucosa dysbiosis lead to the accumulation of different epigenetic alterations predisposing for neoplastic transformation (Fig. 1).

14Chronic inflammation. According to data reported in the literature, approximately 25% of human cancer shares chronic inflammation as a risk factor, indicating that inflammation is one of the most important hallmarks of cancer. Several processes including cell proliferation, angiogenesis, mutagenesis and oncogene activation may be caused or facilitated by chronic inflammatory mediators that alter the normal homeostasis of cells and tissues.

15Some anaerobic oral bacteria including Fusobacterium, Porphyromonas and Prevotella species are associated with periodontal diseases and lead to chronic inflammation. The inflammatory mediators secreted by bacterial cells are able to interact with the cells of different tissues inducing diffused inflammatory processes. Periodontal bacteria influence the paracrine production of different pro-inflammatory mediators, such as interleukins (IL-1, IL-6, IL-17, IL-23), tumor-necrosis factor-α (TNF-α), and proteinases able to deteriorate the extracellular matrix (MMP-8, −9 and −13). The increased production of these inflammatory proteins is responsible for several types of cancer and the overexpression of these proteins (especially IL-6 and MMP-9) predict for a worse prognosis and an aggressive tumor phenotype.

16The upregulation of cytokines and other inflammatory factors lead to the alteration of different molecular pathways, including metabolic pathways, responsible for the modulation of cell metabolism and proliferation. For example, RAGE protein expression changes significantly after periodontal diseases mediated by oral microbiota alterations, leading to carcinogenesis. Moreover, gram-negative bacteria release a pro-inflammatory lipopolysaccharide endotoxin (LPS) able to stimulate the production of IL1-β, IL-6 ant TNF-α by binding the TLR receptor of leucocytes. In particular, these inflammatory cytokines lead to the overexpression of other pro-inflammatory proteins stimulating the release of phospholipase A2, prostaglandins (PG) and acute phase proteins. Other studies demonstrated that high IL-1 levels favor a pro-angiogenetic microenvironment, supporting tumor spread. Simultaneously, IL-1 induces MMP-9, which has been associated with more aggressive phenotypes of carcinoma, higher invasiveness, and low patient survival.

17Other studies demonstrated that tumor spread is also sustained by the overexpression of IL-6, which in turn leads to the upregulation of matrix-metalloproteinases, adhesion molecules and endothelial leukocyte adhesion molecules. All these data showed that interleukins, and in particular IL-6, are strictly involved in neoplastic transformation. Besides interleukins, altered levels of TNF-α, mediated by the alteration of Wnt and NF-κB pathways, were associated with the development of tumors. These data further corroborate the importance of NF-κB in cancer. Indeed, NF-κB acts as an immunostimulant factor against neoplastic cells; however, its protein expression is increased in several cancers acting as an oncogene.

18The abovementioned evidence suggested that dysbiosis-associated cancer may rely on the abnormal activation of NF-κB. Thus, a fundamental role is played also by the immune system, which in the presence of pathogens stimulates the production of NF-κB.

19Oncogenic substances production. Numerous substances produced by bacteria have been suggested to possess a carcinogenic action. Bacterial metabolism leads to the production of sulfur compounds, acids and free radicals, mainly nitric and oxygen reactive species, able to induce pro-tumoral genetic damage. Furthermore, several bacteria have an alcoholic metabolism responsible for the production of acetaldehyde, which sustains neoplastic transformation.

20Regarding reactive oxygen species (ROS) and reactive nitrogen species (RNS), it is well established that alteration of NADPH oxidase and nitric oxide synthase (NOS) activity leads to the accumulation of these harmful substances which promote chronic inflammation and, as described in the above chapter, cancer development. Bacteria also play fundamental roles in these processes. Some peroxygenase oral microorganisms are involved in this process producing hydrogen peroxide (H2O2) and include Bifidobacterium adolescentis, Lactobacillus acidophilus, L. fermentum, L. jensenii, L. minutus, Streptococcus gordonii, S. mitis, S. oligofermentans, S. oralis, and S. sanguinis.

21Other oncogenic substances produced by oral bacteria are represented by sulfides and nitrosamines. Bacteria including Bacteroides and Firmicutes species are capable to ferment the host excessive protein into sulfides and nitrosamines. These harmful substances are able to induce DNA damage in the oncogene or onco-suppressor genes.

22In addition, oral microorganisms, including Bifidobacterium, Lactobacillus, Lactococcus, Leuconostoc, Pediococcus, Peptostreptococcus stomatis and Streptococcus produce several types of acids (lactic, acetic, butyric, isobutyric, isovaleric, and isocaproic acids), which reduce the environmental pH. These acids contribute to the establishment of an ideal tissue microenvironment favorable for cancer cell proliferation and metastatic spread.

23Other studies highlighted the importance of superoxide dismutase (SOD) activity and its expression through the analysis of microbiomes detected in cancer samples and normal mucosa of oral cancer patients. The SOD activity is fundamental for inhibiting the detrimental effects of O2.−. In particular, it was shown that in tumor samples the presence of Fe2+ reacts with H2O2 leading to the production of harmful reactive species that promote neoplastic transformation by inducing DNA mutations affecting key genes involved in the regulation of cell cycle.

24Yost et al reported that in cancer patients, both in tumor or normal sites, microbiome tryptophanase activities are a possible carcinogenetic mechanism. In particular, the higher metabolism of L-tryptophan to secondary metabolites (indole, pyruvate and ammonium) seems to be related to cancer development. In this context, the role of aryl hydrocarbon receptor (AHR) is fundamental. Similarly, other enzymes, such as glutamate dehydrogenase (GDH), are overexpressed in oral cancer patients and their imbalance may contribute to the alteration of the cellular redox state.

25Finally, as stated above, several oral microorganisms (S. gordonii, S. mitis, S. oralis, S. salivarius, S. sanguinis, and Candida yeasts are involved in alcohol metabolizing to acetaldehyde, which has a carcinogenic potential. All these bacteria constitute a risk for OSCC development due to their acetaldehyde production.

26Integrity alteration of epithelial barrier. In a recent review, Pang et al described the role of dysbiosis in the alteration of epithelial barriers in homeostasis and immune activation, as well as the relationship with carcinogenesis. Changes taking place in anatomic structure or in microbial composition and mucus production may lead to an epithelial barrier dysfunction and microenvironment alterations. The consequent imbalance between epithelia/microbiota are key factors both in infections and other microbial diseases, including tumor.

27Moreover, as aforementioned, pro-inflammatory conditions sustained by microbial alterations contribute to epithelial barrier alteration. According to Virchow (1881), the inflammatory events are linked to microbiota and cancer. In addition, inflammation may modify the bacteria population, favor microbial translocation and induce the growth of specific bacteria.

28Specific microbial metabolites (i.e., ROS and hydroxyl radical) and toxins [such as cytolethal distending toxin (CDT)] generate genomic damages inducing the neoplastic transformation of epithelial cells. Moreover, bacteria activate several signal transduction pathways through virulence genes, e.g., AvrA virulence factor. Another factor stimulated by bacteriocins and bacterial proteins is the transforming growth factor β (TGF-β), which induces abnormal cell proliferation.

29Furthermore, TGF-β plays a role as an immunomodulating factor inhibiting dendritic cells (DCs); T-receptor cells thus act as tumor-promoter factors. Notably, the mechanism of TGF-β signaling in promoting tumorigenesis is also associated with the dysregulated inflammation microenvironment actuated by microbiota.

Microbiota-induced epigenetic modulation

30It has been widely demonstrated that environmental factors, including diet, lifestyle habits, and natural compounds, are responsible for both genetic and epigenetic alterations predisposing the development of several diseases, and have beneficial effects in preventing the development of chronic-degenerative disorders. In particular, dietary intake and food consumption modulate several cellular and molecular processes acting in a multifactorial manner. Indeed, the consumption of specific food and nutrients may modulate inflammatory and cell cycle regulatory pathways to maintain the optimal cell homeostasis, preventing the development of diseases. On the contrary, imbalances of nutrient consumption and/or absorption lead to epigenetic changes associated with certain pathologies, including cancer. The way by which food and nutrient intake is able to influence the onset of certain pathologies remains to be determined. However, findings have shown how foods can change the individual's redox state, the oral and gut microbiota, the DNA methylation status and the alteration of microRNA (miRNAs) expression levels.

31In particular, the two latter epigenetic events are now been recognized as key mechanisms of neoplastic transformation and a plethora of diseases. In this context, recent studies have identified different miRNAs, a class of non-coding RNA of 20–22 nucleotides, associated with the development and progression of different tumors. In addition, numerous studies have demonstrated the presence of a dual relationship between microbiota and host microRNAs (miRNAs) and vice versa. Liu and co-workers showed that fecal miRNAs produced by epithelial cells and Hopx-positive cells were able to penetrate bacteria (F. nucleatum and E coli) modulating the gene expressions of bacteria and altering the microbiota composition and bacterial cell growth. These preliminary observations, obtained in Dicer1-deficient mice, allowed the researchers to conclude that fecal miRNAs exert an important role in the regulation of gut microbiota and microbiome suggesting their possible use as novel therapeutic strategies. Fecal miRNAs are not derived only from intestinal cells. Different studies demonstrated that fecal miRNAs can be derived from foods and can be absorbed by intestinal epithelia modulating the expression levels of host genes. These miRNAs are mainly planted exosome-derived miRNAs; however, several studies showed that milk-derived miRNAs play key roles.

32All these food-derived miRNAs can presumably interact with oral and gut microbiota. On this basis, exogenous miRNAs may act as bacterial small RNA to interfere with bacterial gene expression modulating the entire microbiome. However, further studies are needed to deepen the knowledge on interactions between host-miRNAs and oral/gut microbiota. On the other hand, even the microbiota resident in the oral and intestinal mucosa may modulate the expression of specific miRNAs, thus highlighting a dual relationship between miRNAs and microbiota and their ability to influence each other.

33One of the mechanisms by which microbiota alters the expression levels of host-epithelial miRNAs is the production of different metabolites leading to significant changes in host-cell metabolism resulting in the alteration of the gene and miRNA expressions. Pang et al investigated the association among dysbiosis, dysfunction of epithelial barrier and alteration of immune system to evaluate how dysbiosis stimulates carcinogenesis.

Oral bacteria with potential carcinogenetic activity

34According to Zhao et al, oral cancer samples exhibited more bacterial species compared to healthy individuals. Specifically, Catonella, Dialister, Filifactor, Fusobacterium, Parvimonas, Peptococcus and Peptostreptococcus are the most overexpressed bacteria in OSCC samples with previous periodontitis. Notably, the evaluation of Fusobacterium bacteria was proposed as a diagnostic criterium for OSCC. In particular, Fusobacterium nucleatum is responsible, not only for opportunistic infections, but it was recently associated with several kind of cancers.

35In addition, Yost et al performed a preliminary meta-transcriptomic study in order to analyze the oral microbiome in oral squamous cell carcinoma patients and establish the connection with the molecular features of this tumor. Authors of that study found increased expression levels of Fusobacteria transcripts in both tumor and peritumoral tissue samples when compared to healthy individuals. Interestingly, they also showed that Fusobacteria virulence factors may be involved in the pathogenesis of oral cancer. Outcomes of that study are in agreement with findings of Nagy et al who observed some oral bacteria correlated with keratinizing squamous cell carcinomas, including Fusobacterium sp. Moreover, Yang et al correlated the microbiome variations to cancer progression. The Fusobacteria abundance was significantly higher in oral cancer patients showing progression and these data were more evident in stage 4 patients (7.92%) compared to healthy controls (2.98%).

36Lim et al analyzed oral rinse to evaluate the microbiome variations and their correlation oral and head and neck cancers. Those authors identified a panel of bacteria (Capnocytophaga, Corynebacterium, Haemophilus, Oribacterium, Paludibacter, Porphyromonas, and Rothia) to discern oral cavity cancer patients (OCC), oropharyngeal cancer patients (OPC) and healthy subjects. On the basis of results obtained, the authors proposed the detection of these bacteria to predict the risk of OCC and OPC, reaching 100 and 90% sensitivity and specificity, respectively. The outcomes of that study are in agreement with previous studies that indicated Capnocytophaga gingivalis, Peptostreptococcus sp., Porphyromonas gingivalis, Prevotella sp., and Streptococcus sp. as the oral microorganism mostly associated with OSCCs.

37Yost and collaborators demonstrated that among various examined species, Capnocytophaga gingivalis was the more represented in non-tumoral sites. These contrasted results could be due to the different samples examined, as well as to the number of cases enrolled. Other bacteria associated with head, neck, and esophageal cancers were streptococci, of which Streptococcus anginosus represents the most important bacterium.

38Recently, Yang et al investigated the functional role of microbiota changes related to the genetic alterations observed in OSCC patients. The analysis of saliva samples demonstrated an imbalance in the oral cavity taxa showing a relative abundance of Bacteroidetes and Firmicutes in three different groups of oral cancer clustered according to the mutational status. Moreover, significant variations of microorganism diversity were highlighted through analysis of the three groups of patients. Based on these results, the authors proposed a possible association between mutation in OSCC and alteration of microbiota and microbiome. Differences in bacterial composition were also detected between precancerous lesions and cancer samples. The results of that study showed that salivary microbiota patterns were importantly modulated in the three analyzed groups. In particular, the genera Bacillus, Enterococcus, Parvimonas, Peptostreptococcus, and Slackia showed a predictive value for discrimination between precancerous and neoplastic lesions.

Anti-tumoral effects of probiotics

39In recent years, it was widely demonstrated that the consumption of healthy foods enriched with probiotic acid lactic bacteria has positive effects regarding tumor prevention. Probiotics are able to reduce the mutagenic effects of harmful substances while modulating the expression of proteins involved in cell proliferation, apoptosis, inflammation, or immune system activation. Several in vitro experiments performed on cancer cells showed that probiotics possess anti-proliferative and pro-apoptotic effects in these tumor models. Lee and co-workers demonstrated that the cytoplasmic elements of Bifidobacterium longum, L. acidophilus and L. casei exert anti-neoplastic effects in different tumor in vitro models. Besides these probiotics, Bacillus polyfermenticus, Lactobacillus acidophilus 606, LGG/Bb12, LGG/Bifidobacterium animalis subsp. lactis, and Lactobacillus rhamnosus GG possessed anti-neoplastic effects in colorectal cancer cell lines.

40Few data are available on the effects of probiotics on oral cancer. In a recent study, HSC-3 OSCC cell lines were used to determine the effects of Lactobacillus rhamnosus GG (LGG) in increasing the antiblastic effects of geniposide, a derivate of Gardenia jasminoides which in preclinical studies showed important anticancer effects. The results obtained by the authors showed that the combined treatment with geniposide and LGG increased the apoptotic rate of HSC-3 cells. In particular, in a synergistic manner, LGG intensified the antineoplastic action of geniposide, supporting the tentative use of this combined therapy also in clinical practice. In another study, Asoudeh-Fard et al demonstrated that Lactobacillus plantarum was able to inhibit and activate the MAPKs and PTEN pathways, respectively, playing a potential role in the regulation of cancer. Indeed, it is well known that PTEN and MAPKs are associated with the inhibition and the initiation of cancer development, respectively. Consequently, a possible use of L. plantarum for probiotics cancer therapy was proposed.

41In addition, Aghazadeh et al showed that Acetobacter syzygii strain secretions possess anticancer activity promoting the apoptosis induction in oral cancer cells. Interestingly, Acetobacter syzygii products were not involved in the alteration of homeostasis of the epithelial cell line. These findings seem to show the crucial role represented by the microorganism in controlling cancer development in oral tissues and encourage further investigations on the effect of probiotics on OSCC development.

Conclusions

42This review widely discussed how the dysregulation of oral microbiota and oral mucosa homeostasis may represent modifiable risk factors associated with the development of OSCC. In addition, it was shown that certain bacterial strains may play a protective role against oral neoplastic transformation suggesting the possible use of probiotics administration as novel preventive and therapeutic strategies. In this scenario, several species have been strongly correlated with oral carcinoma, such as Capnocytophaga gingivalis, Fusobacterium sp., Streptococcus sp., Peptostreptococcus sp., Porphyromonas gingivalis and Prevotella sp., due to the fact that these bacteria may promote inflammation, cell proliferation and the production of some oncogenic substances. Recent findings have shown that the evaluation of oral microbiota and microbiome may provide important information on oral cancer oncogenesis, outcome prediction and therapeutic response (including immunotherapy). In addition, thanks to the new high-throughput molecular technologies it was possible to define the precise composition and gene expression (microbiome) of oral bacteria in OSCC patients and normal controls identifying specific strains associated with an increased risk of OSCC development. Therefore, the analysis of circulating biomarkers (miRNAs, circulating DNA, specific proteins) represents a good approach for the assessment of oral cancer risk.

43In this respect, the use of probiotics that in appropriate amounts give a health benefit to the host, including anti-tumoral effects, could be useful to promote cancer therapies representing a new step of the evolution of anticancer pharmacological treatments. Although in vitro and in vivo experiments demonstrated the beneficial effects probiotics, few data are available about the efficacy of probiotics in oral cancer. It is reasonable to hypothesize that the beneficial effects exert by probiotics in intestinal and colorectal cancer is similar to those acted in the oral mucosa. Starting from this assumption, future studies are required to explore the involvement of oral microbiota and its relationship with oral cancer.

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Quigley EMM. Microbiota-brain-gut axis and neurodegenerative diseases. Curr Neurol Neurosci Rep. 2017;17:94.
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31.
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Vinciguerra L, Lanza G, Puglisi V, Pennisi M, Cantone M, Bramanti A, Pennisi G, Bella R. Transcranial Doppler ultrasound in vascular cognitive impairment-no dementia. PLoS One. 2019;14:e0216162.
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Impaired Cerebral Haemodynamics in Vascular Depression: Insights From Transcranial Doppler Ultrasonography · 2018
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34.
Lanza G, Cantone M, Musso S, Borgione E, Scuderi C, Ferri R. Early-onset subcortical ischemic vascular dementia in an adult with mtDNA mutation 3316G>A. J Neurol. 2018;265:968-969.
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Bordet R, Ihl R, Korczyn AD, Lanza G, Jansa J, Hoerr R, Guekht A. Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: A consensus report. BMC Med. 2017;15:107.
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Lanza G, Bramanti P, Cantone M, Pennisi M, Pennisi G, Bella R. Vascular cognitive impairment through the looking glass of transcranial magnetic stimulation. Behav Neurol. 2017;2017:1421326.
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Bella R, Cantone M, Lanza G, Ferri R, Vinciguerra L, Puglisi V, Pennisi M, Ricceri R, Di Lazzaro V, Pennisi G. Cholinergic circuitry functioning in patients with vascular cognitive impairment - no dementia. Brain Stimul. 2016;9:225-233.
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Pennisi M, Lanza G, Cantone M, Ricceri R, Spampinato C, Pennisi G, Di Lazzaro V, Bella R. Correlation between motor cortex excitability changes and cognitive impairment in vascular depression: Pathophysiological insights from a longitudinal TMS study. Neural Plast. 2016;2016:8154969.
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Lanza G, Papotto M, Pennisi G, Bella R, Ferri R. Epileptic seizure as a precipitating factor of vascular progressive supranuclear palsy: A case report. J Stroke Cerebrovasc Dis. 2014;23:e379-e381.
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Bella R, Ferri R, Pennisi M, Cantone M, Lanza G, Malaguarnera G, Spampinato C, Giordano D, Alagona G, Pennisi G. Enhanced motor cortex facilitation in patients with vascular cognitive impairment-no dementia. Neurosci Lett. 2011;503:171-175.
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Pennisi G, Ferri R, Cantone M, Lanza G, Pennisi M, Vinciguerra L, Malaguarnera G, Bella R. A review of transcranial magnetic stimulation in vascular dementia. Dement Geriatr Cogn Disord. 2011;31:71-80.
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Bella R, Pennisi G, Cantone M, Palermo F, Pennisi M, Lanza G, Zappia M, Paolucci S. Clinical presentation and outcome of geriatric depression in subcortical ischemic vascular disease. Gerontology. 2010;56:298-302.
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Atanasova KR, Yilmaz O. Looking in the Porphyromonas gingivalis cabinet of curiosities: The microbium, the host and cancer association. Mol Oral Microbiol. 2014;29:55-66.
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Hu X, Zhang Q, Hua H, Chen F. Changes in the salivary microbiota of oral leukoplakia and oral cancer. Oral Oncol. 2016;56:e6-e8.
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Risk factors for cancer of the oral cavity and oro-pharynx in Cuba · 2001
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Pennisi M, Lanza G, Cantone M, Schepis C, Ferri R, Barone R, Bella R. Unusual neurological presentation of nevoid basal cell carcinoma syndrome (Gorlin-Goltz Syndrome). J Clin Neurol. 2017;13:439-441.
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81.
Impact of the gut microbiome on the genome and epigenome of colon epithelial cells: contributions to colorectal cancer development · 2019
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82.
Chronic Inflammation in cancer development · 2012
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83.
Szkaradkiewicz AK. Karpiński TM: Microbiology of chronic periodontitis. J Biol Earth Sci. 2013;3:M14-M20.
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Leonardi R, Talic NF, Loreto C. MMP-13 (collagenase 3) immunolocalisation during initial orthodontic tooth movement in rats. Acta Histochem. 2007;109:215-220.
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85.
MMP-9 as a Candidate Marker of Response to BRAF Inhibitors in Melanoma Patients With BRAFV600E Mutation Detected in Circulating-Free DNA · 2018
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86.
High systemic IL-6 is associated with worse prognosis in patients with non-small cell lung cancer · 2017
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Kossakowska AE, Edwards DR, Prusinkiewicz C, Zhang MC, Guo D, Urbanski SJ, Grogan T, Marquez LA, Janowska-Wieczorek A. Interleukin-6 regulation of matrix metalloproteinase (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase (TIMP-1) expression in malignant non-Hodgkin's lymphomas. Blood. 1999;94:2080-2089.
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Haura EB, Turkson J, Jove R. Mechanisms of disease: Insights into the emerging role of signal transducers and activators of transcription in cancer. Nat Clin Pract Oncol. 2005;2:315-324.
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Karin M. NF-kappaB as a critical link between inflammation and cancer. Cold Spring Harb Perspect Biol. 2009;1:a000141.
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Hussain SP, Hofseth LJ, Harris CC. Radical causes of cancer. Nat Rev Cancer. 2003;3:276-285.
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Brauncajs M, Sakowska D. Krzemiński Z: Production of hydrogen peroxide by lactobacilli colonising the human oral cavity. Med Dosw Mikrobiol. 2001;53:331-336.
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Abranches J, Zeng L, Kajfasz JK, Palmer SR, Chakraborty B, Wen ZT, Richards VP, Brady LJ, Lemos JA. Biology of oral streptococci. Microbiol Spectr. 2018;6:6.
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110.
Microbial pathways in colonic sulfur metabolism and links with health and disease · 2012
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111.
Bhatt AP, Redinbo MR, Bultman SJ. The role of the microbiome in cancer development and therapy. CA Cancer J Clin. 2017;67:326-344.
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Karpiński TM, Szkaradkiewicz AK. Karpiński TM, Szkaradkiewicz AK: Characteristic of bacteriocines and their application. Pol J Microbiol. 2013;62:223-235.
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Acid tolerance properties of dental biofilms in vivo · 2017
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114.
Downes J, Wade WG. Peptostreptococcus stomatis sp. nov., isolated from the human oral cavity. Int J Syst Evol Microbiol. 2006;56:751-754.
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Lunt SJ, Chaudary N, Hill RP. The tumor microenvironment and metastatic disease. Clin Exp Metastasis. 2009;26:19-34.
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117.
Increased virulence of the oral microbiome in oral squamous cell carcinoma revealed by metatranscriptome analyses · 2018
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118.
Franco R, Schoneveld O, Georgakilas AG, Panayiotidis MI. Oxidative stress, DNA methylation and carcinogenesis. Cancer Lett. 2008;266:6-11.
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119.
Murray IA, Patterson AD, Perdew GH. Aryl hydrocarbon receptor ligands in cancer: Friend and foe. Nat Rev Cancer. 2014;14:801-814.
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Jin L, Li D, Alesi GN, Fan J, Kang HB, Lu Z, Boggon TJ, Jin P, Yi H, Wright ER, et al. Glutamate dehydrogenase 1 signals through antioxidant glutathione peroxidase 1 to regulate redox homeostasis and tumor growth. Cancer Cell. 2015;27:257-270.
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Marttila E, Bowyer P, Sanglard D, Uittamo J, Kaihovaara P, Salaspuro M, Richardson M, Rautemaa R. Fermentative 2-carbon metabolism produces carcinogenic levels of acetaldehyde in Candida albicans. Mol Oral Microbiol. 2013;28:281-291.
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Meurman JH, Uittamo J. Oral micro-organisms in the etiology of cancer. Acta Odontol Scand. 2008;66:321-326.
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Elinav E, Nowarski R, Thaiss CA, Hu B, Jin C, Flavell RA. Inflammation-induced cancer: Crosstalk between tumours, immune cells and microorganisms. Nat Rev Cancer. 2013;13:759-771.
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Arthur JC, Perez-Chanona E, Mühlbauer M, Tomkovich S, Uronis JM, Fan TJ, Campbell BJ, Abujamel T, Dogan B, Rogers AB, et al. Intestinal inflammation targets cancer-inducing activity of the microbiota. Science. 2012;338:120-123.
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White RA, Malkoski SP, Wang XJ. TGFβ signaling in head and neck squamous cell carcinoma. Oncogene. 2010;29:5437-5446.
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133.
Lanza G, Centonze SS, Destro G, Vella V, Bellomo M, Pennisi M, Bella R, Ciavardelli D. Shiatsu as an adjuvant therapy for depression in patients with Alzheimer's disease: A pilot study. Complement Ther Med. 2018;38:74-78.
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134.
Lanza G, Bella R, Cantone M, Pennisi G, Ferri R, Pennisi M. Cognitive impairment and celiac disease: Is transcranial magnetic stimulation a trait d'union between gut and brain? Int J Mol Sci. 2018;19:E2243.
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135.
Pennisi M, Bramanti A, Cantone M, Pennisi G, Bella R, Lanza G. Neurophysiology of the ‘Celiac Brain’: Disentangling Gut-Brain Connections. Front Neurosci. 2017;11:498.
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136.
Bella R, Lanza G, Cantone M, Giuffrida S, Puglisi V, Vinciguerra L, Pennisi M, Ricceri R, D'Agate CC, Malaguarnera G, et al. Effect of a gluten-free diet on cortical excitability in adults with celiac disease. PLoS One. 2015;10:e0129218.
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137.
Excitability of the motor cortex in de novo patients with celiac disease. · 2014
Not checked
138.
Pennisi M, Lanza G, Cantone M, Ricceri R, Ferri R, D'Agate CC, Pennisi G, Di Lazzaro V, Bella R. Cortical involvement in celiac disease before and after long-term gluten-free diet: A transcranial magnetic stimulation study. PLoS One. 2017;12:e0177560.
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139.
The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease · 2018
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140.
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Integrated analysis of colorectal cancer microRNA datasets: identification of microRNAs associated with tumor development · 2018
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156.
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157.
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158.
Microbiota Modulate Host Gene Expression via MicroRNAs · 2011
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159.
Peck BCE, Mah AT, Pitman WA, Ding S, Lund PK, Sethupathy P. Functional transcriptomics in diverse intestinal epithelial cell types reveals robust microrna sensitivity in intestinal stem cells to microbial status. J Biol Chem. 2017;292:2586-2600.
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160.
Yuan C, Subramanian S. MicroRNA mediated tumor-microbiota metabolic interactions in colorectal cancer. DNA Cell Biol. 2019;38:281-285.
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164.
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165.
Golan-Gerstl R, Elbaum Shiff Y, Moshayoff V, Schecter D, Leshkowitz D, Reif S. Characterization and biological function of milk-derived miRNAs. Mol Nutr Food Res. 2017;61:1700009.
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Wagner AE, Piegholdt S, Ferraro M, Pallauf K, Rimbach G. Food derived microRNAs. Food Funct. 2015;6:714-718.
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167.
Teng Y, Ren Y, Sayed M, Hu X, Lei C, Kumar A, Hutchins E, Mu J, Deng Z, Luo C, et al. Plant-derived exosomal micrornas shape the gut microbiota. Cell Host Microbe. 2018;24:637-652.e8.
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168.
Adami GR, Tangney CC, Tang JL, Zhou Y, Ghaffari S, Naqib A, Sinha S, Green SJ, Schwartz JL. Effects of green tea on miRNA and microbiome of oral epithelium. Sci Rep. 2018;8:5873.
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169.
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170.
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171.
Yuan C, Steer CJ, Subramanian S. Host-microRNA-microbiota interactions in colorectal cancer. Genes (Basel). 2019;10:E270.
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172.
Epigenetic Regulation at the Interplay Between Gut Microbiota and Host Metabolism · 2019
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173.
Patrignani P, Tacconelli S, Bruno A. Gut microbiota, host gene expression, and aging. J Clin Gastroenterol. 2014;48(Suppl 1):S28-S31.
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174.
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175.
Variations in oral microbiota associated with oral cancer · 2017
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176.
Inflammatory bacteriome featuring Fusobacterium nucleatum and Pseudomonas aeruginosa identified in association with oral squamous cell carcinoma · 2017
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177.
Cervical Microbiome and Cytokine Profile at Various Stages of Cervical Cancer: A Pilot Study · 2016
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178.
Increased Abundance of Clostridium and Fusobacterium in Gastric Microbiota of Patients with Gastric Cancer in Taiwan · 2018
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180.
Oral Microbiota Community Dynamics Associated With Oral Squamous Cell Carcinoma Staging · 2018
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181.
The Performance of an Oral Microbiome Biomarker Panel in Predicting Oral Cavity and Oropharyngeal Cancers · 2018
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182.
Sasaki M, Yamaura C, Ohara-Nemoto Y, Tajika S, Kodama Y, Ohya T, Harada R, Kimura S. Streptococcus anginosus infection in oral cancer and its infection route. Oral Dis. 2005;11:151-156.
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183.
Comparison of oral microbiota in tumor and non-tumor tissues of patients with oral squamous cell carcinoma · 2012
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184.
Galvão-Moreira LV, da Cruz MC. Oral microbiome, periodontitis and risk of head and neck cancer. Oral Oncol. 2016;53:17-19.
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185.
Shiga K, Tateda M, Saijo S, Hori T, Sato I, Tateno H, Matsuura K, Takasaka T, Miyagi T. Presence of Streptococcus infection in extra-oropharyngeal head and neck squamous cell carcinoma and its implication in carcinogenesis. Oncol Rep. 2001;8:245-248.
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Narikiyo M, Tanabe C, Yamada Y, Igaki H, Tachimori Y, Kato H, Muto M, Montesano R, Sakamoto H, Nakajima Y, et al. Frequent and preferential infection of Treponema denticola, Streptococcus mitis, and Streptococcus anginosus in esophageal cancers. Cancer Sci. 2004;95:569-574.
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187.
Yang SF, Huang HD, Fan WL, Jong YJ, Chen MK, Huang CN, Chuang CY, Kuo YL, Chung WH, Su SC. Compositional and functional variations of oral microbiota associated with the mutational changes in oral cancer. Oral Oncol. 2018;77:1-8.
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188.
Kumar M, Kumar A, Nagpal R, Mohania D, Behare P, Verma V, Kumar P, Poddar D, Aggarwal PK, Henry CJ, et al. Cancer-preventing attributes of probiotics: An update. Int J Food Sci Nutr. 2010;61:473-496.
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189.
Yu AQ, Li L. The potential role of probiotics in cancer prevention and treatment. Nutr Cancer. 2016;68:535-544.
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190.
Lee JW, Shin JG, Kim EH, Kang HE, Yim IB, Kim JY, Joo HG, Woo HJ. Immunomodulatory and antitumor effects in vivo by the cytoplasmic fraction of Lactobacillus casei and Bifidobacterium longum. J Vet Sci. 2004;5:41-48.
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191.
Ma EL, Choi YJ, Choi J, Pothoulakis C, Rhee SH, Im E. The anticancer effect of probiotic Bacillus polyfermenticus on human colon cancer cells is mediated through ErbB2 and ErbB3 inhibition. Int J Cancer. 2010;127:780-790.
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Kim Y, Oh S, Yun HS, Oh S, Kim SH. Cell-bound exopolysaccharide from probiotic bacteria induces autophagic cell death of tumour cells. Lett Appl Microbiol. 2010;51:123-130.
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193.
Borowicki A, Michelmann A, Stein K, Scharlau D, Scheu K, Obst U, Glei M. Fermented wheat aleurone enriched with probiotic strains LGG and Bb12 modulates markers of tumor progression in human colon cells. Nutr Cancer. 2011;63:151-160.
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194.
Stein K, Borowicki A, Scharlau D, Schettler A, Scheu K, Obst U, Glei M. Effects of synbiotic fermentation products on primary chemoprevention in human colon cells. J Nutr Biochem. 2012;23:777-784.
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195.
Wan LH, Yao Z, Ni F, Wei M, Zhou Z, Wang HQ, Sun Y, Zhong ZX. Biosynthesis of genipin from gardenoside catalyzed by β-glucosidase in two-phase medium. CIESC J. 2014;65:3583-3591.
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196.
Lactobacillus plantarum induces apoptosis in oral cancer KB cells through upregulation of PTEN and downregulation of MAPK signalling pathways · 2017
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197.
Aghazadeh Z, Pouralibaba F, Yari Khosroushahi A. The prophylactic effect of Acetobacter syzygii probiotic species against squamous cell carcinoma. J Dent Res Dent Clin Dent Prospects. 2017;11:208-214.
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199.
Current Perspectives in Cancer Immunotherapy · 2019
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200.
16S rRNA amplicon sequencing identifies microbiota associated with oral cancer, human papilloma virus infection and surgical treatment · 2016
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201.
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202.
Current and Future Trends on Diagnosis and Prognosis of Glioblastoma: From Molecular Biology to Proteomics · 2019
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203.
Ribeiro IP, de Melo JB, Carreira IM. Head and neck cancer: Searching for genomic and epigenetic biomarkers in body fluids - the state of art. Mol Cytogenet. 2019;12:33.
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204.
Evolution of Cancer Pharmacological Treatments at the Turn of the Third Millennium · 2018
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205.
Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE. Defining the normal bacterial flora of the oral cavity. J Clin Microbiol. 2005;43:5721-5732.
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206.
Chattopadhyay I, Verma M, Panda M. Role of oral microbiome signatures in diagnosis and prognosis of oral cancer. Technol Cancer Res Treat. 2019;18:1533033819867354.
Not in our library10.1177/1533033819867354

Cited by papers we hold 2

An Overview of Physical, Microbiological and Immune Barriers of Oral Mucosa · 2021
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The Oral Microbiome and Cancer · 2020
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