Table 3.
Oral Bacteria and its Association With Diagnosis and Prognosis of HNSCC.
Bacterial Phylum/Genus/Species | Association in Diagnosis and Prognosis of Oral Cancer (Reference No.) |
---|---|
Veillonella, Fusobacterium, Prevotella, Porphyromonas, Actinomyces, Clostridium, Haemophilus, Enterobacteriaceae, and Streptococcus subspecies | Predictive diagnostic marker for premalignant lesion and OSCC51 |
Lactobacillus gasseri: Lactobacillus johnsonii, Lactobacillus vaginalis, Lactobacillus fermentum, Lactobacillus salivarius, and Lactobacillus rhamnosus OTUs | Increased in higher TNM stage of HNSCC55 |
Streptococcus salivarius: Streptococcus vestibularis, Fusobacterium nucleatum, Prevotella oris, and Rothia mucilaginosa were highly abundant in saliva samples of HNSCC. Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans, and Streptococcus mutans were positively related with risk of HNSCC. Fusobacterium periodonticum, Fusobacterium naviforme, F nucleatum_subspecies, Peptostreptococcus stomatis, Parvimonas micra and Eikenella corrodens were significantly enriched in oral cancer |
Predictive diagnostic marker for HNSCC. P gingivalis, Prevotella intermedia, A actinomycetemcomitans, and F nucleatum are responsible produce volatile sulfur compounds VSCs such as genotoxic and mutagenic agent hydrogen sulfide (H2 S) in oral cavity and methyl mercaptan (CH3SH) in the gingival pockets that induce chronic inflammation, cell proliferation, migration, invasion and tumor angiogenesis63 |
Pseudomonas aeruginosa | Inflammation in carcinogenesis induces DNA breaks in epithelial cells that drive chromosomal instability, LasI factor, secreted from P aeruginosa, down regulates the expression of E-cadherin that induces invasion and metastasis65 |
Abundance level of genus Parvimonas | Significantly reduced in low grade (T0-T2) tumor as compared to high grade tumor (T3-T4)60 |
Abundance level of the genus Actinomyces | Significantly increased in low grade (T0-T2) tumor as compared to high grade tumor (T3-T4)60 |
Streptococcus, Actinomyces, Corynebacterium, Enterococcus, Micrococcus and R mucilaginosa | Significantly increased in the tongue tumor tissues57 |
Level of Streptococcus, Haemophilus, Porphyromonas, and Actinomyces | Significantly decreased with the progression of OSCC57 |
Abundant level of F periodonticum, P micra, Streptococcus constellatus, Haemophilus influenza, and Filifactor alocis | Progressively increased from stage 1 to stage 4 of OSCC patients; used as biomarkers for early detection and tracking for the development of OSCC. F alocis induces secretion of pro-inflammatory cytokine and induces apoptosis of gingival epithelial cells through activation of MEK ½ and caspase 3. F alocis modulates host cell response through activation of oncogenes74 |
Neisseria elongata, E corrodens, Oribacterium sp. oral taxon 102, and Dialister pneumosintes | Biomarker for stage 4 of OSCC patients. Due to high alcohol dehydrogenase (ADH) activity, Neisseria produce more acetaldehyde than Streptococcus subspecies, Stomatococcus subspecies, or Moraxella subspecies. Neisseria may play an essential role in alcohol-related oral carcinogenesis62 |
Corynebacterium and Kingella | Involved in xenobiotic biodegradation and metabolism pathways that are capable to metabolize several toxicants found in cigarette smoke67 |
Actinomyces, Granulicatella, Oribacterium, and Campylobacter genera as well as Veillonella dispar, R mucilaginosa, and Haemophilus parainfluenzae | Enriched in patients with HPV-positive cancer64 |
Streptococcus anginosus, Peptoniphilus, and Mycoplasma | Decreased in HPV-positive cancers64 |
Streptococci such as S gordonii, S mitis, S oralis, S salivarius, S sanguinis | Possess the enzyme alcohol dehydrogenase (ADH), which metabolizes alcohol to carcinogenic acetaldehyde which induces development of oral cancer63 |
Abbreviations: HNSCC, head and neck squamous cell carcinoma; HPV, human papilloma virus; OSCC, oral squamous cell carcinoma; VSC, volatile sulfur compounds.