The periodontal diseases are highly prevalent and can affect up to 90% of the worldwide population. Gingivitis, the mildest form of periodontal disease, is caused by the bacterial biofilm (dental plaque) that accumulates on teeth adjacent to the gingiva (gums). However, gingivitis does not affect the underlying supporting structures of the teeth and is reversible. Periodontitis results in loss of connective tissue and bone support and is a major cause of tooth loss in adults. In addition to pathogenic microorganisms in the biofilm, genetic and environmental factors, especially tobacco use, contribute to the cause of these diseases. Genetic, dermatological, haematological, granulomatous, immunosuppressive, and neoplastic disorders can also have periodontal manifestations. Common forms of periodontal disease have been associated with adverse pregnancy outcomes, cardiovascular disease, stroke, pulmonary disease, and diabetes, but the causal relations have not been established. Prevention and treatment are aimed at controlling the bacterial biofilm and other risk factors, arresting progressive disease, and restoring lost tooth support.

At a workshop coordinated by the WHO Collaborating Centre for Oral Cancer and Precancer in the UK issues related to terminology, definitions and classification of oral precancer were discussed by an expert group. The consensus views of the Working Group are presented here. The term, ‘potentially malignant disorders’, was recommended to refer to precancer as it conveys that not all disorders described under this term may transform into cancer. Critically evaluating all definitions proposed so far for oral leukoplakia, the Working Group agreed that the term leukoplakia should be used to recognize ‘white plaques of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer’. An outline was proposed for diagnosing oral leukoplakia that will prevent other oral white disorders being misclassified as leukoplakia. The Working Group discussed the caveats involved in the current use of terminology and classification of oral potentially malignant disorders, deficiencies of these complex systems, and how they have evolved over the past several decades. The terminology presented in this report reflects our best understanding of multi‐step carcinogenesis in the oral mucosa, and aspires to engender consistency in use.

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Background: Head and neck cancers (HNCs) continue to remain a significant public health burden worldwide, causing significant mortality and morbidity despite significant clinical advances enabling their early diagnosis and treatment. Methods: We used data from the GLOBOCAN 2012, Cancer Incidence in Five Continents, World Health Organization Mortality Database and Surveillance, Epidemiology, and End Results programmes to describe the current epidemiology of HNCs. Results: Estimated age-standardised incidence/mortality rates for cancers of the lip and oral cavity among males and females (7.0/2.3 and 2.6/0.6 per 100,000 per annum) in more developed regions are higher compared to those in less developed regions (5.0/2.8 and 2.5/1.4 per 100,000 per annum). Similarly, the estimated rates for cancers of the tonsils and pharynx among males (7.5/2.5 per 100,000 per annum) and females (2.7/0.5 per 100,000 per annum) are reported to be the highest in Western Europe, whereas these rates for cancer of the larynx among males (7.9/4.0 per 100,000 per annum) and females (0.9/0.5 per 100,000 per annum) are reported to be the highest in the Caribbean. Cancer of the nasopharynx represents a significant HNC burden in the Asia-Pacific region and Northern Africa. Conclusion: The current and future estimated burden of HNCs is shifting to less developed regions which may be ill equipped to deal with this increasing burden. This needs urgent attention of policy makers through effective cancer control policy implementation with population-based interventions.

Studies on the possible association between bacteria and oral squamous cell carcinoma (OSCC) remain inconclusive, largely due to methodological variations/limitations. The objective of this study was to characterize the species composition as well as functional potential of the bacteriome associated with OSCC. DNA obtained from 20 fresh OSCC biopsies (cases) and 20 deep-epithelium swabs (matched control subjects) was sequenced for the V1-V3 region using Illumina’s 2 × 300 bp chemistry. High quality, non-chimeric merged reads were classified to species level using a prioritized BLASTN-algorithm. Downstream analyses were performed using QIIME, PICRUSt, and LEfSe. Fusobacterium nucleatum subsp. polymorphum was the most significantly overrepresented species in the tumors followed by Pseudomonas aeruginosa and Campylobacter sp. Oral taxon 44, while Streptococcus mitis, Rothia mucilaginosa and Haemophilus parainfluenzae were the most significantly abundant in the controls. Functional prediction showed that genes involved in bacterial mobility, flagellar assembly, bacterial chemotaxis and LPS synthesis were enriched in the tumors while those responsible for DNA repair and combination, purine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, ribosome biogenesis and glycolysis/gluconeogenesis were significantly associated with the controls. This is the first epidemiological evidence for association of F. nucleatum and P. aeruginosa with OSCC. Functionally, an “inflammatory bacteriome” is enriched in OSSC.

Oral cancer, primarily oral squamous cell carcinoma (OSCC), continues to be a major global health problem with high incidence and low survival rates. While the major risk factors for this malignancy, mostly lifestyle related, have been identified, around 15% of oral cancer cases remain unexplained. In light of evidence implicating bacteria in the aetiology of some cancer types, several epidemiological studies have been conducted in the last decade, employing methodologies ranging from traditional culture techniques to 16S rRNA metagenomics, to assess the possible role of bacteria in OSCC. While these studies have demonstrated differences in microbial composition between cancerous and healthy tissues, they have failed to agree on specific bacteria or patterns of oral microbial dysbiosis to implicate in OSCC. On the contrary, some oral taxa, particularly Porphyromonas gingivalis and Fusobacterium nucleatum, show strong oral carcinogenic potential in vitro and in animal studies. Bacteria are thought to contribute to oral carcinogenesis via inhibition of apoptosis, activation of cell proliferation, promotion of cellular invasion, induction of chronic inflammation, and production of carcinogens. This narrative review provides a critical analysis of and an update on the association between bacteria and oral carcinogenesis and the possible mechanisms underlying it.

The increased focus on the physical health of people with SMI should encompass oral health. Possible interventions could include oral health assessment conducted using standard checklists that can be completed by non-dental personnel, help with oral hygiene, management of iatrogenic dry mouth, and early dental referral.