Ebola virus disease: any risk for oral and maxillo-facial surgery? An overview

The 2014–2015 outbreak of the Ebola virus disease (EVD) in West Africa has been considered a major global health emergency by the WHO. Implications for health care providers including oral and maxillo-facial surgeons have been published by the WHO, the Centers for Disease Control and Prevention (USA), and other medical societies and public health organizations. While the risk of infection with the Ebola virus seems to be rather small in Europe, maxillo-facial and plastic surgeons often travel to Africa to treat patients with facial burns, cleft-lip and palate, and noma. The likelihood of an encounter with patients infected by Ebola virus in subsaharan and West Africa, therefore, has increased during the last 2 years. The purpose of this short overview was to summarize the virology of the Ebola virus, transmission, epidemiology, clinical features, oral manifestations, treatment, and possible implications for maxillo-facial surgeons of EDV.     

Field change and oral cancer: new evidence for widespread carcinogenesis?

Patients with oral squamous cell carcinoma (OSCC) are at risk of developing second or multiple primary cancers as a result of field cancerization in the upper aerodigestive tract. In order to quantify the incidence of field change observable in oral mucosa, 26 consecutive new (untreated) patients presenting with a unilateral OSCC (18) or a premaligant lesion (eight) underwent 'mirror image' biopsies from clinically normal-looking mucosa at corresponding anatomical sites. A total of 15 patients (58%) demonstrated histologically abnormal tissue upon microscopic examination: six showed reactive change/cellular atypia associated with chronic irritation, seven exhibited frank dysplasia, whilst two displayed carcinoma-in-situ (CIS) or microinvasive SCC. Although not statistically significant, there was an observable trend for the lateral/ventral tongue and floor of mouth to display increased vulnerability to dysplastic change.     

Is human papilloma virus associated with salivary gland neoplasms? An in situ-hybridization study

ObjectiveHPV can infect cells of epithelial origin and is closely associated with carcinomas. Studies investigating its presence in salivary gland neoplasms are few and conflicting.MethodsDetection of HPV types 16 &; 18 was done on 34 formalin-fixed, paraffin-embedded archival material of different salivary gland neoplasms using Digene HPV types 16 &; 18 probe using in situ hybridization technique.ResultsEight of neoplastic salivary gland specimens were positively infected by HPV types 16 &; 18. Seven of them were benign (4 Warthin's tumour, 2 pleomorphic adenoma and one myoepithelioma), in addition to one malignant specimen (lymphoma). Correlation was found between the incidence of HPV infection and histological differentiation of salivary gland neoplasms.ConclusionsAn association exists between HPV infections and salivary gland neoplasms. However, given the sparse pattern of reactive cells, it cannot be confirmed that this virus is implicated in the aetiology of this group of tumours.     

Oral infectious diseases: a potential risk factor for HIV virus recrudescence?

As the highly active antiretroviral therapy (HAART) has transitioned human immunodeficiency virus (HIV) infection into a 'chronic disease' management strategy, there is growing evidence that infection with non-HIV pathogens in HIV+ patients may have important public health implications in undermining HAART success and acquired immunodeficiency syndrome progression. Several bacterial and host cell products during infections with non-HIV pathogens have shown the capacity to regulate HIV replication in latently infected cells. A high prevalence of oral infections caused by bacteria, viruses and fungi has been described in HIV+ patients, including periodontal disease. The oral cavity appears to be a site of HIV pathogenesis and potential reservoir for the disease as HIV RNA and DNA forms are present in saliva as well as in gingival crevicular fluid, and oral epithelial cells are susceptible to either cell free or cell-associated HIV infection. The clinical and biological bases of potential associations between chronic oral inflammatory disorders, such as periodontal disease, and exacerbation of HIV viraemia have received little attention. This review attempts to evaluate the current understanding of HIV reactivation as a result of co-infection and/or inflammation induced by non-HIV pathogens in HIV-infected patients, and presents a hypothetic model about the potential role of periodontitis as a global oral infection that potentially contributes to HIV recrudescence.     

Are oral and dental diseases linked to cancer?

Oral Diseases (2011) 17 , 779–784 Objective: Infection and inflammation play a role in carcinogenesis, and highly prevalent oral and dental diseases have been significantly linked to some types of cancer. This article reviews current literature in this area. Materials and Methods: Open literature review using the PubMed database and focused on publications from 2000 to 2010. Results: Numerous potential mechanisms are implicated in the oral disease/carcinogenesis paradigm, including infection‐ and inflammation‐associated cell pathology and microbial carcinogen metabolism. Poor oral hygiene is associated with oral cancer, but there is also evidence of a possible link between oral or dental infections and malignancies in general. Conclusion: Oral infections may trigger malignant transformation in tissues of the mouth and other organs. However, scientific evidence to date remains weak and further well‐conducted studies are warranted before cancer can be properly added to the list of oral infection‐related systemic diseases.     

Extranodal extension in oral cancer: A role for the nodal microenvironment?

Oral squamous cell carcinoma (OSCC) is a significant cause of morbidity and mortality worldwide and accounts for the majority of head and neck cancers. Metastasis of primary tumours, primarily to cervical lymph nodes in the neck, is associated with worsening prognosis. Furthermore, the prognosis of patients with extranodal extension of metastatic tumour from the lymph nodes into the neck tissues is particularly poor. The factors affecting this process are poorly understood, and detection is difficult pre‐surgery. Mounting evidence shows that components of the tumour microenvironment including cancer‐associated fibroblasts, vascular and lymphatic endothelial cells, the extracellular matrix and inflammatory immune cells, are important modulators of tumour behaviour in primary OSCC and other cancers. However, little is known about the lymph node microenvironment, its response to tumour presence and role in extranodal extension. In addition, there are many lymph node‐specific cell types and structures, such as fibroblast reticular cells and high endothelial venules, making the lymph node microenvironment distinct from that found at primary tumour sites, and which contribute to the nodal response to tumour presence. This review details the current knowledge regarding the lymph node tumour microenvironment in OSCC and its role in lymph node metastasis and extranodal extension and relates this to features of the primary tumour. Understanding the role that the lymph node microenvironment plays in promoting tumour development and extranodal extension may aid the identification of novel biomarkers and alternative treatment strategies to improve the prognosis of patients with advanced OSCC.     

Is oral cancer susceptibility inherited? report of five oral cancer families

All the oral cancer patients registered at the Regional Cancer Centre, Trivandrum, during January to July 1995 were subjected to detailed pedigree analysis. This revealed that oral cancer tends to aggregate in families. Like other familial cancers, a family history of oral cancer was associated mostly with an early age of onset of the disease. Family members without habits such as tobacco chewing, smoking or alcohol consumption were also affected. These observations prompt us to suggest the probable inheritance of an oral cancer susceptibility gene in these families. The familial aggregation, mostly site-specific, with an autosomal dominant mode of inheritance, was observed in 0.94% of the total oral cancers. This necessitates the need to undertake studies to elucidate the molecular lesions responsible for oral cancer susceptibility in families.     

Coronally advanced flap procedure: is the interdental papilla a prognostic factor for root coverage?

BACKGROUND: This study was designed to verify if the dimension of the interdental papilla may be a prognostic factor for the clinical outcome of the coronally advanced flap (CAF) in the treatment of gingival recessions. METHODS: Thirty-three Miller Class I recessions were treated in 33 patients using the CAF procedure. Two types of measurements were performed: 1) clinical measurements (probing depth, recession depth, width of keratinized tissue, clinical attachment level) were recorded at baseline and 3 months after surgery and 2) all recessions were photographed and transformed into computer images. A specific software allowed recording of both linear and square measurements. The following digital measurements were recorded at baseline: 1) base, height, and area of the mesial and distal papillae adjacent to the involved tooth and 2) width/depth of the recession and the area of the exposed root surface of the involved tooth. The residual recession area, if any, was recorded 3 months after surgery. The digital measurements of the height and of the area of the papilla were used in statistical analysis (multiple linear regression and logistic regression) to evaluate a possible correlation with root coverage (mm2) and/or with complete root coverage. RESULTS: Root coverage was not significantly correlated to the papilla area (P= 0.3692) or to papilla height (P= 0.0968). The complete root coverage was not correlated to the papilla area (P= 0.3181), but it was correlated to papilla height (P= 0.0499). CONCLUSIONS: This study indicates that the root coverage following CAF procedure is not significantly correlated to papilla dimension. However, complete root coverage is significantly more frequent in sites with lower height of the adjacent papilla.     

The mucosal pellicle – An underestimated factor in oral physiology

Bioadhesion and bio-adsorption of proteins, glycoproteins and other biomolecules are ubiquitous phenomena in the oral cavity. While the protective role of the adsorbed salivary biomolecules on teeth (the acquired enamel pellicle) is well established, it has yet to be defined whether comparable processes occur on the desquamating oral soft tissues. The general term for these layers is pellicle, but due to the different characteristics of the coated surfaces the enamel pellicle and mucosal pellicle are their own entities. There is considerable information on the enamel pellicle, whereas only limited data are available on the mucosal pellicle. This can be attributed to the difficult standardized preparation of this biological structure. Based on the present knowledge the abundant and characteristic components of the mucosal pellicle include secreted soluble mucins (MUC5B, MUC7), membrane-associated epithelial mucins (MUC1), and to a lesser degree CA VI, sIgA, and cystatin. However, it seems to be of completely different ultrastructure as compared with the enamel pellicle. Since it is comprised of larger glycoproteins retaining water, it might be considered as a hydrogel, and it appears to have a lower tenacity than the enamel pellicle. Maturation and turnover are influenced by the delivery of salivary proteins, by the flow of saliva and the underlying desquamating oral epithelium. Its probable functions include lubrication and moisture retention.In general, the mucosal pellicle can be regarded as an underestimated key player in oral physiology.