The role of saliva in oral health problems.
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Biomedical subjects
Publications and source records attributed to C Scully.
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BACKGROUND: In 1997 a new human hepatotropic virus, TT virus (TTV), was identified. The clinical significance of TT virus infection remains unclear. OBJECTIVE: To undertake an initial evaluation of the genoprevalence of TTV DNA among health care workers in the United Kingdom. SETTING: A UK dental hospital. STUDY DESIGN: The sera of 53 dental healthcare workers (9 dentists, 14 dental nurses and 30 office staff) were tested for the presence of TTV DNA using Polymerase Chain Reaction (PCR). RESULTS: TT virus DNA was detected in 3 out of 53 (5.7%) samples. This frequency of TTV carriage is similar to that of blood donors and healthy persons in the UK. CONCLUSION: The present data suggest that dental healthcare workers in the UK are not at increased risk of nosocomial acquisition of TT virus.
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Transmissible spongiform encephalopathies (TSEs) are rare, fatal degenerative brain diseases which affect humans and certain animals, and are caused by inheritance or acquisition of prions (PrPs). Inherited TSEs include Fatal Familial Insomnia (FFI), Gerstmann-Straussler-Scheinker syndrome (GSS) and other less well clinically characterised disorders, while the human infective TSEs include sporadic, iatrogenic and variant Creutzfeldt-Jakob disease (vCJD). The causative prions are found especially in neural tissues and spinal fluid, and in the case of vCJD, in lymphoreticular tissue. Available epidemiological evidence suggests that normal social or routine clinical contact with affected patients does not present a risk to health care workers, relatives or the community. Isolation of patients is not considered necessary. Nevertheless as the prions are resistant to conventional chemical, irradiation and heat sterilisation methods, highly specific cross-infection control measures are required for the dental management of patients with, or at notable risk, of TSE. The present article reviews current knowledge of the clinical consequences of prion disease and provides information regarding necessary changes to the cross-infection routine when managing patients infected, or at risk of, prion disease.
The ability to metabolise carcinogens or pro-carcinogens, repair DNA damage, and control cell signalling and the cell cycle are fundamental to homeostasis. Oral squamous cell carcinoma (oral cancer) and many squamous cell carcinomas of the head and neck (SCCHN) may, under appropriate exposure to mutagens, arise if these mechanisms are defective. SCCHN arise as a consequence of multiple molecular events induced by the effects of various carcinogens from habits such as tobacco use, influenced by environmental factors, possibly viruses in some instances, against a background of heritable resistance or susceptibility. Consequent genetic damage affects many chromosomes and genes, and it is the accumulation of these changes that appears to lead to carcinoma in some instances, sometimes via a clinically evident pre-malignant, or potentially malignant, lesion. Although lifestyle factors play a prominent role in aetiology, some patients appear susceptible because of an inherited trait in their ability or inability to metabolise carcinogens or pro-carcinogens, possibly along with an impaired ability to repair the DNA damage. This is the first of a series of three papers reviewing the advances in the understanding of this area of research since our last review [Scully C, Field JK. Genetic aberrations in squamous cell carcinoma of the head and neck (SCCHN), with reference to oral carcinoma (Review). Int J Oncol 1977;10:5-21] and discusses mainly oral carcinoma in the context of SCCHN.
Carcinogenesis is the result of a series of genetic mutations resulting in unregulated growth of a clone of cells and the development of malignant lesion that is largely monoclonal though, with the evolution of further genetic changes, there develops a degree of heterogeneity in the tumour. DNA technology, especially allelic imbalance (loss of heterozygosity) studies have identified chromosomal changes in oral carcinoma and head and neck squamous cell carcinoma (SCCHN), suggestive of the involvement of tumour suppressor genes (TSGs), particularly in chromosomes 3, 9, 11 and 17. The regions most commonly identified have included 3p, especially 3p14.2 (FHIT); 3p24, and 3p21.3, where the TSGs involved are as yet unidentified; 9p21 where p16 (INK4A/MTS-1] is the main target TSG; and 17p13 where p53 is the major target TSG. Over-expression of oncogenes, genes mainly involved in cell signalling, especially those on chromosome 11 (PRAD-1 in particular) and 17 (H-ras) and mutations in DNA repair genes, have also been implicated in the carcinogenesis of SCCHN.
The molecular changes in malignant epithelium in the head and neck offer possibilities for the development of diagnostic, prognostic and other markers. This article reviews recent developments in this field.