PD2. Oral submucous fibrosis: Pathogenesis and presentation

PD2. Oral submucous fibrosis: Pathogenesis and presentation

Oral Oncology 47 (2011) S5–S14 Contents lists available at ScienceDirect Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology IAOO ...

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Oral Oncology 47 (2011) S5–S14

Contents lists available at ScienceDirect

Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology

IAOO 2011 Panel Discussion Abstracts Panel Discussion #1: PD1. Premalignant lesions Crispian Scully University of Bristol, UK Submucous Fibrosis/Potentially Malignant Lesions Oral cancer appears to be increasing in incidence, and mortality has scarcely improved over past decades. Better understanding of aetiopathogenesis should lead to more accurate and earlier diagnosis and more effective treatments with fewer adverse effects, providing the best chance of a cure. Cancer is the result of DNA mutations arising spontaneously and from the action of various mutagens, especially in tobacco and alcohol. Cancer is a consequence of an interaction of many factors. A sequence of genetic changes leads eventually to loss of growth control and autonomy, but countering these changes are mechanisms to metabolise carcinogens, repair DNA damage, control growth, and defend against cancer. Potentially malignant (premalignant or precancerous) disorders which precede some neoplasms include erythroplasia (erythroplakia) – the most likely lesion to progress to severe dysplasia or carcinoma, leukoplakia, lichen planus and submucous fibrosis. Risk factors include tobacco, betel and alcohol use. Clinical features which suggest a potentially malignant lesion is likely to transform, or has transformed, to carcinoma include: the presence of red lesions (erythroplasia); a verrucous, speckled or granular appearance or an ulcer with fissuring or raised exophytic margins; induration; fixation of the lesion to deeper tissues or to overlying skin or mucosa; cervical lymph node enlargement. Single ulcers, lumps, red patches, or white patches – particularly if any of these are persisting for more than three weeks, may be manifestations of frank malignancy. There should be a high index of suspicion, especially of a solitary lesion present for over 3 weeks: biopsy is invariably indicated. The whole oral mucosa should be examined as there may be widespread dysplastic mucosa (‘‘field change’’) or even a second neoplasm and the cervical lymph nodes must always be examined. Laboratory diagnostic aids increasingly look to detect cellular and now molecular changes. Molecular techniques are being introduced for prognostication. doi:10.1016/j.oraloncology.2011.06.031

PD2. Oral submucous fibrosis: Pathogenesis and presentation Saman Warnakulasuriya Department of Oral Medicine, King’s College London & WHO Collaborating Centre for Oral Cancer, UK

Premalignant or oral potentially malignant disorders (OPMDs) are well documented in the oral cavity and these have variable rates of malignant transformation. A distinctive OPMD that is prevalent in Asia and among Asian migrants to Western countries is ‘‘oral submucous fibrosis’’. Oral submucous fibrosis (OSF) is a chronic, insidious disease that affects the oral mucosa. The disease begins in the lamina propria and as it advances involves tissues deeper in the submucosa of the oral cavity with resulting loss of fibroelasticity. Atrophy of the epithelium is often noted. In the early phase vesicles may appear soon superseded by other markers. The disease manifests with a burning sensation of oral tissues, blanching and marble-like appearance, leathery mucosa, depapilation of tongue, stiffening of the oral mucosa leading to limitation in opening of the mouth. The presence of fibrous bands in lips, cheeks and soft palate is a hallmark of the disease. There is now conclusive evidence that OSF is caused by areca nut, a masticatory substance used by Asians. Several mechanisms and biological pathways have been proposed for the pathogenesis of the disorder, all based on the constituents of areca nut and genetic susceptibility to the disease. In essence the disease could be described as a collagen metabolic disorder with changes observed in the extracellular matrix of the lamina propria and submucosa of the oral cavity due to both increased collagen synthesis and/or reduced collagen degradation. Several chemicals in areca nut including arecoline, tannins and copper appear to upregulate the molecular process of deposition and/or degradation and remodeling of extracellular matrix molecules contributing to collagen deposition underneath the oral epithelium. The process is influenced by increased secretion of inflammatory cytokines and growth factors. In areca nut chewers chronic inflammation is self-perpetuating and the process distorts the microenvironment as a result of aberrantly active transcription factors. Oral screening programmes and public education will provide means for the early detection of OSF. Quitting areca nut use and a diet rich in antioxidants may help to prevent progression of OSF to cancer. doi:10.1016/j.oraloncology.2011.06.032

PD3. Molecular markers of potentially malignant lesions and targeted approach for chemoprevention M. Abraham Kuriakose Department of Surgical Oncology, Chief Head and Neck Oncology Services, Mazumdar Shaw Cancer Center, Bangalore, India Oral cancer in general develops as multi-step, multi-focal disease as a result of various carcinogenic insults on oral mucosa. The lesions often start as premalignant lesions, which over the years