M W Ho1, J M Risk2, J A Woolgar3, E A Field4, J K Field5, J C Steele4, B P Rajlawat4, A Triantafyllou3, S N Rogers6, D Lowe7, R J Shaw8. 1. Regional Maxillofacial Unit, Aintree University Hospital, Liverpool, UK. 2. The University of Liverpool Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, UK. 3. Department of Oral Pathology, Aintree University Hospitals NHS Foundation Trust, UK. 4. Department of Oral Medicine, Liverpool University Dental Hospital, Royal Liverpool and Broadgreen University Hospitals NHS Trust, UK. 5. The University of Liverpool Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, UK; Department of Oral Medicine, Liverpool University Dental Hospital, Royal Liverpool and Broadgreen University Hospitals NHS Trust, UK. 6. Regional Maxillofacial Unit, Aintree University Hospital, Liverpool, UK; Evidence-Based Practice Research Centre (EPRC), Faculty of Health, Edge Hill University, Ormskirk, UK. 7. Evidence-Based Practice Research Centre (EPRC), Faculty of Health, Edge Hill University, Ormskirk, UK. 8. Regional Maxillofacial Unit, Aintree University Hospital, Liverpool, UK; The University of Liverpool Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, UK. Electronic address: richard.shaw@liverpool.ac.uk.
Abstract
BACKGROUND: While the size and clinical appearance are known risk factors for malignant transformation of potentially malignant oral the importance of site, grade of dysplasia and exposure to environmental carcinogens remains controversial. We aim to report the clinical determinants of malignant progression in a series of patients with histopathologically graded oral epithelial dysplasia (OED). METHODS: We recruited patients with a histopathological diagnosis of OED to a longitudinal observational study in a tertiary oral dysplasia clinic. Clinical, histopathological and risk factor data were recorded at baseline. One of three clinical endpoints were determined: malignant transformation, progression of dysplasia grade, remission/stable dysplasia grade. RESULTS: Ninety-one patients meeting the criteria gave consent for inclusion to the cohort, with outcomes reported after a median follow up of 48 months. An estimated 22% (SE 6%) of patients underwent malignant transformation within 5 years, with significant predictors being: non-smoking status (χ(2)=15.1, p=0.001), site (χ(2)=15.3, p=0.002), non-homogeneous appearance (χ(2)=8.2, p=0.004), size of lesion >200 mm(2) (χ(2)=4.7, p=0.03) and, of borderline significance, high grade (χ(2)=5.8, p=0.06). Gender, age, number of lesions and alcohol history did not predict for malignant transformation. CONCLUSIONS: Although a number of these clinical determinants have previously been associated with higher malignant transformation in OED, the high-risk nature of lesions in non-smokers is of particular note and requires a greater emphasis and recognition amongst clinicians dealing with OED. It suggests that those non-smokers with OED, have an inherited or acquired predisposition and should be treated more aggressively; these should form the focus for further investigation.
BACKGROUND: While the size and clinical appearance are known risk factors for malignant transformation of potentially malignant oral the importance of site, grade of dysplasia and exposure to environmental carcinogens remains controversial. We aim to report the clinical determinants of malignant progression in a series of patients with histopathologically graded oral epithelial dysplasia (OED). METHODS: We recruited patients with a histopathological diagnosis of OED to a longitudinal observational study in a tertiary oral dysplasia clinic. Clinical, histopathological and risk factor data were recorded at baseline. One of three clinical endpoints were determined: malignant transformation, progression of dysplasia grade, remission/stable dysplasia grade. RESULTS: Ninety-one patients meeting the criteria gave consent for inclusion to the cohort, with outcomes reported after a median follow up of 48 months. An estimated 22% (SE 6%) of patients underwent malignant transformation within 5 years, with significant predictors being: non-smoking status (χ(2)=15.1, p=0.001), site (χ(2)=15.3, p=0.002), non-homogeneous appearance (χ(2)=8.2, p=0.004), size of lesion >200 mm(2) (χ(2)=4.7, p=0.03) and, of borderline significance, high grade (χ(2)=5.8, p=0.06). Gender, age, number of lesions and alcohol history did not predict for malignant transformation. CONCLUSIONS: Although a number of these clinical determinants have previously been associated with higher malignant transformation in OED, the high-risk nature of lesions in non-smokers is of particular note and requires a greater emphasis and recognition amongst clinicians dealing with OED. It suggests that those non-smokers with OED, have an inherited or acquired predisposition and should be treated more aggressively; these should form the focus for further investigation.