Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology
Oral and Maxillofacial PathologyManagement update of potentially premalignant oral epithelial lesions
Section snippets
Background
Over the last 30 years, there has been a marginal improvement in the 5-year survival rate of patients with oral cancer treated with multimodality contemporary therapy. Current survival rates for all stages range from 50% to 55%.1 The emphasis on early detection, diagnosis, and treatment of premalignant lesions is to prevent their transformation to oral squamous cell carcinoma (OSCC). Early detection is pivotal to increasing the 5-year survival rate because it is directly correlated with stage
Detection and Diagnosis
To date, there have been no reliable and validated in vivo chairside adjuncts that have sufficient sensitivity and specificity to be more superior than clinical examination and tissue biopsy.9 Adjunctive aids include, but are not limited to, photodynamic detection, including autofluorescence, vital staining (toluidine blue, Lugol's iodine), and brush cytology. These techniques are minimally invasive and have virtually no morbidity, but they do carry considerable false-positive and
Treatment
PPOELs can be managed conservatively by observation alone. In theory, medical interventions, such as chemoprevention, are also available, considering the lack of medical therapies approved by the U.S. Food and Drug Administration. Surgical excision is the invasive management of choice for this group of lesions. Factors that influence the type of therapy include patient risk factors for malignancy (age, gender, and habits) and lesion risk factors (classification, size, morphology, malignant
Oral Leukoplakia
OL is defined by the WHO as a white patch that cannot be scraped or wiped off and is not attributable to any pathophysiology or disease process. It is essential to rule out other processes that OL can clinically mimic, such as candidiasis, lichen planus, nicotinic stomatitis, leukoedema, healing aphthous ulcers, white sponge nevus, and frictional keratosis. It is important to keep in mind that OL is a clinical diagnosis and not a histologic one. Various forms of OL have been distinguished in
Oral Erythroplakia
Oral erythroplakia (OE) is morphologically defined as a red, velvety plaque or patch that cannot be attributed to any other pathophysiologic process and is also a diagnosis of exclusion. OE can stand alone or be associated with OL. In the latter case, it is classified as an erythroleukoplakia (Figure 3). The incidence and prevalence of OE is much less than that of OL. However, OE has one of the higher MTRs (up to 50%) of all the PPOELs.26 The histologic study of biopsied homogeneous OE showed
Oral Submucous Fibrosis
OSF is a progressive fibrotic disease of the aerodigestive tract, but mainly affecting the oral cavity. Deranged collagen metabolism is the underlying pathophysiologic process.32, 33 This disease predominantly affects individuals living in the South East Asian countries, has equal gender predilection, and is seen in the second to third decades of life.32 Multiple etiologic factors have been linked to this disease and include nutritional deficiencies, such as those of vitamins, iron, and zinc;
Oral Lichen Planus
Lichen planus is a systemic mucocutaneous disease that commonly affects the oral mucosa but can also affect skin, nails, the scalp, and the vaginal mucosa. It usually manifests at the third to seventh decades of life.34 The disease has a strong female predilection. Intraorally, the buccal mucosa, tongue, and gingiva are the most common sites; lesions are usually bilateral and symmetric.35 The pathophysiology is currently understood as a T cell–mediated autoimmune destruction of the basal cells
Oral Epithelial Dysplasia
It is known that oral epithelial dysplasia (OED) is often the precursor to OSCC. Oral dysplasia is diagnosed histologically and defined by the WHO as a precancerous lesion of stratified squamous epithelium characterized by cellular atypia and loss of normal maturation and stratification short of carcinoma in situ.3, 23, 39 The presence and the grade of dysplasia contribute to the malignant transformation potential for all the above PPOELs.3, 9, 14, 19 OLP, OSF, OL, and OED are the gross
Human Papillomavirus and Dysplasia
Human papillomavirus (HPV) has been identified as a risk factor for the development of oropharyngeal squamous cell carcinoma (OPSCC). Of the several subtypes, HPV-16 and HPV-18 are deemed to pose a high risk for the development of OPSCC.45, 46 Two viral oncoproteins, E6 and E7, derived from the HPV gene, have been isolated, and their presence is necessary for malignant transformation to SCC. These oncoproteins exert their repressive effects on p53 and Rb tumor suppressor activity, respectively.
Prevention and Maintenance
Primary prevention is ideally the best and the first method in the management of premalignancy. Ultimately, the goal is to prevent premalignancy and its progression to malignancy. It is prudent to risk-stratify a patient and provide appropriate counseling and screening for higher-risk individuals. One systematic review study estimated that the population attributable risk for developing SCC was 25% for smoking alone, 18% for alcohol alone, and 40% for combined use of both.49 Both these risk
Conclusions
The management of premalignant lesions is complex, and the current literature regarding the ideal treatment modality is conflicting. The transition from normal mucosa to premalignant or dysplastic mucosa and to finally malignant change is a complex interplay between the environment and the host. Host factors include genetics and immune system function. Environmental factors include exposure to carcinogens, including betel liquid, tobacco, alcohol, and HPV. It is imperative that clinicians
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