Oral dysplasia is a condition characterized by the development of abnormal cells within the lining of the mouth, known as the mucosa. These changes to the soft tissues are not cancerous but are considered a precancerous or potentially malignant condition, meaning they could progress into oral cancer if left unaddressed. The condition indicates that cells in the mouth have undergone harmful changes, often due to damage to their DNA.
Symptoms and Appearance
The most common signs of oral dysplasia are visible patches on the soft tissues inside the mouth. These patches are most often white (leukoplakia) or red (erythroplakia). In some instances, the lesion can be a mixture of red and white, referred to as erythroleukoplakia. The patches vary in size and can appear anywhere in the mouth, including the tongue, gums, floor of the mouth, and inside the cheeks.
A characteristic of these lesions is that they cannot be scraped off. The texture of the patches may vary, appearing flat, slightly raised, thick, or even hardened. An ulcer may occasionally be present within the patch. These lesions are often painless, which can delay detection and makes routine dental examinations a primary method for early identification.
Causes and Associated Risk Factors
The development of oral dysplasia is strongly linked to lifestyle habits and environmental factors. The most prominent causes are tobacco use and heavy alcohol consumption. Tobacco in any form exposes the oral lining to carcinogens that can damage cellular DNA. Alcohol consumption has a similar effect, and the combination of tobacco and alcohol significantly increases the risk.
Chronic irritation is another contributing factor, resulting from poorly fitting dentures, a rough surface on a broken tooth, or habitual cheek biting. For dysplasia that appears on the lips, prolonged and unprotected sun exposure is a known risk. Additionally, certain strains of the human papillomavirus (HPV) have been identified as a cause of cellular changes in the mouth. In a small number of cases, individuals may develop oral dysplasia without any of these risk factors, likely due to a genetic predisposition.
Diagnosis and Grading
A diagnosis of oral dysplasia begins with a visual examination by a dentist or doctor. Because the abnormal cells cannot be seen with the naked eye, a definitive diagnosis requires a biopsy. During this procedure, a small sample of the suspicious tissue is surgically removed and sent to a pathologist for microscopic analysis, which confirms the presence of dysplastic cells.
Once dysplasia is confirmed, it is assigned a grade based on the extent of cellular abnormality. The condition is classified as mild, moderate, or severe. Mild dysplasia indicates that the abnormal cells are confined to the lower layer of the oral lining and the risk of it becoming cancerous is low. Moderate dysplasia involves more significant changes extending into the middle layers. Severe dysplasia means the abnormal cells occupy most of the thickness of the lining, which carries a high risk of progressing to oral cancer.
Management and Treatment Approaches
The management strategy for oral dysplasia is directly informed by its grade. For cases of mild dysplasia, where the risk of cancer development is lower, a “watchful waiting” approach may be adopted. This involves scheduling frequent follow-up visits every few months to monitor the lesion for any changes. This approach is paired with counseling to eliminate contributing risk factors, such as quitting smoking or reducing alcohol intake.
For moderate or severe dysplasia, treatment to remove the abnormal tissue is recommended due to the higher risk of progression. The most common procedure is surgical excision, where a surgeon removes the lesion and a small margin of surrounding healthy tissue. Other removal techniques include laser ablation, which uses a focused beam of light to vaporize the tissue, or cryotherapy, which freezes and destroys the cells. Following treatment, long-term follow-up appointments are necessary to monitor for any signs of recurrence.