Background:

Delay in diagnosis allows tumors to invade deep into local structures and spread to regional lymph nodes in the neck, resulting in this high mortality. When assessing survival, early staged cancers-those less than 4 cm in size and without regional lymph node involvement-are controlled in more than three quarters of the cases.

Routine oral examinations play an important role in controlling oral cancer. Exams can reveal mucosal changes that might be pre-malignant or malignant, thereby accelerating the diagnosis and initiation of early treatment. As carcinomas account for nine of 10 oral cancers, this indicates surface lesions that may be much easier to recognize.

Clinical dentists should think of prevention in two ways:

• early detection to reduce morbidity and mortality; and
• the opportunity to identify and treat pre-malignant lesions.

Major Causes:

Tobacco use (both smoking and chewing) as well as alcohol consumption also contribute to the transformation of normal cells to cells exhibiting malignant behavior. Prevention programs must include measures to control these habits.

A dentist's dilemma in oral diagnosis stems from the multitude of ill-defined, variable appearing, controversial and poorly understood lesions that appear in the mouth. Most lesions are benign, but many present changes that may easily be confused with malignancy. Conversely, early malignancy may be mistaken for a benign change. Inescapably, such clinical uncertainty is involved in the early detection of malignancy as well as in the understanding and management of other lesions that may not always remain benign.

Both public and professional awareness of oral cancer is fundamental for minimizing the time from onset of signs or symptoms to diagnosis. In most instances, patients delay seeking consultation. In some cases, however, delayed diagnosis occurs because a clinician does not suspect a malignant lesion and treats it with inadequate procedures for cancer control.

Symptoms:

Because of the variability of signs and symptoms, even good clinical judgment and experience do not preclude diagnostic errors. Biopsy is the only method to definitively diagnose a cancer.

Types of Lesions:

Though tobacco use increases the risk for oral cancer, paradoxically, in patients with oral leukoplakia, non-smokers appear at higher risk. This finding is hard to explain, but we can speculate that in the absence of tobacco as a causative irritant, there may be a more lethal initiating or potentiating factor.

Some clinical leukoplakias show microscopic cellular changes that are developmentally abnormal (classification of dysplasia). Studies have documented the increased risk for malignant transformation of dysplastic leukoplakic lesions on an unpredictable basis.

There are no associated consistent or reliable clinical signs and symptoms that allow differentiation or prediction of a pre-malignant or early malignant change. Since the clinical appearance of oral leukoplakia-thick or scant, large or small-does not reliably indicate its biologic potential, dentists should suspect all white patches, and carefully evaluate and observe patients with such lesions.

Leukoplakia that clinically has an erythematous or red component (erythroleukoplakia, non-homogeneous) is far more likely to undergo dysplastic or malignant epithelial changes than other forms of leukoplakia. With this in mind, clinicians should biopsy specimens from erythematous areas, particularly if they must choose between red- and white-appearing mucosa.

Conclusion: