Premalignant Lesions

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Premalignant lesions are the unusual or abnormal changes inside the mouth over the cheek, tongue, gums and palate region that are considered to be the initial stages to a fore coming cancerous lesion. There is a risk of these lesion to transform into a cancer but sometimes it is difficult to predict the duration and transformation.

Who are at Risk ?

More commonly detected above age of 40 years, but due to recent change in lifestyle, even younger age group fall into the category. This is due to increase in parafunctional habits. Tobacco and/or heavy alcohol use, paan masala chewing are the main reasons for the cause. Some lesions are idiopathic

  • Duration
  • Non-homogeneous type
  • Size >200 mm squared
  • Site: Tongue, floor of the mouth
  • Leukoplakia in a non-smoker
  • Epithelial dysplasia


How are such lesions detected ?

Patches that are, red, white or mixed \ in color, or that may also be especially when found on “high-risk” sites such as the sides of the tongue, floor of mouth, or at the back of mouth/top of the throat. A white patch that cannot be wiped off with gauze and for which an explanation is not obvious to the dentist may be defined as a leukoplakia.

Similarly, reddish patches with no obvious cause can be defined as erythroplakia and mixed of these two colored areas are termed erythroleukoplakia. Lesions with a red component carry the highest potential for being premalignant or becoming malignant.


Accurate diagnosis can be made by biopsy of that site. There are three possible outcomes: benign (most frequently), premalignant, or cancer. The pathology report will provide- benign diagnoses, epithelial dysplasia (for premalignant lesions), or squamous cell carcinoma (the most common type of cancer seen in the oral cavity).

Types of premalignant lesions
  1. Leukoplakia (idiopathic)
  2. Proliferative verrucous leukoplakia
  3. Erythroplakia
  4. Oral submucous fibrosis
  5. Oral lichen planus
  6. Chronic hyperplastic candidosis


Most common premalignant disorder. One in every 10 cases of oral cancer is known to arise in leukoplakia. These lesions are defined as ‘white plaques of questionable risk having excluded disorders that carry no increased risk for cancer’. These are rare, and thus most persistent white patches are best treated with suspicion until further evaluation.
Clinical variants of leukoplakia include homogenous plaques, nodules, speckled erythroleukoplakia. In India, regions where betel is consumed, prevalence rates reach 5% . The annual risk of malignant transformation is estimated between 1 and 2%. Larger non-homogeneous lesions, especially on the tongue and floor of the mouth, are associated with the highest conversion rates to oral carcinoma.


Similar to leukoplakia, they are red velvety lesions. It is a rare disorder with prevalence between 0.01 and 0.2% but a much higher transformation rate. Clinical appearances are : homogenous, granular and speckled types.

Most common subsides are the palate, the buccal mucosa and the floor of the mouth.

Oral submucous fibrosis

It is the most progressive scarring disorder seen among southeast asia population as its linked to the use of betel products (paan chewing and arecenut content). Additional risk for oral cancer (squamous cell carcinoma) is high by the addition of slaked lime to the betel quid or concurrent use of tobacco. The active ingredients in paan include arecoline, copper and polyphenol fragments such as flavonols, tannins which stimulate an intense acute inflammatory response characterised by a polymorphic infiltrate and vascular dilatation. This gives way to a chronic immune response and constrictive vascular changes that end with obliteration of blood vessels in the affected region.

They are divided into 4 stages based on the severity of the signs and symptoms based on its duration and frequency. Conservative and medical measures are considered for the early stages. This includes physiotherapy, immune modulators steroids and promoters of blood flow such as pentoxifylline.

Surgical options are limited and complete excision unlikely, but surgery is usually indicated for local release of retromolar or buccal scarring to help relieve trismus. Release of trismus is usually necessary at the mouth opening of 25 mm and less and is achieved with incisions, local V–Y flaps and masticator muscle myotomy, resurfacing the defect with the buccal fat pad or other grafts.

Grades in OMFS :
Treatment option for different stages :


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