The potentially malignant oral lesions (PMOL) are morphological alterations that appear in the oral mucosa and have a higher risk of neoplastic transformation, so it is important to understand their epidemiological relevance and to know how to classify them in order to make an accurate diagnosis and follow-up.
- 1 Epidemiological relevance of LOPMs
- 2 Classification of potentially malignant oral lesions
- 3 Etiopathogenic considerations and predisposing factors
- 4 Clinical manifestations of MPLs
- 5 Typical topography of potentially malignant oral lesions
- 6 Diagnostic protocols for LOPMs
- 7 Clinical follow-up and surveillance
- 8 Role of the general dentist in potentially malignant oral lesions
Epidemiological relevance of LOPMs
Oral cancer accounts for about 3% of all malignant neoplasms worldwide and, despite advances in treatment, mortality remains high, mortality remains high: only 40% to 60% of patientsThe mortality rate is still high: only 40% to 60% of patients survive for more than five years, usually due to late diagnosis. These data highlight the importance of opting for a preventive approach to detect potentially malignant oral lesions as early as possible.
Classification of potentially malignant oral lesions
Potentially malignant oral lesions are classified into several types:
- Oral leukoplakia: accounts for 85% of cases. This is further divided into two types, homogeneous and non-homogeneous lesions, the latter being the ones to pay more attention to.
- Oral erythroplasia: usually develops in only 0.2% to 0.83% of individuals, but is attributed with a high probability of risk of malignant transformation, specifically in 14% to 50% of cases.
They are also classified into oral lichen planus, actinic cheilitis, oral submucous fibrosis, palatal lesions in inverse smokers, chronic traumatic ulcer, nicotinic stomatitis, chronic hyperplastic candidiasis, oral lupus erythematosus, syphilitic glossitis and dyskeratosis congenita.
Etiopathogenic considerations and predisposing factors
The increase in LOPM is related to harmful habits such as tobacco consumption, whether smoked or chewed, as well as alcohol consumption and prolonged exposure to ultraviolet radiation. Also due to viral infections by the human papilloma virus (HPV) or Epstein-Barr, alterations in the immune system, chronic trauma due to ill-fitting prostheses or sharp dental edges, nutritional deficiencies, among other habits.
| Injury | Associated factors |
| Oral leukoplakia | Tobacco use, alcohol, HPV infection, Candida albicans or Epstein-Barr, genetic disorders and chronic irritation from poorly adapted dentures. |
| Oral erythroplasia | Similar to the previous one. |
| Oral lichen planus | Its etiology is unknown, it is associated with immunological factors and can be aggravated by alcohol, tobacco, HPV, ultraviolet radiation, immunosuppression, stress, anxiety and betel nut, among others. |
| Actinic cheilitis | Prolonged exposure to ultraviolet radiation, poor oral hygiene, trauma, tobacco or alcohol consumption, allergic reactions, infections or systemic diseases. |
| Oral submucous fibrosis | Its etiology is unknown, it is associated with prolonged consumption of tobacco, chili peppers, lime and betel nut, as well as collagen and immune disorders, or nutritional deficiencies. |
Clinical manifestations of LOPM
Potentially malignant oral lesions present a diverse clinical spectrum:
| Injury | Clinical appearance | Symptoms |
| Oral leukoplakia | White spot that does not peel off when scraped. It can be homogeneous or non-homogeneous: erythroleukoplakia, warty or nodular. | Asymptomatic; smooth or fissured surface; single or multiple. |
| Oral erythroplasia | Velvety red plaque, smooth or granular, well defined edges. | Generally asymptomatic; inflammatory appearance. |
| Oral lichen planus | Wickham's striae on an erythematous background. It may be reticular, erosive or atrophic. | Pain, burning and ulcers. |
| Actinic cheilitis | Affects lower lip; loss of vermilion border, dryness, fissures, desquamation. | Pain, bleeding, occasional blisters. |
| Oral submucous fibrosis | Fibrous bands in mucosa, pale areas. | Burning, limitation of oral opening. |
Typical topography of potentially malignant oral lesions
It is important to keep in mind that the location of potentially malignant oral lesions also influences their risk. areas of the mouth where the epithelium is thinner, is more exposed to irritants or carcinogens, and has a higher rate of cell turnover.There are areas of the mouth where the epithelium is thinner, is more exposed to irritants or carcinogens, and has a higher rate of cell renewal. For example, some of these areas would be the lateral and ventral tongue, the floor of the mouth, the soft palate and the lower lip.
| Injury | Usual location | Highest risk areas |
| Oral leukoplakia | Tongue, lip vermilion, mandibular alveolar mucosa, jugal mucosa. | Tongue, floor of mouth. |
| Oral erythroplasia | Buccal mucosa, palatine mucosa, jugal mucosa. | Floor of mouth, tongue. |
| Oral lichen planus | Tongue, buccal mucosa, lips, gums. | Tongue (erosive forms). |
| Actinic cheilitis | Lower lip. | Lower lip. |
| Oral submucous fibrosis | Jugal mucosa, lips, soft palate, pharynx. | Jugal mucosa. |
Diagnostic protocols for LOPMs
Step 1: Complete history and clinical examination
Dental specialists treating potentially malignant oral lesions should inquire about associated habits and risks, such as smoking or alcohol, and check the entire oral cavity in good light and using both direct and indirect protection.
It is important to take standardized photographs throughout the treatment in order to be able to to be able to compare the evolution of potentially malignant oral lesions.
Step 2: Biopsy and histopathologic study
Biopsy is essential to confirm the diagnosis and to know if there is epithelial dysplasia. whether epithelial dysplasia is present.. If so, a histopathological study will allow classification, as well as detection of atypia, abnormal mitoses or infiltration of the connective tissue.
In some cases, complementary techniques to biopsy, such as exfoliative cytology, toluidine blue staining or autofluorescence, may be used.
Clinical follow-up and surveillance
The frequency of clinical follow-up will depend on the risk, i.e., the degree of dysplasia:
| Type of dysplasia | Recommended monitoring frequency |
| No dysplasia | Every 6 to 12 months. |
| Mild dysplasia | Every 3 to 6 months. |
| Moderate or severe dysplasia | Every 2 or 3 months, even considering surgery. |
At each check-up, it is essential to document the lesion by means of photographs to compare changes in shape, color, texture or size with respect to previous visits. It should also be checked whether the patient has eliminated the causal factor: tobacco, alcohol, sun exposure, irritating prostheses, etc.
If any of these cases occur, the biopsy should be redoneIf the lesion grows, change of color (especially from white to red), hardening or ulceration, appearance of pain or burning, and persistence of the lesion 2 or 3 months after removal of the cause.
Role of the general dentist in potentially malignant oral lesions
Prevention and early detection is key when it comes to LOPM, so, in general, the role of dentists consists of to examine the mouth at every visit, even if the patient has no symptoms, in order to detect warning signs.even if the patient has no symptoms, in order to detect warning signs. It is also important to educate the patient, explaining possible risks and symptoms to watch out for.
It is best to refer to a specialist in oral medicine or maxillofacial surgery when dysplasia or cancer when there is suspicion of dysplasia or cancer, or if the lesion does not disappear after the cause has been eliminated.

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