**3. Erythroplakia**

*Oral Diseases*

**Figure 4.**

palate (**Figure 4**) [4, 6, 11].

nonhomogeneous leukoplakias [4, 6].

dysplasias, thus guiding the treatment [12].

plaque at the onset, which gradually becomes erythematous and exophytic with the progression of the disorder, affecting mainly the gingiva, alveolar mucosa, and

*Proliferative verrucous leukoplakia affecting the hard palate and alveolar ridge. Source: author's file.*

Regarding the histopathological characteristics of leukoplakia, a thick layer of keratin in the epithelium (hyperkeratosis) is present, with or without thickening of the thorny layer (acanthosis). It is still possible to observe in some leukoplakia the presence of hyperkeratosis with epithelial atrophy. Generally, leukoplastic lesions do not exhibit epithelial dysplasias, but the presence of them would be a worrying sign for a possible malignant transformation, a fact that is most observed among

The diagnosis of leukoplakia is basically by excluding other diseases or disorders that do not carry increased risk of malignant transformation. In order to perform an accurate diagnosis of leukoplakia, different levels of leukoplakia must be followed by certainties (factor C) that lead us from a primary clinical diagnosis to the definitive diagnosis based on the histopathological examination of the lesion [4, 6]. Thus, in the van der Waal factor, C1 evidence is obtained in a single visit, in the first contact between the dental surgeon and patient, applying only palpation and inspection as the primary means for diagnosis, in addition to anamnesis to collect data that may make up this provisional clinical diagnosis. In the certainty factor C2, evidence is obtained from negative results of elimination of etiological factors such as mechanical irritation, during a period of follow-up of 2–4 weeks or in the absence of any suspicious etiological factors (definitive clinical diagnosis). Factor C3 is similar to C2 but complemented by incisional biopsy (provisional histopathological diagnosis), and C4 is the evidence obtained from surgical excision of the lesion followed by histopathological examination of the resected specimen (definitive histopathological diagnosis) [11, 12]. Performing biopsy in the diagnosis of leukoplakia is important because only through this examination it is possible to determine whether to perform the histopathological diagnosis or not of epithelial

The treatment of leukoplastic lesions is dependent on the result found in the histopathological examination; in this way, the treatment plan is often individualized according to the histological findings, such as the degree of dysplasia found in the epithelium. The WHO in its latest manual for the classification of head and neck tumors (2017) defines dysplasias as architectural and cytological epithelial changes caused by an accumulation of genetic alterations associated with an increased risk of progression to squamous cell carcinoma. Therefore, in lesions that present mild dysplasia or do not present dysplasia, more conservative measures should be taken,

**78**

Erythroplakia is defined as "a red spot that can't be characterized clinically or pathologically like any other definable disease" [4]. When a mixture of red and white changes occurs, this lesion would be classified as a nonhomogeneous leukoplakia called erythroleukoplakia [10]. Erythroplakia is multifactorial, since no isolated etiological factor has been evident, but several intrinsic and extrinsic etiological factors have contributed to the origin of this disorder, such as smoking, alcohol consumption, candida infection, and even nutritional deficiencies such as iron and vitamin A deficiency [6].

Erythroplakia in comparison to leukoplastic lesions is rare and has a prevalence rate in South and Southeast Asia ranging from 0.02 to 0.83% but presents a high percentage of malignant transformation ranging from 14 to 50%, and about 90% of cases already present moderate or severe dysplasia/carcinoma in situ. Because of the high rates of malignant transformation and the presence of high-grade dysplasias, many specialists have already considered it a primordial clinical sign of squamous cell carcinoma. It is a prevalent disorder in middle-aged adults in the elderly, aged between 45 and 74 years, with no prevalence among the genders [6, 10, 13].

Clinically, erythroplakia presents as a well delimited, asymptomatic, reddish, smooth and shiny stain or plaque with a soft and velvety texture [3, 6]. If hardened areas are observed in the lesion, it is already indicative of the presence of a possible invasive carcinoma at the site. The preferred anatomical location is the floor of the mouth, but it can be observed anywhere in the oral cavity, such as the lip, hard palate, or oral mucosa [3]. The clinical presentation of a solitary lesion is consistently useful to clinically differentiate erythroplakia from erosive lichen planus, lupus erythematosus, and erythematous candidiasis, as these lesions always appear bilaterally and are more or less symmetrical (**Figure 5**) [10].

**Figure 5.** *Erythroplakia affecting palate and superior alveolar ridge. Source: author's file.*

Histopathologically, 90% of erythroplakia present as severe epithelial dysplasias/carcinomas in situ or squamous cell carcinomas. The epithelium will show no production of keratin and is regularly atrophic. This absence of keratin associated with epithelial atrophy allows the underlying microvasculature to be exposed, thereby elucidating the reddish coloration of the lesion. In relation to connective tissue, it regularly exposes chronic inflammation [9].

The diagnosis of erythroplakia, as well as leukoplakias, is made by exclusion. This disorder presents clinically very similar to other lesions commonly found in the oral cavity, such as vascular lesions, candidiasis, mucosites, and even Kaposi's sarcoma. Because it has so many options for differential diagnosis, as in leukoplakia, one can use the steps or factors of analysis guided by Isaac van der Waal (factors C1, C2, C3, and C4) [10]. In addition, lesions on the floor of the mouth and belly regions and lateral border of tongue should be biopsied, since in some anatomical locations, the highest rates of malignant transformation occur and the presence of high degree dysplasia. With the accomplishment of the biopsy, for diagnostic purposes, it will be possible to verify the presence or absence of dysplasias. According to Neville et al. [6], 90% of the erythroplakia already present severe epithelial dysplasias/carcinomas in situ [9].

As in leukoplakias, the treatment plan for erythroplakia is guided by the definitive diagnosis obtained only after the histopathological examination. In the absence of dysplasia or presence of mild dysplasias, the lesion is monitored every 6 months, and if there is any change, perform a biopsy to check if any dysplastic modification has occurred. In lesions presenting moderate to severe dysplasia/ carcinoma in situ, complete removal of the lesion should be done with safety margin. As with leukoplakia, total excision of the lesion does not guarantee that there is no recurrence of erythroplakia; in addition to the fact that this disorder already has high levels of malignant transformation, its removal does not exclude the likelihood of future cancerous lesions on the site or in other oral locations. Something that should be very clear regarding the treatment of erythroplakia and other PMOD is that the patient who has one of these disorders will never be medically released, as these must be followed for life to assess whether or not there was any dysplastic or even the appearance of cancerous lesions in other oral sites [3, 6, 10].

#### **4. Oral lichen planus**

Oral lichen planus is a chronic and systemic mucocutaneous disease often found in the oral cavity, but it can also affect other body parts such as the skin, nails, scalp, and vaginal mucosa. The British physician, Erasmus Wilson, in 1869, was the first to describe lichen planus, and he believed that the cause of this disorder would be fungal infections [6, 14]. Thus, the pathophysiology of OLP for years has been a mystery, but it is known that this disorder occurs due to T-cell-mediated autoimmune destruction of the basal cells of the epithelium. Recently it was considered a PMOD, after several discussions among scholars, due to the fact that the lesion shows a low degree of malignant transformation, around 0.5% [13, 14].

The etiological factors for this disorder are still unknown, but it is believed to be related to stress, anxiety, diabetes, autoimmune diseases, and genetic predisposition [15]. Stress and anxiety may not have total influence on the pathogenesis of lichen planus, but it has been observed that patients with this disorder are usually subjected to high levels of stress [6].

**81**

**Figure 7.**

**Figure 6.**

*Potentially Malignant Oral Disorders*

*DOI: http://dx.doi.org/10.5772/intechopen.88580*

tation of oral bullous lichen planus [6].

*Lichen planus on jugal mucosa, showing Wickham striations. Source: author's file.*

*Erosive lichen planus on jugal mucosa. Source: author's file.*

Oral lichen planus affects between 0.5 and 2% of the population, having a predilection for women between the ages of 30 and 60 years, being a rare disorder in children [6, 15]. The main intraoral sites of lichen planus are the jugal mucosa, tongue, and gingiva. An important feature of this lesion is bilaterality and symmetry [14]. Clinically, oral lichen planus is characterized by six distinct forms: reticular, erosive, bullous, plaque, papular, and atrophic, with reticular and erosive forms being the most prevalent. The reticular OLP is routinely present in the posterior jugal mucosa bilaterally. Other anatomical areas may be affected, such as the lateral border and back of the tongue, gingiva, palate, and vermilion lips [6, 15]. This type of OLP is much more common than erosive, but the latter is the most studied because it is symptomatic, which leads more patients to seek treatment specialists [6]. The reticular type is thus defined by its appearance of intertwined and asymptomatic white striations, the pathognomonic sign of the disorder being the Wickham striae (**Figure 6**). In the erosive type, erythematous and atrophic areas are observed, with varying degrees of central ulceration, and at the periphery of the atrophic regions, fine irradiated white streaks are usually observed (**Figure 7**) [6, 14, 15]. If the erosive state is aggravated, a separation between the epithelium and the underlying connective tissue may occur, resulting in a rare clinical presen-

#### *Potentially Malignant Oral Disorders DOI: http://dx.doi.org/10.5772/intechopen.88580*

*Oral Diseases*

Histopathologically, 90% of erythroplakia present as severe epithelial dysplasias/carcinomas in situ or squamous cell carcinomas. The epithelium will show no production of keratin and is regularly atrophic. This absence of keratin associated with epithelial atrophy allows the underlying microvasculature to be exposed, thereby elucidating the reddish coloration of the lesion. In relation to connective

The diagnosis of erythroplakia, as well as leukoplakias, is made by exclusion. This disorder presents clinically very similar to other lesions commonly found in the oral cavity, such as vascular lesions, candidiasis, mucosites, and even Kaposi's sarcoma. Because it has so many options for differential diagnosis, as in leukoplakia, one can use the steps or factors of analysis guided by Isaac van der Waal (factors C1, C2, C3, and C4) [10]. In addition, lesions on the floor of the mouth and belly regions and lateral border of tongue should be biopsied, since in some anatomical locations, the highest rates of malignant transformation occur and the presence of high degree dysplasia. With the accomplishment of the biopsy, for diagnostic purposes, it will be possible to verify the presence or absence of dysplasias. According to Neville et al. [6], 90% of the erythroplakia already present severe epithelial

As in leukoplakias, the treatment plan for erythroplakia is guided by the definitive diagnosis obtained only after the histopathological examination. In the absence of dysplasia or presence of mild dysplasias, the lesion is monitored every 6 months, and if there is any change, perform a biopsy to check if any dysplastic modification has occurred. In lesions presenting moderate to severe dysplasia/ carcinoma in situ, complete removal of the lesion should be done with safety margin. As with leukoplakia, total excision of the lesion does not guarantee that there is no recurrence of erythroplakia; in addition to the fact that this disorder already has high levels of malignant transformation, its removal does not exclude the likelihood of future cancerous lesions on the site or in other oral locations. Something that should be very clear regarding the treatment of erythroplakia and other PMOD is that the patient who has one of these disorders will never be medically released, as these must be followed for life to assess whether or not there was any dysplastic or even the appearance of cancerous lesions in other oral

Oral lichen planus is a chronic and systemic mucocutaneous disease often found in the oral cavity, but it can also affect other body parts such as the skin, nails, scalp, and vaginal mucosa. The British physician, Erasmus Wilson, in 1869, was the first to describe lichen planus, and he believed that the cause of this disorder would be fungal infections [6, 14]. Thus, the pathophysiology of OLP for years has been a mystery, but it is known that this disorder occurs due to T-cell-mediated autoimmune destruction of the basal cells of the epithelium. Recently it was considered a PMOD, after several discussions among scholars, due to the fact that the lesion

The etiological factors for this disorder are still unknown, but it is believed to be related to stress, anxiety, diabetes, autoimmune diseases, and genetic predisposition [15]. Stress and anxiety may not have total influence on the pathogenesis of lichen planus, but it has been observed that patients with this disorder are usually

shows a low degree of malignant transformation, around 0.5% [13, 14].

tissue, it regularly exposes chronic inflammation [9].

dysplasias/carcinomas in situ [9].

sites [3, 6, 10].

**4. Oral lichen planus**

subjected to high levels of stress [6].

**80**

Oral lichen planus affects between 0.5 and 2% of the population, having a predilection for women between the ages of 30 and 60 years, being a rare disorder in children [6, 15]. The main intraoral sites of lichen planus are the jugal mucosa, tongue, and gingiva. An important feature of this lesion is bilaterality and symmetry [14].

Clinically, oral lichen planus is characterized by six distinct forms: reticular, erosive, bullous, plaque, papular, and atrophic, with reticular and erosive forms being the most prevalent. The reticular OLP is routinely present in the posterior jugal mucosa bilaterally. Other anatomical areas may be affected, such as the lateral border and back of the tongue, gingiva, palate, and vermilion lips [6, 15]. This type of OLP is much more common than erosive, but the latter is the most studied because it is symptomatic, which leads more patients to seek treatment specialists [6]. The reticular type is thus defined by its appearance of intertwined and asymptomatic white striations, the pathognomonic sign of the disorder being the Wickham striae (**Figure 6**). In the erosive type, erythematous and atrophic areas are observed, with varying degrees of central ulceration, and at the periphery of the atrophic regions, fine irradiated white streaks are usually observed (**Figure 7**) [6, 14, 15]. If the erosive state is aggravated, a separation between the epithelium and the underlying connective tissue may occur, resulting in a rare clinical presentation of oral bullous lichen planus [6].

```
Figure 6.
Lichen planus on jugal mucosa, showing Wickham striations. Source: author's file.
```
**Figure 7.** *Erosive lichen planus on jugal mucosa. Source: author's file.*

Lichen planus has typical histopathological characteristics, but they are not specific for the lesion. Its epithelium has varying degrees of orthokeratosis and parakeratosis, and depending on whether the lesion is reticular or erosive, the thickness of the thorny layer may vary. Epithelial ridges may be absent, atrophic, or hyperplastic but usually exhibit sharp, serrate-like progressions. Another striking feature is the presence of hydropic degeneration, that is, the destruction of the basal cell layer of the epithelium and an intense infiltration of banded inflammatory cells predominantly composed of T lymphocytes. Some lesions of lichen planus may show some degree of dysplasia, being able to present aberrant mitoses and nuclear and cellular pleomorphisms, among other dysplastic alterations [6, 16].

The diagnosis of OLP is basically made by clinical findings, mainly in the reticular type, by the presence of the pathognomonic signal (Wickham striae). In addition to the clinical diagnosis, the histopathological examination may be requested for a definitive diagnosis. One thing that can make it difficult to diagnose OLP is the existence of candidiasis overlapping with lichen lesion, and for this, it is recommended that the treatment for candidiasis be carried out first and only subsequently the definitive diagnosis of OLP and the respective treatment plan of the same [6, 15].

As the reticular type does not present symptoms, there is no need for specific treatment, but as already mentioned, candidiasis can occur overlapping with lesions of lichen planus; in this way it is proposed that the antifungal treatment be performed based on topical nystatin, and mouthwash with nystatin or application of Miconazole gel is recommended. In erosive lichen planus, because it has painful symptomatology, treatment with topical corticosteroids initially, such as triamcinolone acetonide and beclomethasone, is suggested. The second line of treatment would be the use of retinoids, cyclosporine, and calcineurin inhibitors prescribed for about 2 weeks. In addition to drug treatment, photodynamic therapy is usually used to relieve symptoms [6, 13]. Lastly, patients with this disorder should be evaluated periodically for 3–6 months, especially in atypical cases with some degree of dysplasia [6].
