Oral Health and Dental Management

Analysis of Oral Leukoplakia in Relation to HPV Infection

Alba Tejero-Mas^* Department of Oral Medicine Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA
^*Correspondence: Alba Tejero-Mas, Department of Oral Medicine Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA, Email:

Received: 27-Sep-2022, Manuscript No. OHDM-22-18681; Editor assigned: 30-Sep-2022, Pre QC No. OHDM-22-18681(PQ); Reviewed: 14-Oct-2022, QC No. OHDM-22-18681; Revised: 21-Oct-2022, Manuscript No. OHDM-22-18681(R); Published: 27-Oct-2022, DOI: 10.35248/2247-2452.22.21.1025

Description

Leukoplakia, the most frequent potentially cancerous lesion of the oral cavity, can be categorized as homogenous or nonhomogenous based on its clinical appearance. The two most frequent risk factors for oral leukoplakia are tobacco and areca nut consumption, either separately or in combination. However, some cases of oral leukoplakia are idiopathic. Some sectors of the precancerized oral epithelium contain keratinocytes that may be in various stages of cytogenetic change when leukoplakia develops there. Unpredictably regressing, remaining stable, or developing into carcinoma are all possible outcomes for leukoplakia. Idiopathic leukoplakia, non-homogenous leukoplakia, leukoplakia affecting the floor of the mouth, the ventrolateral surface of the tongue, the maxillary retromolar, and the adjacent soft palate (collectively referred to as high-risk sites), leukoplakia with high-grade epithelial dysplasia, and leukoplakia in which the keratinocytes carry cytogenetic changes. Although there seems to be a connection between oral leukoplakia and Human Papilloma Virus (HPV), there is little proof to suggest that either HPV infection causes oral leukoplakia or that HPV-infected leukoplakic keratinocytes lead to their carcinomatous transformation.

There is a direct correlation between the frequency and duration of cigarette, pipe, and cigar smoking and the prevalence of oral leukoplakia. About 70%-90% of oral leukoplakias are linked to smoking and areca nut consumption, either alone or in combination. Unknown variables may be involved in the development of idiopathic leukoplakia. However, there is minimal proof that either Human Papilloma Virus (HPV) infection or excessive alcohol drinking causes oral leukoplakia. Instead, it is probable that both oral epithelium infection with HPV and excessive alcohol consumption may be related to the condition. A proper diagnosis of oral leukoplakia has been said to require the histological exclusion of other oral keratotic lesions recognized as distinct entities as well as the exclusion of any additional etiological agents outside tobacco or areca nut consumption. Oral leukoplakia can be divided into two primary clinical types: homogeneous and non-homogeneous, based on how it appears. Clinically, either type may manifest as a single lesion or a cluster of lesions. The size of the leukoplakic lesion can vary.

Non-homogeneous leukoplakia can be nodular or verrucous with a wrinkled or corrugated surface, or it might be a mixture of white and red patches known as erythroleukoplakia. Homogeneous leukoplakia is a flat, uniformly white plaque with a smooth or moderately smooth surface. Oral leukoplakia’s clinical appearance may alter over time. While some homogeneous lesions may enlarge or become non-homogeneous, most oral leukoplakias will remain stable or regress and a small number may develop into carcinomas. The prevalence of oral leukoplakia rises with age, and it is typically diagnosed in middle age. The majority of the remaining 90% of oral leukoplakias are linked to tobacco or areca nut usage, with approximately 10% of cases being idiopathic. Because men consume tobacco more frequently than women, so they are affected more frequently than women. In 25% of instances, the buccal mucosa, 20% of cases, the mandibular gingiva, 10% of cases, the tongue, 10% of cases, and other oral locations make up the remaining cases.

A helpful indicator of the possibility of developing carcinomatous transformation, epithelial dysplasia in oral leukoplakia serves as a crucial therapeutic care guide. However, because dysplasia can be stable for a long time, it cannot be utilized to forecast the development of carcinomatous transformation with certainty. According to their genotype, Human Papilloma Viruses (HPVs) exclusively attack mucosal squamous epithelium but can also infect the skin. Based on their epidemiological relationship with cancer of the cervix uteri, those that infect the mucosal epithelium have either been classified as high-risk kinds (such as HPV-16, 18, 31, 33, and 35) or low-risk category. These classifications have been widely used in research on the cancer-causing potential of HPV infection in all upper aerodigestive tracts of anatomical regions.

Low-risk HPV genotypes have been linked to the development of benign oral proliferative epithelial lesions, including squamous cell papilloma, condyloma acuminatum, and focal epithelial hyperplasia (Heck disease), whereas high-risk genotypes have been linked to precancerous and cancerous oral and oropharyngeal epithelial lesions. Numerous studies looking into the connection between HPV and squamous cell carcinoma of the upper aerodigestive tract used PCR techniques for HPV DNA detection also without measuring the viral load. Small DNA fragments that may indicate sample contamination or a physiologically inconsequential HPV infection can be found using PCR. These results have been presented as if they were noteworthy from a pathogen perspective. The prevalence of HPV is likely to be 10%, 20.2%, 26.2%, and 46.5%, respectively, in normal oral mucosa, nondysplastic leukoplakias, dysplastic leukoplakias, and other precancerous intraepithelial oral neoplasms. This shows that there may be a connection between oral precancerous and cancerous lesions and HPV infection.

Conclusion

All oral leukoplakias should ideally be treated since they are potentially cancerous and because some of them will unexpectedly develop into carcinoma. The preferred course of treatment for two or three circumscribed accessible lesions is surgical excision. Leukoplakias will, however, reappear in up to 30% of treated cases, regardless of the severity of the lesion or the type of treatment used, and some leukoplakias may progress to squamous cell carcinoma despite treatment. Idiopathic leukoplakia, non-homogeneous leukoplakia, leukoplakia affecting high-risk oral sites, leukoplakia displaying moderate or severe grades of epithelial dysplasia, and especially leukoplakias where a combination of these factors affects the risk of carcinomatosis, should be aggressively treated. Additional leukoplakias arising at fresh oral locations and changes in color, texture, or size are early signs that a carcinomatous transformation may occur.