Hairy Leukoplakia: Causes, Symptoms, Management & Treatment

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It wasn’t until 1984 that the disease of the mucosa known as hairy leukoplakia (HL) was first described. It is believed to be caused by the Epstein-Barr virus (EBV), which is also referred to as human herpesvirus 4. It is detected most frequently in persons who are infected with HIV, although it is also possible to find it in people who do not have HIV. Patients with this condition are typically people who have undergone a transplant of an organ or bone marrow, suffer from an immunocompromised disease, or have hematological cancer.

This exercise highlights the role of the interprofessional team in enhancing treatment for patients who have hairy leukoplakia and covers the evaluation and management of the disorder known as hairy leukoplakia.

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Objectives

The pathophysiology of hairy leukoplakia needs to be described.

The presentation of a patient who had hairy leukoplakia can be summed up as follows:

Outline the concerns that should be made while treating patients who have hairy leukoplakia.

To better the results for patients afflicted with hairy leukoplakia, please explain why it is so important to improve care coordination among the many members of the interdisciplinary team.

Introduction

It wasn’t until 1984 that the disease of the mucosa known as hairy leukoplakia (HL) was first described.

It is believed to be caused by the Epstein-Barr virus (EBV), which is also referred to as human herpesvirus 4. It is detected most frequently in persons who are infected with HIV, although it is also possible to find it in people who do not have HIV. Patients who fit this profile have typically undergone an organ or bone marrow transplant or been diagnosed with an immunodeficiency condition or hematological cancer.

On the other hand, it has also been documented in people who do not have a weakened immune system.

It has been demonstrated that immunocompetent patients who have been taking inhaled, topical, or systemic corticosteroids for an extended period of time are at an increased risk of developing the illness.

This condition has been categorized as a Category-B clinical marker of HIV illness by the Center for Disease Control and Prevention (CDC) because it has a definite predictive value in determining whether or not an individual would go on to acquire AIDS.

Etiology

The presence of HIV infection and/or immunosuppression is typically shown to be associated with the development of hairy leukoplakia. It has been shown that the likelihood of having hairy leukoplakia increases by practically a factor of two with every fall in the CD4 count of 300 units. It has also been observed in patients who have other types of severe immunodeficiencies, such as those who are undergoing chemotherapy, those who have leukemia, or those who have received an organ transplant. In immunocompetent patients, it has only very rarely been observed.

In addition, hairy leukoplakia has been linked to Behcet syndrome as well as ulcerative colitis in some cases. When looking at HIV-positive men, a positive correlation has been found between smoking more than one pack of cigarettes per day and the development of hairy leukoplakia.

Epidemiology

The condition known as hairy leukoplakia is quite common in HIV-positive homosexual males, especially those who are smokers. Studies have revealed that patients who are not receiving any therapy for HIV, particularly those patients whose CD4 count has dropped to less than 0.3 x 10/L, have an increased risk of developing HL. This risk can reach as high as fifty percent. There does not appear to be a correlation between age or race and the development of hairy leukoplakia.

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Pathophysiology

The pathophysiology of this illness is complex, necessitating an interplay of different elements such as coinfection with EBV in addition to its productive replication, virulence, genetic evolution, and specific EBV genes that are expressed while they are in a dormant state. Hairy leucoplakia is caused by all of these causes, which are exacerbated by a local as well as a systemic deficit of the host’s immune system. [6] In the beginning, the virus will only infect the basal cells of the epithelium that lines the pharynx. At this point, it enters a condition of replication, which causes the infectious virus to be released into the saliva. This process continues for the entirety of the infected person’s life span. It is also possible for the virus to infiltrate the B cells of the pharynx, which is where it will remain dormant for an undetermined amount of time. Cytotoxic T cells are necessary for keeping the EBV infection in a dormant condition, despite the fact that they are unable to completely eradicate the virus from the body. Reactivation of the dormant virus in B lymphocytes results in the production of virions by the virus. Because of the release of these virions, the circulating monocytes become infected. These monocytes then go to the lamina propria of the mucosa of the oral cavity, where they eventually differentiate into macrophages and progenitors of the Langerhans cell. After this, they travel into the oral epithelium, where they are found predominately in the basal and/or parabasal layers. After the virus has been reactivated, it travels through the dendritic processes of the Langerhans cells in order to reach the keratinocytes that are located in the spinosum and granulosum layer. The replication process of the virus begins once it reaches these layers.

Additionally, it has been discovered that hairy leukoplakia biopsy tissues include either a significant decrease in the number of Langerhans cells or none at all. Langerhans cells are antigen-presenting immune cells that are essential for the immune system’s response to viral infections.

Their absence may make it possible for EBV to multiply repeatedly and avoid being recognized by the immune system.

Because the lateral edge of the tongue is more prone to being injured by mechanical trauma, it is simple for EBV to gain access to the prickle cell receptors in this area. weakened immunological condition of the host in addition to a significant decrease in the number of Langerhans cells. then contribute to the propagation of EBV in the oral epithelium and its subsequent effective establishment.

Histopathology

The histological image of the disorder reveals five primary characteristics, which are as follows:

This is caused by a modification in the pattern of expression of keratin in the squamous cells that make up the epithelium, which results in hyperkeratosis of the superficial layer of the epithelium. It is possible for this hyperkeratotic thick layer to split from the cells that lie beneath it, which will result in projections that give the lesion its characteristic “hairy” appearance. This hyperkeratinized epithelium has the potential for developing a superficial infection from bacteria or Candida.

An increase in the number of hyperparakeratotic cells in the epithelium’s superficial layer: Incomplete squamous differentiation can be identified by the aberrant persistence of nuclei of the cell in this layer of the epithelium. It is possible that this layer will demonstrate the presence of several Candida hyphae.

Acne of the upper stratum spinosum or prickle cell layer: acanthosis This aberrant enlargement of cells manifests themselves as layers of cells that resemble koilocytes or cells that have blown out. The nuclei may have an overall look similar to ground glass, and they may have eosinophilic intranuclear inclusions that are surrounded by a halo (Cowdry type A).

There was no evidence of inflammation in the epithelium, and there was very little to no evidence of inflammation in the lamina propria. There was also no evidence of inflammatory mononuclear cell infiltration.

Histologically normal epidermal basal cells include the following: It is necessary to have the BZLF1 gene present in order to bring about the intracellular shift from the dormant to the infectious productive state. The BZLF1 gene is confined to the cells of the stratum spinosum and stratum granulosum in cases of hairy leukoplakia. The cells that make up these layers are the ones that carry the gene for Blimp1, which is a transcription factor that is active during the last stage of keratinocyte differentiation. Because neither Blimp1 nor BZLF1 can be found in the basal cell layer of the oral epithelium, it is presumed that this layer is not involved in the development of hairy leukoplakia.

Even though the aforementioned characteristics point to hairy leukoplakia, none of the aforementioned histologic characteristics are typical of hairy leukoplakia and are seen solely in this lesion. It is for this reason that a histologic appearance, in addition to the proof of DNA, RNA, or protein of Epstein-Barr virus within the epithelial cells, is required to arrive at a conclusive diagnosis of hairy leukoplakia.

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History and Physical History

Due to the fact that hairy leukoplakia is frequently asymptomatic, many people are unaware that they have the condition. They may describe a white plaque along the lateral edge of the tongue that is not painful and does not itch. It’s possible that the lesion will appear and then fade on its own. Some patients may experience moderate pain, dysesthesia, a change in their sensitivity to the temperature of food, a change in the taste sensation due to a modification in their taste buds, and the psychological impact of the unattractive aesthetic look of the condition.

An examination of the body

White lesions, either unilateral or bilateral, that are painless and found intraorally are most commonly observed on the lateral margin of the tongue.

The appearance of the lesion can range from a smooth, flat, and tiny lesion to an uneven “hairy” or “feathery” lesion with obvious folds or projections. This is because the lesion is caused by an abnormal growth of cells. Along the lateral border of the tongue, it can manifest as either a continuous or a discontinuous lesion, and it is frequently asymmetrical on both sides of the tongue. The size, severity, and surface characteristics of the lesions can vary from patient to patient.

Because the lesion is attached to the surface, it is impossible to remove it via scraping. There are no indications of an erythematous or edematous alteration in the tissue that is around the lesion. There is a possibility that hairy leukoplakia will spread to other surfaces of the tongue, as well as the buccal mucosa and/or the gingiva. In this case, it may have a flat look with a smooth surface and will not have the characteristic “hairy” appearance of the lesion.

Evaluation

In most cases, a clinical examination is all that is required to establish a diagnosis of hairy leukoplakia. Nevertheless, a histological investigation and the confirmation of DNA, RNA, or protein of the Epstein-Barr virus located within the epithelial cells are necessary for arriving at a diagnosis that is 100 percent certain. There are a number of kits available for purchase that can be used for this purpose.

The detection of EBV can be accomplished through the use of a number of distinct methods, including polymerase chain reaction, electron microscopy, immunohistochemistry, and in situ hybridization. The in situ hybridization method is regarded as the most reliable and accurate of all of these many approaches. A tissue biopsy can be performed, but it is not necessary unless the lesion has a peculiar look or is ulcerated, both of which are signs that it could be cancer.

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Proceed to the Treatment and Management page.

Because hairy leukoplakia is a benign disorder with a low morbidity rate and a tendency to resolve itself on its own, it is not necessary to precisely treat every instance of the condition. When the patient wants to treat the disease for cosmetic reasons or to provide relief for symptoms that are caused by the condition, treatment is administered. Anti-retroviral medication is one of the available treatment choices. In most cases, highly active antiretroviral therapy medications will lessen the appearance of hairy leukoplakia; nevertheless, the condition may return if the dosage of the drug is decreased.

Within seven to fourteen days of starting treatment, the illness is typically cured when it is managed systemically with antiviral medications. Oral treatment with an antiviral medicine such as acyclovir needs to be administered in a high dosage of around 4,000 milligrams per day in divided dosages for at least seven days in order to obtain the requisite therapeutic levels.

It is also possible to make use of other medications, such as valacyclovir and famciclovir. Orally administered, these new antiviral medications have a bioavailability that is relatively superior to that of the medicine acyclovir and requires a relatively lower dosage. They are taken in quantities of 3000 mg and 1500 mg per day, respectively, with the dosages being divided. These medications work by inhibiting the reproduction of productive EBV through their mechanism of action; however, they do not completely eliminate the latent infection. The condition, however, may frequently return a few weeks after treatment with these drugs has been discontinued, which is a drawback.

Podophyllin resin can be applied topically as a therapy for the condition. The problem is typically cured after a few applications of this resin solution, which is administered at a concentration of 25 percent.

Although Podophyllin is known to have cytotoxic effects on the cells, the precise method by which it improves the disease is not yet understood. However, just like with other medications, there is a possibility of the condition returning following therapy with this method. Additionally, there is a possibility that the therapy will momentarily cause pain and discomfort in the places where it is applied, as well as dysgeusia.

In addition, retinoic acid can be applied topically as a kind of treatment. Tretinoin, or vitamin A at a concentration of 0.1 percent, is often applied twice or three times daily until the patches have completely disappeared. Acid retinoic slows down or stops the process of the virus replicating. However, even after being successfully treated with retinoic acid for a period of several weeks, the disease continues to return.

It has also been claimed that cryotherapy, which uses liquid nitrogen, can resolve hairy leukoplakia; however, this treatment technique is not utilized very frequently.

Go to: Differential Diagnosis

The following are examples of alternative diagnoses for hairy leukoplakia:

Candidiasis

Oral leukoplakia

White sponge nevus

Keratosis is caused by oral friction

Smoker’s keratosis

Verrucous proliferative leukoplakia of the skin

Lichen planus

Reactions involving lichenes

Condyloma acuminatum

Go to:

Prognosis

When hairy leukoplakia is detected, the majority of patients who present with the condition tend to have considerable suppression of their immune systems. The condition manifests itself not too long after HIV seroconversion, i.e., prior to the development of AIDS. When the disease is first identified, the CD4 count could be anywhere from 235 to 468 microL on average at that time. According to the findings of several studies, the life expectancy of AIDS patients who also have hairy leukoplakia is significantly lower than that of AIDS patients who do not show indications of this lesion. In addition, if these patients are also infected with the hepatitis B virus, their condition may deteriorate, which could lead to the early development of AIDS.

Glosspopyrosis is a complication that can arise from hairy leukoplakia, which can be caused by an infrequent candidal superinfection (burning tongue). Alterations to one’s sense of taste are still another difficulty, albeit an uncommon one. When taken topically for an extended period of time, retinoids can cause a sensation similar to burning on the skin.

Because of the patient’s changed speech, difficulties in mastication and deglutition, and/or pain, the existence of oral lesions has a substantial impact on the patient’s overall quality of life as it relates to their health. This could make the patient’s nutrition-related difficulties even worse, which would be another step in the patient’s health decline. As a result, patients must be educated adequately regarding the oral lesions linked with HIV as well as their general oral health.

Having a robust immune system is the first step in eliminating the risk of developing hairy leukoplakia. Patients need to be taught about the need of following the HIV treatment plan as well as the oral hygiene practice that is prescribed to them. Additionally, measures need to be done in order to keep up a healthy way of life. It is important for the patient to be educated on this topic because those who are infected with HIV and have a smoking habit have a higher risk of contracting the virus as compared to those who do not smoke.

Visit Improving the Results Obtained by Healthcare Teams.

If the dentists have comprehensive knowledge regarding the treatment of oral disorders associated with HIV infection, such as hairy leukoplakia, the treatment success, in general, can be improved. The dentist, along with the other members of the patient’s interprofessional health care team, should devise a plan of suitable follow-up care after reviewing the patient’s medical history, physical exam, and laboratory findings. Education and training of a fundamental nature are insufficient to fulfill the responsibilities of health care workers. It extends to supplying the patients with the appropriate knowledge and information regarding oral lesions, as well as the development of reinforcing educational programs because the early diagnosis and management of these lesions play an important role in reducing the impact of the disease on the patient. Patients are educated by nurses who have received specialty training in AIDS and otolaryngology. These nurses also arrange for patients to receive follow-up care and encourage communication among the team. Pharmacists confer with clinicians to ascertain the right agent(s) and dosage, evaluate prescriptions, investigate potential drug interactions, and provide patients with information. The results for patients will be improved as a result of these interprofessional efforts.