**3. Hairy leukoplakia**

## **3.1 Background**

OHL (Oral hairy leukoplakia) is caused by Epstein-Barr virus and was first described in 1984. 50% of individuals with HIV present with this condition and it is a very good indicator of immunosuppression. The lesion usually presents itself when the CD4 cell counts fall below 0.3\*109/L (Bravo, et al., 2006). According to the CDC (Centers for Disease Control and Prevention), this condition has a clear prognostic value in predicting the future development of AIDS ("1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS among Adolescents and Adults," 1992).

#### **3.2 Pathogenesis**

The pathogenesis of OHL is due to the replication of Epstein-Barr virus and increased virulence in conjunction with a decrease in local and systemic host immunity.

#### **3.3 Clinical features**

OHL present themselves as white, corrugated lesions on the lateral surface of the tongue and are not painful. There has been a decrease in the incidence of OHL due to the potent anti-retroviral drugs. However, if OHL is seen in an HIV-infected person, it may indicate failure of current therapy. Differential diagnosis of this condition includes oral candidiasis, lichen planus, other forms of leukoplakia, HPV (human papilloma virus) associated intraepithelial neoplasia, and oral squamous cell carcinoma.

Fig. 6. Oral Hairy Leukoplakia

#### **3.4 Treatment**

84 Global View of HIV Infection

OHL (Oral hairy leukoplakia) is caused by Epstein-Barr virus and was first described in 1984. 50% of individuals with HIV present with this condition and it is a very good indicator of immunosuppression. The lesion usually presents itself when the CD4 cell counts fall below 0.3\*109/L (Bravo, et al., 2006). According to the CDC (Centers for Disease Control and Prevention), this condition has a clear prognostic value in predicting the future development of AIDS ("1993 Revised Classification System for HIV Infection and Expanded

The pathogenesis of OHL is due to the replication of Epstein-Barr virus and increased

OHL present themselves as white, corrugated lesions on the lateral surface of the tongue and are not painful. There has been a decrease in the incidence of OHL due to the potent

Surveillance Case Definition for AIDS among Adolescents and Adults," 1992).

virulence in conjunction with a decrease in local and systemic host immunity.

Fig. 5. Angular Chelitis

**3. Hairy leukoplakia** 

**3.1 Background** 

**3.2 Pathogenesis** 

**3.3 Clinical features** 

OHL is a relatively benign condition with low morbidity and does not require any specific treatment. Most of the time, these lesions resolve spontaneously. However, several treatment options are available for those who feel uncomfortable or have cosmetic concerns due to the lesion. Since the lesion is caused by multiplication of the Epstein-Barr virus topical and systemic anti-viral agents work effectively in resolving the lesion. High doses of Acyclovir (800 mg 5 times a day) (Resnick, et al., 1988), Valacyclovir (1000 mg 3 times a day), and Famciclovir (500 mg 3 times a day) have all been shown to resolve the lesions in 1-2 weeks (Schofer, et al., 1987). However, once the effect of the anti-viral agent wears off, the lesions can recur several weeks later.

Topical application of Podophyllin resin in 25% solution has produced resolution of the lesion in 1-2 weeks (Gowdey, et al., 1995). Topical therapy with retinoic acid has also been shown to cause resolve the lesions due to inhibition of Epstein-Barr virus replication. Ablative and cryotherapy have also had success in treatment of the lesions. Although the above treatment options are effective in resolving the lesion, OHL can recur several weeks after treatment since none of these agents eliminate the latent state of infection.

Individuals with HIV/AIDS: Clinical Manifestations in the Oral Cavity in the Post-HAART Era 87

indicated for lesions on the face, hands and upper extremities, obstructive lymphadenopathy, periorbital edema, lesions on soles of the feet, anorectal or genital lesions, oral lesions and ulcerating cutaneous lesions. Radiotherapy shows merits in symptomatic disease where systemic treatment is not necessary and expensive chemotherapy can be avoided (Swift, 1996). If an active opportunistic infection is observed, chemotherapeutic agents should be considered. Systemic chemotherapeutic treatment is indicated in extensive KS of oral cavity, widespread skin involvement, pedal or scrotal edema, symptomatic visceral involvement and flare induced by immune reconstitution inflammatory syndrome (Osoba, et al., 2001). Individuals may suffer from neutropenia and thrombocytopenia and hence controlled therapy should be the choice of treatment. Only nodular and symptomatic lesions of oropharynx should be treated with radiation. Recombinant and non-recombinant alpha interferons can be used for treatment

HPV is the leading cause of orpharyngeal carcinomas (D'Souza, et al., Rosenquist, 2005). HPV16 is a common cause for the majority of oropharyngeal carcinomas (Kreimer, et al., 2005) . HPV-positive individuals are most frequently Caucasian and belong to high socioeconomic status (Gillison, et al., 2008). HIV-infected individuals have two to four-fold increase in risk for developing HPV-related oral cancers (Gilbert, et al.). HPV has also been considered as one of the etiologic factors for OHL (oral hairy leukoplakia) (Fejerskov, et al., 1977), as shown by identification of HPV antigens and HPV DNA (Loning, et al., 1985). HPV-induced OL shows prevalence ranged from 17% to 68.6% (Shroyer, et al., 1993,

of epidemic KS (De Wit, et al., 1988).

Fig. 7. Kaposi's Sarcoma

Sugiyama, et al., 2003).

**5.1 Background** 

**5. Human Papilloma Virus (HPV) infections** 
