Human papillomavirus in the oral cavities of children and adolescents.

OBJECTIVE: The purpose of this pilot study was to determine the frequency of human papillomavirus (HPV) in the oral cavities of children and adolescents and to identify potential risk factors for HPV infection. STUDY DESIGN: Sociodemographic information was obtained on 268 healthy infants, children, and adolescents who were < or = 20 years old. Oral squamous cells were collected from swabs with young children and from oral saline solution rinses with older children and adolescents. Extracted DNA was evaluated for HPV by polymerase chain reaction, dot blot hybridization, and DNA sequencing. Factors associated with the presence of HPV were tested by using chi(2), Fisher's exact test, and logistic regression tests. RESULTS: HPV was detected in 6.0% of the participants. HPV frequency among young children (<7 years old) was 8.7% (11/127), and among adolescents (13-20 years old) it was 5.2% (5/97). HPV was not detected in children aged 7 to 12 years old (0/44). Fifty-four percent (6/11) of HPV-positive children were 1 year of age or less; 3 of the HPV-positive children (<7 years old) were delivered by cesarean section. No statistically significant association was found between the detection of HPV in the oral cavity and method of delivery or gender; parent's race, education, HPV-related conditions, smoking history, or number of sex partners; or adolescent's smoking history or history of sexual activity. CONCLUSIONS: This study suggests that HPV is present in the oral cavity primarily in children 2 years old and younger and in adolescents 13 years and older. Cesarean delivery was not protective against oral HPV infection; in fact, half of the HPV-positive infants were born by cesarean delivery.

Human papillomavirus and risk of laryngeal cancer.

We determined the relationship between human papillomavirus (HPV) infection and the HPV types detected in 44 patients with squamous cell carcinoma, 10 laryngeal leukoplakia patients, and 12 patients evaluated for benign laryngeal conditions (controls). The sources of HPV DNA were from brushings from the upper respiratory tract and lesion (benign or malignant), oral rinses, and biopsies of patient lesions. Polymerase chain reaction (PCR) and DNA sequencing were used to identify and type HPV. We detected HPV in 25.0% (11/44) of patients with laryngeal cancer, in 30.0% (3/10) of patients with laryngeal leukoplakia, and in 16.7% (2/12) of noncancer controls. Patients with cancer were not more likely to be identified with oncogenic HPV types ( 18.2%) than either the leukoplakia group (20%) or the control group (16.7%). An increased risk of disease was associated with current tobacco use and former alcohol drinking in cancer patients versus controls and in leukoplakia patients versus controls (all p < .05). After we controlled for tobacco and alcohol effects on the risk of disease, exposure to oncogenic HPV types was associated with an increased risk of laryngeal cancer (odds ratio = 3.0) and of laryngeal leukoplakia (odds ratio = 6.0) compared to controls, although the results were not statistically significant. This study suggests that although HPV infection and HPV oncogenic types are not found at a higher frequency in laryngeal cancer or laryngeal leukoplakia as compared to controls, infection is associated with an increased risk of disease after controlling for the effects of alcohol and tobacco use.

p53 polymorphism, human papillomavirus infection in the oral cavity, and oral cancer.

OBJECTIVES: Human papillomavirus (HPV) infection has emerged as a risk factor in oral carcinogenesis. An arginine-coding polymorphism of the tumor suppressor protein p53 at codon 72 is more readily degraded by the HPV oncoprotein E6. Our objective was to evaluate the association between p53 polymorphism at codon 72 and HPV infection in the oral cavity, as well as its association with oral cancer. STUDY DESIGN: Oral squamous cells from 202 patients with oral cancer and 333 age-sex frequency matched controls were evaluated by polymerase chain reaction for the presence and type of HPV and for alleles of codon 72 in p53. Fisher exact test and chi(2) tests were used to evaluate the data. RESULTS: The p53 codon 72 polymorphism is not associated with HPV infection, whether comparing HPV-negative controls with HPV-positive controls or comparing HPV-negative cases with HPV-positive cases. Additionally, we found no association with the codon 72 polymorphism and oral cancer, whether comparing HPV-negative controls with HPV-negative cases or comparing HPV-positive controls with HPV-positive cases. CONCLUSIONS: There is no association between p53 codon 72 polymorphism and HPV infection or between the p53 polymorphism and the risk of oral cancer.