Prevalence of human papillomaviruses in the healthy oral mucosa of women with high‐grade squamous intra‐epithelial lesion and of their partners as compared to healthy controls

Abstract

Oral human papillomavirus (HPV) carriage rates were investigated in relation to genital HPV carriage in women with HPV-associated cervical lesions and male partner of such women, including several couples, in comparison with healthy individuals. Buccal and lingual mucosa of 60 males and 149 females with healthy oral mucosa and without known genital lesion, genital and oral mucosa of further 40 females with cervical high-grade squamous intraepithelial lesion (HSIL) and 34 male sexual partners of women with HSIL (including 20 couples) were sampled. HPV DNA was detected using MY/GP PCR. Genotype was determined by sequencing or restriction fragment length polymorphism. Virus copy numbers were determined by real-time PCR. Overall, oral HPV carriage rate was 5.7% (12/209) in healthy individuals; average copy number was 5.8 × 10(2) copies/1 μg DNA; male and female rates were comparable. Oral carriage in women with HSIL was significantly higher, 20.0% (8/40, P = 0.003); males with partners with HSIL showed a carriage rate of 17.6% (6/34), copy numbers were similar to the healthy controls. In contrast, genital carriage rate (52.9%, 18/34 vs. 82.5%, 33/40; P = 0.006) and average copy number were lower in males (5.0 × 10(5) vs. 7.8 × 10(5) copies/1 μg DNA; P = 0.01). Oral copy numbers in these groups and in healthy individuals were comparable. High-risk genotypes were dominant; couples usually had the same genotype in the genital sample. In conclusion, genital HPV carriage is a risk factor of oral carriage for the individual or for the sexual partner, but alone is not sufficient to produce an oral HPV infection in most cases.

PCR Technique Assisting the Early Diagnosis of Human Papillomavirus A retrospective clinical study

“…The presence of the HPV 16 genotype in the oral cavity can be considered a risk factor of oral malignancy, similar to smoking that can increase the risk of oral cancer by 13 times [14]. In the current study, HPV 16 was the most often identified out of the high risk HPV group (HR-HPV), that could be isolated from almost half of the female genital samples (10 cases, which result is comparable to those obtained by Tatar et al [24]. Out of HR HPV genotypes HPV 16 was identified in three-fourths of the male genital samples (3 cases), and in each of the oral samples (4 cases, 2 male, 2 female).…”

“…Out of the 48 female participants HPV DNA was identified in the genital sample in 38 cases (79.20%) and a total of 11 cases (22.90%) of oral HPV positivity were identified, therefore genital HPV infection in women is significantly more common than oral HPV infection This is in line with the data published by Meyer et al [25], who compared the genital and oral HPV status of 129 women and found that 54.3% had genital HPV DNA positivity 5.4% had oral HPV infection. Almost a third of HPV positive oral samples originated from women with genital HPV infection and no HPV DNA was found in the oral samples of women who had no genital HPV infection, which correlates with a number of studies [24,25,28,29]. Meyer et al (2014) found HPV DNA in the oral samples of 5.7% of women with genital HPV infection and in 5.1% of genitally HPV negative women.…”

“…Szarka et al (2009) studied the HPV DNA copy numbers in samples from malignant oral squamous cell tumours, oral precancerous lesions and from exfoliated cells of clinically healthy oral mucosa from the same patients as well as from healthy individuals and found that the copy number of the virus had a correlation with the severity of the lesions [19]. Besides they also studied the number of copies of HPV DNA in genital and oral samples and found that in women suffering from HSIL the copy of the virus DNA was significantly higher in the genital tract than in their partners' genital samples, but the viral load of the oral mucosa did not show a significant difference according to sex [24]. It is important to determine what viral load has a clinical relevance and a prognostic value in predicting the development and prognosis of oral lesions, which would necessitate further long term follow-up studies in large populations.…”

Atividade mucosotrópica do Papilomavírus Humano (HPV) no processo carcinogênico em diferentes sítios de infecção.

“…Ademais, se o modelo da carcinogênese amplamente aceito para a patogênese do câncer cervical é aplicável para a carcinogênese oral mediada pelo HPV, então a mucosa saudável é o passo inicial na cavidade oral, com isso a prevalência e a dinâmica da infecção oral pelo HPV torna-se um tópico significativo para ser abordado para elucidar o papel do HPV na carcinogênese oral (TATÁR et al, 2015).…”

“…Alguns citam uma provável disseminação do vírus no organismo, mas não levantam questionamentos sobre quais seriam as possíveis vias de disseminação e não relatam o sangue como um possível agente disseminador no organismo (MARQUES et al, 2015;OLIVEIRA et al, 2016;SAINI et al, 2010;TATÁR et al, 2015;VIDOTI et al, 2014).…”