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Aim: Epidemiological and molecular studies have demonstrated that high risk
HPV types are not only related to the development of cervical cancer but also
associated with certain types of head and neck cancers. However, its role in the
development of oral precancerous and cancerous lesions is less well defined.
In an attempt to contribute to the understanding of pathogenesis of oral lesions,
and additionally to evaluate the presence of HPV DNA in saliva and genital area
in general population we investigated the rate of detection of HPV genotypes: a)
in 68 saliva samples of patients with oral squamous cell carcinoma (OSCC), b) in
4 saliva and 4 histological samples of patients with precancerous oral lesions
(leukoplakia), c) 34 saliva samples of HIV-seropositive patients with normal oral
mucosa, d) 43 saliva and 43 cervical scrapings of individuals with normal oral
mucosa.
Methods: The detection and genotyping of the HPV DNA was performed by
polymerase chain reaction method ...
Aim: Epidemiological and molecular studies have demonstrated that high risk
HPV types are not only related to the development of cervical cancer but also
associated with certain types of head and neck cancers. However, its role in the
development of oral precancerous and cancerous lesions is less well defined.
In an attempt to contribute to the understanding of pathogenesis of oral lesions,
and additionally to evaluate the presence of HPV DNA in saliva and genital area
in general population we investigated the rate of detection of HPV genotypes: a)
in 68 saliva samples of patients with oral squamous cell carcinoma (OSCC), b) in
4 saliva and 4 histological samples of patients with precancerous oral lesions
(leukoplakia), c) 34 saliva samples of HIV-seropositive patients with normal oral
mucosa, d) 43 saliva and 43 cervical scrapings of individuals with normal oral
mucosa.
Methods: The detection and genotyping of the HPV DNA was performed by
polymerase chain reaction method (PCR) and consensus primers MY09/11,
followed by the restriction fragment length polymorphism (RFLP). Saliva and
cervical samples of the healthy subjects as well as the histological samples of
precancerous lesions were examined with consensus PCR and nested PCR
(NPCR) for additional sensitivity. Statistical analysis was performed using two
tailed Fisher’s exact test and the calculation of odds ratios (OR).
Results: HPV DNA was detected in saliva samples of normal oral mucosa
individuals, OSCC patients, leukoplakia patients and HIV-seropositive individuals,
with rates 11.6%, 10.3%, 25%, and 35.3% respectively, using consensus PCR
method. High risk HPV types were found in 60%, 71.4%, 100%, and 75%
respectively of the above study groups. HPV 16 was the predominant type
(40.0%, 42.8%, 100%, and 50%) of the HPV positive samples in the above
subject groups. The HIV positive individuals was the only group which indicated a
statistically significant difference (P=0.025; OR 4.145; 95% CI 1.329-12.813)
compared to the healthy subjects. Additionally, with the application of NPCR
method on histological samples of leukoplakia, HPV DNA was detected in 100% of the examined samples. In the group of sexually active women with normal oral
mucosa the presence of HPV DNA was simultaneously investigated in saliva and
cervical scrapings, using two methods of detection: consensus PCR and NPCR.
Oral HPV DNA was detected in 11.6% of saliva samples and in 51.2% of cervical
samples using consensus PCR, while the detection rate with NPCR was 44.2%
and 60.5% respectively. The results showed a significant deference on the
detection rate of HPV DNA between saliva and cervical samples (P < 0.001, OR:
0.126, 95% CI: 0,043 - 0371) and a statistically significant deference (P=0.001;
OR 6.017; 95% CI 2.036-17.603) in the detection rate of HPV in saliva between
consensus and nested PCR. The sensitivity of consensus PCR in the detection of
HPV DNA in saliva samples reached only 26.3% compared to NPCR method,
while in cervical samples it reached 84.6% of the NPCR. In addition, 100% of
HPV-positive saliva women with consensus PCR had also a positive PAP-test,
while the possibility of having a positive PAP-test in women with a NPCR-positive
saliva test was 8.5 times higher (P = 0.009, 95% CI: 1.74 – 39.70).
Conclusion: a) HPV DNA was detected in saliva of patients with oral lesions as
well as the general population with normal oral mucosa. The incidence rate of
detected HPV DNA in the above studied subjects did not indicate a statistically
significant difference, probably due to low viral load in saliva and the limited
detection ability of consensus PCR. However, the etiologic role of the virus in oral
carcinogenesis cannot be excluded, considering the higher incidence of HPV
DNA in patients with precancerous lesions and the significant higher rate of HPV
detection in saliva of HIV-seropositive individuals, which is probably associated
with some degree of immunosuppression in this particular group.
b) In the majority of cases there was detected at least one common HPV type in
saliva and cervical samples of the same individual. This finding supports the
hypothesis of the HPV tropism for the genital and oral mucosa, as well as the
potential sexual transmission from the genital area.
c) The presence of HPV DNA in saliva of sexually active women may be
associated with a positive PAP-test.
d) The detection of HPV DNA in the oral mucosa though, cannot clearly prove the
etiologic role of the virus in the development of oral disease considering latent infection, which is being detected with sensitive molecular methods. However,
persistence of HPV infection in the oral cavity in combination with some degree
of immunosuppression, genetic predisposition, tobacco, or alcohol abuse might
be considered as an additional risk factor in the development of oral disease.
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