Hpv and oral cancer,can you treat herpes naturally video,herpes 2 outbreak - How to DIY

admin 28.11.2014

Oral squamous cell carcinoma (OSCC) is a com­mon cancer whose significant risk factors are smoking, alcohol, betel quid use, sun exposure and immunosuppression. In this study we demonstrated HPV-53 infection in an invasive, oral squamous cell carcinoma. Oral cancer has historically been attributed at the highest rates to smokers.  However, with smoking on the decrease, HPV is expected to take over the role as the biggest contributor to certain types of oral cancer (oropharyngeal) in the coming years. Why is oral cancer on the rise among younger people?  Studies show that most cases of oral cancer among young people are caused by HPV.  Therefore, as the incidence of the virus grows, so does the incidence of oral cancer. Please note that this information is intended to inform, not scare.  Although oropharyngeal cancers are increasing in incidence, they are still a very small risk in our world.  Be informed and be proactive!
To our knowledge, this is the first report of detection of HPV-53 in a malignant lesion of the oral mucosa. The rarity of reports on HPV-53 in malignant tumors rendered it difficult to define the oncogenic status of the virus. There was no evidence of infection by other HPV types, especially, high-risk types such as HPV-16, 18, 31, 33 or 35.

Butura, DDS provides Dental Implants, Wisdom Teeth Removal, Bone Grafting, Extractions, Oral Pathology, and BOTOX® in the Phoenix Metro Area including Scottsdale, Sun City, Glendale, Mesa, Tempe, Gilbert, and Carefree. If you require further details regarding the transaction data, please contact the supplier directly. While it is well known that HPV infec­tion is a significant risk factor for cervical cancer, its relationship with oral malignant tumors has not been fully characterized yet.
This virus had originally been detected in benign lesions of female genitalia and leukoplakia.
The singular presence of HPV-53 in an invasive OSCC in a patient with no other risk factors, supports the recent suggestion that HPV-53 is a probable high-risk type associated with malignant progression of epithelial lesions. In 1985, de Villier first detected HPV DNA in oral carcinoma, and many studies have confirmed this finding.
Until now, only six cases have been reported in the literature where HPV-53 was isolated from cancer lesions. In particular, it was unique that HPV-53 had been isolated from a malignant tumor of the oral cavity such as OSCC, other than from cervical cancer.

A review of articles from 1982 to 1997 showed that the detection rate of HPV in OSCC was up to 46.5%.
The specimens were all from cervical squamous cell carcinoma, among which only two were found to have a single infection of that virus. We tried to determine the HPV status of the previous verrucous carcinoma, but have failed to detect any HPV in that lesion. The most frequently detected types were HPV 16 and 18, suggesting an important role for these viruses in malignant transformation. Further studies on more HPV-53 positive cancers are required to define the oncogenicity of HPV-53. Other various types of HPV were detected in oral cancers, although their detection rates were much lower than those of HPV- 16 and 18.

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