Dear Arnavaz, have you checked other risk factors like alcohol, or somehow, poor oral hygiene? by the way, we can check HPV in specimen. If anybody has a recommendation, please let me know
Although there is some association with oncogenic HPV and oral cavity SCC, the association between HPV and HNSCC is much stronger in oropharynx, especially tonsil. HPV tumours are typically not well differentiated. If you wanted to investigate this further, the easiest method would be to look for p16 overexpression in pathological specimen.
Actually, in our department of Oral and Maxillofacial-Head and Neck Surgery from the University Hospital Infanta Cristina, Badajoz, SPAIN, we are observing an increasing rate of young patients (below 50 y-o) among the oral cancer population. When studying their habits, it is not rare to do not find tobacco or alcohol consumption. We are now systematically asking for HPV colonization among these patients to the pathologist. Although we have no results yet, our impression is similar to yours.
KAMINAGAKURA, E. ; VILLA, L. L. ; ANDREOLI, M. A. ; SIMAO, J. ; VARTANIAN, J. G. ; SOARES, F. A. ; NISHIMOTO, I. N. ; ROCHA, A. C. ; KOWALSKI, L. P. . High-risk HPV in oral squamous cell carcinoma of young patients. International Journal of Cancer (Print), v. 130, p. 1726-1632, 2012.
Actually white lesions is now increasing among populations, but specifically oral lesions of HPV origin in my opinion have correlation with anal lesions , it is dominant in female anus so anal suckling may be most of transmission in recent years.Also transformation to cancer is due to the neglect of immediate treatment or even biopsy resulted in conflict with other lesions.The typing 16 is dominant in both oral and female anal infections treatment based on either of sites may be beneficial to reduce cancer.
An youngster with White lesion/Carcinoma without any habits probably has 2 chances for occurrence.
History of familial occurrence of carcinoma has to be probed. Transmitted genetic defects tend to cause Ca in younger age groups.
HPV associated lesions often tend to occur in oropharynx rather than anterior part of the mouth. Such suspicious lesions need to be checked, Sexual history probed to elicit the probable etiology.
However till demonstration of viral particles by any method, all other alternatives need to be considered as they would be a "high risk" and vulnerable group.
SEAR studies details the increasing occurrence as early as 1990's.
There really is no debate about the association between HPV 16/18 and head and neck cancer. Mainly affects lingual and palatine tonsils. Much higher in younger males and there is a definite association with oral sex. Very good research at John Hopkins, USA Dept ORL, Westera W, Pai S, Also see clinics of North America Aug 2012.
Please see links below. We are running a conference in Galway, may 17th.
HPV is definitely becoming an increasing problem in HNSCC. In our department we routinely determine status of p16 oncoprotein in all oral and oropharyngeal carcinomas. Furthermore we observed that HPV related carcinomas mostly present in early T category but usually have cervical lymph node metastases. Therefore you can look to this combination if you want further clinical signs of HPV related carcinomas. Our study will be published soon.
the two cases ive seen recently were at base of the tongue and had cervical lymph nodes enlarged.
I would be interested in knowing more about your study.
Ivan, im sorry but i havent been following the posts for a few days..i want to visit ireland and attending the galway conference would have been a good opportunity to combie learning and a holiday.
Unfortunately, this year will be difficult as my daughter is appearing for the pre-medical test(its an entrance exam) due in next may.
But pl keep posting..its good to read all opinions and findings from everywhere.
Details of issue are below - it was June! We have also uploaded our presentations from our HPV conference onto youtube. I will try to paste link below.
not sure what exactly you're searching for, but you could check the GLOBOCAN website for graphics and figures - you can choose by cancer type or region or both:
sorry I didnot see your querstion. p16 can be determined with immunohistochemistry:
* "An HPV infection in tumor tissue was retrospectively determined using p16 immunohistochemistry as a highly sensitive and specific surrogate marker for HPV-associated carcinogenesis [7]. P16 immunohistochemistry was performed using a primary antibody retrieved from Santa Cruz Biotechnology (clone JC8, dilution: 1:100). Tumors were considered positive for p16 when strong nuclear and cytoplasmic staining was present in >60% of cells."
* Prognostic factors in limited (T1-2, N0-1) oropharyngeal carcinoma treated with surgery ± adjuvant therapy. Psychogios G, Mantsopoulos K, Agaimy A, Koch M, Zenk J, Waldfahrer F, Iro H. Head Neck. 2013 Mar 6. doi: 10.1002/hed.23229. [Epub ahead of print]
I am not an expert in this area, but it seems to me that a lot of the answers are obfuscating and over-complicating what should be obvious, that unphysiological sexual activity bypasses the body's normal protective mechanisms and gives viruses a free rein in uncustomary places. Is it only someone like Michael Douglas who is prepared to say this in public?
I think you just say the same thing in other words: oral sex gives HPV the possibility to infect the oropharyngeal region and leads to oropharyngeal carcinoma in some cases.
Unfortunately "physiologic sexual activity" does neither offer any protection for HPV as the number of genital condylomas and cervix cancer patients shows. So I don’t really think that there is a "normal protective mechanism" against HPV.
So only protective possibilities are to have no sex at all or to get the HPV vaccine.
Btw does anyone have an opinion about safety of HPV vaccine?
My comment was a general one applicable to any organism, viral or not, that causes sexual infections. There is clearly a baseline risk of catching infection from standard (physiological) sex, but is there any organism where the risk of spreading or developing infection is not raised with unphysiological sex activity?
Relatively few oral cancer are HPV positive, but many oropharyngeal ones are. And they are located in the tonsil and the base of the tongue (lymphatcic tissue). These patients are younger than the usual (drinking-smoking) oral cancer pateints, but never "youngsters".
All "youngsters" we have see with oral cancer (tongue), aged 20-30 were HPV negative.
"These patients are younger than the usual (drinking-smoking) oral cancer pateints, but never "youngsters". All "youngsters" we have see with oral cancer (tongue), aged 20-30 were HPV negative."
So what activity do such younsters particularly engage in that would expose them to unusual viruses outside their natural habitat? The epidemiology is surely giving the vital clue.
There is no activity we might coin as a trigger or risk factor.
They do not smoke nor drink, but even if they did, the habit would have been during a period of only few years since they are 20 and 22 years and this would probably be only a coincidence. I guess the same applies for HPV: oral sex will not induce a tumor within few years.