* 1. Summary
* 2. Summary
* 3. Introduction
* 5. Result
* 6. Discussion
* 7. Conclusions
* 8. References
The Oral Papillomavirus is one of the most common lesions of the mouth and is produced by the human papillomavirus. Therefore, this study aimed to determine the frequency of oral Papilloma in the population that attends the Dental Clinic of the Faculty of Dentistry at the Universidad Central de Venezuela, in the period July 1988 in July 1998. Through the medical records of patients with presumptive clinical diagnosis of oral papilloma, underwent histopathological examination to confirm the final diagnosis of the lesion. Of the 250 stories with buccal papilloma presumptive diagnosis was obtained with a total of 57 indicated definitive diagnosis (59.6%). The female (68.42%) is the most affected, the most common location was the tongue (31.6%), the ethnic group is the Mestizo (56.1%) and the most common age was between 50 and 59 years (24.6%). The oral papilloma is a relatively common injury in the population that attends the Dental Clinic of the Faculty of Dentistry at the Central University of Venezuela, with higher prevalence in females between the third and fifth decade of life and frequent location in the language and easily confused clinically with traumatic fibrosis.
Keywords. Papillomavirus, HPV, oral mucosa, retrospective study of oral mucosal papillomavirus.
Oral Papilloma is one of the MOST frequent injuries of the mouth and is produced by the human papilloma virus of. The present work had as an objective to determine the frequency of the oral papilloma in the population That goes to the Service of Estomatologic Clinic of the Faculty of Dentistry of the Central University of Venezuela Between July 1988 to 1998. Through clinical histories of patients with presumptive clinical diagnosis of oral papilloma, a histopathologic study was performed to confirm the definitive diagnosis of the lesions. From 250 histories with presumptive diagnosis of oral papilloma, a total of 57 with Indicated Were Obtained definitive diagnosis (59.6%). Female sex (68.42%) is the more Affected, the location turned out to be the tongue (31.6%), the ethnic group corresponds With The half-breed (56.1%) and the MOST frequent age was Between the 50 and 59 years old (24.6%). The oral papilloma is a Relatively frequent injuries in the population That goes to the service of the Clinic of the Faculty Estomatologic of Dentistry of the Central University of Venezuela, with Greater Prevalence in the female sex Between the third and fifth decade of the life and of frequent location in the tongue and Easily with traumatic fibrosis Clinically confusing.
Key words Human Papilloma Virus, HPV, Oral Mucosa, Clinico-Pathological Retrospective Study.
The papillomavirus is one of the most common epithelial lesions in the oral cavity. (1), and today it is accepted that it is caused by the human papilloma virus (HPV), which was isolated in animals (2) and its presence in human lesions have been widely demonstrated (1). HPV infection in the oral mucosa, was first demonstrated in animals for over fifty years. (3). This virus is transmitted by direct contact, and most lesions of the oral cavity are due to direct contact orogenital autoinoculation and relationships, this gives rise to the growth of HPV may be in skin and mucosa (face, the body, and oral cavity). (4). Human Papilloma Virus (HPV) belongs to a group of DNA viruses, double stranded helical protected capsid proteins containing fixing surface enabling the virus to susceptible cells. (5). This virus induces the formation of hyperplastic lesions, papillomatous and warty skin and mucous membranes of animals. (6-7) Similar results have been reported in different parts of the human body including the anogenital tract, urethra, skin, tracheobronchial mucosa, nasal cavity , sinuses, oral cavity, esophagus and conjunctiva. (8-9).
Has been isolated from a variety of benign, premalignant and malignant lesions of the mouth from which we papilloma, condyloma acuminatum, verruca vulgaris, Multifocal epithelial hyperplasia, papillomatous hyperplasia, fibrous hyperplasia, squamous cell carcinoma, lichen planus and leukoplakia. Their presence has been demonstrated by techniques Histopathology, ultrastructure, molecular biology technique (Molecular Hybridization, Immunohistochemistry and Chain Reaction Polymerase) (10-11).
Currently have identified more than 95 types of HPV, which show variable oncogenic potential malignancy (12-13). Thus the type 6 and 11 is common genital condylomata acuminata type and respiratory papillomas (14). The types 16,18,31,33,35,45 and 56 are isolated from anogenital lesions and malignant buccal and type 5 and 8 are associated with skin cancer in patients with hereditary dysplasia verruciformis. (15).
Papillomaviruses are classified according to the host and the relationship of their nucleic acids (3). The virus isolated from the same species are subclassified into types according to the homology of their nucleic acid sequence. Any virus isolated having a sequence of less than 50% approval with existing, is designated as a new type and the number is assigned according to the order of discovery, if the homology is greater than 50% is considered a subtype but if the homology reaches 100% with only a few differences in the nucleotide sequence are considered as a variant of the same type of virus. HPV viral particles are identical in appearance both in animals and in humans, and is a DNA core enclosed within a viral capsid protein to be observed by electron microscopy. Viral reproduction occurs when the virus penetrates the cell alive and to be in the intracellular environment and loses its capsid genome enters the nucleus and the ability to encode gain structure and synthesise cellular proteins which give rise to capsid, nucleic acids and enzymes necessary to produce new virus, the which are released to infect new cells and when cell death occurs not possibly give rise to chronic infection (16).
In recent years there has been an increase in the incidence of disease caused by HPV, which may be due to changes in sexual habits and promiscuity among the population in the last two decade. Another form of infection at oral occurs through improper sterilization of medical and surgical instruments for endoscopic examination and oral, although infection may also occur during childbirth or transplacental contamination (17). The risk of infection increases in gay, bisexual, chronic smoking, promiscuous, drug addicts, immunosuppressed patients and in those patients taking oral contraceptives, progesterone and / or steroids (18).
The incubation period is three to six months, beginning immediately after the initial sexual contact with an infected person, but when HPV is transmitted from person to person, the virus infects the top layers of the skin and can remain inactive or dormant for months or years before appearing a wart or other signs of infection. The spread of infection can be horizontal by sexual transmission also occurs through the smoke generated during electrocoagulaciones the cervix, which may displace the viral particles that may contaminate the nasal passages and sinuses physician Handler, (19). Vertical, is non-sexual and occurs through intrauterine infection of the fetus (20).
The clinical features of oral papillomas most is that they are small and do not exceed centimeter (3) although sometimes larger lesions can be found. Clinically have a rough surface whose color varies from pink to white, depending on the degree of keratinization of the mucosa may be sessile or pedunculated, arising at any age between the third and fifth decade of life (3). Studies of incidence by age in our country have shown a rise from 25 years, down to 34 years, when stabilized to descend again after 50 years. (21). It can appear anywhere in the mouth being the most common inner lip, hard and soft palate, uvula and lateral border of tongue. (22-23-3).
For diagnosis we use various methods, such as observation by light microscopy, in this specific changes are observed in the cell tissue in the pattern of growth and appearance of the core, with the electron microscope can observe icosahedral structure and the diameter of the viral particles with an accuracy of 10 to 50% and more accurate techniques using molecular biology methods (immunohistochemistry and hybridization techniques chain reaction of the polymerase.).
The aim of this study was to determine the frequency of oral mucosa papilloma in the population attends the Dental Clinic of the Faculty of Dentistry at the Universidad Central de Venezuela, and make comparisons with data collected and published in our country as in the literature, in order to determine if there are similarities or differences that establish patterns of behavior of the disease in Venezuela.p align = “center”>
4. Materials and methods.
This paper is a retrospective clinical pathological lesions with presumptive diagnosis of oral papilloma in 250 individuals of a total population of 30,000 patients treated at the Department of Clinical Stomatology, Faculty of Dentistry, Central University of Venezuela, in a 10-year period, from July 1988 to July 1998.
The information on this population was obtained from the registers of clinical consultation service for patients, there was obtained the data from the name, the number of patient records, and file history is chair of Dental Clinic collected the data needed to establish the research variables.
Medical records were reviewed and discarded those where there was no doubt confirmed or presumptive clinical diagnosis of papilloma, once selected medical records data were transferred to the investigation form, developed for this purpose, which contains the following data namely: Name, age, ethnicity, gender, occupation, location of injury, provisional diagnosis and definitive diagnosis.
These 250 patients with presumptive diagnosis of oral papilloma histopathology was performed to confirm the diagnosis thus resulting provisional total of 57 patients with diagnosis of oral papilloma, the rest were for other disease entities.
Of the 250 stories with presumptive clinical diagnosis of oral papilloma, we found that 57 individuals underwent biopsy for definitive diagnosis of the lesion studied. In this group of records, it was found that 18 were males and 39 to 31.58% female, which gives a percentage of 68.42% (Figure 1).
As for the final diagnosis of the 57 stories was found that only 34 to 59.6% were oral papillomas, 21 with 36.8% of fibroids, 1 to nevi and another verruca vulgaris to 1.8% each. (Figure 2).
With respect to the location of the lesions were located in the tongue 18 lesions that corresponded to 31.6% 16 28.1% lips, hard palate 12 corresponding to 21.0%, on inside of cheeks 2 to 3.5% and marginal gingiva with 15.8% in September. (Figure 3).
With regard to the ethnic group most affected must be Caucasoid group 23 cases were observed for 40.4%, 32 injuries mestizos corresponding to 56.1% and 2 black ethnicity injuries to 3.5%. (Figure 4).
In terms of age, the patients studied were between 16 and 70 years and between 16 and 19 years found one case to 1.8%, between 20 and 29 years 10 to 17.5 cases %, between 30 and 39 years 11 cases were found to be 19.3%, the same percentage was achieved between 40 and 49 years, between 50 and 59 years were 14 cases with 24.6%, from 60 and 69 reported 8 cases and finally 14.0% between 70 and 80 years old 2 cases with 3.5% (Figure 5).
Papilloma of the oral cavity is considered by many authors as a neoplasm of epithelial origin (24). However, Batsakis, 1979 (25), describes the papillomavirus as a localized reaction.
Its etiology is not well defined, most authors agree that there is no correlation between the development of this injury trauma and infections, however Cheville and Olson, 1964 (2), tested the oral papilloma viral origin in experimental animals. Studies Frithof and Werson, 1967 (26), and Jenson et al., 1982 (27) among others, have demonstrated the presence of viral particles and antigens associated with human papillomavirus (HPV), and in 1984 Syrjanen et al. , (1), were able to isolate these virus particles and antigen detection techniques HPV DNA in the human oral papilloma.
Knapp, 1971 (28); Premoli and Christensen, 1985 (22), described as an entity that appears frequently in the oral cavity. The frequency found in this study, was 57 cases in a retrospective review of 10 years, where we reviewed 250 stories, which equates to a 24.8% frequency. This shows a high frequency, to compare it with other studies reported in the country as of Lamura and Premoli, 1989 (23), in a review period of 20 years, with 147 lesions with an incidence of 2.1%.
Regarding the age groups of patients, this study shows that the most commonly found between the third and fifth decade of life, which is consistent with previous studies by Greer results and Goldman, 1974 (29) , and Premoli and Christensen, 1985 (22), which reported that the average age is 38 years with a peak incidence between 30 and 50 years.
As for the location of the lesion was found, that the site is the most prevalent language, followed by the inside of the lower lip and the hard palate, according to authors such as Greer and Goldman, 1974 (29), and Abbey and Col., 1980 (30), who found that the place of greatest appearance of the lesion was in tongue, palate and lips and in Venezuela with previous studies by Lamura and Premoli, 1989 (23) and Jimenez et al ., 1998 (21), who reported that the most common site is the tongue, followed by the lip, palate and gums.
In the 57 cases studied, it was observed that corresponded to 39 female and 18 male, meaning that most often occurs in women (a ratio of 2,11:1), but in most of the literature studied is no association with sex as occurs in both at the same frequency. Abbey et al., 1980 (30) reported a slight bias towards males in a ratio of 1.04:1, in a review of 464 lesions; Kohn et al., 1963 (31), speak of a higher incidence in males by a ratio of 3:1. As seen in previous studies was a slight predominance of men over women in other countries. However, in studies of similar frequency in Venezuelan populations reported a higher prevalence in females, which is consistent with data reported by Lamura and Premoli, 1989 (23) and Jimenez et al., 1998 (21). It is important to note that of the 57 cases, 21 were diagnosed clinically as fibroma, which suggests that not being keratinized surface and whitish lack of an error may occur in the clinical diagnosis given to be easily confused with the fibroid , found a case with a provisional diagnosis of pigmented nevus, which was misdiagnosed because of size, as it reaches a few millimeters and presenting pigmentation, plus a case with the provisional diagnosis of wart, this being a HPV lesion. with similar clinical appearance. We can conclude that there is a margin of error in the compactness index of clinical diagnosis and histopathological, which may be due to lack of clinical experience by students who bring their patients to the service or lack of calibration between staff Teachers attending the service.
With respect to ethnic groups affected, it was observed that the highest percentage is in the mestizos, which is easily explained by the amalgamation of ethnic groups that are crossed in our population.
The papilloma is a relatively common injury in the population that goes to service Dental Clinic, Faculty of Dentistry, UCV, between July 1988 and July 1998 with the highest incidence in females, between the third and fifth decade of life.
The most common site of injury was the language with 31.6% followed by the inner lips of 28.1%.
Clinically, the lesion may be confused with the fibroid by 36.8% of the cases studied.
None of the lesions studied were related to previous trauma or infection.
1. Syrjanen.K, Happonen.RP, Syrjanen.F, Colonius.B Human papilloma virus (HPV) and Local inmunologic antiges reactivity in oral squamous cell tumor and hyperplasia. Scand J Dent.1984; 92:358-370.
2. Cheville. NF, Olson.C. CarCine Citoly of the oral papilloma. Am J.Pathol.1964; 45:849-872.
3. Chang.F, Syrjanen.S, Kellookoski.J. Human Papillomavirus (HPV) and Their Associations with infevtions oral disease. J. Oral Pathol Med 1991; 20 305-17
4. Perrone. M. Viral Infections of dental interest. Venezuelan Dental Act. 1988, 26 (2) 33-35.
5. Jawetz.W, Melnick.JL, Adelberg.EA. Viral Infections Modern Medical Microbiology Handbook SA . Mexico DF Ed 1992.14, pp. 608-611.
6. Pfister H. Biology and biochemistry of papillomavirus types. Rev Physiol Biochem Pharmacol. 1984, 99 (1) :12-81.
7. Pfister.H, Krubke.J, Dietrich.W, Ifter.T, Fuchs.P. Classification of the papillomaviruses-mapping the genome. Ciba found symp.1986, 120: 3-119.
8. Zur Hausen. Human Papillomaviruses and Their rolein squamous cell carcinomas possible. Curr Top Microbiol immunol.1977, 78 1-30.
9. Chang. F, Shen. Q, Zhoul. J, Wang.C, Wang.D, Syrjanen.S, Syrrjanen.K. Detection of Human Papillomavirus DNA in cytologic specimens derived from sopliageal precancer lesions and Cancer. Scand J. Gastroenterol. 1990, 25: 383-8.
10. Syrjanen.k, Syrjanen.S, Lamberg.M, Pyrhourn.S, Niutinen.J. Morphological and immunohistochemical evidence suggesting human papillomavirus (HPV) in oral squamos involvethent cell carcinogenesis. J.Oral Surg. 1983, 12:418-24.
11. Scully. C; Cox.MF, Primer.SS, Manitand.NJ. Papillomaviruses. The current status in relation to oral disease. Surg.OralMed.Oral Oral Pathol. 1988, 65:526-32.
12. DeVilliers.EM, Gissman.L, Zurhausen.H. Human Papillomavirus types 6 and 11 DNA sequences in genital and larygeal papillomas and in some cervical Cancers, molecular cloning of viral DNA from human genital warts. J.Virol. 1981, 40:932-935.
13. Hageusee.M. Human papillomavirus vaccine. Infect Urol 1999, 12 (11) 518-19.
14. Firzloff.JM, Gallowag.DA, Eiseman.RN. The E7 protein of human papillomavirus type 16 is phosphaylated by casein Kinese II. New Biol 1989, 1: 44-53.
15. Ostrow.RS, Bender.M, Dimura.N. Human papillomavirus DNA in cutaneous primary and metastasized squamous cell carcinomas from patients with epidermodysplasia verruciformis. Proc.Natl.Acad. USA.1998 Sci, 79:1634-1638.
16. Da Costa. JJ, Silveira.FR, Batista.JM, Birman.EG. Human Papillomavirus – ITS Epthelial Association with proliferative lesions. Braz Dent J. 1994; 5:5-10.
17. Balsdon. MJ, Herane.MI. Genital Wart papilloma virus infection in Humano.Bol.Hosp .. San Juan de Dios. 1995, 42 (2): 64-71.
18. Gross.G. Human Papilloma Virus. Microbiology. 1990 Cap 4 pp 837.
19. Kashima.HK. Recurrent respiratory papillomatosis. Obstetrics and Gynecology. C.D. Clincs of North America 1996, 23:699-703.
20. Ferenczy, A; Bergeron., C. Human Papillomavirus DNA in fomites on objects used for management of patients with genital human papillomavirus infections. Obsted Gynecol. 1989, 74:950.
21. Jimnez.C, Correnti.M. Detection and typing of Human Papillomavirus in a group of Venezuelan patients with benign clinical entities of the oral cavity. 1998.; Thesis Venezuela. Central University of Venezuela.
22. Premoli. G, Christense.C. A clinical study of virus induced Histological human papillomavirus. 1985 Thesis University of California USA. Los Angeles California.
23. Lamura.A, Premoli.G. Epidemiological Study of 147 cases of oral papilloma (Venezuela) 1st. Party. Dental Act Venezolana.27 :27-32.
24. Shaffer.WG, Hine.ML, Levy. BM. Oral Pathology. 4th edition 1983 Philaderphia W.B. Saunders.
25. Batsakis.JG. Tumor of head and neck. Clinical and pathologic considerations. 1979, 2 nd edition. Baltimore. Williams and Wilkins, pp. 76.
26. Frithof.L and Warsall.J. Pasticles like Virus in human oral papilloma. Otorrinolaringol Act 1967, 64:263-266.
27. Jenson. AB, Lancaster. WD, Hostman.DP, Shaffer.EL. Frecunency and distribution of papillomavirus structural antigens in verrucae, multiple papillomas and condylomata of the oral cavity. Am.J Pathol.1982; 107:212-218.
28. Knapp.MJ. Oral disease in the consecutive oral examinations. J. Dent Assoc. 1971, 83: 1288-1293.
29. Greer.RO and Goldman. Oral papillomas, restropective clinicopathologic evaluation and examination for dyskeratosis in 110 lesions. Oral Surg Oral Med Oral Pathol. 1974, 38:435-440.
30. Abbey. LM, Page.RG and Sawyer.DR. The clinical and histopathological factors of a series of 464 oral squamous cell papillomas. Oral Surg Oral Med Oral Pathol. 1980, 49:419-428.
31. Kohn.EM, Dahlin.DC and Erick.K. Primary Neoplasms of the SOST and palates and the uvula staff Clinc.1963 Meet Magician; 38:233-241.
Prez Jimnez and Celenia2 Cecilia1 –
Added 1Profesor. Chair of Clinical Stomatology. Faculty of Dentistry. Central University of Venezuela. Founding Member of the Society of Oral Pathology.
Associate 2Professor. Chair of Clinical Stomatology. Faculty of Dentistry, Central University of Venezuela. Founding Member of the Society of Oral Pathology.