INVESTIGATION OF HSV1, HSV2, HPV, HPV16, EBV AND HHV8 MARKERS IN TERMS OF THE PATHOLOGICAL CHANGES IN DENTAL FOLLICLES OF HIV NEGATIVE PERSONS

Year 2019, , 16 - 21, 04.03.2019

Serap Keskin Tunç , Cennet Neslihan Eroğlu , Sevinç Şahin

https://doi.org/10.17343/sdutfd.399350

Abstract

Several viruses have been suggested to play a role in the pathogenesis of oral cancers in the literature. However, this issue has not yet been clarified. The aim of this study is to investigate the presence of possible precancerous viral markers (HPV, HHV8, HSV1, HSV2 and EBV) in the impacted teeth follicles. Material and Method 100 patient aged 18 years or older was included in the study. Following the tooth extraction, the dental follicle was removed and fixed in 10% formaldehyde. HPV (HPV 8, HPV 11 and HPV 18), p16 (HPV 16), HHV8, HSV1, HSV2 and EBV antibodies were used for histopathological and immunohistochemical studies. In addition, the immunohistochemical results were evaluated by Chi-square test in relation to clinicopathological information (age, sex and smoking status). Total of 55 men and 45 women were included in the survey. Results The age of the patients who participated in the study ranged between 17 and 56 (mean: 25). Histopathologically, inflammation, granulation tissue and pseudoepitheliomatous hyperplasia were investigated. No dysplasia or neoplasm was found. Immunohistochemical staining showed p16% 62, EBV 32% and HSV-1 26% positivity. In all cases HPV, HSV2 and HHV-8 are immunonegative. It is the first study to show the presence of HPV 16, EBV and HSV1 in dental follicles. Conclusion We can claim that these viruses can act as reservoirs to show tropism in dental follicles. Although dysplasia or neoplastic changes were not detected in this study, viral effects (especially for HPV16 and EBV) may be seen as a threat leading to dysplasia and neoplasia in long term impacted wisdom teeth . As a result, for the possible viral oncogenesis and tumorigenesis, the impacted teeth should be removed and histopathologic examination of all follicles should be performed. 

Keywords

Dental follicle, HPV, p16, HSV1, HSV2, EBV, HHV8

HIV NEGATİF BİREYLERİN DENTAL FOLİKÜLLERINDE PATOLOJİK DEĞİŞİM RİSKİ AÇISINDAN HSV1, HSV2, HPV, HPV16, EBV VE HHV8 MARKIRLARININ ARAŞTIRILMASI

Abstract

Giriş:
Literatürde çeşitli virüslerin ağız kanserlerinin patogenezinde rol aldığı öne
sürülmektedir. Ancak bu konu henüz tam olarak açıklanamamıştır. Bu çalışmanın
amacı gömülü diş foliküllerinde olası prekanseröz viral markırların (HPV, HHV8,
HSV1, HSV2, and EBV) varlığının araştırılmasıdır.

Materyal
ve Metod: 18 yaşından büyük 100 gönüllü hasta araştırmaya
dahil edildi. Gömülü diş çekimi sonrasında diş folikülü çıkartılarak %10’luk
formaldehit içinde fikse edildi. Histopatolojik ve immünohistokimyasal
araştırma için HPV (HPV 8, HPV 11 ve HPV 18), p16 (HPV 16), HHV8, HSV1, HSV2,
EBV antikorlar kullanılmıştır. Ayrıca immünohistokimyasal sonuçların
klinikopatolojik veriler (yaş, cinsiyet ve sigara içme durumu) ile ilişkisi
Ki-Kare Testi ile değerlendirilmiştir. 55 erkek ve 45 kadın araştırmaya dahil
edildi.

Bulgular:
Araştırmaya katılan hastaların yaşları 17-56 (ortalama:25) arasında
değişmekteydi. Histopatolojik olarak inflamasyon, granülasyon dokusu ve
psodöepitelyomatöz hiperplazi varlığı araştırıldı. Displazi veya neoplaziye
rastlanmadı. İmmünohistokimyasal boyamada p16 %62 oranında, EBV %32 oranında ve
HSV-1 %26 oranında pozitiflik saptanmıştır. Tüm vakalarda HPV, HSV-2 ve HHV-8
immünonegatiftir. Bu bilinen diş folikülünde HPV 16, EBV ve HSV1 varlığını gösteren ilk çalışmadır.

Sonuç:
Bu virüslerin gömülü diş foliküllerinde tropizmi göstermek için rezervuar
olarak işlev gördüklerini ileri sürebiliriz.  Herhangi bir displazi veya neoplastik değişim tespit edilmemesine karşın
viral etkilerin (özellikle HPV16 ve EBV için) uzun süre gömülü kalan dişlerde
displazi ve neoplazm için tehdit olarak kabul edilebilir. Sonuç olarak
olası viral onkogenezi ve tümörgenezi önlemek için gömülü kalan dişlerin çekimi
yapılmalı ve sonrasında tüm foliküllerin histopatolojik incelenmesi
yapılmalıdır.

Keywords

diş, germ, HPV, p16, HSV2, HSV1, EBV, HHV

References

• Adelsperger J, Campbell JH, Coates DB, Summerlin DJ, Tomich CE (2000). Early soft tissue pathosisassociated with impacted third molars without pericoronal radiolucency. Oral Surgery Oral Medicine Oral Pathology Oral Radiology Oral Endodontics. 2000; 89(4):402-406.
• Adeyemo WL. Do the pathologies associated with impacted lower third molars justify prophylactic removal? A critical review of literature. Oral Surgery Oral Medicine Oral Pathology Oral Radiology Endodontic. 2006;102:448-452.
• Leitner C, Hoffmann J, Kröber S Reinert S. Low-grade malignant fibrosarcoma of the dental follicle of an unerupted third molar without clinical evidence of any follicular lesion. Journal of Cranio-Maxillofacial Surgery. 2007;35:48-51.
• Gillison ML, Koch WM, Capone RB, Spafford M, Westra WH, Wu L, Zahurak ML, Daniel RW, Viglione M, Symer DE, Shah KV, Sidransky D. Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. J Natl Cancer Inst. 2000;92(9):709-20.
• Chen G, Stenlund A. The E1 initiator recognizes multiple overlapping sites in the papillomavirus origin of DNA replication. J Virol. 2001;75(1):292-302.
• Slots J, Saygun I, Sabeti M, Kubar A. Epstein-Barr virus in oral diseases. J Periodontal Res. 2006;41(4):235-44. Review.
• Regezi JA, Sciubba JJ, Jordan RCK. Oral Pathology Clinical Pathologic Correlations. 4th ed., Sounders, St. Louis, 2003; p. 1-11.
• Pérez CL, Tous MI, Zala N, Camino S. Human herpesvirus 8 in healthy blood donors, Argentina. Emerg Infect Dis. 2010;16(1):150-1.
• Becker G, Bottke D. Radiotherapy in the management of Kaposi's sarcoma. Onkologie. 2006;29(7):329-33
• Reyes M, Rojas-Alcayaga G, Pennacchiotti G, Carrillo D, Muñoz JP, Peña N, Montes R, Lobos N, Aguayo F. Human Papillomavirus infection in oral Squamous cell carcinomas from Chilean patients. Experimental and Molecular Pathology. 2015;6(99,1):95-99.
• Elamin F, Steingrimsdottir H, Wanakulasuriya NJ, Tavassoli M. Prevalence of human papillomavirus infection in prremalignant and malignant lesions of the oral cavity in U.K. subjects: a novel method of detection. Oral Oncology.1998;34:191-197.
• Ostwald C, Rutsatz K, Schweder J, Schmidt W, Gundlach K ve Barten M. Human Papillomavirus 6/11, 16 and 18 in oral carcinomas and benign oral lesions. Medical Microbiology and Immunology. 2003;192:145-148.
• Portugal LG, Goldenberg JD, Wenig BL ve Ferrer KT. Human papilloma expression and p53 gene mutations in squamous cell carcinoma. Archieves of Otolaryngology Head Neck Surgery. 1997;123:1230-1234.
• Lambropoulos AF, Dimitrakopoulos J, Frangoulides E, Katopodi R, Kotsis A, Karakasis D. Incidence of human papillomavirus 6, 11, 16, 18 and 33 in normal oral mucosa of a Greek population. European Journal of Oral Science. 1997;105: 294-297.
• Balaram P, Nalinakumari KR, Abraham E, Balan A, Hareendran NK, Bernard HU, Chan SY. Human papillomaviruses in 91 oral cancers from Indian betel quid chewers--high prevalence and multiplicity of infections. Int J Cancer. 1995;61(4):450-4.
• Lazzari CM, Krug LP, Quadros OF, Baldi CB, Bozzetti MC. Human papillomavirus frequency in oral epithelial lesions. Journal of Oral Pathology Medicine. 2004;33:260-265.
• Smith EM, Ritchie JM, Summersgill KF, Klussmann JP, Lee JH, Wang DH Haugen TH, Turek LP. Age, sexual behavior and human papillomavirus infection oral cavity and oropharyngeal cancers. International Journal of Cancer. 2004;108:766-772.
• Antonsson A, Neale RE, Boros S, Lampe G, Coman WB, Pryor DI, Porceddu SV, Whiteman DC. Human papillomavirus status and p16(INK4A) expression in patients with mucosal squamous cell carcinoma of the head and neck in Queensland, Australia. Cancer Epidemiology. 2015;39(2):174-181.
• Rosen BJ, Walter L, Gilman RH, Cabrerra L, Gravitt PE, Marks MA. Prevalence and correlates of oral human papillomavirus infection among healthy males and females in Lima, Peru. Sex Transm Infect. 2015;8:14.
• Polz-Gruszka D, Morshed K, Stec A, Polz-Dacewicz M. Prevalence of Human papillomavirus (HPV) and Epstein-Barr virus (EBV) in oral and oropharyngeal squamous cell carcinoma in south-eastern Poland. Infect Agent Cancer. 2015;12(10):37.
• Klemenc P, Skalerič U, Artnik B, Nograšek P, Marin J. Prevalence of some herpesviruses in gingival crevicular fluid. Journal Clinic Virology. 2005;34(2): 147-152.
• Cassai E, Galvan M, Trombelli L, Rotola A. HHV-6, HHV-7, HHV-8 in gingival biopsies from chronic adult periodontitis patients. A case-control study. Journal of Clinical Periodontology. 2003;30(3):184-191.
• Madinier I, Doglio A, Cagnon L, Lefèbvre JC, Monteil RA. Epstein-Barr virus DNA detection in gingival tissues of patients undergoing surgical extractions. British Journal Oral Maxillofacial Surgery. 1992;30(4):237-243.
• Kuruppu D, Tanabe KK. HSV-1 as a novel therapy for breast cancer meningeal metastases. Cancer Gene Ther. 2015;22(10):506-8.
• Skeate JG, Porras TB, Woodham AW, Jang JK, Taylor JR, Brand HE, Kelly TJ, Jung JU, Da Silva DM, Yuan W, Kast WM. Herpes Simplex Virus downregulation of secretory leukocyte protease inhibitor enhances Human Papillomavirus type 16 infection. J Gen Virol. 2015;11:10.
• Skeate JG, Porras TB, Woodham AW, Jang JK, Taylor JR, Brand HE, Kelly TJ, Jung JU, Da Silva DM, Yuan W, Kast WM. Herpes Simplex Virus downregulation of secretory leukocyte protease inhibitor enhances Human Papillomavirus type 16 infection. J Gen Virol. 2015;11:10.
• Schwartz RA. Kaposi's sarcoma: an update. J Surg Oncol. 2004;87(3):146-51.
• Régulier EG, Reiss K, Khalili K, Amini S, Zagury JF, Katsikis PD, Rappaport J. T-cell and neuronal apoptosis in HIV infection: implications for therapeutic intervention. Int Rev Immunol. 2004;23(1-2):25-59.
• Mardirossian A, Contreras A, Navazesh M, Nowzari H, Slots J. Herpesviruses 6, 7 and 8 in HIV- and non-HIV-associated periodontitis. Journal of Periodontal Research. 2000;35(5):278-284.