Chronic Periodontitis−Human Papillomavirus Synergy in Base of Tongue Cancers

Tezal, Miné; Nasca, Maureen Sullivan; Stoler, Daniel L.; Melendy, Thomas; Hyland, Andrew; Smaldino, Philip J.; Rigual, Néstor R.; Loree, Thom R.

doi:10.1001/archoto.2009.6

Cited by 76 publications

(88 citation statements)

References 26 publications

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“…Whether periodontal disease is related to oral HPV infection remains controversial (20)(21)(22), though the presence of such inflammatory diseases may serve an important role in the biology of HPV infection. On the other hand, HPV may be involved in deterioration associated with periodontal disease (i.e., increased alveolar bone loss) in accordance with other pathogenic factors (18). Similarly, the presence of human viruses, including the herpes virus and Epstein-Barr virus, in periodontal sites may worsen periodontal disease (23,24).…”

Section: Discussionmentioning

confidence: 99%

“…However, a significant association between smoking and HPV viral copy number was not identified in the present study (data not shown). On the other hand, gingivitis and periodontal disease are also potential risk factors for oral HPV infection (16)(17)(18), indicating that poor oral hygiene may induce the risk of HPV infection in gingival pockets. A comparison of denture wearers and non-wearers demonstrated a higher HPV infection rate in the former, indicating that mucosal injury or poor dental hygiene associated with denture use is importantly involved in HPV infection (8,9).…”

Section: Discussionmentioning

confidence: 99%

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High HPV16 E6 viral load in the oral cavity is associated with an increased number of bacteria: A preliminary study

et al. 2017

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Abstract. In a previous study, the present research group reported that males had a significantly higher prevalence of human papillomavirus (HPV)16 than females in oral rinse samples. The objective of the present study was to examine the relationship between HPV16 viral load and clinical factors, including remaining teeth, denture use and numbers of oral bacteria. A total of 124 patients (48 males and 76 females; mean age, 61.6 years; age range, 20-97 years) who visited the Department of Oral and Maxillofacial Reconstructive Surgery of Hiroshima University Hospital (Hiroshima, Japan) between November 2016 and August 2017 were analyzed. None of the patients had evidence of oral cancer or pre-malignant lesions, including epithelial dysplasia and leukoplakia. Quantitative polymerase chain reaction (qPCR) analysis was employed to examine the number of HPV16 viral copies. Furthermore, the number of oral bacteria was determined using the dielectrophoretic impedance measurement method. HPV16 was below the limit of detection in qPCR findings for samples obtained from 30 of the 124 subjects, thus the association of HPV16 viral copy number with clinical parameters was examined in the remaining 94 patients. The average number of HPV16 E6 DNA copies was 1.65±3.47 copies/cell (range, 0.07-25.3 copies/cell) and was significantly higher in subjects with a high oral bacteria count [≥10 6.5 colony forming unit (CFU)/ml] than in those with a low count (<10 6.5 CFU/ml) (0.79±0.98 vs. 2.06±4.11 copies/cell; P=0.030). The present results indicated that HPV16 viral load may be related to an increased bacterial number in the oral cavity. Further investigations are required to clarify the correlation between oral HPV load and oral hygiene status. IntroductionHuman papillomavirus (HPV) infection is a major cause of cervical cancer and is also associated with the development of oropharyngeal cancer and prognosis in affected patients (1-3). To date, >170 HPV genotypes have been reported, of which ~50 are known to infect the anogenital and oral mucosa regions (4-6). As for oral cancer, a previous study conducted by the present research group indicated that ~80% of patients with HPV16-positive moderate epithelial dysplasia progressed to oral squamous cell carcinoma (OSCC), indicating that oral HPV16 infection may also be associated with the development of oral cancer (7). However, few epidemiologic studies have focused on oral HPV prevalence in non-OSCC cases and the risk factors for oral HPV infection have not been fully elucidated. Hence, we previously performed a meta-analysis, which demonstrated that sexual behavior and smoking are significant risk factors for oral HPV infection in cancer-free individuals (8). In addition, other factors, such as poor oral hygiene related to periodontitis and gingivitis, have been indicated to be associated with oral HPV infection (8).In order to examine the correlation between HPV16 prevalence in the oral cavity and clinical factors, we also investigated HPV16 prevalence using oral rinse samples obtaine...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

High HPV16 E6 viral load in the oral cavity is associated with an increased number of bacteria: A preliminary study

et al. 2017

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“…Tezal et al found an association with HPV+ status and alveolar bone loss on evaluation of tongue cancer biopsy specimens for HPV+ or HPV− status from 30 participants and determined periodontal status by the panoramic radiographic alveolar bone loss. [7] In the present case report, a final diagnosis of squamous cell papilloma with mild dysplasia was made on the basis of clinical presentation and histopathology of the lesion. On histopathological evaluation lesion present as papillary projections lined by stratified squamous epithelium.…”

Section: Discussionmentioning

confidence: 89%

The squamous cell papilloma of gingiva with mild dysplasia: A case report

Dhavan¹,

Shiggaon²,

Waghamre³

et al. 2017

IJMDCR

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Squamous papillomas are benign proliferating lesions caused by human papillomavirus. Periodontitis is a multifactorial disease affecting the oral cavity with main etiologic factor as a microbial biofilm. Recently, viruses have shown association with periodontitis. Periodontal pockets and gingival sulcus of patients with periodontal diseases exhibit the presence of human papillomaviruses (HPV). This could link periodontitis to HPV associated squamous cell carcinoma. HPV most commonly affects the oral cavity with a predilection for the tongue, hard and soft palate, gingiva, buccal mucosa, and uvula. Hence, we present a case report of chronic periodontitis patient with squamous cell papilloma of gingiva with mild dysplasia.

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“…proliferation following low level (e.g., 5%,v/v, 50 mg/mL.) ETOH treatment will increase expression of Annexin A2, and EGFR to also enhance HPV 16 entry [13,14,[18][19][20][21][22][23][24][25][26][27][28][29][30][31][32].…”

Section: Set Of Comparative Assays To Examine Associations Of S Salimentioning

confidence: 99%

“…Among human populations AA is a product of both tobacco (e.g., smoke and E-cigarette) [21] and alcohol metabolism which increases risk for oral disorders such as premalignant and malignant carcinoma [21][22][23][24][25][26][27]. AA facilitates these problems by entering epithelium through membrane to induce DNA damage, bulky adduct formation; N 2 -acetaldehyde deoxyguanine.…”

Section: Introductionmentioning

confidence: 99%

Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

2014

J Oral Biol

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Background: Oropharyngeal carcinoma is often associated with human papilloma virus subtype 16 (HPV) infections; however events that lead to HPV entry and carcinoma are poorly understood. We simulated a clinical situation in the laboratory by examining human epithelial and oral keratinocyte (HOK) responses to oral commensal bacteria (Streptococcus spp.) and metabolism of ethyl alcohol (ETOH). These studies led us to conclude that oral bacteria and ethyl alcohol through keratinocyte membrane signals act as co-factors for HPV 16 entry. Methods:We tested ETOH exposure responses of Streptococcus spp., ETOH-sensitive, acetaldehyde (AA) producers: S. mutans (LT11), S. salivarius strain, 109-2 and S. gordonii (V2016; wild type). In comparison to ETOH-resistant, non-producers of AA: S. salivarius strain, 101-7 or S. gordonii (adh ABE mutant). 5×105 per cfu/mL of bacteria were exposed to ETOH (5%,v/v) for 1h and then co-incubated for 3h with epithelial targets: immortalized: 293TT; HPV 16 (HOK/HPV 16B cells), or telomerase: hTERT HOK. Streptococci spp. attachment to epithelial cells and subsequent effects were enumerated with immune cytochemistry; Western immunoblotting, and immunoprecipitation techniques. These methods delineated expressions of syndecans-1, 4; phospho-L-tyrosine epidermal growth factor receptor (EGFR), and furin convertase (FC) with HPV 16 pseudo virus (PsV) entry into 293TT, hTERT HOKs and oral squamous cell carcinoma (SCC-25). To verify these relationships we used inhibitors of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and FC.Results: Streptococcus spp. metabolism of ETOH released AA to trigger HOK expressions of syndecans 1 and 4 and heparin sulfate binding proteins were degraded by heparanase. Following these events enhanced phosphorylated EGFR expression and HPV 16 entry through FC activity were recorded.Conclusions: Some oral Streptococcus spp. response to ETOH mediates epithelial cell susceptibility to HPV 16 entry. This occurs through membrane associated expression changes of proteoglycans and EGFR. Moreover, oral cancer cell differentiation and growth may be dependent upon these associations.

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Chronic Periodontitis−Human Papillomavirus Synergy in Base of Tongue Cancers

Abstract: Chronic periodontitis may be a significant factor in the natural history of HPV infection in patients with base of tongue cancers. Additional confirmation in larger studies is required.

Cited by 76 publications

References 26 publications

High HPV16 E6 viral load in the oral cavity is associated with an increased number of bacteria: A preliminary study

High HPV16 E6 viral load in the oral cavity is associated with an increased number of bacteria: A preliminary study

The squamous cell papilloma of gingiva with mild dysplasia: A case report

Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

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