Periodontal Disease and Risk of Head and Neck Cancer: A Meta-Analysis of Observational Studies

Zeng, Xian‐Tao; Deng, Aiping; Li, Cheng; Xia, Lingyun; Niu, Yu‐Ming; Li, Weidong

doi:10.1371/journal.pone.0079017

Cited by 106 publications

(101 citation statements)

References 28 publications

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“…(39,40) hem diş kaybı hem de periodontal hastalığın baş-boyun kanserlerinde bağımsız risk faktörleri olduğunu ortaya koymuştur. Benzer şekilde, Tezal ve ark.…”

Section: -Oral Kavite Ve Orofarinks Kanseri Ile Hpv Ilişkisiunclassified

Relationship between human papilloma virus and benign and malign lesions of oral cavity and oropharynx, current approach

Sarısoy¹,

Yıldırım²,

Sarisoy³

et al. 2018

Okmeydani Medical Journal

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ÖZ GİRİŞPapillomavirus enfeksiyonu insanlarda çok sık görü-len ve esas olarak cinsel yolla bulaşan bir hastalık-tır. Enfeksiyonlar geçici ve asemptomatiktir, ancak enfeksiyon devam ederse, Human Pailloma Virüse (HPV) bağlı olarak deri ve mukozal membranlarda zedelenmeler ortaya çıkabilir (1) .HPV enfeksiyonu sırasında, hücreler tarafından bağışıklık sistemine lokal ya da sistemik viral antijen sunumu minimaldir, enfeksiyon, klinik olarak tanın-madan aylarca ya da yıllarca devam eder. İmmün yanıtların HPV enfeksiyonlarında önemli bir rol oynadığı bilinmektedir; Cilt siğilleri genellikle kendiliğinden gerilemektedir ve HPV ile indüklenen deri veya mukozal enfeksiyon insidansı, bağışıklığı yetersiz kişilerde daha yüksektir (2) .HPV enfeksiyonunun gelişimi, uterus serviksi, diğer alt genital bölge mukozası ve oral mukozadan başlayabilir. HPV nin invazyonu ve oral epitelin dö-nüşümü çok katlı skuamoz bir epitelden ve yoğun bağ dokusuna sahip lamina propriadan oluşan oral kavitenin histolojisine bağlı olarak değişir. Gingiva, sert damak, dil sırtı tamamen keratinizeyken dudak epiteli, yanak, vestibül, alveolar mukoza, ağız tabanı ve yumuşak damakta keratinizasyon yoktur. Bu

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“…(39,40) hem diş kaybı hem de periodontal hastalığın baş-boyun kanserlerinde bağımsız risk faktörleri olduğunu ortaya koymuştur. Benzer şekilde, Tezal ve ark.…”

Section: -Oral Kavite Ve Orofarinks Kanseri Ile Hpv Ilişkisiunclassified

Relationship between human papilloma virus and benign and malign lesions of oral cavity and oropharynx, current approach

Sarısoy¹,

Yıldırım²,

Sarisoy³

et al. 2018

Okmeydani Medical Journal

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“…53 Among the rural school children between 5 to 15 years, the prevalence of dental caries, plaque, gingival bleeding and bleeding on probing was 69.6%, 91.6%, 66.8 % and 64% respectively. 54 The Link between PD and CAD Periodontitis has been found to be associated with a number of systemic diseases and conditions, including stroke, 55 peripheral arterial disease, 56 type 2 diabetes, 57 rheumatoid arthritis, 58 chronic kidney disease, 59 and chronic obstructive pulmonary disease, 60 Alzheimer's disease, 61 cancers, 62 anaemia, 63 and low-birth weight baby. [64][65] Currently, however, there is a lack of consensus among experts on the nature of these associations and confusion among health care providers and the public on how to interpret this rapidly growing body of science.…”

Section: (Figure 1)mentioning

confidence: 99%

Link between Periodontal Disease and Coronary Artery Disease: Bangladesh Perspective

et al. 2014

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Coronary artery disease (CAD) is an increasingly important medical and public healthproblem, and is the leading cause of mortality in Bangladesh. Besides conventional risk factors and ethnicity, a number of emerging risk factors may explain the undue prevalence of CAD in this population. Periodontal disease (PD) is one of them, with prevalence of approximately 50%. As with many other diseases, PD is associated with CAD, and the association is independent of conventional risk factors. Low socioeconomic condition, illiteracy and ignorance, metabolic syndrome, nutritional deficiencies including hypovitaminosis D presumably contribute to the prevalence of PD in Bangladesh. In fact, PD and CAD share some cardiometabolic risk factors including diabetes mellitus, obesity and metabolic syndrome. Future research will hopefully explore different aspects of both public health problems, namely, PD and CAD in the country. The information gathered thereby, will help formulate policy to promote good oral health and tackle the deadly epidemic of CAD more efficiently. DOI: http://dx.doi.org/10.3329/cardio.v7i1.20800 Cardiovasc. j. 2014; 7(1): 44-54

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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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Periodontal Disease and Risk of Head and Neck Cancer: A Meta-Analysis of Observational Studies

Cited by 106 publications

References 28 publications

Relationship between human papilloma virus and benign and malign lesions of oral cavity and oropharynx, current approach

Relationship between human papilloma virus and benign and malign lesions of oral cavity and oropharynx, current approach

Link between Periodontal Disease and Coronary Artery Disease: Bangladesh Perspective

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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