Acetaldehyde production and microbial colonization in oral squamous cell carcinoma and oral lichenoid disease

Marttila, Emilia; Uittamo, Johanna; Rusanen, Peter; Lindqvist, Christian; Salaspuro, Mikko; Rautemaa, Riina

doi:10.1016/j.oooo.2013.02.009

Cited by 55 publications

(52 citation statements)

References 40 publications

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“…Microbes cultured from samples of smokers produced significantly higher amounts of acetaldehyde than those of non-smokers. The study thus highlights the importance of good oral hygiene, especially with potentially malignant lesions in the oral cavity [50].…”

Section: Possible Role Of Malodorous Gases In Carcinogenesismentioning

confidence: 67%

“…In a study of 30 subjects with oral squamous cell carcinoma, 30 with oral lichenoid disease, and 30 who were healthy, the oral microbiota from each lesion or control site showed the ability to produce carcinogenic levels of acetaldehyde ( 4100 μM) [45,50]. Microbes cultured from samples of smokers produced significantly higher amounts of acetaldehyde than those of non-smokers.…”

Section: Possible Role Of Malodorous Gases In Carcinogenesismentioning

confidence: 99%

See 1 more Smart Citation

Oral malodorous gases and oral microbiota: From halitosis to carcinogenesis

Tanda

Hoshikawa

Ishida

et al. 2015

Journal of Oral Biosciences

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Section: Possible Role Of Malodorous Gases In Carcinogenesismentioning

confidence: 67%

Section: Possible Role Of Malodorous Gases In Carcinogenesismentioning

confidence: 99%

Oral malodorous gases and oral microbiota: From halitosis to carcinogenesis

Tanda

Hoshikawa

Ishida

et al. 2015

Journal of Oral Biosciences

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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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“…По результатам исследований также было уста-новлено, что формирование дисбиоза на СОПР при красном плоском лишае и красной волчанке в зна-чительной степени повышает риск развития малиг-низации с трансформацией дерматозов в плоско-клеточный рак [14,15].…”

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State-of-the-art capabilities of improving the treatment of the diseases of the oral mucosa

Perlamutrov¹,

Trofimova²,

Glebova³

et al. 2015

Klin. dermatol. venerol.

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Слизистая оболочка полости рта является уникальной эконишей, на микробиоценоз которой воздействует большое количество экзогенных и эндогенных факторов. Цель настоящего исследования -оценка эффективности препарата Фурасол в терапии дерматозов и воспалительных заболеваний с локализацией на слизистой оболочке полости рта. Материал и методы. В исследовании приняли участие 96 больных с заболеваниями слизистой оболочки полости рта. Всем пациентам проводили клинический осмотр с определением гигиенического статуса и лечение. Для выявления особенностей микробного пейзажа полости рта использовали культуральный метод исследования. Результаты. Назначение препарата Фурасол (3 раза в день в течение 5-7 дней) способствовало сокращению сроков лечения и эрадикации патогенной микробиоты у большинства пациентов. Ключевые слова: слизистая оболочка полости рта, красный плоский лишай, многоформная экссудативная эритема, токсидермия, гингивит, стоматит, Фурасол, клиническая эффективность.The oral mucosa is a unique econiche, whose microbiocenosis is affected by a large number of exogenous and endogenous factors. Objective. This study is aimed at assessing the efficacy of Furasol in treatment of dermatoses and inflammatory diseases localized on the oral mucosa. Material and methods. The study involved 96 patients with oral mucosa diseases. All patients underwent clinical examination, including assessment of hygienic status, and treatment. The culture method was used to identify the characteristics of the microbial landscape of the oral cavity. Results. The use of Furasol (3 times per day during 5-7 days) contributed to reducing the duration of treatment and eradication of pathogenic microbiota in most patients.

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Acetaldehyde production and microbial colonization in oral squamous cell carcinoma and oral lichenoid disease

Cited by 55 publications

References 40 publications

Oral malodorous gases and oral microbiota: From halitosis to carcinogenesis

Oral malodorous gases and oral microbiota: From halitosis to carcinogenesis

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

State-of-the-art capabilities of improving the treatment of the diseases of the oral mucosa

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