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• W2904005611 endingPage "115" @default.
• W2904005611 startingPage "115" @default.
• W2904005611 abstract "The human body is naturally colonized by a huge number of different commensal microbial species, in a relatively stable equilibrium. When this microbial community undergoes dysbiosis at any part of the body, it interacts with the innate immune system and results in a poor health status, locally or systemically. Research studies show that bacteria are capable of significantly influencing specific cells of the immune system, resulting in many diseases, including a neoplastic response. Amongst the multiple different types of diseases, pancreatic cancer and liver cirrhosis were significantly considered in this paper, as they are major fatal diseases. Recently, these two diseases were shown to be associated with increased or decreased numbers of certain oral bacterial species. These findings open the way for a broader perception and more specific investigative studies, to better understand the possible future treatment and prevention. This review aims to describe the correlation between oral dysbiosis and both pancreatic cancer and liver cirrhotic diseases, as well as demonstrating the possible diagnostic and treatment modalities, relying on the oral microbiota, itself, as prospective, simple, applicable non-invasive approaches to patients, by focusing on the state of the art. PubMed was electronically searched, using the following key words: “oral microbiota” and “pancreatic cancer” (PC), “liver cirrhosis”, “systemic involvement”, and “inflammatory mediators”. Oral dysbiosis is a common problem related to poor oral or systemic health conditions. Oral pathogens can disseminate to distant body organs via the local, oral blood circulation, or pass through the gastrointestinal tract and enter into the systemic circulation. Once oral pathogens reach an organ, they modify the immune response and stimulate the release of the inflammatory mediators, this results in a disease. Recent studies have reported a correlation between oral dysbiosis and the increased risk of pancreatic and liver diseases and provided evidence of the presence of oral pathogens in diseased organs. The profound impact that microbial communities have on human health, provides a wide domain towards precisely investigating and clearly understanding the mechanism of many diseases, including cancer. Oral microbiota is an essential contributor to health status and imbalance in this community was correlated to oral and systemic diseases. The presence of elevated numbers of certain oral bacteria, particularly P. gingivalis, as well as elevated levels of blood serum antibodies, against this bacterial species, was associated with a higher risk of pancreatic cancer and liver cirrhosis incidence. Attempts are increasingly directed towards investigating the composition of oral microbiome as a simple diagnostic approach in multiple diseases, including pancreatic and liver pathosis. Moreover, treatment efforts are concerned in the recruitment of microbiota, for remedial purposes of the aforementioned and other different diseases. Further investigation is required to confirm and clarify the role of oral microbiota in enhancing pancreatic and liver diseases. Improving the treatment modalities requires an exertion of more effort, especially, concerning the microbiome engineering and oral microbiota transplantation." @default.
• W2904005611 created "2018-12-22" @default.
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• W2904005611 date "2018-12-11" @default.
• W2904005611 modified "2023-10-11" @default.
• W2904005611 title "Oral Dysbiosis in Pancreatic Cancer and Liver Cirrhosis: A Review of the Literature" @default.
• W2904005611 cites W1518286619 @default.
• W2904005611 cites W1566844255 @default.
• W2904005611 cites W1572705565 @default.
• W2904005611 cites W1642873092 @default.
• W2904005611 cites W1756046628 @default.
• W2904005611 cites W1825346247 @default.
• W2904005611 cites W1869714721 @default.
• W2904005611 cites W1930644939 @default.
• W2904005611 cites W1933981076 @default.
• W2904005611 cites W1949755594 @default.
• W2904005611 cites W1964027278 @default.
• W2904005611 cites W1966827834 @default.
• W2904005611 cites W1967507143 @default.
• W2904005611 cites W1971439989 @default.
• W2904005611 cites W1972798849 @default.
• W2904005611 cites W1975391560 @default.
• W2904005611 cites W1975691929 @default.
• W2904005611 cites W1977428675 @default.
• W2904005611 cites W1978862810 @default.
• W2904005611 cites W1981185465 @default.
• W2904005611 cites W1981247190 @default.
• W2904005611 cites W1981761407 @default.
• W2904005611 cites W1983159706 @default.
• W2904005611 cites W1986718102 @default.
• W2904005611 cites W1992031722 @default.
• W2904005611 cites W1992378251 @default.
• W2904005611 cites W1997072139 @default.
• W2904005611 cites W2001458398 @default.
• W2904005611 cites W2003750215 @default.
• W2904005611 cites W2007110604 @default.
• W2904005611 cites W2008294135 @default.
• W2904005611 cites W2008733625 @default.
• W2904005611 cites W2010508425 @default.
• W2904005611 cites W2010592372 @default.
• W2904005611 cites W2012049965 @default.
• W2904005611 cites W2012179517 @default.
• W2904005611 cites W2013067182 @default.
• W2904005611 cites W2013330518 @default.
• W2904005611 cites W2015161836 @default.
• W2904005611 cites W2022649181 @default.
• W2904005611 cites W2031365879 @default.
• W2904005611 cites W2034786222 @default.
• W2904005611 cites W2042295984 @default.
• W2904005611 cites W2046118138 @default.
• W2904005611 cites W2051961396 @default.
• W2904005611 cites W2056246809 @default.
• W2904005611 cites W2056354437 @default.
• W2904005611 cites W2058793213 @default.
• W2904005611 cites W2062627337 @default.
• W2904005611 cites W2064186191 @default.
• W2904005611 cites W2064212629 @default.
• W2904005611 cites W2066673924 @default.
• W2904005611 cites W2068084277 @default.
• W2904005611 cites W2070981217 @default.
• W2904005611 cites W2072515653 @default.
• W2904005611 cites W2074819592 @default.
• W2904005611 cites W2076219872 @default.
• W2904005611 cites W2076728075 @default.
• W2904005611 cites W2078397257 @default.
• W2904005611 cites W2079758378 @default.
• W2904005611 cites W2082411151 @default.
• W2904005611 cites W2090211843 @default.
• W2904005611 cites W2093574752 @default.
• W2904005611 cites W2095566926 @default.
• W2904005611 cites W2098488968 @default.
• W2904005611 cites W2098555833 @default.
• W2904005611 cites W2100635712 @default.
• W2904005611 cites W2101866230 @default.
• W2904005611 cites W2101867417 @default.
• W2904005611 cites W2102675446 @default.
• W2904005611 cites W2105329195 @default.
• W2904005611 cites W2105871378 @default.
• W2904005611 cites W2108666079 @default.
• W2904005611 cites W2112931540 @default.
• W2904005611 cites W2120563211 @default.
• W2904005611 cites W2120715581 @default.
• W2904005611 cites W2121470572 @default.
• W2904005611 cites W2121748291 @default.
• W2904005611 cites W2123497942 @default.
• W2904005611 cites W2127743008 @default.
• W2904005611 cites W2129690444 @default.
• W2904005611 cites W2130785878 @default.
• W2904005611 cites W2132692852 @default.

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