Periodontitis From Dysbiotic Microbial Immune Response to Systemic Inflammation

Periodontitis is an infection-induced inflammatory disease accounting for huge healthcare costs and socio-economic impacts. Bacteria from the indigenous oral flora colonize the interspace between the tooth and the connective tissue, which induces an inflammatory response. If the bacteria proliferate...

Full description

Saved in:
Bibliographic Details
Other Authors: Johansson, Anders (Editor)
Format: Electronic Book Chapter
Language:English
Published: Basel, Switzerland MDPI - Multidisciplinary Digital Publishing Institute 2020
Subjects:
Online Access:DOAB: download the publication
DOAB: description of the publication
Tags: Add Tag
No Tags, Be the first to tag this record!

MARC

LEADER 00000naaaa2200000uu 4500
001 doab_20_500_12854_69297
005 20210501
003 oapen
006 m o d
007 cr|mn|---annan
008 20210501s2020 xx |||||o ||| 0|eng d
020 |a books978-3-03943-508-1 
020 |a 9783039435074 
020 |a 9783039435081 
040 |a oapen  |c oapen 
024 7 |a 10.3390/books978-3-03943-508-1  |c doi 
041 0 |a eng 
042 |a dc 
072 7 |a M  |2 bicssc 
100 1 |a Johansson, Anders  |4 edt 
700 1 |a Johansson, Anders  |4 oth 
245 1 0 |a Periodontitis  |b From Dysbiotic Microbial Immune Response to Systemic Inflammation 
260 |a Basel, Switzerland  |b MDPI - Multidisciplinary Digital Publishing Institute  |c 2020 
300 |a 1 electronic resource (122 p.) 
336 |a text  |b txt  |2 rdacontent 
337 |a computer  |b c  |2 rdamedia 
338 |a online resource  |b cr  |2 rdacarrier 
506 0 |a Open Access  |2 star  |f Unrestricted online access 
520 |a Periodontitis is an infection-induced inflammatory disease accounting for huge healthcare costs and socio-economic impacts. Bacteria from the indigenous oral flora colonize the interspace between the tooth and the connective tissue, which induces an inflammatory response. If the bacteria proliferate and release virulence factors, they cause an imbalance in the host inflammatory response that induces degenerative processes in the surrounding tissues. This process is often slow, and the disease affects mainly older people, but the process could be rapid and affect young individuals if certain pathogens colonize the area. The two most studied periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, express virulence factors, including proteases and exotoxins. Periodontal bacteria and their products can be translocated to the peripheral circulation and are therefore linked to the risk pattern of several systemic diseases. However, it is not known if the increased risk for systemic disease associated with periodontitis is an effect of the invading bacteria and/or their released products, the release of components from the local inflammatory response, or a common host susceptibility pattern. The most studied periodontitis-associated systemic diseases are cardiovascular diseases and rheumatoid arthritis. Here, we want to shed light on mechanisms behind the associations of periodontal infections with systemic inflammation. 
540 |a Creative Commons  |f https://creativecommons.org/licenses/by/4.0/  |2 cc  |4 https://creativecommons.org/licenses/by/4.0/ 
546 |a English 
650 7 |a Medicine  |2 bicssc 
653 |a apical periodontitis 
653 |a adaptive immunity 
653 |a saliva 
653 |a serum 
653 |a antibody 
653 |a Aggregatibacter actinomycetemcomitans 
653 |a invasiveness 
653 |a leukotoxin 
653 |a cytolethal distending toxin 
653 |a serum resistance 
653 |a outer membrane vesicles 
653 |a oral microbiome 
653 |a nitric oxide 
653 |a nitrate 
653 |a nitrite 
653 |a periodontal disease 
653 |a alveolar bone loss 
653 |a gingiva 
653 |a bacteria 
653 |a biofilm 
653 |a immunity 
653 |a inflammation 
653 |a smoking 
653 |a Rheumatoid arthritis 
653 |a Porphyromonas gingivalis 
653 |a periodontitis 
653 |a citrullination 
653 |a peptidylarginine deiminase 
653 |a ACPA 
653 |a anti-CCP 
653 |a host response 
653 |a infection 
653 |a oral microbiota 
653 |a virulence factors 
653 |a metabolites 
653 |a TREM-1 
653 |a intervention 
653 |a LP17 
653 |a IL-17 
653 |a RANKL 
653 |a OPG 
653 |a cardiovascular diseases 
653 |a rheumatoid arthritis 
653 |a inflammatory response 
856 4 0 |a www.oapen.org  |u https://mdpi.com/books/pdfview/book/3087  |7 0  |z DOAB: download the publication 
856 4 0 |a www.oapen.org  |u https://directory.doabooks.org/handle/20.500.12854/69297  |7 0  |z DOAB: description of the publication