English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Periodontitis is an inflammatory disease induced by a dysbiotic oral microbiome. Probiotics of the genus  Bifidobacterium  may restore the symbiotic microbiome and modulate the immune response, leading to periodontitis control. We evaluated the effect of two strains of  Bifidobacterium  able to inhibit  Porphyromonas gingivalis  interaction with host cells and biofilm formation, but with distinct immunomodulatory properties, in a mice periodontitis model. Experimental periodontitis (P+) was induced in C57Bl/6 mice by a microbial consortium of human oral organisms.  B. bifidum  162 2A  [B+ (1622)] and  B. breve  110 1A  [B+ (1101)] were orally inoculated for 45 days. Alveolar bone loss and inflammatory response in gingival tissues were determined. The microbial consortium induced alveolar bone loss in positive control (P + B-), as demonstrated by microtomography analysis, although  P. gingivalis  was undetected in oral biofilms at the end of the experimental period. TNF-α and IL-10 serum levels, and Treg and Th17 populations in gingiva of SHAM and P + B- groups did not differ.  B. bifidum  162 2A , but not  B. breve  110 1A , controlled bone destruction in P+ mice.  B. breve  110 1A  upregulated transcription of  Il-1β ,  Tnf-α ,  Tlr2 ,  Tlr4 , and  Nlrp3  in P-B+(1101), which was attenuated by the microbial consortium [P + B+(1101)]. All treatments downregulated transcription of  Il-17 , although treatment with  B. breve  110 1A  did not yield such low levels of transcripts as seen for the other groups.  B. breve  110 1A  increased Th17 population in gingival tissues [P-B+ (1101) and P + B+ (1101)] compared to SHAM and P + B-. Administration of both bifidobacteria resulted in serum IL-10 decreased levels. Our data indicated that the beneficial effect of  Bifidobacterium  is not a common trait of this genus, since  B. breve  110 1A  induced an inflammatory profile in gingival tissues and did not prevent alveolar bone loss. However, the properties of  B. bifidum  162 2A  suggest its potential to control periodontitis.

Bifidobacterium Strains Present Distinct Effects on the Control of Alveolar Bone Loss in a Periodontitis Experimental Model