Oral Administration of Lactobacillus acidophilus LA5 Prevents Alveolar Bone Loss and Alters Oral and Gut Microbiomes in a Murine Periodontitis Experimental Model.

Periodontitis is a destructive inflammatory response triggered by dysbiosis. Lactobacillus acidophilus LA5 (LA5) may impair microbial colonization and alter the host. Thus, we evaluated the effect of LA5 on alveolar bone loss in a periodontitis murine model and investigated its effect on the oral and gut microbiomes. Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, and Streptococcus gordonii were inoculated in C57BL/6 mice (P+), with LA5 (L+). SHAM infected controls (P- and/or L- groups) were also evaluated. After 45 days, alveolar bone loss in the maxilla and oral and gut microbiomes were determined. The administration of LA5 controlled the microbial consortium-induced alveolar bone loss. Periodontopathogens infection resulted in shifts in the oral and gut microbiomes consistent with dysbiosis, and LA5 reshaped these changes. The oral microbiome of P+L- group showed the increased abundance of Enterococaccea, Streptoccocaceae, Staphylococcaceae, Moraxellaceae, and Pseudomonadaceae, which were attenuated by the administration of LA5 to the infected group (P+L+). The administration of LA5 to otherwise non-infected mice resulted in the increased abundance of the superphylum Patescibacteria and the family Saccharamonadaceae in the gut. These data indicate L. acidophilus LA5 as a candidate probiotic for the control of periodontitis.

Lactobacilli Attenuate the Effect of Aggregatibacter actinomycetemcomitans Infection in Gingival Epithelial Cells.

Probiotics may be considered as an additional strategy to achieve a balanced microbiome in periodontitis. However, the mechanisms underlying the use of probiotics in the prevention or control of periodontitis are still not fully elucidated. This in vitro study aimed to evaluate the effect of two commercially available strains of lactobacilli on gingival epithelial cells (GECs) challenged by Aggregatibacter actinomycetemcomitans. OBA-9 GECs were infected with A. actinomycetemcomitans strain JP2 at an MOI of 1:100 and/or co-infected with Lactobacillus acidophilus La5 (La5) or Lacticaseibacillus rhamnosus Lr32 (Lr32) at an MOI of 1:10 for 2 and 24 h. The number of adherent/internalized bacteria to GECs was determined by qPCR. Production of inflammatory mediators (CXCL-8, IL-1ß, GM-CSF, and IL-10) by GECs was determined by ELISA, and the expression of genes encoding cell receptors and involved in apoptosis was determined by RT-qPCR. Apoptosis was also analyzed by Annexin V staining. There was a slight loss in OBA-9 cell viability after infection with A. actinomycetemcomitans or the tested probiotics after 2 h, which was magnified after 24-h co-infection. Adherence of A. actinomycetemcomitans to GECs was 1.8 × 107 (± 1.2 × 106) cells/well in the mono-infection but reduced to 1.2 × 107 (± 1.5 × 106) in the co-infection with Lr32 and to 6 × 106 (± 1 × 106) in the co-infection with La5 (p < 0.05). GECs mono-infected with A. actinomycetemcomitans produced CXCL-8, GM-CSF, and IL-1ß, and the co-infection with both probiotic strains altered this profile. While the co-infection of A. actinomycetemcomitans with La5 resulted in reduced levels of all mediators, the co-infection with Lr32 promoted reduced levels of CXCL-8 and GM-CSF but increased the production of IL-1ß. The probiotics upregulated the expression of TLR2 and downregulated TLR4 in cells co-infected with A. actinomycetemcomitans. A. actinomycetemcomitans-induced the upregulation of NRLP3 was attenuated by La5 but increased by Lr32. Furthermore, the transcription of the anti-apoptotic gene BCL-2 was upregulated, whereas the pro-apoptotic BAX was downregulated in cells co-infected with A. actinomycetemcomitans and the probiotics. Infection with A. actinomycetemcomitans induced apoptosis in GECs, whereas the co-infection with lactobacilli attenuated the apoptotic phenotype. Both tested lactobacilli may interfere in A. actinomycetemcomitans colonization of the oral cavity by reducing its ability to interact with gingival epithelial cells and modulating cells response. However, L. acidophilus La5 properties suggest that this strain has a higher potential to control A. actinomycetemcomitans-associated periodontitis than L. rhamnosus Lr32.

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

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 1622A [B+ (1622)] and B. breve 1101A [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 1622A, but not B. breve 1101A, controlled bone destruction in P+ mice. B. breve 1101A upregulated transcription of Il-1ß, 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 1101A did not yield such low levels of transcripts as seen for the other groups. B. breve 1101A 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 1101A induced an inflammatory profile in gingival tissues and did not prevent alveolar bone loss. However, the properties of B. bifidum 1622A suggest its potential to control periodontitis.

Oral yeast colonization in patients with eating disorders: commensal acquisition or due to purgative habits?

Oral problems are common in patients diagnosed with Eating Disorders (ED) and still require better elucidation. We aimed to analyze the prevalence of oral Candida spp in individuals with ED. The sample of the study was comprised of 30 women with purgative habits and 15 without purgative habits. Samples of the oral cavity were collected by sterile cotton swab rubbed on soft tissues and teeth. Yeasts were isolated on Sabouraud dextrose agar. Yeasts were isolated from the oral cavity of 53% of the patients yielding 75 yeast isolates; of these, 43 were identified by conventional mycological methods: C. parapsilosis (n=19), C. glabrata (n=16), Rhodotorula sp (n= 6), C. famata (n=2). The remaining 32 isolates were presumptively identified as C. albicans or C. dubliniensis and required mass spectrometry for the final differentiation: 28 isolates were confirmed as C. albicans and four as C. dubliniensis. Among the control group, only four subjects (26.7%) were found to harbor C. albicans. The four C. dubliniensis isolates were from two patients, one that was only colonized and the other, with severe ED, was diagnosed with an oral candidiasis as demonstrated by the presence of pseudohyphae on the direct mycological exam from different sites. The increased rate of isolation of non-albicans species, such as C. glabrata, C. parapsilosis, and C. dubliniensis in the oral cavity from ED patients with nutritional deficiency may suggest that purgative habits of these patients can lead to changes in normal flora and predispose to oral candidiasis.

Oral profile of eating disorders patients: Case series.

Oral alterations in patients diagnosed with eating disorders (ED) are reported in the literature, but few articles demonstrate these changes in a specific population. This study aims to summarize the findings of 26 patients with ED in a Brazilian dental clinic, through analyzing the body mass index and oral conditions (decayed, missing and filled teeth-DMFT, dental wear, salivary flux, xerostomia, oral hygiene-OHI-S, oral lesions, and the prevalence of candidiasis), in order to facilitate recognition and enable accurate diagnosis for the general dentist. Probably, the premature diagnosis of ED resulted in lower DMFT and oral lesions.