Systemic administration of probiotics reduces the severity of apical periodontitis

Cosme‐Silva, Leopoldo; Dal‐Fabbro, Renan; Cintra, Luciano Tavares Ângelo; Santos, Vagner Rodrigues; Duque, Cristiane; Ervolino, Edílson; Bomfim, Srm; Gomes‐Filho, João Eduardo

doi:10.1111/iej.13192

Cited by 34 publications

(43 citation statements)

References 58 publications

(116 reference statements)

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“…A number of studies have demonstrated that LPS-induced overproduction of IL-1β, il-6 and TnF-α contributes to the majority of inflammatory responses that are involved in the pathogenesis of inflammatory-stimulated oral bone diseases, including periodontitis (35), peri-implantitis (36) and apical periodontitis (37). By contrast, our previous studies identified that NAC inhibited LPS-mediated synthesis of IL-1β, il-6 and TnF-α (10,26).…”

Section: Discussionmentioning

confidence: 71%

N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway

Wang

Jiang

et al. 2020

Mol Med Rep

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n-acetyl cysteine (nac) has been used to inhibit lipopolysaccharide (LPS)-induced inflammation. However, the molecular mechanism underlying its anti-inflammatory effects remains to be elucidated. The present study aimed to determine the effect of NAC on the LPS-induced inflammatory response in bone marrow mesenchymal stem cells (BMSCs) and elucidate the underlying molecular mechanism. First, BMSCs were stimulated by LPS following pretreatment with NAC (0, 0.1, 0.5, 1 or 2 mM). A Cell Counting Kit 8 assay was used to determine the number of viable cells and 1 mM NAC was selected as the experimental concentration. Then, the secretion of inflammatory factors, including interleukin (IL)-1β, IL-6 and tumor necrosis factor-α was evaluated by enzyme-linked immunosorbent assay. Finally, the expression levels of mRNA and proteins, including apoptosis-associated speck-like protein containing a CARD (ASC), nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), caspase-1, thioredoxin-interacting protein (TXNIP), and thioredoxin (TRX), were evaluated by reverse transcription-quantitative PCR and western blot analysis, respectively. The results demonstrated that the secretion of inflammatory factors, which was increased by the administration of LPS, was reduced by pretreatment with NAC. Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX. To conclude, NAC had anti-inflammatory effects on LPS-stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL-1β signaling pathway. Thus, NAC may be a promising treatment to attenuate the inflammatory response in LPS-induced BMSCs.

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Section: Discussionmentioning

confidence: 71%

N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway

Wang

Jiang

et al. 2020

Mol Med Rep

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“…Administration of probiotics can also elevate Treg cells in the bone marrow of OVX mice, and thus suppress bone loss [73,74]. Although mechanisms are still unclear, bene cial local effects of probiotics on in ammatory alveolar bone loss have also been reported [38,[75][76][77]. Our previous study also shown that administration of berberine, a natural alkaloid with well-known ecological effect on gut microbiota, can enrich butyrate-generating bacteria and elevate the generation of gut-derived SCFAs, which promote gut barrier function and attenuate OVX-exacerbated periodontal bone loss [41].…”

Section: Discussionmentioning

confidence: 99%

“…Although speci c mechanisms are still unclear, oral administration of Lactobacillus rhamnosus GG, Bi dobacterium animalis subsp. Lactis, and Akkermansia muciniphila have shown the effectiveness in suppressing alveolar bone loss and reducing the severity of CP and AP in animal models [37][38][39][40]. Our previous work showed that berberine, a natural alkaloid, was able to ameliorate periodontal bone loss by regulating gut microbiota of OVX rats [41], underscoring the importance of gut microbiota modulation in the reversion of alveolar bone resorption.…”

Section: Introductionmentioning

confidence: 92%

Probiotics Ameliorate Alveolar Bone Loss by Regulating Gut Microbiota

Jia

et al. 2020

Preprint

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BackgroundEstrogen deficiency is an etiological factor of postmenopausal osteoporosis (PMO), which not only decreases bone density in vertebrae and long bone, but also aggravates inflammatory bone loss in alveolar bone. Recent evidence has suggested the critical role of gut microbiota in osteoimmunology, and modulation of gut microbiota may have positive influence on bone metabolisms. The present study aimed to evaluate the therapeutic effects of probiotics on alveolar bone loss under estrogen-deficient condition. Inflammatory alveolar bone loss induced by either chronic periodontitis or apical periodontitis was established in ovariectomized (OVX) rats, which were gavage-fed with probiotics daily until sacrifice. Gut microbiota and gut permeability, as well as alveolar bone loss and the related osteoimmune were evaluated to investigate the effects and underlying mechanisms by which probiotics counter the alveolar bone loss under estrogen-deficiency. ResultsWe found that administration of probiotics significantly prevented periodontal and apical bone resorption in OVX rats. Administration of probiotics significantly enriched butyrate-producing genera and enhanced gut butyrate production, resulting in improved intestinal barrier and decreased gut permeability in the OVX rats. Furthermore, the estrogen deprivation-induced inflammatory responses were suppressed in probiotics-treated OVX rats, as reflected by reduced serum levels of inflammatory cytokines and a balanced distribution of CD4+IL-17A+Th17 cells and CD4+CD25+Foxp3+Treg cells in the bone marrow. ConclusionOur data demonstrate that probiotics can effectively attenuate alveolar bone loss by modulating gut microbiota and further regulating osteoimmune, and thus represent a promising adjuvant in the treatment of alveolar bone loss under estrogen-deficiency.

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“…Considering possible animal deaths, three more animals were added in each group, resulting in ten rats per group (Cosme‐Silva et al . 2019).…”

Section: Methodsmentioning

confidence: 99%

Relationship between apical periodontitis and atherosclerosis in rats: lipid profile and histological study

et al. 2020

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Aim To investigate the relationship between apical periodontitis and atherosclerosis in rats by lipid profile and carotid artery intima tunic measurement, and histological and histometric evaluation of periapical lesions. Methodology Forty male Wistar rats were allocated into four groups: control (C), with apical periodontitis (AP), with atherosclerosis (AT) and with AP and AT (AP + AT). Atherosclerosis was induced using a high‐lipid diet associated with a surgical ligature in the carotid artery and a super dosage of vitamin D3. AP was induced via pulp exposure to the oral environment. At 45 and 75 days, serum levels of total cholesterol (TC), triglycerides (TG), high‐density lipoprotein cholesterol (HDL‐C) and low‐density lipoprotein cholesterol (LDL‐C) were measured. The maxillary and mandibular jaws and carotid artery were collected and processed for histological analysis. The Kruskal–Wallis or Mann–Whitney test was performed for nonparametric data, and the Tukey’s or Student’s t‐test was performed for parametric data (P < 0.05). Results In nonatherosclerotic animals, the induction of apical periodontitis increased TG levels significantly, from 63.1 ± 11.4 mg dL−1 in group C to 88.2 ± 7.9 mg dL−1 in the AP group (P < 0.05). The induction of AP was associated with a trend for higher TC and LDL‐C levels in atherosclerotic animals (P > 0.05); however, it only significantly increased TG levels, from 93.2 ± 18.0 mg dL−1 in AT group to 121.9 ± 14.5 mg dL−1 in the AP + AT group (P < 0.05). Animals in the AP + AT group had a 36.5% increase in the thickness of the carotid intima tunic when compared with the AT group (P < 0.05). The intensity of the inflammatory infiltrate was significantly larger in the AP + AT group when compared with AP group (P < 0.05). The AP + AT group exhibited significantly greater alveolar bone loss, with a periapical lesion size of 206.4 ± 56.3 × 104 μm2, compared with 151.4 ± 49.1 × 104 μm2 in the AP group (P < 0.05). Conclusion Apical periodontitis influenced triglyceride levels, increasing them even in the absence of atherosclerosis, and influenced the increase in the thickness of the carotid artery intima tunic in the presence of atherosclerosis. Atherosclerosis intensified the inflammatory reaction and increased bone resorption in periapical lesions.

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Systemic administration of probiotics reduces the severity of apical periodontitis

Cited by 34 publications

References 58 publications

N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway

N‑acetyl cysteine inhibits the lipopolysaccharide‑induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL‑1β signaling pathway

Probiotics Ameliorate Alveolar Bone Loss by Regulating Gut Microbiota

Relationship between apical periodontitis and atherosclerosis in rats: lipid profile and histological study

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