Postmenopausal osteoporosis (PMO) is a risk factor for periodontitis, and current therapeutics against PMO prevent the aggravated alveolar bone loss of periodontitis in estrogen-deficient women. Gut microbiota is recognized as a promising therapeutic target for PMO. Berberine extracted from Chinese medicinal plants has shown its effectiveness in the treatment of metabolic diseases such as obesity and diabetes via regulating gut microbiota. Here, we hypothesize that berberine ameliorates periodontal bone loss by improving the intestinal barriers by regulating gut microbiota under an estrogen-deficient condition. Experimental periodontitis was established in ovariectomized (OVX) rats, and the OVX-periodontitis rats were treated with berberine for 7 wk before sacrifice for analyses. Micro-computed tomography and histologic analyses showed that berberine treatment significantly reduced alveolar bone loss and improved bone metabolism of OVX-periodontitis rats as compared with the vehicle-treated OVX-periodontitis rats. In parallel, berberine-treated OVX-periodontitis rats harbored a higher abundance of butyrate-producing gut microbiota with elevated butyrate generation, as demonstrated by 16S rRNA sequencing and high-performance liquid chromatography analysis. Berberine-treated OVX-periodontitis rats consistently showed improved intestinal barrier integrity and decreased intestinal paracellular permeability with a lower level of serum endotoxin. In parallel, IL-17A-related immune responses were attenuated in berberine-treated OVX-periodontitis rats with a lower serum level of proinflammatory cytokines and reduced IL-17A cells in alveolar bone as compared with vehicle-treated OVX-periodontitis rats. Our data indicate that gut microbiota is a potential target for the treatment of estrogen deficiency-aggravated periodontal bone loss, and berberine represents a promising adjuvant therapeutic by modulating gut microbiota.
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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.
Food hardness is one of the dietary features that may impact brain functions. We performed a systematic review to evaluate the effect of food hardness (hard food versus soft food diet) on behavior, cognition, and brain activation in animals and humans (PROSPERO ID: CRD42021254204). The search was conducted on 29 June 2022 using Medline (Ovid), Embase, and Web of Science databases. Data were extracted, tabulated by food hardness as an intervention, and summarized by qualitative synthesis. The SYRCLE and JBI tools were used to assess the risk of bias (RoB) of individual studies. Of the 5427 studies identified, 18 animal studies and 6 human studies met the inclusion criteria and were included. The RoB assessment indicated that 61% of animal studies had unclear risks, 11% had moderate risks, and 28% had low risks. All human studies were deemed to have a low risk of bias. The majority (48%) of the animal studies showed that a hard food diet improved behavioral task performance compared to soft food diets (8%). However, 44% of studies also showed no differential effects of food hardness on behavioral tests. It was also evident that certain regions of the brain were activated in response to changes in food hardness in humans, with a positive association between chewing hard food, cognition performance, and brain function. However, variations in the methodologies of the included studies hindered the meta-analysis execution. In conclusion, our findings highlight the beneficial effects of dietary food hardness on behavior, cognition, and brain function in both animals and humans, however, this effect may depend on several factors that require further understanding of the causality.
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