scholarly journals Probiotics Ameliorate Alveolar Bone Loss by Regulating Gut Microbiota

2020 ◽  
Author(s):  
Leming Jia ◽  
Ye Tu ◽  
Xiaoyue Jia ◽  
Qian Du ◽  
Xin Zheng ◽  
...  
Keyword(s):  
Bone Loss ◽  
Gut Microbiota ◽  
Alveolar Bone ◽  
Critical Role ◽  
Alveolar Bone Loss ◽  
Estrogen Deficiency ◽  
Long Bone ◽  
Therapeutic Effects ◽  
Gut Permeability ◽  
Ovx Rats

Abstract 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.

scholarly journals Berberine Ameliorates Periodontal Bone Loss by Regulating Gut Microbiota

2018 ◽  
Vol 98 (1) ◽  
pp. 107-116 ◽  
Author(s):  
X. Jia ◽  
L. Jia ◽  
L. Mo ◽  
S. Yuan ◽  
X. Zheng ◽  
...  
Keyword(s):  
Bone Loss ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Alveolar Bone ◽  
Intestinal Barrier ◽  
Alveolar Bone Loss ◽  
Micro Computed Tomography ◽  
Ovx Rats ◽  
Obesity And Diabetes ◽  
Periodontal Bone Loss

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.

scholarly journals Probiotics ameliorate alveolar bone loss by regulating gut microbiota

2021 ◽  
Author(s):  
Leming Jia ◽  
Ye Tu ◽  
Xiaoyue Jia ◽  
Qian Du ◽  
Xin Zheng ◽  
...  
Keyword(s):  
Bone Loss ◽  
Gut Microbiota ◽  
Alveolar Bone ◽  
Alveolar Bone Loss

scholarly journals Effects of Chronic Ethanol Consumption and Ovariectomy on the Spontaneous Alveolar Bone Loss in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Priscila Cunha Nascimento ◽  
Leonardo Oliveira Bittencourt ◽  
Soraya O. Pinto ◽  
Luana N. S. Santana ◽  
Renata Duarte Souza-Rodrigues ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Estrogen Deficiency ◽  
Female Rats ◽  
Chronic Ethanol Consumption ◽  
Female Wistar Rats ◽  
Postmenopausal Estrogen ◽  
Post Hoc ◽  
One Way Anova

Postmenopausal estrogen deficiency and ethanol (EtOH) abuse are known risk factors for different diseases including bone tissues. However, little is known about the synergic effects of EtOH abuse and estrogen deficiency on alveolar bone loss in women. The present study evaluated the effects of EtOH chronic exposure and ovariectomy on the alveolar bone loss in female rats. For this, 40 female Wistar rats were randomly divided into 4 groups: control, EtOH exposure, ovariectomy (OVX), and OVX plus EtOH exposure. Initially, half of the animals were ovariectomized at 75 days of age. After that, the groups received distilled water or EtOH 6.5 g/kg/day (20% w/v) for 55 days via gavage. Thereafter, animals were sacrificed and the mandibles were collected, dissected, and separated into hemimandibles. Alveolar bone loss was evaluated by measuring the distance between the cementoenamel junction and the alveolar bone crest through a stereomicroscope in 3 different anatomical regions of the tissue. One-way ANOVA and post hoc Tukey were used to compare groups ( p < 0.05 ). The results showed that the ovariectomy and EtOH exposure per se were able to induce alveolar bone loss, and their association did intensify significantly the effect. Therefore, OVX associated with heavy EtOH exposure increase the spontaneous alveolar bone loss in rats.

scholarly journals Therapeutic effects of caffeic acid phenethyl ester on alveolar bone loss in rats with endotoxin-induced periodontitis

2019 ◽  
Vol 14 (4) ◽  
pp. 339-345
Author(s):  
Alper Kızıldağ ◽  
Taner Arabacı ◽  
Mevlüt Albayrak ◽  
Ufuk Taşdemir ◽  
Erman Şenel ◽  
...  
Keyword(s):  
Bone Loss ◽  
Caffeic Acid ◽  
Alveolar Bone ◽  
Caffeic Acid Phenethyl Ester ◽  
Alveolar Bone Loss ◽  
Therapeutic Effects

Diet-induced obesity, gut microbiota and bone, including alveolar bone loss

2017 ◽  
Vol 78 ◽  
pp. 65-81 ◽  
Author(s):  
Sathima Eaimworawuthikul ◽  
Parameth Thiennimitr ◽  
Nipon Chattipakorn ◽  
Siriporn C. Chattipakorn
Keyword(s):  
Bone Loss ◽  
Gut Microbiota ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Diet Induced Obesity

scholarly journals Involvement of SOCS3 in Regulation of CD11c+ Dendritic Cell-Derived Osteoclastogenesis and Severe Alveolar Bone Loss

2009 ◽  
Vol 77 (5) ◽  
pp. 2000-2009 ◽  
Author(s):  
Xiaoxia Zhang ◽  
Mawadda Alnaeeli ◽  
Bhagirath Singh ◽  
Yen-Tung A. Teng
Keyword(s):  
T Cells ◽  
Dendritic Cell ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Expression Profiles ◽  
Critical Role ◽  
Alveolar Bone Loss ◽  
Cytokine Signaling ◽  
Periodontal Inflammation ◽  
Socs3 Expression

ABSTRACT To investigate the role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediated dendritic cell (DC)-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4+ T cells and the effect of SOCS3 expression in CD11c+ DCs during periodontal inflammation-induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice. Our results of ex vivo and in vitro analyses showed that (i) there is significantly higher SOCS3 expression associated with RANKL+ T-cell-mediated bone loss in correlation with increased CD11c+ DC-mediated osteoclastogenesis; (ii) the transfection of CD11c+ DC using an adenoviral vector carrying a dominant negative SOCS3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP expression, bone resorption, and SOCS3 activity are not associated with any detectable change in the expression levels of TRAF6 and mitogen-activated protein kinase signaling adaptors (i.e., Erk, Jnk, p38, and Akt) in RANKL+ T cells. We conclude that SOCS3 plays a critical role in modulating cytokine signaling involved in RANKL-mediated DC-derived osteoclastogenesis during immune interactions with T cells and diabetes-associated severe inflammation-induced alveolar bone loss. Therefore, the development of SOCS3 inhibitors may have therapeutic potential as the target to halt inflammation-induced bone loss under pathological conditions in vivo.

scholarly journals Influence of different durations of estrogen deficiency on alveolar bone loss in rats

2011 ◽  
Vol 25 (6) ◽  
pp. 538-543 ◽  
Author(s):  
Susana Ungaro Amadei ◽  
Daniela Martins de Souza ◽  
Adriana Aigotti Haberbeck Brandão ◽  
Rosilene Fernandes da Rocha
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Estrogen Deficiency

scholarly journals Estrogen deficiency and periodontal condition in rats: a radiographic and macroscopic study

2006 ◽  
Vol 17 (3) ◽  
pp. 201-207 ◽  
Author(s):  
Ana Lia Anbinder ◽  
Marcela de Almeida Prado ◽  
Marianne Spalding ◽  
Ivan Balducci ◽  
Yasmin Rodarte Carvalho ◽  
...  
Keyword(s):  
Risk Factor ◽  
Bone Loss ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Estrogen Deficiency ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Furcation Involvement ◽  
The Impact

The purpose of this study was to evaluate the impact of ovariectomy-induced estrogen deficiency as a risk factor of periodontal disease in rats. Forty 90-day old female rats were either ovariectomized (OVX; n=20) or sham operated (SHAM; n=20). After 30 days, periodontitis was induced by placement of a cotton ligature around the upper second molars of 10 OVX and 10 SHAM animals. All animals were sacrificed 5 weeks later. Body weight was assessed before all surgical procedures. The left hemimaxillas were removed and the percentage of periodontal bone support was determined radiographically and buccal alveolar bone loss was determined macroscopically using an image-analysis software. Furcation involvement was also evaluated. Data were analyzed statistically by ANOVA at 5% significance level. Within the evaluated period, the ovariectomized rats gained more weight than the sham-operated animals (p<0.001). The animals in which periodontitis was induced had less bone support, greater alveolar bone loss and furcation involvement than those without ligature (p<0.001). However, there was no difference between ovariectomized and sham-operated animals (p>0.05). Based on the findings of this study, estrogen deficiency could not be considered as a risk factor for periodontal disease.

Effects of Estrogen Deficiency and/or Caffeine Intake on Alveolar Bone Loss, Density, and Healing: A Study in Rats

2013 ◽  
Vol 84 (6) ◽  
pp. 839-849 ◽  
Author(s):  
Joyce Pinho Bezerra ◽  
Ariane de Siqueira ◽  
Amanda Gonçalves Pires ◽  
Marcelo Rocha Marques ◽  
Poliana Mendes Duarte ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Estrogen Deficiency ◽  
Caffeine Intake

scholarly journals Prevention of Alveolar Bone Loss in an Osteoporotic Animal Model via Interference of Semaphorin 4d

2014 ◽  
Vol 93 (11) ◽  
pp. 1095-1100 ◽  
Author(s):  
Y. Zhang ◽  
L. Wei ◽  
R.J. Miron ◽  
Q. Zhang ◽  
Z. Bian
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Height Loss ◽  
Emission Computed Tomography ◽  
Therapeutic Effects ◽  
Semaphorin 4D ◽  
Bone Targeting ◽  
Number Of Patients ◽  
Bone Height

Semaphorin 4d (Sema4d) has been proposed as a novel target gene for the treatment of osteoporosis. Recently, we fabricated a site-specific bone-targeting system from polymeric nanoparticles that demonstrates an ability to prevent bone loss in an osteoporotic model by interfering with Sema4d gene expression using small interference RNA (siRNA) molecules. The aim of the present investigation was to determine the effects of this targeting system on the periodontium, an area of high bone turnover. We demonstrated, by single photon emission computed tomography, that intravenous injection of this molecule in ovariectomized Balb/C mice is able to target alveolar bone peaking 4 hr post-injection. We then compared, by histological analysis, the bone volume/total volume (BV/TV), alveolar bone height loss, immunohistochemical expression of Sema4d, and total number of osteoclasts in mandibular alveolar bone. Four treatment modalities were compared as follows: (1) sham-operated, (2) OVX-operated, (3) OVX+estrogen replacement therapy, and (4) OVX+siRNA-Sema4d animals. The results from the present study demonstrate that an osteoporotic condition significantly increases alveolar bone height loss, and that the therapeutic effects via bone-targeting systems featuring interference of Sema4d are able to partly counteract alveolar bone loss caused by osteoporosis. While the future therapeutic demand for the large number of patients suffering from osteoporosis faces many challenges, we demonstrate within the present study an effective drug-delivery moiety with anabolic effects on the bone remodeling cycle able to locate and target alveolar bone regeneration.

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