Influence of oestrogen deficiency on the development of apical periodontitis

Brasil, Sabrina C.; Santos, Rachel Moreira Morais dos; Fernandes, Arlete; Alves, Flávio R.F.; Pires, Fábio Ramôa; Siqueira, José F.; Armada, Luciana

doi:10.1111/iej.12612

Cited by 15 publications

(19 citation statements)

References 30 publications

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“…, Brasil et al . , Jara et al . ), but they did not consider the role of specific pathogenic microorganisms in CAP.…”

Section: Discussionmentioning

confidence: 99%

“…Long-standing periapical bone destruction is a sign of post-treatment endodontic disease and the manifestation of CAP without persistent clinical symptoms (Yuanita et al 2018). Most rodent CAP models have explored the mechanisms of CAP through an access cavity open to the oral environment (Azuma et al 2017, Brasil et al 2017, Jara et al 2018), but they did not consider the role of specific pathogenic microorganisms in CAP. The study of specific pathogens laid the foundation for seeking the best method for bacterial clearance.…”

Section: Discussionmentioning

confidence: 99%

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Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

et al. 2019

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Aim To conduct three‐dimensional micro‐CT analysis of bone destruction, periapical sclerotic changes and inflammatory root resorption (IRR) to compare the differences between Enterococcus faecalis (Ef)‐ and Porphyromonas gingivalis (Pg)‐induced chronic apical periodontitis (CAP). Methodology Mono‐species bacteria‐induced CAP was established in the first and second molars of the right maxilla and mandible of male Sprague–Dawley rats. Fifteen animals were divided into three groups with five rats in each group: control group, Ef‐CAP group and Pg‐CAP group. The maxilla and mandible were harvested and then scanned by micro‐CT. Alveolar bone destruction was evaluated by measuring the volume of alveolar bone resorption, bone volume fraction (BV/TV), trabecular thickness (Tb. Th), trabecular number (Tb. N) and trabecular spacing (Tb. Sp). The results were analysed using one‐way analysis of variance and Fisher's least significant difference methods (LSD). The sclerotic changes in the periapical bone were graded and the IRR indexes were scored. The data were analysed using the chi‐square test. Results The alveolar bone resorption volume of the Pg‐CAP group was significantly larger than that of the Ef‐CAP group (P < 0.01). In the maxilla, both Pg‐CAP and Ef‐CAP groups had a significant decrease in BV/TV and increase in Tb. Sp (P < 0.01) with the more significant changes of trabecular bone in the Pg‐CAP group. A significant reduction of Tb. N was only found in the Pg‐CAP group (P < 0.05). There was no significant change in Tb. Th in either group (P > 0.05). In the mandible, except for an increase in Tb. Sp in the Pg‐CAP group (P < 0.05), there was no significant change in BV/TV, Tb. Th or Tb. N (P > 0.05). No obvious sclerotic change was observed. IRR was detected in significantly more root surfaces in the Pg‐CAP group (240 surfaces, 60%) than those in the Ef‐CAP group (178 surfaces, 44.5%) (P < 0.001). The IRR extension was also significantly more advanced in the Pg‐CAP group (P < 0.05). Conclusions Pg‐CAP caused more substantial alveolar bone destruction and IRR than Ef‐CAP. The maxilla was more susceptible to CAP in terms of microstructural changes of trabecular bone than the mandible. Tb. Sp was the most sensitive index for evaluating the residual alveolar bone of CAP.

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“…, Brasil et al . , Jara et al . ), but they did not consider the role of specific pathogenic microorganisms in CAP.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

et al. 2019

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“…It is important to emphasize although the studied genetic polymorphisms were not associated with PAP, it is possible that estrogen play an important role in this endodontic phenotype. Estrogen deficiency after ovariectomy or menopause plays an important role in the early alterations in the turnover of cancellous bone, leading to both the early and late forms of osteoporosis in women (48) and in animals with induced apical periodontitis, they presented a larger lesion (16)(17)(18). Therefore, it is possible that estrogen deficiency in humans could be involved in the PAP.…”

Section: Discussionmentioning

confidence: 99%

“…These factors increase bone resorption and are downregulated by estrogen (15). Studies performed in estrogen deficiency rats with experimental apical periodontitis showed that they have a significantly increased bone loss (16)(17)(18). Estrogen binds to either ERα (estrogen receptor alpha) or ERβ (estrogen receptor beta) stimulating ER-positive cell lines (19).…”

Section: Introductionmentioning

confidence: 99%

Association between Estrogen, Vitamin D and Microrna17 Gene Polymorphisms and Periapical Lesions

et al. 2020

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This study evaluated the association between polymorphisms in genes encoding estrogen receptors 1 (ESR1) and 2 (ESR2), vitamin D receptor (VDR) and in microRNA17 (which binds to ESR1 and VDR) with persistent apical periodontitis (PAP) after the endodontic treatment. We included 162 patients who completed endodontic treatment at least one year ago and presented apical periodontitis at the beginning of the root canal therapy. Clinical and radiographic exams were performed to evaluate the presence of PAP or healthy periradicular tissues (healed). Saliva samples were collected as a genomic DNA. The genotyping of ESR1 (rs2234693 and rs9340799), ESR2 (rs1256049 and rs4986938), VDR (rs739837 and rs2228570) and miRNA17 (rs4284505) were performed by real-time PCR. Chi-square test was used to the distribution of genotype and allele frequencies. Haplotype analysis was also performed. Eighty-nine patients were included in the “healed” group and 73 in the “PAP” group. No association was found between the allelic and genotypic polymorphisms studied and PAP (p>0.05). Haplotype analysis also did not demonstrated an association (p>0.05). In conclusion, the genetic polymorphisms in ESR1, ESR2, VDR and miRNA17 are not associated with PAP.

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“…Chronic periodontitis (CP) and apical periodontitis (AP) are polymicrobial infectious disease characterized with local in ammatory response within the supporting tissue of teeth, leading to alveolar bone loss [15,16]. Despite the common lesion of osteoporosis in long bones and vertebras, many studies have reported the exacerbate alveolar bone resorption under estrogen-de ciency [17][18][19][20], imposing challenges to the clinical treatment of these diseases. Conventional therapies of CP and AP mainly rely on mechanical removal of plaque bio lm and root canal therapy.…”

Section: Introductionmentioning

confidence: 99%

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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Influence of oestrogen deficiency on the development of apical periodontitis

Abstract: Ovariectomized rats had significantly larger apical periodontitis lesions after 40 days of pulp exposure when compared with controls. These findings suggest that bone alterations as a result of long periods of oestrogen deficiency can influence the progression of apical periodontitis.

Cited by 15 publications

References 30 publications

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

Association between Estrogen, Vitamin D and Microrna17 Gene Polymorphisms and Periapical Lesions

Probiotics Ameliorate Alveolar Bone Loss by Regulating Gut Microbiota

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