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1.
Pol J Vet Sci ; 24(3): 365-373, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34730299

RESUMO

Periodontitis is a highly prevalent, chronic immune-inflammatory disease of the periodontium that results in the periodontium and alveolar bone loss's progressive destruction. In this study, the induction of periodontal disease via retentive ligature, lipopolysaccharide, and their combination at three different times were compared in a rat model. Seventy-two Sprague Dawley rats were distributed into four treatment groups: 1) control group with no treatment; 2) application of 4/0 nylon ligature around second maxillary molars; 3) combination of ligature and LPS injection (ligature-LPS); 4) intragingival injection of Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) to the palatal mucosa of the second maxillary molars. Six rats were sacrificed from each group after 7, 14, and 30 days of periodontal disease induction. Alveolar bone loss, attachment loss, number of inflammatory cells, and blood vessels were evaluated histologically. A micro-CT scan was used as a parameter to know the rate of alveolar bone loss. Parametric data were analyzed using two-way ANOVA followed by Bonferroni correction with a significance set at 5%. Non-parametric data were analyzed using Kruskal-Wallis, followed by multiple comparisons with Bonferroni correction. The histological results revealed significant destructive changes in the periodontal tissues and alveolar bone following the ligature and ligature-LPS induction techniques. These changes were evident as early as seven days, maintained until 14 days post-treatment, and declined with time. The ligature technique was effective in inducing acute periodontal disease. The LPS injection technique did not induce alveolar bone loss, and its combination to ligature added insignificant effects.


Assuntos
Modelos Animais de Doenças , Lipopolissacarídeos/toxicidade , Doenças Periodontais/etiologia , Perda do Osso Alveolar/patologia , Animais , Ligadura , Masculino , Doenças Periodontais/patologia , Periodontite/patologia , Ratos , Ratos Sprague-Dawley
2.
PLoS One ; 16(10): e0258109, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34618843

RESUMO

PURPOSE: Previous studies have found that Epstein-Barr virus (EBV) is associated with periodontitis, though some controversy remains. This meta-analysis aimed to clarify and update the relationship between EBV and periodontitis as well as clinical parameters. METHODS: A comprehensive search was conducted in the PubMed and Scopus databases in December 2020. Original data were extracted according to defined inclusion and exclusion criteria. Outcomes were analyzed, including overall odds ratios (ORs) and 95% confidence intervals (CIs). A random-effects model was used, and publication bias was assessed by Egger's and Begg's tests. Sensitivity analysis was used to evaluate the stability of the outcome. RESULTS: Twenty-six studies were included in the present meta-analysis, involving 1354 periodontitis patients and 819 healthy controls. The included studies mostly showed high quality. The overall quantitative synthesis for the association between EBV and periodontitis was an increased odds ratio when subgingival EBV was detected OR = 7.069, 95% CI = 4.197-11.905, P<0.001). The results of subgroup analysis suggested that the association of EBV with periodontitis was significant in Asian, European, and American populations (P<0.001; P = 0.04; P = 0.003, respectively) but not in African populations (P = 0.29). Subgroup analysis by sample type showed that subgingival plaque (SgP), tissue and gingival crevicular fluid GCF were useful for EBV detection (P<0.001). EBV detection amplification methods included nested PCR, multiplex PCR and PCR (P<0.001; P = 0.05, P<0.001, respectively), but EBV detection by real-time PCR and loop-mediated isothermal amplification presented no significant result (P = 0.06; P = 0.3, respectively). For the clinical parameters of periodontitis, pocket depth (PD) and bleeding of probing (BOP) percentages were higher in the EBV-positive sites than in the EBV-negative sites (MD 0.47 [0.08, 0.85], P = 0.02; MD 19.45 [4.47, 34.43], P = 0.01). CONCLUSIONS: A high frequency of EBV detection is associated with an increased risk of periodontitis. The EBV association was particularly significant in all populations except in African populations. Subgigival plaque (SgP), tissue and GCF were not significantly different useful material for detecting EBV in periodontitis. Nested PCR and multiplex PCR are reliable methods for this purpose. In the presence of EBV, PD and BOP are reliable clinical parameters for gingival inflammation. However, some caution in such interpretation is justified due to heterogeneity among studies. A suggested extension could assess the parallel influence of other human herpesviruses.


Assuntos
Infecções por Vírus Epstein-Barr/genética , Gengivite/epidemiologia , Herpesvirus Humano 4/patogenicidade , Periodontite/epidemiologia , Adulto , Citomegalovirus/isolamento & purificação , Citomegalovirus/patogenicidade , DNA Viral/genética , Infecções por Vírus Epstein-Barr/complicações , Infecções por Vírus Epstein-Barr/epidemiologia , Infecções por Vírus Epstein-Barr/virologia , Feminino , Líquido do Sulco Gengival/virologia , Gengivite/genética , Gengivite/patologia , Gengivite/virologia , Herpesvirus Humano 4/genética , Humanos , Masculino , Pessoa de Meia-Idade , Técnicas de Diagnóstico Molecular , Técnicas de Amplificação de Ácido Nucleico , Periodontite/genética , Periodontite/patologia , Periodontite/virologia
3.
Am J Physiol Heart Circ Physiol ; 321(5): H948-H962, 2021 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-34597184

RESUMO

Oral and gum health have long been associated with incidence and outcomes of cardiovascular disease. Periodontal disease increases myocardial infarction (MI) mortality by sevenfold through mechanisms that are not fully understood. The goal of this study was to evaluate whether lipopolysaccharide (LPS) from a periodontal pathogen accelerates inflammation after MI through memory T-cell activation. We compared four groups [no MI, chronic LPS, day 1 after MI, and day 1 after MI with chronic LPS (LPS + MI); n = 68 mice] using the mouse heart attack research tool 1.0 database and tissue bank coupled with new analyses and experiments. LPS + MI increased total CD8+ T cells in the left ventricle versus the other groups (P < 0.05 vs. all). Memory CD8+ T cells (CD44 + CD27+) were 10-fold greater in LPS + MI than in MI alone (P = 0.02). Interleukin (IL)-4 stimulated splenic CD8+ T cells away from an effector phenotype and toward a memory phenotype, inducing secretion of factors associated with the Wnt/ß-catenin signaling that promoted monocyte migration and decreased viability. To dissect the effect of CD8+ T cells after MI, we administered a major histocompatibility complex-I-blocking antibody starting 7 days before MI, which prevented effector CD8+ T-cell activation without affecting the memory response. The reduction in effector cells diminished infarct wall thinning but had no effect on macrophage numbers or MertK expression. LPS + MI + IgG attenuated macrophages within the infarct without effecting CD8+ T cells, suggesting these two processes were independent. Overall, our data indicate that effector and memory CD8+ T cells at post-MI day 1 are amplified by chronic LPS to potentially promote infarct wall thinning.NEW & NOTEWORTHY Although there is a well-documented link between periodontal disease and heart health, the mechanisms are unclear. Our study indicates that in response to circulating periodontal endotoxins, memory CD8+ T cells are activated, resulting in an acceleration of macrophage-mediated inflammation after MI. Blocking activation of effector CD8+ T cells had no effect on the macrophage numbers or wall thinning at post-MI day 1, indicating that this response was likely due in part to memory CD8+ T cells.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Memória Imunológica , Lipopolissacarídeos , Ativação Linfocitária , Infarto do Miocárdio/imunologia , Miocárdio/imunologia , Periodontite/imunologia , Porphyromonas gingivalis , Cicatrização , Animais , Linfócitos T CD8-Positivos/metabolismo , Células Cultivadas , Modelos Animais de Doenças , Feminino , Mediadores da Inflamação/metabolismo , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Macrófagos/metabolismo , Masculino , Camundongos , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/patologia , Miocárdio/metabolismo , Miocárdio/patologia , Periodontite/induzido quimicamente , Periodontite/metabolismo , Periodontite/patologia , Fagocitose , Fenótipo , Fatores de Tempo
4.
Hua Xi Kou Qiang Yi Xue Za Zhi ; 39(5): 518-523, 2021 Oct 01.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-34636198

RESUMO

OBJECTIVES: To investigate the effect of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) on liver injury induced by periodontitis in rats. METHODS: Twenty-four male Wistar rats were randomly divided into two groups: control group and periodontitis group, twelve per group. In periodontitis group, the periodontitis models were established for the maxillary first molars in rats by means of "wire ligation+vaccinationwith Porphyromonas gingivalis", the control group was inoculated with the equal volume of 2% sodium carboxymethyl cellulose in the same position, for 6 weeks. The probing depth, tooth mobility and sulcus bleeding index were detected. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of liver tissues in rats. The quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) were used to detect the gene and protein expression levels of PGC-1α, nuclear factor erythroid 2-related factor 2 (Nrf2) and mitochondrial transcription factor A (TFAM) in liver tissues of rats. RESULTS: The probing depth, tooth mobility and sulcus bleeding index in periodontitis group were significantly higher than that in control group. HE staining showed in periodontitis group, hepatic cords ranged disorderly and there were vacuoles in cells and inflammatory cells infiltrated in liver tissues of rats, and there was no obvious abnormality in control group. The qRT-PCR results showed that the mRNA expression levels of Pgc-1α, Nrf2 and Tfam in liver tissues of rats in periodontitis group were lower obviously than that in control group. IHC results showed that the protein expression level of PGC-1α in liver tissues of rats in periodontitis group was decreased significantly than that in control group. CONCLUSIONS: PGC-1α may be involved in the process of periodontitis-induced liver injury in rats.


Assuntos
Fígado/lesões , PPAR gama , Periodontite , Animais , Masculino , Periodontite/patologia , Ratos , Ratos Wistar
5.
Int J Mol Sci ; 22(19)2021 Sep 26.
Artigo em Inglês | MEDLINE | ID: mdl-34638690

RESUMO

Periodontal inflammation is a common inflammatory disease associated with chronic inflammation that can ultimately lead to alveolar attachment loss and bone destruction. Understanding autophagy and pyroptosis has suggested their significant roles in inflammation. In recent years, studies of differentiated embryo-chondrocyte expressed genes 1 and 2 (Dec1 and Dec2) have shown that they play important functions in autophagy and in pyroptosis, which contribute to the onset of periodontal inflammation. In this review, we summarize recent studies on the roles of clock genes, including Dec1 and Dec2, that are related to periodontal inflammation and other diseases.


Assuntos
Autofagia , Fatores de Transcrição Hélice-Alça-Hélice Básicos/biossíntese , Regulação da Expressão Gênica , Proteínas de Homeodomínio/biossíntese , Periodontite/metabolismo , Piroptose , Animais , Humanos , Inflamação/metabolismo , Inflamação/patologia , Periodontite/patologia
6.
Life Sci ; 284: 119938, 2021 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-34506837

RESUMO

AIMS: The relationship between stress to endoplasmic reticulum (ER) and periodontitis has been known, and ER stress induced by Porphyromonas gingivalis results in the loss of alveolar bone. Salubrinal is a small synthetic compound and attenuates ER stress through inhibition of de-phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α). In this study, we examined whether salubrinal attenuates periodontitis in a mouse model of experimental periodontal disease. MATERIALS AND METHODS: We evaluated loss of alveolar bone and attachment levels in periodontium using micro-computed tomography (µCT) and hematoxylin-eosin (HE) staining, respectively. Furthermore, we measured osteoclast numbers using tartrate-resistant acid phosphatase (TRAP) staining and osteoblast numbers using HE staining for bone resorption and for bone formation, respectively. To examine the inhibitory effects of salubrinal against pro-inflammatory cytokines, we measured TNF-α and IL1-ß score in periodontium using immunohistostaining. KEY FINDINGS: The results revealed that salubrinal suppressed loss of alveolar bone and attachment levels in periodontium induced by periodontitis. It decreased osteoclast numbers and increased osteoblasts. It also suppressed the expression levels of TNF-α in periodontium. SIGNIFICANCE: These results show that salubrinal alleviates periodontitis through suppression of alveolar bone resorption and the pro-inflammatory cytokine, and promotion of the bone formation. Since salubrinal has been shown to have these beneficial effects for periodontal disease, it may provide a novel therapeutic possibility for the disease.


Assuntos
Perda do Osso Alveolar/tratamento farmacológico , Cinamatos/uso terapêutico , Tioureia/análogos & derivados , Perda do Osso Alveolar/complicações , Perda do Osso Alveolar/diagnóstico por imagem , Perda do Osso Alveolar/patologia , Animais , Contagem de Células , Cinamatos/administração & dosagem , Cinamatos/farmacologia , Modelos Animais de Doenças , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Interleucina-1beta/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Osteoblastos/efeitos dos fármacos , Osteoblastos/patologia , Periodontite/complicações , Periodontite/tratamento farmacológico , Periodontite/patologia , Tioureia/administração & dosagem , Tioureia/farmacologia , Tioureia/uso terapêutico , Fator de Transcrição CHOP/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Microtomografia por Raio-X
7.
Int J Mol Sci ; 22(16)2021 Aug 18.
Artigo em Inglês | MEDLINE | ID: mdl-34445604

RESUMO

Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.


Assuntos
Modelos Animais de Doenças , Microbioma Gastrointestinal , Ligadura/efeitos adversos , Doenças Periodontais/patologia , Periodontite/patologia , Animais , Carga Bacteriana , Camundongos , Doenças Periodontais/etiologia , Periodontite/etiologia
8.
Front Immunol ; 12: 663328, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34220811

RESUMO

Periodontitis is an oral inflammatory disease in which the polymicrobial synergy and dysbiosis of the subgingival microbiota trigger a deregulated host immune response, that leads to the breakdown of tooth-supporting tissues and finally tooth loss. Periodontitis is characterized by the increased pathogenic activity of T helper type 17 (Th17) lymphocytes and defective immunoregulation mediated by phenotypically unstable T regulatory (Treg), lymphocytes, incapable of resolving the bone-resorbing inflammatory milieu. In this context, the complexity of the immune response orchestrated against the microbial challenge during periodontitis has made the study of its pathogenesis and therapy difficult and limited. Indeed, the ethical limitations that accompany human studies can lead to an insufficient etiopathogenic understanding of the disease and consequently, biased treatment decision-making. Alternatively, animal models allow us to manage these difficulties and give us the opportunity to partially emulate the etiopathogenesis of periodontitis by inoculating periodontopathogenic bacteria or by placing bacteria-accumulating ligatures around the teeth; however, these models still have limited translational application in humans. Accordingly, humanized animal models are able to emulate human-like complex networks of immune responses by engrafting human cells or tissues into specific strains of immunodeficient mice. Their characteristics enable a viable time window for the study of the establishment of a specific human immune response pattern in an in vivo setting and could be exploited for a wider study of the etiopathogenesis and/or treatment of periodontitis. For instance, the antigen-specific response of human dendritic cells against the periodontopathogen Porphyromonas gingivalis favoring the Th17/Treg response has already been tested in humanized mice models. Hypothetically, the proper emulation of periodontal dysbiosis in a humanized animal could give insights into the subtle molecular characteristics of a human-like local and systemic immune response during periodontitis and support the design of novel immunotherapeutic strategies. Therefore, the aims of this review are: To elucidate how the microbiota-elicited immunopathogenesis of periodontitis can be potentially emulated in humanized mouse models, to highlight their advantages and limitations in comparison with the already available experimental periodontitis non-humanized animal models, and to discuss the potential translational application of using these models for periodontitis immunotherapeutics.


Assuntos
Modelos Animais de Doenças , Suscetibilidade a Doenças , Camundongos Transgênicos , Periodontite/etiologia , Animais , Gerenciamento Clínico , Suscetibilidade a Doenças/imunologia , Interações entre Hospedeiro e Microrganismos , Humanos , Hospedeiro Imunocomprometido , Transfusão de Linfócitos , Camundongos , Microbiota , Transplante de Órgãos , Periodontite/patologia , Periodontite/terapia , Transplante de Células-Tronco
9.
Biomolecules ; 11(6)2021 06 12.
Artigo em Inglês | MEDLINE | ID: mdl-34204680

RESUMO

Here, we assess the association between homocysteine (Hcy) serum levels and periodontal status in a large representative sample of the National Health and Nutrition Examination Survey (NHANES). Using the 2001-2002 and 2003-2004 NHANES databases, participants with a periodontal examination, medical self-reported data, blood pressure (BP) and blood samples to determine complete blood count, C-reactive protein (CRP) and Hcy levels. We then calculated the periodontal inflamed surface area (PISA) and the periodontal epithelial surface area (PESA). Multivariable regression analysis explored the association between Hcy, periodontal measures and BP. Mediation analysis was performed to understand the effect of PISA and PESA in the link between Hcy and BP. 4021 participants fulfilled the inclusion criteria. Hcy levels showed significant correlations with systolic BP, diastolic BP, PISA, PESA and age. PESA showed to be significantly associated with Hcy both for the crude and adjusted models (p < 0.01), but not PISA (p > 0.05). In the association of Hcy with systolic BP, PISA significantly mediated 17.4% and PESA 0.9%. In the association of Hcy with diastolic BP, PISA significantly mediated 16.3% and PESA 47.2%. In conclusion, Hcy and periodontitis are associated. Further, both PISA and PESA significantly mediated the association of Hcy with systolic BP and diastolic BP. Future studies shall deepen the mechanisms by which Hcy levels increase in a clinical situation of periodontitis.


Assuntos
Pressão Sanguínea , Homocisteína/sangue , Periodontite/sangue , Periodontite/fisiopatologia , Periodonto/metabolismo , Adulto , Idoso , Proteína C-Reativa/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Periodontite/patologia , Periodonto/patologia
10.
J Leukoc Biol ; 110(3): 475-484, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34184309

RESUMO

Neutrophil plays a critical role in the progression of periodontitis. In general, its chemotaxis and activation are benefit for the host defense of bacterial infection and inflammation. However, previous studies have reported that the hyperactive and reactive neutrophils appear to be one of the reasons for tissue destruction in periodontitis tissues. In this study, we investigated an isoquinoline alkaloid Litcubanine A (LA), which from the Traditional Chinese medicinal plant, Litsea cubeba. We found LA showed significant activity in inhibiting neutrophils chemotaxis in the zebrafish yolk sac microinjection model in vivo and in mouse neutrophils in vitro. Further investigation proved that LA could inhibit the expression levels of neutrophil respiratory burst-related and inflammation-related genes CYBB and NCF2, as well as inhibit the activation of MAPK signaling pathway. Moreover, using LA, we successfully achieved the effect of reducing periodontitis bone loss by regulating neutrophil chemotaxis and related functions in a mouse ligature-induced periodontitis model.


Assuntos
Alcaloides/uso terapêutico , Quimiotaxia , Isoquinolinas/uso terapêutico , Neutrófilos/patologia , Periodontite/tratamento farmacológico , Alcaloides/farmacologia , Animais , Reabsorção Óssea/patologia , Quimiotaxia/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Interleucina-8/metabolismo , Isoquinolinas/farmacologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Camundongos Endogâmicos C57BL , Microinjeções , Infiltração de Neutrófilos/efeitos dos fármacos , Neutrófilos/efeitos dos fármacos , Periodontite/diagnóstico por imagem , Periodontite/patologia , Receptores de Quimiocinas/genética , Receptores de Quimiocinas/metabolismo , Explosão Respiratória/efeitos dos fármacos , Saco Vitelino/efeitos dos fármacos , Saco Vitelino/metabolismo , Peixe-Zebra
11.
J Med Life ; 14(2): 287-294, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34104255

RESUMO

A hopeless tooth from a periodontal point of view, with severe bone resorption, mobility and abnormal tooth migration, is often extracted. In advanced cases, function and esthetics are impaired, and an interdisciplinary treatment is requested. Retaining or not these teeth is based on clinician judgment. A growing body of evidence claims that prognosis has great potential to be improved in a motivated patient with good oral hygiene and regular maintenance. This case report aims to present a periodontal regenerative technique combining enamel matrix protein derivatives and a particulated xenograft to treat intraosseous defects caused by periodontitis. The patient healed uneventfully, and no complications were recorded after the surgical procedure. To correct abnormal tooth migration and improve function and esthetics, orthodontic treatment was instituted. Tooth prognosis improved from hopeless to questionable. This approach extended the life span of a compromised tooth, improving periodontal support and decreasing tooth mobility. This could be an alternative to extraction and implant.


Assuntos
Dente/patologia , Feminino , Seguimentos , Humanos , Pessoa de Meia-Idade , Periodontite/diagnóstico por imagem , Periodontite/patologia , Prognóstico , Suturas , Dente/diagnóstico por imagem , Dente/cirurgia , Extração Dentária
12.
PLoS One ; 16(6): e0252859, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34153036

RESUMO

Patients with rheumatoid arthritis (RA) experience a higher prevalence of periodontitis. This study aimed to examine the variation of periodontitis experienced with different serotypes suffered by RA patients and to examine the relationship between the different medications taken for RA that may influence this relationship. Two hundred and sixty RA and control participants underwent standardized periodontal examinations. Medical, serological and radiological (Sharp/van der Heijde) records were assessed. Functional status was assessed using the administered Health Assessment Questionnaire. Moreover, disease parameters, including disease activity (DAS28-ESR) and anti-citrullinated protein antibodies (ACPA) and rheumatoid factor (RF) seropositivity were evaluated. Periodontitis was higher in RA (71.54%) compared with controls (54.62%). The stage of periodontitis experienced by ACPA-positive participants were higher than APCA-negative participants. The probing pocket depth and recession experienced by RF-positive participants were higher than those who were RF-negative. RA participants on methotrexate had lower clinical attachment loss and lower periodontal probing depth compared with participants on a combination methotrexate and other disease-modifying antirheumatic drugs. Participants taking corticosteroids had lower gingival index scores. The association between seropositivity and the type of medications taken with periodontal health parameters in this group of patients suggests that both seropositivity and medications taken are important modifiers in the relationship between periodontitis and RA.


Assuntos
Anticorpos Anti-Proteína Citrulinada/metabolismo , Antirreumáticos/farmacologia , Artrite Reumatoide/fisiopatologia , Osteoartrite/fisiopatologia , Periodontite/epidemiologia , Sorogrupo , Artrite Reumatoide/sangue , Artrite Reumatoide/tratamento farmacológico , Estudos de Casos e Controles , Feminino , Humanos , Malásia/epidemiologia , Masculino , Metotrexato/farmacologia , Pessoa de Meia-Idade , Osteoartrite/sangue , Osteoartrite/tratamento farmacológico , Periodontite/metabolismo , Periodontite/patologia
13.
Int J Mol Sci ; 22(10)2021 May 14.
Artigo em Inglês | MEDLINE | ID: mdl-34069164

RESUMO

BACKGROUND: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. METHODS: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. RESULTS: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). CONCLUSION: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.


Assuntos
Densidade Óssea/genética , Periodontite/genética , Receptor Tipo 1 de Angiotensina/genética , Receptor Tipo 2 de Angiotensina/genética , Animais , Modelos Animais de Doenças , Lipopolissacarídeos/toxicidade , Masculino , Camundongos Knockout , Óxido Nítrico Sintase Tipo II/genética , Periodontite/induzido quimicamente , Periodontite/diagnóstico por imagem , Periodontite/patologia , Porphyromonas gingivalis/patogenicidade , Ligante RANK/metabolismo , Microtomografia por Raio-X
14.
Int J Mol Sci ; 22(11)2021 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-34064286

RESUMO

During the last few decades, it has been established that messenger ribonucleic acid (mRNA) transcription does not inevitably lead to protein translation, but there are numerous processes involved in post-transcriptional regulation, which is a continuously developing field of research. MicroRNAs (miRNAs) are a group of small non-coding RNAs, which negatively regulate protein expression and are implicated in several physiological and pathological mechanisms. Aberrant expression of miRNAs triggers dysregulation of multiple cellular processes involved in innate and adaptive immune responses. For many years, it was thought that miRNAs acted only within the cell in which they were synthesised, but, recently, they have been found outside cells bound to lipids and proteins, or enclosed in extracellular vesicles, namely exosomes. They can circulate throughout the body, transferring information between cells and altering gene expression in the recipient cells, as they can fuse with and be internalised by the recipient cells. Numerous studies on miRNAs have been conducted in order to identify possible biomarkers that can be used in the diagnosis of periodontal disease. However, as therapeutic agents, single miRNAs can target several genes and influence multiple regulatory networks. The aim of this review was to examine the molecular role of miRNAs and exosomes in the pathophysiology of periodontal disease and to evaluate possible clinical and future implications for a personalised therapeutical approach.


Assuntos
MicroRNAs/genética , Periodontite/genética , Periodontite/patologia , Animais , Exossomos/genética , Regulação da Expressão Gênica/genética , Humanos , Biossíntese de Proteínas/genética , RNA Mensageiro/genética
15.
Int J Mol Sci ; 22(11)2021 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-34070915

RESUMO

Systemic inflammation induced by periodontitis is suggested to be the link between periodontitis and cardiovascular disease. The aim of this work was to explore the oral microbiome in periodontitis in relation to disease severity and systemic inflammation. The saliva and subgingival microbiome from periodontal pocket samples of patients with severe (n = 12) and mild periodontitis (n = 13) were analyzed using metagenomic shotgun sequencing. The taxa and pathways abundances were quantified. The diversity was assessed and the abundances to phenotype associations were performed using ANCOM and linear regression. A panel of inflammatory markers was measured in blood and was associated with taxa abundance. The microbial diversity and species richness did not differ between severe and mild periodontitis in either saliva or periodontal pockets. However, there were significant differences in the microbial composition between severe and mild periodontitis in the subgingival microbiome (i.e., pocket samples) and, in a lower grade, in saliva, and this is positively associated with systemic inflammatory markers. The "red complex" and "cluster B" abundances in periodontal pockets were strongly associated with inflammatory markers interleukin-6 and the white blood cell count. Our data suggest that systemic inflammation in severe periodontitis may be driven by the oral microbiome and may support the indirect (inflammatory) mechanism for the association between periodontitis and cardiovascular disease.


Assuntos
Metagenoma , Microbiota/genética , Periodontite/microbiologia , Periodonto/microbiologia , Idoso , Biomarcadores/metabolismo , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/imunologia , Doenças Cardiovasculares/microbiologia , Doenças Cardiovasculares/patologia , Feminino , Expressão Gênica , Variação Genética , Humanos , Inflamação , Proteína Antagonista do Receptor de Interleucina 1/genética , Proteína Antagonista do Receptor de Interleucina 1/imunologia , Interleucina-6/genética , Interleucina-6/imunologia , Leucócitos/imunologia , Leucócitos/microbiologia , Masculino , Pessoa de Meia-Idade , Periodontite/complicações , Periodontite/imunologia , Periodontite/patologia , Periodonto/imunologia , Periodonto/patologia , Fenótipo , Filogenia , Índice de Gravidade de Doença
16.
Biomed Pharmacother ; 139: 111677, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33965727

RESUMO

Periodontitis is a chronic inflammatory disease that affects the tooth-supporting tissues. This study evaluated the anti-inflammatory and antiresorptive effects of milk kefir (MK) on periodontitis in rats. Micro-Raman spectroscopy was performed on MK at different fermentation times to verify the presence of Lactobacillus kefiri. From these results, Wistar rats were divided into the following groups: C (Control); EP (experimental periodontitis); K1 (animals that received MK with one day of fermentation); K1+EP; K4 (animals without EP using MK with four days of fermentation) and K4+EP. MK was administered 28 days before EP induction and during the disease development period (11 days). On day 28, in the EP groups, periodontitis was induced. The animals were euthanized on day 39. The hemimaxillae were removed and the following parameters were evaluated: micro-Raman analysis of the presence of inflammation; histomorphometric analysis to quantify alveolar bone loss and immunohistochemistry for IL-6, TNF-α, IL-Iß and IL-10 in the periodontal ligament. Micro-Raman analysis showed that four days fermentation MK has a higher intensity spectrum of L. kefiri. Furthermore, the administration of this probiotic reduced the intensity of the inflammation spectrum when compared to one day fermentation MK. It was observed that the animals from the K4+EP group showed significant reduction of alveolar bone loss, as well as a lower IL-6, TNF-α and IL-Iß immunoexpression and a higher IL-10 immunoexpression, when compared to EP groups. We conclude that MK has anti-inflammatory and antiresorptive effects on periodontitis in rats and that these effects are fermentation time dependent.


Assuntos
Perda do Osso Alveolar/tratamento farmacológico , Inflamação/tratamento farmacológico , Kefir , Periodontite/tratamento farmacológico , Probióticos/uso terapêutico , Perda do Osso Alveolar/patologia , Animais , Reabsorção Óssea/patologia , Reabsorção Óssea/prevenção & controle , Citocinas/metabolismo , Fermentação , Inflamação/patologia , Masculino , Ligamento Periodontal/patologia , Periodontite/patologia , Periodonto/patologia , Ratos , Ratos Wistar , Microtomografia por Raio-X
17.
Front Immunol ; 12: 664756, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34012448

RESUMO

Periodontitis is a chronic inflammatory disease associated with the formation of dysbiotic plaque biofilms and characterized by the progressive destruction of the alveolar bone. The transition from health to disease is characterized by a shift in periodontal immune cell composition, from mostly innate (neutrophils) to adaptive (T lymphocytes) immune responses. Resolvin E1 (RvE1) is a specialized pro-resolution mediator (SPMs), produced in response to inflammation, to enhance its resolution. Previous studies have indicated the therapeutic potential of RvE1 in periodontal disease; however, the impact of RvE1 in the microbial-elicited osteoclastogenic immune response remains uncharacterized in vivo. In the present study, we studied the impact of RvE1 on the gingival inflammatory infiltrate formation during periodontitis in a mouse model. First, we characterized the temporal-dependent changes of the main immune cells infiltrating the gingiva by flow cytometry. Then, we evaluated the impact of early or delayed RvE1 administration on the gingival immune infiltration and cervical lymph nodes composition. We observed a consistent inhibitory outcome on T cells -particularly effector T cells- and a protective effect on regulatory T cells (Tregs). Our data further demonstrated the wide range of actions of RvE1, its preventive role in the establishment of the adaptive immune response during inflammation, and bone protective capacity.


Assuntos
Ácido Eicosapentaenoico/análogos & derivados , Gengivite/etiologia , Gengivite/metabolismo , Linfócitos T/imunologia , Linfócitos T/metabolismo , Perda do Osso Alveolar/etiologia , Perda do Osso Alveolar/metabolismo , Perda do Osso Alveolar/patologia , Animais , Modelos Animais de Doenças , Progressão da Doença , Ácido Eicosapentaenoico/farmacologia , Gengivite/tratamento farmacológico , Gengivite/patologia , Imunofenotipagem , Linfonodos/imunologia , Linfonodos/metabolismo , Linfonodos/patologia , Camundongos , Neutrófilos/imunologia , Neutrófilos/metabolismo , Periodontite/etiologia , Periodontite/metabolismo , Periodontite/patologia , Linfócitos T/patologia
18.
J Leukoc Biol ; 110(3): 577-583, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34028883

RESUMO

Periodontitis is a chronic infectious disease characterized by loss of periodontal attachment and resorption of alveolar bone. Dysregulated oral microbial community is the initial factor of periodontitis and causes excessive infiltration of immune cells in periodontal tissues. Macrophage, as an important part of the innate immune system, interacts continually with oral pathogens. Macrophages can recognize and phagocytize pathogens and apoptotic neutrophils and produce the specialized pro-resolving mediators (SPMs) playing an important role in maintaining the homeostasis of tissue microenvironment. However, macrophages may also induce abnormal immune responses with the overstimulation from pathogens, leading to the destruction of periodontal tissues and alveolar bone. Looking for targeted drugs that can regulate the activities of oral pathogens and the functions of macrophages provides a new idea for periodontitis treatment. This review summarizes the interaction between macrophages and periodontal pathogens in periodontitis, focusing on the pro-inflammation and anti-inflammation phenotypes of macrophages, and briefly concludes potential new methods of periodontitis therapy targeted at oral pathogens and macrophages.


Assuntos
Macrófagos/patologia , Periodontite/microbiologia , Periodontite/patologia , Periodonto/microbiologia , Periodonto/patologia , Animais , Humanos , Inflamação/patologia , Modelos Biológicos , Periodontite/terapia , Receptores Toll-Like/metabolismo
19.
J Leukoc Biol ; 110(3): 565-576, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34043832

RESUMO

Periodontitis is characterized by the periodontium's pathologic destruction due to the host's overwhelmed inflammation to the dental plaque. The bacterial infections and subsequent host immune responses have shaped a distinct microenvironment, which generally affects resident periodontal ligament stem cells (PDLSCs). Interestingly, recent studies have revealed that impaired PDLSCs may also contribute to the disturbance of periodontal homeostasis. The putative vicious circle underlying the interesting "positive feedback" of PDLSCs in the periodontitis niche remains a hot research topic, whereas the inseparable interactions between resident PDLSCs and the periodontitis niche are still not fully understood. This review provides a microscopic view on the periodontitis progression, especially the quick but delicate immune responses to oral dysbacterial infections. We also summarize the interesting crosstalk of the resident PDLSCs with their surrounding periodontitis niche and potential mechanisms. Particularly, the microenvironment reduces the osteogenic properties of resident PDLSCs, which are closely related to their reparative activity. Reciprocally, these impaired PDLSCs may disrupt the microenvironment by aggravating the host immune responses, promoting aberrant angiogenesis, and facilitating the osteoclastic activity. We further recommend that more in-depth studies are required to elucidate the interactions of PDLSCs with the periodontal microenvironment and provide novel interventions for periodontitis.


Assuntos
Comunicação Celular , Ligamento Periodontal/patologia , Periodontite/patologia , Células-Tronco/patologia , Humanos , Imunidade , Modelos Biológicos , Periodontite/imunologia
20.
BMC Oral Health ; 21(1): 279, 2021 05 28.
Artigo em Inglês | MEDLINE | ID: mdl-34049546

RESUMO

BACKGROUND: Immunoglobulin G4-related disease (IgG4-RD) is a chronic inflammatory systemic disease of unknown etiology that can affect one or multiple organs. The disease can mimic many infectious and inflammatory diseases, mainly causing organ enlargement or hyperplasia. Its diagnosis primarily relies on clinical, serologic, and histological features (lymphoplasmacytic infiltrates, storiform fibrosis, and obliterative phlebitis of IgG4 + plasma cells). Here, we report a rare case of IgG4-related periodontitis, and review the relevant literatures. CASE PRESENTATION: A 38-year-old Chinese man visited the Department of Periodontics with gingival enlargement, loose teeth, and tooth loss. The patient had very poor oral hygiene and a large amount of calculus. Gingivae were edematous with deep periodontal pockets and attachment loss. Panoramic radiography showed alveolar bone loss. Serologic examination showed that IgG was 23.70 g/L and IgG4 concentration was 2.800 g/L. There was significant lymphoplasmacytic infiltration, a storiform pattern of fibrosis, and mitotic figures with hematoxylin and eosin staining; immunohistochemical staining showed 10 scattered IgG4-positive plasma cells in a high-power field. The patient was diagnosed as IgG4-related periodontitis. He received a course of corticosteroids with periodontal therapy, and the enlargement was significantly improved without recurrence. CONCLUSION: IgG4-RD in the oral and maxillofacial region mainly involves salivary glands, but this rare case was characterized by enlarged gingivae. The differential diagnosis of IgG4-RD should be based on the clinical features and serologic (IgG4) and histopathological examinations. Corticosteroid therapy is effective for most IgG4-RD patients. Taken together, we hope this case report and the literature review can help dentists to improve their understanding of the IgG4-RD.


Assuntos
Doença Relacionada a Imunoglobulina G4 , Periodontite , Adulto , Fibrose , Humanos , Imunoglobulina G , Doença Relacionada a Imunoglobulina G4/diagnóstico , Doença Relacionada a Imunoglobulina G4/tratamento farmacológico , Doença Relacionada a Imunoglobulina G4/patologia , Masculino , Periodontite/patologia , Plasmócitos
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