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1.
Braz. oral res. (Online) ; 34: e038, 2020. tab, graf
Article in English | LILACS, BBO | ID: biblio-1100932

ABSTRACT

Abstract The possible role of B-cell growth and differentiation-related cytokines on the pathogenesis of diabetes-related periodontitis has not been addressed so far. The aim of this study was to evaluate the effects of diabetes mellitus (DM) on the gene expression of proliferation-inducing ligand (APRIL) and B-lymphocyte stimulator (BLyS), two major cytokines associated to survival, differentiation and maturation of B cells in biopsies from gingival tissue with periodontitis. Gingival biopsies were obtained from subjects with periodontitis (n = 17), with periodontitis and DM (n = 19) as well as from periodontally and systemically healthy controls (n = 10). Gene expressions for APRIL, BLyS, RANKL, OPG, TRAP and DC-STAMP were evaluated using qPCR. The expressions APRIL, BLyS, RANKL, OPG, TRAP and DC-STAMP were all higher in both periodontitis groups when compared to the control group (p < 0.05). Furthermore, the expressions of BLyS, TRAP and RANKL were significantly higher in the subjects with periodontitis and DM when compared to those with periodontitis alone (p < 0.05). The mRNA levels of BLyS correlated positively with RANKL in the subjects with periodontitis and DM (p < 0.05). BLyS is overexpressed in periodontitis tissues of subjects with type 2 DM, suggesting a possible role of this cytokine on the pathogenesis DM-related periodontitis.


Subject(s)
Humans , Male , Female , Adult , Aged , Periodontitis/immunology , Periodontitis/pathology , Diabetes Mellitus, Type 2/complications , B-Cell Activating Factor/analysis , Osteogenesis/immunology , Reference Values , Biopsy , RNA, Messenger/analysis , Biomarkers/analysis , Case-Control Studies , Gene Expression , Cytokines/analysis , Cytokines/physiology , Statistics, Nonparametric , Diabetes Mellitus, Type 2/immunology , Tumor Necrosis Factor Ligand Superfamily Member 13/analysis , Real-Time Polymerase Chain Reaction , Gingiva/immunology , Gingiva/pathology , Middle Aged
2.
Actual. osteol ; 15(1): 34-43, ene. abr. 2019. ilus.
Article in Spanish | LILACS | ID: biblio-1049002

ABSTRACT

La brucelosis es una de las enfermedades zoonóticas más importantes a nivel mundial capaz de producir enfermedad crónica en los seres humanos. La localización osteoarticular es la presentación más común de la enfermedad activa en el hombre. Sin embargo, algunos de los mecanismos moleculares implicados en la enfermedad osteoarticular han comenzado a dilucidarse recientemente. Brucella abortus induce daño óseo a través de diversos mecanismos en los cuales están implicados TNF-α y RANKL. En estos procesos participan células inflamatorias que incluyen monocitos/macrófagos, neutrófilos, linfocitos T del tipo Th17 y linfocitos B. Además, B. abortus puede afectar directamente las células osteoarticulares. La bacteria inhibe la deposición de la matriz ósea por los osteoblastos y modifica el fenotipo de estas células para producir metaloproteinasas de matriz (MMPs) y la secreción de citoquinas que contribuyen a la degradación del hueso. Por otro lado, la infección por B. abortus induce un aumento en la osteoclastogénesis, lo que aumenta la resorción de la matriz ósea orgánica y mineral y contribuye al daño óseo. Dado que la patología inducida por Brucella afecta el tejido articular, se estudió el efecto de la infección sobre los sinoviocitos. Estos estudios revelaron que, además de inducir la activación de estas células para secretar quemoquinas, citoquinas proinflamatorias y MMPs, la infección inhibe la muerte por apoptosis de los sinoviocitos. Brucella es una bacteria intracelular que se replica en el retículo endoplásmico de los macrófagos. El análisis de los sinoviocitos infectados con B. abortus indicó que las bacterias también se multiplican en el retículo endoplasmático, lo que sugiere que la bacteria podría usar este tipo celular para la multiplicación intracelular durante la localización osteoarticular de la enfermedad. Los hallazgos presentados en esta revisión intentan responder a preguntas sobre los mediadores inflamatorios implicados en el daño osteoarticular causado por Brucella. (AU)


Brucellosis is one of the most important zoonotic diseases that can produce chronic disease in humans worldwide. Osteoarticular involvement is the most common presentation of human active disease. The molecular mechanisms implicated in bone damage have started to be elucidated. B. abortus induces bone damage through diverse mechanisms in which TNF-α and RANKL are implicated. These processes are driven by inflammatory cells, including monocytes/macrophages, neutrophils, Th17 lymphocytes and B cells. Also, Brucella abortus (B. abortus) can directly affect osteoarticular cells. The bacterium inhibits bone matrix deposition by osteoblast and modifies the phenotype of these cells to produce matrix methalloproteinases (MMPs) and cytokine secretion that contribute to bone matrix degradation. B. abortus also affects osteoclast increasing mineral and organic bone matrix resorption and contributing to bone damage. Since the pathology induced by Brucella species involves joint tissue, experiments conducted in sinoviocytes revealed that besides inducing the activation of these cells to secrete chemokines, proinflammatory cytokines and MMPS, the infection also inhibits sinoviocyte apoptosis. Brucella is an intracellular bacterium that replicate in the endoplasmic reticulum of macrophages. The analysis of B. abortus infected sinoviocytes indicated that bacteria also replicate in their reticulum suggesting that the bacterium could use this cell type for intracellular replication during the osteoarticular localization of the disease. The findings presented in this review try to answer key questions about the inflammatory mediators involved in osteoarticular damage caused by Brucella. (AU)


Subject(s)
Humans , Animals , Osteoarthritis/pathology , Brucella abortus/pathogenicity , Brucellosis/pathology , Osteoarthritis/immunology , Osteoblasts/pathology , Osteocytes/microbiology , Osteogenesis/immunology , Brucella abortus/immunology , Brucellosis/etiology , Brucellosis/immunology , B-Lymphocytes/pathology , Cytokines/adverse effects , Tumor Necrosis Factor-alpha/adverse effects , Matrix Metalloproteinases/chemical synthesis , RANK Ligand/adverse effects , Th17 Cells/pathology , Synoviocytes/immunology , Macrophages/pathology , Neutrophils/pathology
3.
Full dent. sci ; 1(3): 224-230, abr.-jun. 2010. ilus
Article in Portuguese | LILACS, BBO | ID: lil-642943

ABSTRACT

O reparo de defeitos ósseos é um desafio para diversas áreas, pois a invasão de células fibroblásticas no defeito, resulta em tecido conjuntivo cicatricial. Assim, os princípios de Regeneração Tecidual Guiada (RTG) estão bem estabelecidos para tratamento de defeitos ósseos. Essa técnica consiste na utilização de biomembranas que agem como barreiras e evitam a invasão dos fibroblastos e permite o povoamento com células osteoprogenitoras. O presente trabalho propôs-se avaliar o crescimento e potencial regenerativo em defeitos ósseos através de avaliações macroscópicas e radiográficas. Para tanto, 27 coelhos foram divididos em 3 grupos experimentais de acordo com o tratamento: Controle (A), Látex (B) e PTFE (C). Então, subdivididos em 3 grupos para análise de neoformação periódica: 15 (I); 30 (II) e 60 dias (III). As cobaias foram submetidas à cirurgia para confecção de defeitos ósseos críticos em calvária e tratamento específico de cada grupo. Após os períodos os animais foram sacrificados e obtidas as peças anatômicas para as radiografias pelo método Digora e fotografias digitais. As análises macroscópicas permitiram observar crescimento ósseo e áreas radiopacas sugestivas de tecido ósseo. No período de 15 dias a densidade óssea nos grupos experimentais no defeito foi semelhante. Contudo, aos 60 dias, verificou-se formação óssea homogênea para Látex e vários níveis de radiopacidade para PTFE e controle. Dentro das limitações, conclui-se que biomembranas são bem indicadas em processos cirúrgicos para regeneração óssea, visto que as barreiras impedem ou dificultam a migração de células incompatíveis com o tecido a ser neoformado e promove a osteogênese.


The repair of bone defects is challenge for many areas, since the invasion of fibroblast cells in the defect, resulting in scar tissue. Thus, the principles of Guided Tissue Regeneration (GTR) are well established for treatment of bone defects. This technique is the use of bio-membranes that act as barriers and prevent the invasion of fibroblasts and allows the placement of osteoprogenitor cells. The proposition of this study is evaluate the mechanical growth and regenerative potential in bone defects by macroscopic and radiographic analyses. Twenty-seven rabbits were divided into 3 groups according to treatment: control (A), Latex (B) and PTFE (C). Then divided into 3 groups for analysis of periodic neoformation: 15 (I), 30 (II) and 60 days (III). The animals were subjected to surgical preparation of bone defects in critical calvaria and specific treatment of each group. After the period, they were sacrificed and collected the body parts for X-rays by the Digora method and digital photographs. Macroscopic analysis allowed observed bone growth and areas suggestive of bone tissue. During 15 days of bone density in the experimental groups in the defect was similar. However, after 60 days, there was bone formation for homogeneous in group of Latex and various levels of radiopacity to PTFE and control. Within the experimental conditions, the biomembranes are well indicated in surgical procedures for bone regeneration, since the barriers preventing or hindering cell migration incompatible with the tissue to be newly formed and promotes osteogenesis.


Subject(s)
Animals , Rabbits , Bone Regeneration , Guided Tissue Regeneration , Latex/analysis , Membranes/transplantation , Osteogenesis/immunology , Polytetrafluoroethylene , Diagnostic Imaging , Materials Testing
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