Comportamiento de la enfermedad periodontal inmunoinflamatoria crónica. Jovellanos. Matanzas / Behavior of the chronic immunoinflammatory periodontal disease. Jovellanos. Matanzas

RESUMEN Introducción: Para la Organización Mundial de la Salud, la enfermedad periodontal representa un problema de salud pública en países industrializados y en los que están en vías de desarrollo. Afecta la calidad de vida de quienes las sufren. Este término agrupa una serie de entidades que afectan los tejidos de protección e inserción del diente, dentro de las cuales se encuentra la periodontitis, proceso inmunoinflamatoria crónico. Objetivo: estimar la prevalencia de la enfermedad periodontal inmunoinflamatoria crónica en el municipio de Jovellanos, provincia de Matanzas. Materiales y métodos: con el objetivo de estimar la prevalencia de la enfermedad periodontal inmunoinflamatoria crónica, en el municipio de Jovellanos, provincia de Matanzas se realizó un estudio observacional, descriptivo transversal, en el período comprendido entre el mes junio del 2009 a junio del 2010. Resultados: el 54,5 % de la población no presentó la enfermedad estudiada. El grupo de 5 a 11 años fue el que más aportó a este resultado. La enfermedad fue diagnosticada en el 45,5 % de la población examinada, la cual comenzó a manifestarse a partir del grupo de edad de 15 a 18 años. El 92,9 % de los individuos de 60 a 74 años fueron los más afectados. Conclusiones: en cuanto a la enfermedad periodontal inmuno inflamatoria la cantidad de pacientes sanos, desde el punto de vista periodontal, estuvo entre un 49,4 % y un 59,6 % del total de la población. La incidencia de la enfermedad aumenta con la edad. La presencia de bolsas resultó mayor a partir de los 35 años y causó gran afectación en los individuos de 60 a 74 años.

ABSTRACT Introduction: According to the World Health Organization, periodontal disease represents a public health problem in the developed countries and in the developing ones. It affects the life quality of people suffering it. This term groups together several entities affecting the tooth´s insertion and protection tissues; periodontitis, a chronic immunoinflammatory process, is found among them. Objective: estimate the prevalence of periodontal disease inmunoinflamatoria chronic in the municipality of Jovellanos, province of Matanzas. Materials and methods: a cross-sectional descriptive, observational study was carried out in the municipality of Jovellanos, province of Matanzas from June 2009 to June 2010 for the sake of estimating the prevalence of the chronic immunoinflammatory periodontal disease. Results: 54.5 % of the population did not present the studied disease. The 5-11-years-old group was the one contributing more to these results. The disease was diagnosed in 45.5 % of the studied population, and started to manifest beginning from the 15-18-years-old age group. 92.9 % of the individuals aged 60 to 74 years were the most affected ones. Conclusions: from the periodontal point of view, the quantity of healthy patients oscillated between 49.4 % and 59.6 % of the total population. The disease incidence increases with age. The presence of pockets was higher from the age of 35 years on, and caused great affectation in individuals aged 60-74 years.

Periodontal condition and immunological aspects of individuals hospitalized in the intensive care unit

Abstract There are few studies on the clinical and immunological periodontal status of intensive care unit (ICU) in-patients. The aim of the present study was to evaluate the periodontal condition among ICU in-patients through clinical and immunological periodontal parameters. From the sample of 373 hospitalized ICU patients, 182 were submitted' to a thorough clinical periodontal and immunological evaluation. Data on bleeding on probing (BOP), probing depth (PD), and clinical attachment level (CAL) were collected and gingival sulcular fluid samples were quantified through ELISA on IL-1, IL-6, and MMP-2 for immunological evaluation. Data was statistically analyzed by Chi-square, Fisher's exact, Mann-Whitney tests, and Sperman's correlation and multivariate logistic regression analysis. A high dental plaque index and a high prevalence of periodontitis (48.3%), mostly in moderate and localized chronic form, were observed. Individuals with periodontitis presented higher levels of IL-1 and MMP-2, while individuals with cardiovascular disease (CVD) and individuals with two or more systemic diseases (MSD) presented higher levels of IL-1; diabetes mellitus (DM) and MSD individuals presented higher levels of IL-6. A positive association was found between the severity of periodontitis and CVD (OR 2.2; CI = 1.11-4.42). This study reported a 48.3% of the prevalence of periodontitis in ICU patients and a positive association between the severity of periodontitis and CVD. Additionally, higher levels of IL-1 and MMP-2 were found in individuals with periodontitis, higher levels of IL-6 were found in individuals with DM, and higher levels of IL-1 were found in individuals with CVD.

Resumo Existem poucos estudos sobre o estado clínico periodontal e imunológico de pacientes em unidade de terapia intensiva (UTI). O objetivo do presente estudo foi avaliar a condição periodontal entre os pacientes internados na UTI através de parâmetros clínicos periodontais e imunológicos. De uma amostra inicial de 373 pacientes internados em UTI, 183 foram submetidos a exame periodontal completo e análise imunológica. Os dados sobre o sangramento na sondagem (BOP), profundidade de sondagem (PD) e nível clínico de inserção (CAL) foram coletados e as amostras de fluido sulcular gengival foram quantificadas para avaliação imunológica através de ELISA para IL-1, IL-6 e MMP-2. Os dados foram analisados estatisticamente pelos testes de Qui-quadrado, exato de Fischer, Mann-Whitney, correlação de Sperman e análise de regressão logística multivariada. Foi observado um alto índice de placa dental e uma alta prevalência de periodontite (48,3%), principalmente na forma crônica moderada e localizada. Os indivíduos com periodontite apresentaram níveis mais altos de IL-1 e MMP-2, enquanto indivíduos com doença cardiovascular (CVD) e com mais de duas doenças sistêmicas (MSD) apresentaram níveis mais altos de IL-1 e os com diabetes mellitus (DM) e MSD apresentaram níveis mais elevados de IL-6. Foi encontrada associação positiva entre a gravidade da periodontite e CVD (OR 2.2; IC = 1,11-4,42). Este estudo reportou uma prevalência de periodontite em 48.3% dos pacientes em UTI e uma associação positiva entre ocorrência de periodontite e CVD. Além disso, níveis mais elevados de IL-1 e MMP-2 foram encontrados em indivíduos com periodontite, de IL-6 em indivíduos com DM e de IL-1 em indivíduos com CVD.

Association between periodontal disease and polycystic ovary syndrome: a scoping review

Background: polycystic ovary syndrome (PCOS) is one of the most prevalent endocrine disorders in women. it is believed that sex hormones play a role in the maintenance of bone mass and directly or indirectly influence several cell types, including periodontal cells. objective: to evaluate the association between periodontal disease and PCOS according to the evidence reported in the last decade. material and method: a search was made in the biomedical databases: Pubmed, Embase, Scopus, SciELO, Science Direct and SIGLE for the 2007-2017 period. selection criteria: prospective and retrospective studies reporting the relationship between periodontal disease and PCOS. the methodological quality of the studies was analyzed using the critical appraisal skills program scale. results: 10 articles were found: 1 clinical trial and 9 case-control studies. the number of patients ranged from 48 to 196, mean age between 23.3 and 28.1 years, age range between 15 and 45 years. studies were conducted in Turkey, India and Iran. all the studies presented good methodological quality and a positive association between PCOS and periodontal disease. conclusion: PCOS shows a positive and significant association with the clinical and molecular parameters of periodontal diseases.

Evolution of Periodontal Disease: Immune Response and RANK/RANKL/OPG System

Abstract The aim of this study was to evaluate markers of bone loss and immune response present in evolution of periodontal disease. One hundred and two Wistar rats were divided into three animals groups: PD0, without ligation and PD15 days and PD60 days, submitted to ligation placement with a sterile 3-0 silk cord in the cervical region of the upper first molar on both sides. Samples were obtained from the gingival tissue for histomorphometric analysis, immunohistochemical analysis of RANK, RANKL, OPG, characterization of the inflammatory infiltrate, quantification of nitric oxide, MCP-1, RANTES, IP10 chemokines, and expression of the TGF-b1, VEG, and bFGF. The number of inflammatory cells in gingival tissue was higher in PD60 samples. The collagen content and the area occupied by birefringent collagen fibers were lower for PD60. Differential leukocyte counting showed that there was a significantly higher polymorphonuclear influx in group PD15, while PD60 showed a greater number of lymphocytes. PD60 showed higher RANTES, IP-10, MCP-1 gene transcripts, as well as a higher nitric oxide concentration. Clinical evaluation revealed that the PD60 group presented an increase in furcal area. In conclusion, in this animal model the increase of RANK/RANKL and HGF markers is related to a specific immune response, and probably contributed to the evolution of periodontal disease. Investigating the effect of these biomarkers can help in targeted therapy for bone resorption, since blocking these can inhibit bone loss.

Resumo Este estudo avaliou marcadores de perda óssea e da resposta imune presentes na evolução da doença periodontal. Cento e dois ratos Wistar foram divididos em três grupos de animais: PD0, sem ligadura e PD15 dias e PD60 dias, submetidos a colocação de ligadura com um fio de seda estéril 3-0 na região cervical do primeiro molar superior em ambos os lados. Foram obtidas amostras de tecido gengival para análise histomorfométrica, análises imunohistoquímicas de RANK, RANKL, OPG, caracterização do infiltrado inflamatório, quantificação de óxido nítrico, expressão de quimiocinas MCP-1, RANTES, IP10 e do TGF-b1, VEGF e bFGF . O número de células inflamatórias no tecido gengival foi maior nas amostras PD60. O teor de colágeno na área ocupada pelas fibras de colágeno birrefringentes foram menores para PD60. A contagem diferencial de leucócitos mostrou que houve um influxo polimorfonuclear significativamente maior no grupo PD15, enquanto que PD60 mostrou número maior de linfócitos. PD60 apresentou transcritos de genes RANTES, IP-10, MCP-1 mais elevados, bem como uma maior concentração de óxido nítrico. A avaliação clínica revelou que o grupo PD60 apresentou aumento da área óssea exposta na região da furca. Em conclusão, neste modelo animal o aumento dos marcadores RANK/RANKL e HGF está relacionado a uma resposta imunológica específica e provavelmente contribuiu para a evolução da doença periodontal. Investigar o efeito destes biomarcadores pode ajudar na terapia dirigida para a reabsorção óssea, uma vez que bloquear estes pode inibir a perda óssea.

Cuidados preventivos periódicos em pacientes com risco a doenças periodontais: alcoolismo e tabaco / Preventive care for patients with risks for periodontal disease (alcoholism and tobbaco) ­ a case report

O objetivo desse estudo foi demonstrar novas modalidades de tratamento e a atualização de condutas de diagnóstico clínico e laboratorial da doença periodontal. Em um período de seis meses, esse estudo acompanhou a condição periodontal de um paciente do sexo masculino, com 35 anos de idade, na tentativa de associar a condição sistêmica do mesmo com os fatores modifi cadores e de risco das doenças periodontais, levando em consideração a perda de inserção e a ausência de profundidades de sondagem significativas, por meio de um relato de caso. O álcool e a nicotina modulam as funções imunológicas do hospedeiro (o uso crônico ou agudo esporádico de álcool pode estar ligado à combinação da diminuição da resposta inflamatória), diminuindo as funções dos neutrófi los, monócitos e, consequentemente, reduzindo a resposta imune. O alcoolismo e o tabaco estão associados à gravidade da doença periodontal, porém, com uma terapia de suporte e manutenção adequada, pode-se reduzir ou até mesmo impedir a progressão da doença, preservando assim parâmetros clínicos compatíveis com a saúde periodontal. Além disso, os resultados mostram que o paciente necessita de um acompanhamento contínuo, podendo ter recaídas no controle da relação doença periodontal, alcoolismo e tabaco.

The objective of this study was to demonstrate new treatment modalities and to update the clinical and laboratory diagnosis of periodontal disease. In a six-month period, this study followed the periodontal condition of a 35-year-old male patient in an attempt to associate his systemic condition with the modifying and risk factors of periodontal diseases, taking into account the loss of insertion and absence of signifi cant probing depths, by means of a case report. Alcohol and nicotine modulate the host's immune functions (chronic or acute sporadic use of alcohol may be linked to a combination of decreased infl ammatory response), decreasing the function of neutrophils, monocytes, and consequently reducing the immune response. Alcoholism and tobacco are associated with the severity of periodontal disease, but with adequate supportive and maintenance therapy, disease progression can be reduced or even prevented, thus preserving clinical parameters consistent with periodontal health. In addition, the results show that the patient needs continuous follow-up, and may have recurrences in the control of periodontal disease, alcoholism and tobacco control. Key words:

Péptidos antimicrobianos y mediadores lipídicos: rol en las enfermedades periodontales / Antimicrobial peptides and lipid mediators: their role in periodontal diseases

En la actualidad existe consenso en que el daño de los tejidos de soporte dentario que se produce durante la periodontitis es un proceso complejo en el cual la presencia de los patógenos periodontales es necesaria, pero no suficiente, para explicar en su totalidad la extensión y severidad de dicho daño. Asimismo, la destrucción del tejido de soporte periodontal es en gran medida producida por el desbalance de la respuesta inmune generada por el paciente frente a antígenos y factores de virulencia derivados de los patógenos periodontales. Esta respuesta inmune, desencadenada por las bacterias periodontopatógenas, incluye tanto mecanismos asociados a inmunidad innata como adaptativa, siendo el rol de los péptidos antimicrobianos y mediadores lipídicos aspectos relacionados con ambas ramas de la inmunidad y que no han sido completamente dilucidados en relación con sus mecanismos de acción contra los patógenos periodontales. En esta revisión se describe el rol de los péptidos antimicrobianos y de los mediadores lipídicos en la enfermedad periodontal, enfocándonos en su contribución tanto a la protección como a la destrucción del tejido de soporte dentario durante la infección periodontal. Se destaca además la importancia de considerarlos dentro del complejo escenario de la respuesta inmune durante las enfermedades periodontales, ya que forman parte fundamental de la respuesta inmune del hospedero. Analizar la enfermedad periodontal ampliando la perspectiva de estudio a este tipo de moléculas que participan de la respuesta inmune permitiría en el futuro lograr un nuevo enfoque terapéutico de las enfermedades periodontales.

Currently, there is consensus that the damage of the tooth support tissues that occurs during periodontitis is a complex mechanism, in which the presence of specific periodontal pathogens is necessary, but not sufficient, to fully explain the extent and severity of the observed periodontal destruction. Moreover, the destruction of periodontal support tissue is largely the effect of the imbalance in the patient immune response, triggered by periodontal pathogen-derived antigens and virulence factors. The immune response elicited by periodontal pathogenic bacteria includes mechanisms associated with both innate and adaptive responses, where the role of antimicrobial peptides and lipid mediators are related to these two arms of immunity, and have not been fully elucidated in relation to their mechanisms of action against periodontal pathogens. In this review, a discussion is presented on the characteristics of these molecules and their role in periodontal disease in relation to both protection and destruction of tooth supporting tissue during periodontal infection. The relevance of considering these mediators within the complex scenario of the immune response during periodontal diseases is also highlighted, since they are a fundamental part of the host immune response. Periodontal diseases should be analysed in a broader perspective, where the study of these types of molecules involved in the immune response of periodontal tissues, may help to develop new therapeutic approaches to periodontal diseases in the future.

Marcadores de remodelamiento óseo en pacientes con enfermedad periodontal / Bone remodeling biomarkers in patients with periodontal disease

La Fosfatasa Alcalina Ósea (FAO) es una isoforma de la Fosfatasa Alcalina (FAL). La medición de su actividad en saliva es una medida indirecta del proceso de formación ósea, más sensible y específica que la FAL. La catepsina K es la principal colagenasa del proceso de resorción ósea, es capaz de degradar al colágeno tipo I en varios sitios dando lugar a pequeños péptidos N- y C- terminales. El telopéptido C-terminal (CTx) es el marcador más sensible y específico en el aumento de la resorción ósea, ya que el colágeno tipo I constituye más del 90 por ciento de la matriz orgánica del hueso...

Enfermedad periodontal y síndrome de Down / Periodontal disease and Down´s syndrome

El síndrome de Down es un factor de riesgo no modificable para la enfermedad periodontal; los individuos con síndrome de Down tienen una mayor prevalencia y severidad de enfermedad periodontal que no puede ser explicada únicamente por una higiene bucal deficiente, y diversos estudios sugieren que esto se debe a cambios en su respuesta inmune y en la composición microbiológica de su biofilm. En este trabajo se hará una revisión de las siguiente anormalidades del sistema inmune que fueron encontradas: - defectos en la quimiotaxis de los neutrófilos - fagocitosis parcial de los leucocitos contra los estafilococos - distribución alterada de subclases de IgG en saliva - aumentados niveles de prostaglandinas E2 - aumentada cantidad de metaloproteinasas de la matriz en el fluido gingival crevicular - reducida expresión de IL-10. Por estos motivos, la atención periodontal de los pacientes son síndrome de Down es ligeramente diferente...

Efectos del tabaquismo en la microbiota y tejido periodontal: revisión de la literatura / Effects of smoking on the microbiota and periodontal tissue: literature review

La Periodontitis es una enfermedad inflamatoria local crónica de los tejidos de soporte delos dientes que conduce a la pérdida progresiva del ligamento periodontal y del hueso alveolar. El tabaquismo es un factor de riesgo conocido para muchas enfermedades y la evidencia creciente sugiere que el tabaquismo afecta negativamente a la salud periodontal. El hábito del tabaquismo provoca el aumento de la flora bacteriana periodonto patógenas, aumentando su patogenicidad y alteraciones en el tejido periodontal, sin embargo el efecto del tabaquismo no es directamente a estas bacterias. La nicotina provoca una disminución del flujo sanguíneo y disminución de capilares lo que dificulta la respuesta inmune contra las bacterias patógenas. Además el sistema inmune se ve suprimido frente al tabaquismo, por lo que la acción de los leucocitos es escasamente eficaz para combatir la enfermedad periodontal. Como conclusión, el tabaquismo, principalmente la nicotina, afecta al flujo sanguíneo gingival, la producción de citocinas, la función de los neutrófilos, el recambio de tejido conectivo y como consecuencia de estos factores, aumenta el número de bacterias periodonto patógenas lo que afecta negativamente al tejido periodontal.

Periodontitis is a chronic local inflammatory disease of tissue supporting the teeth that leads to progressive loss of periodontal ligament and alveolar bone. Smoking is a known risk factor for many diseases and increasing evidence suggests that smoking negatively affects periodontal health. Cigarette smoking increased periodontal pathogenic bacterial flora, increasing their pathogenicity and alterations in the periodontal tissue, however the effect of smoking is not directly to these bacteria. Nicotine causes a decreased blood flow and decreased capillary hindering the immune response against pathogenic bacteria. In addition, the immune system is suppressed, so the action of leukocytes is poorly effective against periodontal disease. In conclusion, smoking, mainly nicotine, affects the gingival blood flow, cytokine production, the neutrophil function, replacement of connective tissue and because of these factors, increases the number of periodontal pathogenic bacteria which negatively affects the periodontal tissue.

La modulación de la expresión de IL-10 por el polimorfismo IL-10-592C/A (rs1800872) es independiente de la presencia y carga bacteriana de los periodontopatógenos clásicos / Modulation of IL-10 mRNA levels in periodontal lesions by IL-10-592C/A polymorphism (rs1800872) is independent of the frequency and load of classic periodontopathic bacteria

Objetivo: Reportamos la asociación entre el polimorfismo de nucleótido simple de IL-10-592C/A (rs1800872) y la detección/abundancia relativa de los periodontopatógenos Porfiromonas gingivalis, Tenerella forsythia, Treponema denticola y Aggregatibacter actinomycetemcomitans. Además investigamos la influencia de los determinantes genéticos y microbiológicos en los niveles de expresión de IL-10 en lesiones periodontales. Metodología Fueron reclutados 117 pacientes con periodontitis crónica y 58 controles. Luego del examen clínico fueron obtenidas muestras microbiológicas y la presencia/carga bacteriana de especies de periodontopatógenos fue cuantificada por RT-PCR. El genotipo para IL-10-592C/A fue determinado mediante restriction fragment length polymorphism. Resultados La distribución alélica del SNP rs1800872 en la población investigada cumplió con el equilibrio de Hardy-Weinberg (p = 0,64). Como ya ha sido reportado, los sujetos polimórficos demostraron menor expresión de IL-10 y riesgo aumentado de sufrir periodontitis crónica. El polimorfismo IL-10-592C/A no demostró relación con la detección o carga bacteriana de ninguna de las bacterias investigadas, además los niveles de expresión de IL-10 no fueron influenciados por el perfil microbiológico, sino que se correlacionaron directamente con el genotipo para el polimorfismo IL-10-592C/A.

Objective: A study was conducted to investigate the possible influence of the single nucleotide polymorphism (SNP) IL-10-592 C/A on the occurrence and load of the periodontal pathogens: P. gingivalis, T. forsythia, T. denticolaand A. Actinomycetemcomitans; as well to investigate the influence of microbial and genetic factors on the modulation of local IL-10 mRNA levels. Methodology The study included 117 cases and 58 controls. After clinical examination microbiological samples were obtained and the detection/quantification of the target bacterial species was performed by RT-PCR. SNP rs1800872 was assayed by restriction fragment length polymorphism (RFLP). Results Allele distribution of rs1800872 was in Hardy-Weinberg equilibrium (P = 64). As previously reported, polymorphic subjects demonstrated decreased IL-10 expression and increased risk of suffering chronic periodontitis. IL-10-592C/A rs1800872 SNP was not associated with the detection or the bacterial load of the investigated pathogens. Moreover, the presence/load of bacteria at periodontal sites did not influence IL-10 expression, which was determined by the genetic background of the study subjects. IL-10-592C/A SNP was not associated with detection/bacterial load of pathogenic bacteria. IL-10 expression levels were determined by the genetic background and were independent of the bacterial microenvironment.

Host response mechanisms in periodontal diseases

Periodontal diseases usually refer to common inflammatory disorders known as gingivitis and periodontitis, which are caused by a pathogenic microbiota in the subgingival biofilm, including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Treponema denticola that trigger innate, inflammatory, and adaptive immune responses. These processes result in the destruction of the tissues surrounding and supporting the teeth, and eventually in tissue, bone and finally, tooth loss. The innate immune response constitutes a homeostatic system, which is the first line of defense, and is able to recognize invading microorganisms as non-self, triggering immune responses to eliminate them. In addition to the innate immunity, adaptive immunity cells and characteristic cytokines have been described as important players in the periodontal disease pathogenesis scenario, with a special attention to CD4+ T-cells (T-helper cells). Interestingly, the T cell-mediated adaptive immunity development is highly dependent on innate immunity-associated antigen presenting cells, which after antigen capture undergo into a maturation process and migrate towards the lymph nodes, where they produce distinct patterns of cytokines that will contribute to the subsequent polarization and activation of specific T CD4+ lymphocytes. Skeletal homeostasis depends on a dynamic balance between the activities of the bone-forming osteoblasts (OBLs) and bone-resorbing osteoclasts (OCLs). This balance is tightly controlled by various regulatory systems, such as the endocrine system, and is influenced by the immune system, an osteoimmunological regulation depending on lymphocyte- and macrophage-derived cytokines. All these cytokines and inflammatory mediators are capable of acting alone or in concert, to stimulate periodontal breakdown and collagen destruction via tissue-derived matrix metalloproteinases, a characterization of the progression of periodontitis as a stage that presents a significantly host immune and inflammatory response to the microbial challenge that determine of susceptibility to develop the destructive/progressive periodontitis under the influence of multiple behavioral, environmental and genetic factors.

O efeito adjunto de uma suplementação alimentar à base de ômega-3 no tratamento da periodontite: um estudo clínico e imunológico / The adjunctive effects of Omega-3 dietary supplementation in the treatment of periodontitis: a clinical and immunological study

O objetivo foi avaliar se a suplementação com ômega (ω)-3 no tratamento não cirúrgico da periodontite melhora os resultados clínicos e imunológicos. Avaliar os níveis séricos dos ω-3 e ω-6 na doença periodontal, investigar se o tratamento periodontal associado ou não a suplementação com ω-3 afeta os níveis séricos destes. Assim como avaliar a expressão de um painel de citocinas relacionadas a osteoclatogênese no fluido gengival (FG) de sítios dos pacientes com gengivite e periodontite, adicionalmente relacionar estas citocinas a densidade óptica do osso alveolar destes sítios. Por fim, investigar se as terapias propostas neste estudo afetam os parâmetros clínicos periodontais, a densidade óptica do osso alveolar e a expressão das citocinas no FG. Para isso foi realizado um ensaio clínico piloto, randomizado, duplo-cego, controlado-placebo, com vinte e um pacientes com periodontite e dezesseis com gengivite. Estes foram investigados para os níveis séricos dos ácidos graxos poli-insaturados de cadeia longa (AGPI-CL), ácido eicosapentaenóico (EPA), ácido docosahexaenóico (DHA), ácidos docosapentaenóico (DPA), o ácido araquidônico (AA) usando cromatografia gasosa. O FG dos sítios controle-gengivite, controle-periodontite e destruído de pacientes com periodontite foi avaliado para Receptor ativador do fator nuclear kappa-B ligante (RANK-L), osteoprotegerina (OPG), a osteocalcina (OC), fator de necrose tumoral (TNF)-α, interferon (IFN)-γ, interleucina (IL) -1ß, IL-4, IL-6 e IL-10, utilizando imunoensaio multiplex. Pacientes com periodontite foram subagrupados em grupos com e sem Síndrome Metabólica para avaliação dos AGPI-CL. Sítios dos pacientes com periodontite foram subagrupados em sítios sem e com considerável desmineralização ópticas baseado na avaliação da densidade óptica alveolar representada pelos valores de pixels das radiografias intraorais digitais para avaliação das citocinas no FG. Pacientes com periodontite foram randomizados em raspagem e alisamento radicular mais suplementação com ω-3 (RAR+ω-3) ou placebo (RAR+placebo), e foram reavaliados depois de quatro meses para AGPI-CL no soro, citocinas no FG e densidade alveolar óptica. Os níveis significativamente maiores dos AGPI-CLs foram observados em pacientes com periodontite em comparação com gengivite. A profundidade de bolsa mostrou uma correlação positiva significativa com DHA, DPA e AA. Após RAR+ω-3, DPA, AA, AA/EPA e AA/DHA reduziram significativamente, e depois da RAR+placebo todos os níveis dos AGPI-CLs reduziram significativamente. Os níveis das citocinas, IFN-γ, IL-4, IL-10, RANK-L e OC, no FG de sítios controle-gengivite foram menores comparados aos sítios controle-periodontite e destruído. O mesmo resultado foi observado para os níveis da IL-1ß, IL-6 e OPG em comparação com sítios destruídos. Pacientes com periodontite apresentaram níveis mais baixos de IL-1ß e OPG em sítios controle-periodontite comparado aos destruídos. Após RAR+ω-3, o nível da IL-4 aumentou e os níveis de OC, IFN-γ e IL-10 diminuíram. Não houve diferenças significativas entre os grupos experimentais para a densidade alveolar óptica e parâmetros. Em conclusão, os níveis séricos dos AGPI-CLs são afetados pela gravidade de doença periodontal e diferem com a presença da síndrome metabólica. Citocinas relacionadas a osteoclatogênese no FG refletem a gravidade periodontal e diferem com densidade óptica alveolar alterada. A suplementação com ω-3 não melhora clinica ou imunologicamente o resultado do tratamento periodontal.

The aim was to test whether omega (ω)-3 supplementation associated to non-surgical treatment of periodontitis improves clinical and immunological results. Evaluate the serum levels of ω-3 and ω-6 in periodontal disease, hence, to investigate whether periodontal treatment with or without ω-3 supplementation affects serum levels of these. Therefore, to evaluate the expression of a panel of cytokines related to osteoclastogenesis in the gingival crevicular fluid (GCF) sites of patients with gingivitis and periodontitis, additionally relate these cytokines with optical alveolar bone density in these sites. Finally, to investigate whether the therapies proposed in this study affect the clinical periodontal parameter, the optical density of the alveolar bone and the expression of cytokines in GCF. Then was conducted a pilot clinical trial, randomized, double-blind, placebo-controlled, with twenty-one patients with periodontitis and sixteen with gingivitis. These were investigated for blood levels of long chain polyunsaturated fatty acids (LC-PUFA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), arachidonic acid (AA) using gas chromatography. The GCF of the sites of control-gingivitis, control-periodontitis and destroyed from patients periodontitis were evaluated for receptor activator of kappa-B ligand nuclear factor (RANK-L), osteoprotegerin (OPG), osteocalcin (OC), tumor necrosis factor (TNF) -α, interferon (IFN) -γ, interleukin (IL) -1ß, IL-4, IL-6 and IL-10 using multiplex immunoassay. Patients with periodontitis were subgrouped in groups with and without metabolic syndrome to evaluate the LC-PUFA. Sites of patients with periodontitis were subgrouped at sites with and without considerable optical demineralization based on the evaluation of alveolar optical density represented by the pixel values of the digital intraoral radiographs for evaluation of cytokines in GCF. Patients were randomized into the periodontal scaling and root planing more ω-3 supplementation (ω-3 SRP +) or placebo (SRP + placebo), and were assessed after four months to LC-PUFA in serum, cytokines in GCF and alveolar optical density. The significantly higher levels of LC-PUFA were observed in patients with periodontitis compared to gingivitis. The pocket depth showed a significant positive correlation with DHA, DPA and AA. After RAR + ω-3, APD, AA, AA / AA and EPA / DHA reduced significantly, and, after SRP + placebo, all levels of LC-PUFA reduced significantly. The levels of cytokines, IFN-γ, IL-4, IL-10, and OC RANK-L, from controlgingivitis sites GCF were lower compared to control-periodontitis and destroyed sites. The same result was observed for levels of IL-1ß, IL-6 and OPG compared to destroyed sites. Periodontitis patients had lower levels of IL-1ß and OPG in control-periodontitis compared to destroyed sites. After SRP + ω-3, the level of IL-4 and OC increased and levels of IFN-γ and IL-10 decreased. There were no significant differences between the experimental groups to optical density and clinical parameters. In conclusion, serum levels of LC-PUFA are affected by periodontal disease severity and differ in the presence of the metabolic syndrome. Cytokines related to osteoclastogenesis in GCF reflect the periodontal severity and differ with impaired alveolar optical density. Ω-3 supplementation does not improve clinical or immune result of non-surgical periodontal treatment.

Revisión sistemática sobre polimorfismos genéticos de interleucina 1-ß en pacientes con periodontitis agresiva

La forma agresiva es la expresión clínica menos frecuente de laperiodontitis (0,1-1%). La inflamación, respuesta inmune del hospedador a la agresión delas bacterias periodontopatógenas del biofilm subgingival, conduce a la destrucción tisularmediante reclutamiento leucocitario y liberación de citocinas siendo Interleuquina-1 (IL-1)la principal citocina proinflamatoria y tiene 2 genotipos: IL-1α e IL-1β.OBJETIVO: Elaborar una síntesis del conocimiento científico disponible sobre el grado deasociación entre polimorfismos genéticos de IL-1β y periodontitis agresiva (PA) medianterevisión sistemática de estudios observacionales de casos y controles.MÉTODOS: Se realizó una revisión sistemática en base a búsqueda bibliográfica electrónicaen Bireme, MEDLINE, The Cochrane, SciELO, LILACS, BBO-Odontología (Brasil), CENTRALregistrode ensayos clínicos controlados, IBECS (España), Med Carib, DARE-RevisionesSistemáticas Avaladas y DeCS- Descriptores en Ciencias de la Salud, de estudios publicadosentre enero de los años 2003 y 2013 que estudiaron polimorfismos genéticos de IL- 1 β ysu asociación con PA.RESULTADOS: Se seleccionó cada artículo según criterios de inclusión. La búsqueda arrojó1.656 trabajos que incluían Meta-análisis (MA) y Artículos Originales (AO), de los cuales, 22estudios cumplieron los criterios de inclusión de esta revisión sistemática de la evidenciacientífica (RSEC). Ningún estudio corroboró asociación entre IL-1β C[+3953/4]T y PA. Un MAque incluyó 16 de estos estudios en poblaciones caucásicas y asiáticas resultó en OR=0,95;IC 95%=0,75/1,19. Los datos se organizaron en tablas para facilitar la interpretación,análisis y síntesis cualitativa del conocimiento aportado por la selección de artículos...

Aggressive periodontitis (AP) is the least common clinical expression ofthis disease (0.1-1%). The inflammation, which is the immune response of the host to theaggression of the periodontal pathogenic bacteria of the subgingival bio film, leads totissular destruction through leukocyte recruitment and cytokine liberation.Interleukine-1(IL-1) is the main proinflammatory cytokine, having 2 genotypes: IL-1α and IL-1β.AIM: To synthesize the available scientific knowledge as regards the degree of associationbetween IL-1β genetic polymorphysm and aggresive periodontitis (AP), by making asystematic revision of cases- control observational studies.METHODS: A systematic bibliographic search and revision was carried out from studiespublished in Bireme, MEDLINE, The Cochrane, SciELO, LILACS, BBO-Odontología (Brazil),CENTRAL- controlled clinical trials register , IBECS ( Spain), Med Carib, DARE-EndorsedSystematic Revisions and DeCS- Health Science Descritors, from studies published betweenJanuary 2003 and January 2014 such works examine IL-1β genetic polymorphysm and theirassociation with AP.RESULTS: Each article was selected according to inclusion criteria. The search yielded 1,656studies that included Meta-analysis (MA) and Original Articles (OA), 22 of which fulfilledthe inclusion criteria of this RSEC. No study was found to confirm the association betweenIL-1β C[+3953/4]T and AP. A MA that included 16 of these studies in Caucasian and Asianpopulations turned out to be in OR=0.95; CI 95%=0.75/1.19. The collected data weredistributed in tables to facilitate their interpretation, their analysis and the qualitativesynthesis of the knowledge gathered from the selected articles...

Modulación de la respuesta del huésped en el tratamiento periodontal: revisión de la literatura / Host response modulation in periodontal treatment: a review of the literature

En la enfermedad periodontal, la acumulación de bacterias gramnegativas, genera una respuesta inmunoinflamatoria que es modulada por el mecanismo de defensa del paciente. El tratamiento de modulación del huésped (TMH), ha sido incorporado como una opción farmacológica para el control de la enfermedad periodontal. El objetivo de la revisión fue investigar los efectos de los inhibidores de la colagenasa tisular y de los analgésicos antiinflamatorios no esteroides (AINES) como agentes moduladores de la enfermedad periodontal. A tal fin, se realizó una búsqueda de estudios de casos, controles y revisiones, empleando las bases de datos Medline-PubMed, LILACS y Dialnet. Se encontró que los resultados de las terapias de modulación del huésped tienen como blanco los mediadores proinflamatorios y enzimas destructivas que degradan el colágeno y destruyen tejido óseo, equilibrando y aumentando las acciones antiinflamatorias y protectivas. Los fármacos usados en el TMH regulan los procesos destructivos de la respuesta inmunoinflamatoria en presencia de placa dental, sobre todo en pacientes susceptibles.

Fosfatasa alcalina como marcador bioquímico de la enfermedad periodontal / Alkaline phosphatase as a biochemical marker of periodontal disease

La fosfatasa alcalina (ALP) es una enzima relacionada con la enfermedad periodontal (EP). Se encuentra en los polimorfonucleares (PMN), osteoblastos, fibroblastos y diversas céluals del tejido conjuntivo. Juega un papel importante en el remodelado del tejido óseo y del ligamento periodontal. Los niveles de ALP son elevados en los sitios con pérdida de inserción, permitiendo el diangóstico de EP y la vigilancia del tratamiento periodontal

La enfermedad periodontal asociada al paciente con síndrome de Down / Periodontal disease associated to the Down´s syndrome patient

El síndrome de Down es una de las condiciones de discapacidad más comunes. Dentro de las patologías bucales más prevalentes, la enfermedad periodontal es una de las asociadas con este síndrome. Se cxonsidera que la persona con síndrome de Down presenta una mayor susceptibilidad a contraer esta enfermedad. En este artículo se describen los factores etiológicos y las características clínicas de la enfermedad en este paciente.

Oral coinfection can stress peripheral lymphocyte to inflammatory activity in leprosy

INTRODUCTION: This study evaluated the intracellular profile of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-10 (IL-10) and interferon-γ (IFN-γ) in peripheral blood mononuclear cells (PBMCs) from leprosy patients based on oral infections presence to determine whether these coinfections could be associated with pro-inflammatory activity in leprosy. METHODS:Leprosy patients regardless of clinical form and specific leprosy treatment (n=38) were divided into two groups: Group I - leprosy patients with oral infections (n=19), and Group II - leprosy patients without oral infections (n=19). Non-leprosy patients presenting oral infections were assigned to the control Group (n=10). Intracellular IL-2, IL-4, IL-10 and IFN-γ production was evaluated by flow cytometry (FACS) before and 7 days after controlling the oral infection in the Group I, before and 7 days after dental prophylaxis in the Group II, and during oral infection process in control Group. RESULTS: Low percentages of CD3+ lymphocytes bearing IL-2, IL-10 and IFN-γ were observed in the Group I and Group II at baseline and 7 days after therapy or prophylaxis compared to controls. Group I showed reduced percentages of IL-4 at baseline and 7 days after therapy compared to controls, or at baseline of Group II, and the Group II showed reduced percentages of CD3+ cells bearing IL-4 compared to control. An increase of the percentages of CD3+cells bearing IL-4 was observed in the Group I after the oral infections treatment. CONCLUSIONS: The occurrence of oral infections favors the intracellular cytokines expression and, probably, the inflammatory reaction operating as a stimulatory signal triggering the leprosy reactions.

Leptina, péptido pleiotrópico: características y su relación con la enfermedad periodontal: revisión de la literatura / Leptin, pleiotropic peptide: general features and its relationship with periodontal disease: review of literature

La leptina es un péptido que inicialmente fue caracterizado como un factor regulador del apetito y se creía que era producido sólo por el tejido adiposo, sin embargo, actualmente se conoce que es sintetizado en diferentes tejidos y posee receptores a lo largo de toda la economía del organismo, mostrando así múltiples funciones, dentro de las que cabe destacar su participación en la regulación del metabolismo lipídico y de los carbohidratos, el crecimiento óseo y la respuesta inmunológica, siendo estos últimos, procesos involucrados en la génesis de la enfermedad periodontal. Por tal motivo, en la presente revisión, se esbozan las principales características tanto estructurales como funcionales de este péptido, y su participación en diferentes roles a nivel sistémico, haciendo énfasis en el moldeado óseo y la respuesta inmunológica, para luego adentrarse en diferentes hallazgos encontrados a nivel bucal, que pudiesen indicar su posible participación en la génesis y el desarrollo de la enfermedad periodontal

Leptin is a peptide that was initially characterized as an appetite regulatory factor and it was believed that it was only produced by adipose tissue, however, it ?s currently known that is synthesized in different tissues and posses receptors throughout the body economy, showing multiple functions, such as involvement in the regulation of lipid and carbohydrate metabolism, bone growth and immune response, being the latter processes, involved in the genesis of periodontal disease. Therefore, the present review outlines the main structural and functional characteristics of this peptide, and their participation in various capacities at the systemic level, with emphasis on bone shaping and the immune response, and then goes into different findings at the oral level that could indicate their possible role in the genesis and periodontal disease development

Modulation of host cell signaling pathways as a therapeutic approach in periodontal disease

Recently, new treatment approaches have been developed to target the host component of periodontal disease. This review aims at providing updated information on host-modulating therapies, focusing on treatment strategies for inhibiting signal transduction pathways involved in inflammation. Pharmacological inhibitors of MAPK, NFκB and JAK/STAT pathways are being developed to manage rheumatoid arthritis, periodontal disease and other inflammatory diseases. Through these agents, inflammatory mediators can be inhibited at cell signaling level, interfering on transcription factors activation and inflammatory gene expression. Although these drugs offer great potential to modulate host response, their main limitations are lack of specificity and developments of side effects. After overcoming these limitations, adjunctive host modulating drugs will provide new therapeutic strategies for periodontal treatment.

Avaliação do papel dos receptores TLR2 e TLR4 na produção de citocinas por fibroblastos humanos periodontais deficientes desses receptores / The role of TLR2 and TLR4 in cytokines production by human periodontal fibroblasts knocked down for these receptors

Os fibroblastos são atualmente considerados componentes ativos da resposta imune porque estas células expressam receptores do tipo Toll (TLRs), são capazes de reconhecer padrões moleculares associados a patógenos e mediar a produção de citocinas e quimiocinas durante a inflamação. A resposta imune inata do hospedeiro a lipopolissacarídeos (LPS) de Porphyromonas gingivalis é incomum, já que diferentes estudos relataram que este LPS pode ser um agonista para TLR2 e um antagonista ou agonista para TLR4. A sinalização por TLRs envolve proteínas adaptadoras, como MyD88 e TRAM, que são necessárias para a transdução do sinal até o núcleo para que ocorra a transcrição de RNAm para os mediadores da inflamação. O objetivo deste estudo foi investigar e comparar se a sinalização por meio de TLR2 ou TLR4 poderia afetar a produção de Interleucina (IL)-6, IL-8 e CXCL12 em fibroblastos humanos gengivais (HGF) e fibroblastos humanos de ligamento periodontal (HPLF). Objetivamos também comparar a participação das moléculas adaptadoras MyD88 e TRAM na expressão do RNAm dos mesmos alvos. Material e Métodos: Após silenciamento mediado por RNA de interferência de TLR2, TLR4, MyD88 ou TRAM, confirmado por RT-qPCR, HGF e HPLF, provenientes de três dadores voluntários, foram estimulados com LPS de Porphyromonas gingivalis ou com dois agonistas sintéticos de TLR2, Pam2CSK4 e Pam3CSK4, por 6 horas. A expressão do RNAm e das proteínas IL-6, IL-8, e CXCL12 foram avaliados por qRT-PCR e ELISA, respectivamente. Resultados: A expressão do RNAm de TLR2 foi regulada em HGF, mas não em HPLF por todos os estímulos. O silenciamento de TLR2 diminuiu IL-6 e IL-8 em resposta ao LPS de P. gingivalis, Pam2CSK4 e Pam3CSK4 de maneira semelhante, em ambas as subpopulações de fibroblastos (p<0,05). Por outro lado, a produção de CXCL12 permaneceu inalterada pelo silenciamento de TLR2 ou TLR4. No caso do silenciamento de MyD88 e TRAM, em ambos os subtipos de fibroblastos, o RNAm para os mesmos alvos também...

Fibroblasts are now seen as active components of the immune response because these cells express Toll-like receptors (TLRs), recognize pathogen associated molecular patterns and mediate the production of cytokines and chemokines during inflammation. The innate host response to lipopolysaccharide (LPS) from Porphyromonas gingivalis is unusual in that different studies have reported that it can be an agonist for TLR2 and an antagonist or agonist for TLR4. TLRs signaling pathway involves adaptor proteins, like MyD88 and TRAM, which are crucial for signal transduction to the nucleus and mRNA expression of inflammatory mediators. This study investigated and compared whether signaling through TLR2 or TLR4 could affect the production of IL-6, IL-8 and CXCL12 in both human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPLF). The role of MyD88 and TRAM on the mRNA expression of the same targets were also evaluated. Methods: After small interfering RNA-mediated silencing of TLR2, TLR4, MyD88 or TRAM, confirmed by RT-qPCR, HGF and HPLF from three volunteer donors were stimulated with P. gingivalis LPS or with two synthetic ligands of TLR2, Pam2CSK4 and Pam3CSK4, for 6 hours. IL-6, IL-8, and CXCL12 mRNA expression and protein production were evaluated by RT-qPCR and ELISA, respectively. Results: TLR2 mRNA expression was upregulated in HGF but not in HPLF by all the stimuli applied. Knockdown of TLR2 decreased IL-6 and IL-8 in response to P. gingivalis LPS, Pam2CSK4 and Pam3CSK4 in a similar manner in both fibroblasts subpopulations. Conversely, CXCL12 remained unchanged by TLR2 or TLR4 silencing. For MyD88 or TRAM silencing, IL-6 and IL-8 mRNA were also decreased, in both fibroblasts subtypes. However CXCL12 mRNA constitutive expression was increased by siMyD88 or siTRAM. Conclusion: These results suggest that signaling through TLR2 by fibroblasts, the most numerous resident cells in gingiva and periodontal...