Abstract Objectives: Dental composites release unreacted resin monomers into the oral environment, even after polymerization. Periodontal cells are, therefore, exposed to substances that potentially elicit the immune inflammatory response. The underlying molecular mechanisms associated with the interaction between resin monomers and human immune cells found in the gingival crevicular fluid are not fully understood yet. This study investigated the ability of bisphenol A-glycidyl methacrylate (BISGMA), urethane dimethacrylate (UDMA) and triethylene glycol dimethacrylate (TEGDMA) to induce apoptosis and cytokine release by human leukocytes stimulated with a periodontal pathogen. Methodology: Peripheral blood mononuclear cells (PBMC) from 16 healthy individuals were included in this study. To determine the toxicity, the PBMC were incubated for 20 hours, with monomers, for the analysis of cell viability using MTT assay. To evaluate cell death in the populations of monocytes and lymphocytes, they were exposed to sub-lethal doses of each monomer and of heat-inactivated Porphyromonas gingivalis (P. gingivalis) for 5 hours. Secretions of IL-1β, IL-6, IL-10 and TNF-α were determined by ELISA after 20 hours. Results: UDMA and TEGDMA induced apoptosis after a short-time exposure. Bacterial challenge induced significant production of IL-1β and TNF-α (p<0.05). TEGDMA reduced the bacterial-induced release of IL-1β and TNF-α, whereas UDMA reduced IL-1β release (p<0.05). These monomers did not affect IL-10 and IL-6 secretion. BISGMA did not significantly interfere in cytokine release. Conclusions: These results show that resin monomers are toxic to PBMC in a dose-dependent manner, and may influence the local immune inflammatory response and tissue damage mechanisms via regulation of bacterial-induced IL-1β and TNF-α secretion by PBMC.

RESUMO Objetivo: Avaliar a influência do tratamento periodontal sobre a atividade da doença na artrite reumatoide. Métodos: Pesquisaram-se as bases de dados Medline/PubMed, The Cochrane Library, Clinical Trials, SciELO e Lilacs em busca de estudos publicados até dezembro de 2014. Incluíram-se estudos prospectivos que avaliaram pacientes com mais de 18 anos diagnosticados com periodontite e artrite reumatoide submetidos a tratamento periodontal não cirúrgico; os estudos deveriam ter também um grupo controle não submetido a tratamento periodontal. Os resultados dos estudos deveriam contar com pelo menos um marcador da atividade da doença na artrite reumatoide. A qualidade metodológica dos estudos foi avaliada com a escala PEDro. Reuniram-se os dados quantitativos em uma metanálise estatística com o uso do Review Manager 5. Resultados: Incluíram-se quatro artigos. O tratamento periodontal não cirúrgico esteve associado a uma redução significativa no DAS-28 (OR: -1,18; IC 95%: -1,43 a -0,93; p < 0,00001). A velocidade de hemossedimentação, a proteína C-reativa, a avaliação da atividade reumatoide pela escala visual analógica e as contagens de articulações sensíveis e inchadas apresentaram uma tendência de redução (não estatisticamente significativa). Conclusões: A redução no DAS-28 em pacientes com artrite reumatoide após tratamento periodontal sugere que a melhoria na condição periodontal é benéfica a esses pacientes. São necessários mais ensaios clínicos randomizados controlados para confirmar esse achado.

ABSTRACT Objective: To evaluate the influence of periodontal treatment on rheumatoid arthritis activity. Methods: MEDLINE/PUBMED, The Cochrane Library, Clinical Trials, SciELO and LILACS were searched for studies published until December 2014. Included articles were: prospective studies; including patients older than 18 years, diagnosed with periodontitis and rheumatoid arthritis submitted to non-surgical periodontal treatment; with a control group receiving no periodontal treatment; with outcomes including at least one marker of rheumatoid arthritis activity. Methodological quality of the studies was assessed using PEDro scale. Quantitative data were pooled in statistical meta-analysis using Review Manager 5. Results: Four articles were included. Non-surgical periodontal treatment was associated with a significant reduction of DAS28 (OR: -1.18; 95% CI: -1.43, -0.93; p < 0.00001). Erythrocyte sedimentation rate, C-reactive protein, patient's assessment of rheumatoid activity using visual analogical scale, tender and swollen joint counts showed a trend toward reduction (not statistically significant). Conclusions: The reduction of DAS 28 in patients with rheumatoid arthritis after periodontal treatment suggests that the improvement of periodontal condition is beneficial to these patients. Further randomized controlled clinical trials are necessary to confirm this finding.

Resumo A doença periodontal resulta da interação entre bactérias patogênicas que colonizam os filmes supra e subgengival e o hospedeiro e deflagram uma resposta inflamatória local, com efeitos sistêmicos, que leva à destruição imunomediada dos tecidos de sustentação dos dentes e do osso alveolar. Vias imunológicas e fatores genéticos predisponentes comuns à doença periodontal e às doenças reumáticas, entre elas o lúpus eritematoso sistêmico, vêm sendo descritos. Relatos de caso sugeriram maior gravidade da doença periodontal em pacientes com lúpus eritematoso sistêmico. No entanto, estudos que avaliaram as influências do tratamento de uma sobre as manifestações da outra apresentaram resultados conflitantes.

Abstract Periodontal disease results from the interaction between pathogenic bacteria that colonize supragingival and subgingival biofilms and the host, triggering an inflammatory response, with systemic effects leading to immune-mediated destruction of the attachment apparatus and loss of supporting alveolar bone. Immunological pathways and predisposing genetic factors common to periodontal disease and rheumatic diseases, including systemic lupus erythematosus, have been described. Case reports have suggested greater severity of periodontal disease in patients with systemic lupus erythematosus. However, studies evaluating the influence of the treatment of one disease on the clinical and laboratory manifestations of the other have yielded conflicting results.

Alguns estudos têm relacionado a presença de quimiocinas com estágios iniciais da doença de Alzheimer (ALZ). A identificação desses mediadores pode contribuir para um diagnóstico precoce. O objetivo deste estudo foi avaliar os níveis de beta-amiloide (BA), tau, fosfo-tau (p-tau) e quimiocinas (CCL2, CXCL8 e CXCL10) no líquido cefalorraquidiano dos pacientes com ALZ e controles saudáveis e a correlação destes marcadores com parâmetros clínicos. Os níveis de p-tau foram maiores nos pacientes com ALZ em relação aos controles, enquanto a razão tau/p-tau foi menor. Houve um aumento significativo de CCL2. Uma correlação positiva foi encontrada entre os níveis de BA e todas as quimiocinas estudadas e também entre os níveis de CCL2 e p-tau. Nossos resultados sugerem que a presença de CCL2 está envolvida na patogênese da ALZ e que esta quimiocina pode ser um marcador adicional para monitorar a progressão da doença.

Some studies have linked the presence of chemokines to the early stages of Alzheimer's disease (AD). Then, the identification of these mediators may contribute to diagnosis. Our objective was to evaluate the levels of beta-amyloid (BA), tau, phospho-tau (p-tau) and chemokines (CCL2, CXCL8 and CXCL10) in the cerebrospinal fluid (CSF) of patients with AD and healthy controls. The correlation of these markers with clinical parameters was also evaluated. The levels of p-tau were higher in AD compared to controls, while the tau/p-tau ratio was decreased. The expression of CCL2 was increased in AD. A positive correlation was observed between BA levels and all chemokines studied, and between CCL2 and p-tau levels. Our results suggest that levels of CCL2 in CSF are involved in the pathogenesis of AD and it may be an additional useful biomarker for monitoring disease progression.