A influência do sexo e da idade na prevalência de bolsas periodontais

The aim of this study was to evaluate the influence of risk factors on the prevalence of periodontal pockets in patients attending the clinic of the School of Dentistry of Piracicaba - Unicamp. The sample consisted of 100 patients attended by the students from the third and fourth years of undergraduation. The data were taken from anamneses and clinical - periodontal records. Probing depths were considered to be 3, 5, 7 and 10 mm, according to the WS diagnosis system (SALLUM, 1996). The results were compared regarding pockets depths and the risk factors age and gender. Also, the distribution of pockets among the sextants was observed. This study indicated a major prevalence of periodontal pockets in men and an increase in probing depth in patients older than 31 years. The distribution of pockets among the sextants was relatively uniform in all studied groups.Este trabalho teve como objetivo avaliar a influência dos fatores de risco na prevalência de bolsas periodontais em pacientes atendidos na clínica do terceiro e quarto anos da Faculdade de Odontologia de Piracicaba - Unicamp. Foram avaliados 100 pacientes através do levantamento dos dados contidos nas fichas clínico-anamnésicas, sendo consideradas bolsas de profundidade: 3 mm, 5 mm, 7 mm e 10 mm, de acordo com o sistema diagnóstico WS (SALLUM; SALLUM27, 1996). Os resultados foram comparados entre as profundidades de sondagem e as variáveis idade, sexo, bem como sua distribuição por sextantes. Observou-se maior prevalência de bolsas periodontais no sexo masculino, bem como maior profundidade de sondagem em pacientes acima de 31 anos. A distribuição de bolsas periodontais entre os sextantes foi homogênea

RG108 increases NANOG and OCT4 in bone marrow-derived mesenchymal cells through global changes in DNA modifications and epigenetic activation. RG108 increases NANOG and OCT4 through epigenetic activation.

Human bone marrow-derived mesenchymal stem cells (hBMSCs) are important for tissue regeneration but their epigenetic regulation is not well understood. Here we investigate the ability of a non-nucleoside DNA methylation inhibitor, RG108 to induce epigenetic changes at both global and gene-specific levels in order to enhance mesenchymal cell markers, in hBMSCs. hBMSCs were treated with complete culture medium, 50 μM RG108 and DMSO for three days and subjected to viability and apoptosis assays, global and gene-specific methylation/hydroxymethylation, transcript levels' analysis of epigenetic machinery enzymes and multipotency markers, protein activities of DNMTs and TETs, immunofluorescence staining and western blot analysis for NANOG and OCT4 and flow cytometry for CD105. The RG108, when used at 50 μM, did not affect the viability, apoptosis and proliferation rates of hBMSCs or hydroxymethylation global levels while leading to 75% decrease in DNMTs activity and 42% loss of global DNA methylation levels. In addition, DNMT1 was significantly downregulated while TET1 was upregulated, potentially contributing to the substantial loss of methylation observed. Most importantly, the mesenchymal cell markers CD105, NANOG and OCT4 were upregulated being NANOG and OCT4 epigenetically modulated by RG108, at their gene promoters. We propose that RG108 could be used for epigenetic modulation, promoting epigenetic activation of NANOG and OCT4, without affecting the viability of hBMSCs. DMSO can be considered a modulator of epigenetic machinery enzymes, although with milder effect compared to RG108

Necessidade de tratamento periodontal avaliada pelo CPITN e sua relação com a qualidade de acabamento cervical das restaurações

Irregularities of the cervical margin of restorations facilitate the retention of bacterial plaque, hindering plaque control through the habitual procedures of oral hygiene and favoring the development of periodontal disease. The aim of this study was to evaluate the periodontal condition and treatment needs (applying CPITN) in relation to the cervical margin of dental restorations. Three hundred and sixty-seven teeth with class II and V cavities restored with amalgam, class III cavities restored with composite resin, cast metal restorations and unitary prostheses were examined. With a WHO periodontal probe, the position of the cervical margins of restorations was verified (supragingival, subgingival or at the gingival margin level); the presence of defects (lack or excess of restoring material) and the presence of score 2 of CPITN were also assessed. After the analysis of the data, it was possible to conclude that: 1) supragingival margins offered the best marginal adaptation and the lowest frequency of score 2; 2) both the lack and the excess of restoring material favor the development of score 2, despite the utilized material and 3) in subgingival margins, incorrect marginal adaptation was the most frequent event, mainly due to excess of restoring material, and in these cases there was higher frequency of score 2 of CPITN.Irregularidades do acabamento cervical de restaurações constituem fatores de retenção de placa bacteriana, dificultando o controle de placa pelos procedimentos habituais de higiene bucal, favorecendo o desenvolvimento da doença periodontal. O objetivo deste estudo foi avaliar as condições periodontais e a necessidade de tratamento em função do acabamento cervical de restaurações dentais. Foram examinados 367 dentes restaurados com classes II e V de amálgama, classe III em resina, restauração metálica fundida e próteses unitárias. Utilizando-se sonda periodontal (OMS), verificou-se a posição do término da restauração (supragengival, subgengival ou ao nível da margem gengival); a qualidade das restaurações (falta ou excesso de material restaurador) e a presença de grau 2 do CPITN. Após a análise dos dados, foi possível concluir que: 1) o término supragengival ofereceu a melhor adaptação marginal e a menor freqüência de grau 2 do CPITN; 2) a falta ou excesso de material restaurador favorecem o desenvolvimento de grau 2, independentemente do material utilizado e 3) nos términos subgengivais, foi maior a freqüência de adaptação marginal incorreta, principalmente casos de excesso de material restaurador, sendo estes casos de maior ocorrência de grau 2 do CPITN

Central Role of Pyrophosphate in Acellular Cementum Formation

Background: Inorganic pyrophosphate (PPi) is a physiologic inhibitor of hydroxyapatite mineral precipitation involved in regulating mineralized tissue development and pathologic calcification. Local levels of PPi are controlled by antagonistic functions of factors that decrease PPi and promote mineralization (tissue-nonspecific alkaline phosphatase, Alpl/TNAP), and those that increase local PPi and restrict mineralization (progressive ankylosis protein, ANK; ectonucleotide pyrophosphatase phosphodiesterase-1, NPP1). The cementum enveloping the tooth root is essential for tooth function by providing attachment to the surrounding bone via the nonmineralized periodontal ligament. At present, the developmental regulation of cementum remains poorly understood, hampering efforts for regeneration. To elucidate the role of PPi in cementum formation, we analyzed root development in knock-out ((-/-)) mice featuring PPi dysregulation. Results: Excess PPi in the Alpl(-/-) mouse inhibited cementum formation, causing root detachment consistent with premature tooth loss in the human condition hypophosphatasia, though cementoblast phenotype was unperturbed. Deficient PPi in both Ank and Enpp1(-/-) mice significantly increased cementum apposition and overall thickness more than 12-fold vs. controls, while dentin and cellular cementum were unaltered. Though PPi regulators are widely expressed, cementoblasts selectively expressed greater ANK and NPP1 along the root surface, and dramatically increased ANK or NPP1 in models of reduced PPi output, in compensatory fashion. In vitro mechanistic studies confirmed that under low PPi mineralizing conditions, cementoblasts increased Ank (5-fold) and Enpp1 (20-fold), while increasing PPi inhibited mineralization and associated increases in Ank and Enpp1 mRNA. Conclusions: Results from these studies demonstrate a novel developmental regulation of acellular cementum, wherein cementoblasts tune cementogenesis by modulating local levels of PPi, directing and regulating mineral apposition. These findings underscore developmental differences in acellular versus cellular cementum, and suggest new approaches for cementum regeneration

Impact of supragingival therapy on subgingival microbial profile in smokers versus non-smokers with severe chronic periodontitis

The aim of this study was to assess subgingival microbiological changes in smokers versus non-smokers presenting severe chronic periodontitis after supragingival periodontal therapy (ST).Non-smokers (n=10) and smokers (n=10) presenting at least nine teeth with probing pocket depth (PPD) (≥5 mm), bleeding on probing (BoP), and no history of periodontal treatment in the last 6 months were selected. Clinical parameters assessed were plaque index (PI), BoP, PPD, relative gingival margin position (rGMP) and relative clinical attachment level (rCAL). Subgingival biofilm was collected before and 21 days after ST. DNA was extracted and the 16S rRNA gene was amplified with the universal primer pair, 27F and 1492R. Amplified genes were cloned, sequenced, and identified by comparison with known 16S rRNA sequences. Statistical analysis was performed by Student's t and Chi-Square tests (α=5%).Clinically, ST promoted a significant reduction in PI and PPD, and gain of rCAL for both groups, with no significant intergroup difference. Microbiologically, at baseline, data analysis demonstrated that smokers harbored a higher proportion of Porphyromonas endodontalis, Bacteroidetes sp., Fusobacterium sp. and Tannerella forsythia and a lower number of cultivated phylotypes (p<0.05). Furthermore, non-smokers featured significant reductions in key phylotypes associated with periodontitis, whereas smokers presented more modest changes.Within the limits of the present study, ST promoted comparable clinical improvements in smokers and non-smokers with severe chronic periodontitis. However, in smokers, ST only slightly affected the subgingival biofilm biodiversity, as compared with non-smokers

Neuropilin controls endothelial differentiation by mesenchymal stem cells from the periodontal ligament

Background: Periodontal ligament (PDL) has been reported to be a source of mesenchymal stem cells (MSCs). New vascular networks from undifferentiated cells are essential for repair/regeneration of specialized tissues, including PDL. The current study aims to determine potential of CD105(+)-enriched cell subsets of periodontal ligament cells (PDLSCs) to differentiate into endothelial cell (EC)-like cells and to give insights into the mechanism involved. Methods: CD105(+)-enriched PDLSCs were induced to EC differentiation by endothelial growth medium 2 (EGM-2) for 3, 7, 14, and 21 days, with mRNA/protein levels and functional activity assessed by: 1) real-time polymerase chain reaction; 2) Western blotting; 3) fluorescence-activated cell sorting; 4) immunohistochemistry; 5) immunofluorescence; 6) matrigel; and 7) small interfering RNA assays. Results: Data analyses demonstrated that EGM-2 treated PDLSCs presented increased expression of EC markers, including: 1) CD105; 2) kinase domain-containing receptor; and 3) Ulex europaeus agglutinin 1, and were able to form cord/tube-like structures. Gene and protein expression analysis showed that neuropilin 2 (NRP2), a key factor for vascular development, was significantly downregulated during EC differentiation. NRP2 was constitutively expressed in mouse PDL tissues by immunohistochemistry analysis, and NRP2 knockdown in CD105(+)-enriched PDLSCs resulted in increased cord/tube-like structures in a matrigel assay. Conclusion: These findings demonstrated the potential of CD105(+)-enriched PDLSCs to support angiogenesis, and NRP2 as a pivotal factor regulating this process.877E138E147COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPES02426/09-

GTR in class III furcation defects with resorbable polylactic acid membranes. A histomorphometric study in dogs

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Membrane proteome characterization of periodontal ligament cell sets from deciduous and permanent teeth

Physiological roles for the periodontal ligament (PDL) include tooth eruption and anchorage, force absorption, and provision of proprioceptive information. Despite the advances in understanding the biology of PDL cells, there is a lack of information regarding the molecular signature of deciduous (DecPDL) and permanent (PermPDL) PDL tissues. Thus, the present study was designed to characterize the membrane proteome of DecPDL and PermPDL cells. Primary PDL cells were obtained (n = 6) and a label-free quantitative proteome of cell membrane-enriched components was performed. Proteome findings were validated by quantitative polymerase chain reaction and Western blot assays in fresh human tissues (n = 8) and primary cell cultures (n = 6). In addition, confocal microscopy was used to verify the expression of target factors in the PDL cell cultures. Comparative gene ontology enrichment analysis evidenced that most stickling differences involved "endomembrane system" (PICALM, STX4, and LRP10), "hydrolase activity" (NCSTN and XRCC6), "protein binding" (PICALM, STX4, GPNMB, VASP, extended-synaptotagmin 2 [ESYT2], and leucine-rich repeat containing 15 [LRRC15]), and "isomerase activity" (FKBP8). Data are available via ProteomeXchange with identifier PXD010226. At the transcript level, high PICALM in DecPDL and ESYT2 and LRRC15 in PermPDL were confirmed in fresh PDL tissues. Furthermore, Western blot analysis confirmed increased levels of PICALM, LRRC15, and ESYT2 in cells and/or fresh tissues, and confocal microscopy confirmed the trends for PICALM and LRRC15 expression in PDL cells. We report the first comprehensive characterization of the membrane protein machinery of DecPDL and PermPDL cells, and together, we identified a distinct molecular signature for these cell populations, including unique proteins for DecPDL and PermPDL907775787CNPQ - Conselho Nacional de Desenvolvimento Científico e TecnológicoFAPESP – Fundação de Amparo à Pesquisa Do Estado De São Paulo304680/2014-12016/13786-0; 2016/02942-1; 2015/06372-