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1.
Braz. oral res. (Online) ; 31: e16, 2017. tab, graf
Article in English | LILACS | ID: biblio-839530

ABSTRACT

Abstract Recent studies investigating protease-activated receptor type 2 (PAR-2) suggest an association between the receptor and periodontal inflammation. It is known that gingipain, a bacterial protease secreted by the important periodontopathogen Porphyromonas gingivalis can activate PAR-2. Previous studies by our group found that PAR-2 is overexpressed in the gingival crevicular fluid (GCF) of patients with moderate chronic periodontitis (MP). The present study aimed at evaluating whether PAR-2 expression is associated with chronic periodontitis severity. GCF samples and clinical parameters, including plaque and bleeding on probing indices, probing pocket depth and clinical attachment level, were collected from the control group (n = 19) at baseline, and from MP patients (n = 19) and severe chronic periodontitis (SP) (n = 19) patients before and 6 weeks after periodontal non-surgical treatment. PAR-2 and gingipain messenger RNA (mRNA) in the GCF of 4 periodontal sites per patient were evaluated by Reverse Transcription Polymerase Chain Reaction (RT-qPCR). PAR-2 and gingipain expressions were greater in periodontitis patients than in control group patients. In addition, the SP group presented increased PAR-2 and gingipain mRNA levels, compared with the MP group. Furthermore, periodontal treatment significantly reduced (p <0.05) PAR-2 expression in patients with periodontitis. In conclusion, PAR-2 is associated with chronic periodontitis severity and with gingipain levels in the periodontal pocket, thus suggesting that PAR-2 expression in the GCF reflects the severity of destruction during periodontal infection.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Gingival Crevicular Fluid/chemistry , Receptor, PAR-2/analysis , Chronic Periodontitis/pathology , Reference Values , Severity of Illness Index , Cysteine Endopeptidases/analysis , Biomarkers/analysis , Case-Control Studies , Gene Expression , Periodontal Index , Dental Plaque Index , Periodontal Attachment Loss , Porphyromonas gingivalis , Statistics, Nonparametric , Adhesins, Bacterial/analysis
3.
Rev. bras. hipertens ; 8(1): 76-88, jan.-mar. 2001. ilus, tab
Article in Portuguese | LILACS | ID: lil-284129

ABSTRACT

O endotélio sadio exerce funçöes anticoagulante, vasodilatadora e antiinflamatória que säo essenciais para a manutençäo da homeostasia. Em várias doenças cardiovasculares, entre elas a hipertensäo arterial, ocorre disfunçäo endotelial. O endotélio normal tem funçäo protetora contra o desenvolvimento de lesöes vasculares mantendo a vasodilataçäo, inibindo a agregaçäo plaquetária, a adesäo leucocitária e a proliferaçäo das células musculares lisas. Essas açöes säo exercidas principalmente pelo óxido nítrico, considerado o mais importante fator endotelial, ou EDRF (do inglês Endothelial-Derived Relaxing Factor), ao lado da prostaciclina e do fator hiperpolarizante derivado do endotélio. O endotélio pode também gerar fatores contráteis conhecidos por EDCFs, como as endotelinas, a angiotensina II, as prostaglandinas vasoconstritoras e espécies reativas de oxigênio. A disfunçäo endotelial na hipertensäo leva a desequilíbrio da produçäo/liberaçäo dos fatores contráteis e relaxantes e: 1) provoca diminuiçäo da geraçäo de óxido nítrico/aumento das espécies reativas de oxigênio, aumentando dessa forma o tônus vascular; 2) contribui para o aumento da permeabilidade vascular levando à formaçäo de edema subendotelial; 3) aumenta a expressäo de moléculas de adesäo com conseqüente aumento da aderência leucocitária à parede vascular; 4) acelera a coagulaçäo intravascular; 5) aumenta a proliferaçäo de células musculares lisas, levando à hipertrofia/hiperplasia da parede vascular. Torna-se evidente assim que o endotélio tem papel central na hipertensäo, controlando a permeabilidade vascular, a adesäo leucocitária, a proliferaçäo de células musculares lisas, a coagulaçäo e o equilíbrio entre fatores endoteliais (os EDRFs e os EDCFs).


Subject(s)
Humans , Animals , Endothelium/physiology , Hypertension , Nitric Oxide/physiology , Angiotensin II
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