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1.
J Periodontol ; 80(3): 492-8, 2009 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-19254133

RESUMO

BACKGROUND: Neutrophil formylpeptide receptors (FPRs) play an important role in bacterial recognition and chemotaxis. Defective FPR1 expression and impaired polymorphonuclear leukocyte chemotaxis toward bacterial formylpeptides are associated with aggressive periodontitis (AgP). The objective of this study was to determine whether single nucleotide polymorphisms (SNPs) in FPR1 are associated with AgP. METHODS: Genomic DNA was isolated from blood samples obtained from African Americans (30 subjects with AgP and 33 healthy controls) and Turks (75 subjects with AgP and 63 healthy controls). A highly polymorphic fragment of the FPR1 gene was amplified by polymerase chain reaction and sequenced for analysis of SNPs. RESULTS: Five previously identified SNPs were detected in African Americans, whereas six were detected in Turkish subjects. The frequency of synonymous SNP c.348T>C was significantly higher in African Americans with AgP than in controls (P = 0.029). The 348T allele was significantly associated with AgP (P = 0.010). Seven of the subjects with AgP, but none of the controls, were homozygous for 348T. FPR1 haplotypes 348T.568A, 348T.576T, and 348T.568A.576T were significantly increased in African Americans with AgP (P <0.02). The Turkish population did not exhibit significant differences in FPR1 SNP frequencies between subjects with AgP and controls. CONCLUSIONS: FPR1 SNP c.348T>C is associated with AgP in African Americans. Individuals who are homozygous for 348T may have an increased risk for developing this disorder.


Assuntos
Periodontite Agressiva/genética , Citosina , Neutrófilos/metabolismo , Polimorfismo de Nucleotídeo Único/genética , Receptores de Formil Peptídeo/genética , Timina , Adolescente , Adulto , Negro ou Afro-Americano/genética , Alelos , Etnicidade/genética , Feminino , Frequência do Gene/genética , Haplótipos , Homozigoto , Humanos , Masculino , Pessoa de Meia-Idade , Perda da Inserção Periodontal/genética , Bolsa Periodontal/genética , Fatores de Risco , Turquia , Adulto Jovem
2.
Acta Odontol Scand ; 67(2): 65-73, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19031159

RESUMO

OBJECTIVE: Periodontal regeneration is histologically defined as regeneration of the tooth supporting structures, including alveolar bone, periodontal ligament, and cementum. Cells in the remaining periodontal tissues need optimal conditions if they are to perform their functions in the regeneration process. The present study is an investigation of the molecular effects of ABM/P-15 on human periodontal ligament cells (PDL) in vitro. MATERIAL AND METHODS: PDL cells obtained from healthy subjects were used for in vitro experiments. Cell proliferation, morphology, and mineralization using Von kossa staining were evaluated. mRNA expressions for transforming growth factor-beta (TGF-beta), insulin-like growth factor-I (IGF-I), basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), bone morphogenic protein-2 (BMP-2), platelet-derived growth factor (PDGF), and type 1 collagen (COL1) were assessed on days 3 and 7 using RT-PCR. RESULTS: ABM/P-15 enhanced proliferation of cultured PDL cells. It increased the mRNA expression of TGF-beta and BMP-2 in cultured PDL cells on days 3 and 7. IGF-I and b-FGF mRNA expressions showed a slight decrease, while PDGF expression was observed to have increased on day 3. VEGF and COL1 mRNA expressions were found not to be different on days 3 and 7. No differences were observed in the mineralization properties of cultured PDL cells treated with or without ABM/P-15. CONCLUSIONS: Based on the results of this in vitro study, it may be concluded that ABM/P-15 enhanced the regenerative capacity of PDL by regulating specific gene expressions of cells during early wound healing.


Assuntos
Substitutos Ósseos/farmacologia , Colágeno/farmacologia , Regeneração Tecidual Guiada Periodontal/métodos , Hidroxiapatitas/farmacologia , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Fragmentos de Peptídeos/farmacologia , Ligamento Periodontal/metabolismo , Animais , Matriz Óssea , Proteína Morfogenética Óssea 2/efeitos dos fármacos , Proteína Morfogenética Óssea 2/genética , Proteína Morfogenética Óssea 2/metabolismo , Bovinos , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Colágeno Tipo I/efeitos dos fármacos , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Combinação de Medicamentos , Fator 2 de Crescimento de Fibroblastos/efeitos dos fármacos , Fator 2 de Crescimento de Fibroblastos/genética , Fator 2 de Crescimento de Fibroblastos/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/fisiologia , Humanos , Fator de Crescimento Insulin-Like I/efeitos dos fármacos , Fator de Crescimento Insulin-Like I/genética , Fator de Crescimento Insulin-Like I/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/genética , Ligamento Periodontal/citologia , Ligamento Periodontal/efeitos dos fármacos , Fator de Crescimento Derivado de Plaquetas/efeitos dos fármacos , Fator de Crescimento Derivado de Plaquetas/genética , Fator de Crescimento Derivado de Plaquetas/metabolismo , RNA Mensageiro/análise , Valores de Referência , Alicerces Teciduais , Fator de Crescimento Transformador beta/efeitos dos fármacos , Fator de Crescimento Transformador beta/genética , Fator de Crescimento Transformador beta/metabolismo , Fatores de Crescimento do Endotélio Vascular/efeitos dos fármacos , Fatores de Crescimento do Endotélio Vascular/genética , Fatores de Crescimento do Endotélio Vascular/metabolismo
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