目的分析牙龈卟啉单胞菌及其毒力因子牙龈蛋白K在青少年正畸治疗早期的变化。方法随机收集青少年正畸牙龈正常者45例,分别取矫治器戴入前,戴入后1、2、3、6个月龈沟液标本,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌及其毒力...目的分析牙龈卟啉单胞菌及其毒力因子牙龈蛋白K在青少年正畸治疗早期的变化。方法随机收集青少年正畸牙龈正常者45例,分别取矫治器戴入前,戴入后1、2、3、6个月龈沟液标本,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌及其毒力因子牙龈蛋白K;采用SPSS17.0软件包对数据进行统计分析,牙龈卟啉单胞菌及牙龈蛋白K各组间检出率比较用χ2检验;牙龈卟啉单胞菌、牙龈蛋白K的检出率与牙龈炎症之间的关系用Spearman等级相关分析。结果牙龈卟啉单胞菌在矫治前与戴入后1个月有显著性差异(P<0.05),与2个月、3个月之间有极显著性差异(P<0.01);戴入后1个月与2个月之间有显著性差异(P<0.05);牙龈蛋白K在矫治器戴入前与戴入后1个月、6个月之间无显著性差异,与戴入后2个月、3个月之间有显著性差异(P<0.05);从第2个月开始牙龈卟啉单胞菌与牙龈蛋白K的检出率下降,到6个月时检出率已基本接近矫治器戴入前。结论青少年正畸治疗过程中在矫治器戴入早期可引发牙龈卟啉单胞菌及牙龈蛋白K的增加,出现牙龈炎症反应,当增加到一定时间即2个月后开始逐渐下降,到6个月时已基本接近矫治器戴入前。展开更多
目的:分析牙龈蛋白K(gingipain K,Kgp)在正畸治疗中对牙龈炎性反应的影响。方法:选择青少年牙龈健康者45例,分别取矫治器戴入前与矫治器戴入后3个月的龈沟液,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌(P.g)及Kgp,采用SPSS17....目的:分析牙龈蛋白K(gingipain K,Kgp)在正畸治疗中对牙龈炎性反应的影响。方法:选择青少年牙龈健康者45例,分别取矫治器戴入前与矫治器戴入后3个月的龈沟液,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌(P.g)及Kgp,采用SPSS17.0软件包对数据进行统计学分析。结果:矫治器戴入前Kgp检出率为35.71%,矫治器戴入后Kgp检出率为67.86%,两者之间差异显著(P<0.05)。结论:正畸治疗患者在矫治器戴入后Kgp检出率增加,出现牙龈炎性反应。展开更多
Alzheimer’s disease has proven to be largely intractable to treatment,despite years of research,and numerous trials of therapies that target the hallmarks of the disease-amyloid plaques and neurofibrillary tangles.Th...Alzheimer’s disease has proven to be largely intractable to treatment,despite years of research,and numerous trials of therapies that target the hallmarks of the disease-amyloid plaques and neurofibrillary tangles.The etiology of Alzheimer’s disease remains elusive.There is a growing body of evidence for an infectious trigger of Alzheimer’s disease,and,in particular,the focus has been on the oral pathogen Porphyromonas gingivalis(P.gingivalis).Reports of the expression of a misfolded form of p53 in non-neuronal cells(fibroblasts,peripheral blood mononuclear cells,and B cells)and serum,which appears several years before clinical symptoms manifest,may provide further support for the role of bacteria in general,and P.gingivalis in particular,in the initiation of the disease.This review presents a model of the pathway from initial oral infection with P.gingivalis to amyloid plaque formation and neuronal degeneration,via the steps of chronic periodontitis;secretion of the inflammagens lipopolysaccharide and gingipains into the bloodstream;induction of an inflammatory response in both peripheral cells and tissues;disruption of the blood-brain barrier,and entry into the central nervous system of the inflammagens and the P.gingivalis bacteria themselves.In this model,the misfolded p53(or“unfolded p53”;up53)is induced in non-neuronal cells and upregulated in serum as a result of oxidative stress due to lipopolysaccharide from P.gingivalis.up53 is therefore a potential biomarker for early diagnosis of the presence of a causative agent of Alzheimer’s disease.Fastidious dental hygiene and aggressive antibiotic treatment may prevent the patient progressing to clinical Alzheimer’s disease if serum up53 is detected at this pre-symptomatic stage.展开更多
文摘目的分析牙龈卟啉单胞菌及其毒力因子牙龈蛋白K在青少年正畸治疗早期的变化。方法随机收集青少年正畸牙龈正常者45例,分别取矫治器戴入前,戴入后1、2、3、6个月龈沟液标本,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌及其毒力因子牙龈蛋白K;采用SPSS17.0软件包对数据进行统计分析,牙龈卟啉单胞菌及牙龈蛋白K各组间检出率比较用χ2检验;牙龈卟啉单胞菌、牙龈蛋白K的检出率与牙龈炎症之间的关系用Spearman等级相关分析。结果牙龈卟啉单胞菌在矫治前与戴入后1个月有显著性差异(P<0.05),与2个月、3个月之间有极显著性差异(P<0.01);戴入后1个月与2个月之间有显著性差异(P<0.05);牙龈蛋白K在矫治器戴入前与戴入后1个月、6个月之间无显著性差异,与戴入后2个月、3个月之间有显著性差异(P<0.05);从第2个月开始牙龈卟啉单胞菌与牙龈蛋白K的检出率下降,到6个月时检出率已基本接近矫治器戴入前。结论青少年正畸治疗过程中在矫治器戴入早期可引发牙龈卟啉单胞菌及牙龈蛋白K的增加,出现牙龈炎症反应,当增加到一定时间即2个月后开始逐渐下降,到6个月时已基本接近矫治器戴入前。
文摘目的:分析牙龈蛋白K(gingipain K,Kgp)在正畸治疗中对牙龈炎性反应的影响。方法:选择青少年牙龈健康者45例,分别取矫治器戴入前与矫治器戴入后3个月的龈沟液,应用16S r DNA PCR技术检测各样本中的牙龈卟啉单胞菌(P.g)及Kgp,采用SPSS17.0软件包对数据进行统计学分析。结果:矫治器戴入前Kgp检出率为35.71%,矫治器戴入后Kgp检出率为67.86%,两者之间差异显著(P<0.05)。结论:正畸治疗患者在矫治器戴入后Kgp检出率增加,出现牙龈炎性反应。
文摘Alzheimer’s disease has proven to be largely intractable to treatment,despite years of research,and numerous trials of therapies that target the hallmarks of the disease-amyloid plaques and neurofibrillary tangles.The etiology of Alzheimer’s disease remains elusive.There is a growing body of evidence for an infectious trigger of Alzheimer’s disease,and,in particular,the focus has been on the oral pathogen Porphyromonas gingivalis(P.gingivalis).Reports of the expression of a misfolded form of p53 in non-neuronal cells(fibroblasts,peripheral blood mononuclear cells,and B cells)and serum,which appears several years before clinical symptoms manifest,may provide further support for the role of bacteria in general,and P.gingivalis in particular,in the initiation of the disease.This review presents a model of the pathway from initial oral infection with P.gingivalis to amyloid plaque formation and neuronal degeneration,via the steps of chronic periodontitis;secretion of the inflammagens lipopolysaccharide and gingipains into the bloodstream;induction of an inflammatory response in both peripheral cells and tissues;disruption of the blood-brain barrier,and entry into the central nervous system of the inflammagens and the P.gingivalis bacteria themselves.In this model,the misfolded p53(or“unfolded p53”;up53)is induced in non-neuronal cells and upregulated in serum as a result of oxidative stress due to lipopolysaccharide from P.gingivalis.up53 is therefore a potential biomarker for early diagnosis of the presence of a causative agent of Alzheimer’s disease.Fastidious dental hygiene and aggressive antibiotic treatment may prevent the patient progressing to clinical Alzheimer’s disease if serum up53 is detected at this pre-symptomatic stage.
