目的比较异种胶原蛋白基质(XCM)和自体结缔组织移植瓣(CTG)用于牙周软组织增量的效果。方法检索PubMed、Web of Science、EMBASE、Cochrane、CNKI、CBM、万方数据库、中文科技期刊全文数据库,查找利用XCM和CTG进行牙周软组织增量效果的...目的比较异种胶原蛋白基质(XCM)和自体结缔组织移植瓣(CTG)用于牙周软组织增量的效果。方法检索PubMed、Web of Science、EMBASE、Cochrane、CNKI、CBM、万方数据库、中文科技期刊全文数据库,查找利用XCM和CTG进行牙周软组织增量效果的临床随机对照研究。利用RevMan 5.3软件分析、比较两者牙周软组织增量的效果,包括角化龈宽度增量、角化龈厚度增量、平均根面覆盖率和手术时间。结果共纳入10篇临床随机对照研究。Meta分析结果显示,两组患者在术后6个月时角化龈宽度增量及根面覆盖率方面效果的差异无统计学意义(P>0.05),术后12个月时XCM效果不如CTG(P<0.05);术后12个月XCM的角化龈厚度增量效果不如CTG(P<0.05);XCM的手术时间短于CTG(P<0.05)。结论有限的证据表明,在增加角化龈宽度和提高根面覆盖率方面,XCM与CTG无差异;在增加角化龈厚度方面,无足够证据表明XCM不如CTG;但XCM的手术时间显著短于CTG。尚需随访时间更长的、多中心、大样本、前瞻性随机对照临床研究来进一步验证该问题。展开更多
Aortic dissection （AD） is a devastating, heterogeneous condition of aorta. The homeostasis between collagens and matrix metalloproteases （MMPs）/tissue inhibitors of MMPs （TIMPs） system in the extracellular matri...Aortic dissection （AD） is a devastating, heterogeneous condition of aorta. The homeostasis between collagens and matrix metalloproteases （MMPs）/tissue inhibitors of MMPs （TIMPs） system in the extracellular matrix plays an important role for structure and functions of aorta. However, our knowledge on association between variants of genes in this system and pathogenesis of AD is very limited. We analyzed all yet known coding human genes of collagens （45 genes）, MMPs/TIMPs （27 genes） in 702 sporadic AD patients and in 163 matched healthy controls, by using massively targeted next-generation and Sanger sequencing. To define the pathogenesis of potential disease-causing candidate genes, we performed transcriptome sequencing and pedigree co-segregation analysis in some genes and generated Col5a2 knockout rats. We identified 257 pathogenic or likely pathogenic variants which involved 88.89% （64/72） genes in collagens-MMPs/TIMPs system and accounted for 31.05% （218/702） sporadic AD patients. In them, 84.86% patients （185/218） carried one variant, 12.84% two variants and 2.30% more than two variants. Importantly, we identified 52 novel probablY pathogenic loss-of-function （LOF） variants （20 nonsense, 16 frameshift, 14 splice sites, one stop-loss, one initiation codon） in 11.06% （50/452） AD patients, which were absent in 163 controls （P=2.5-10-5）. Transcriptome sequencing revealed that identified variants induced dyshomeostasis in expression of collagens-TIMPs/MMPs systems. The Col5a2-/- rats manifested growth retardation and aortic dysplasia. Our study provides a first comprehensive map of genetic alterations in collagens-MMPs/TIMPs system in sporadic AD patients and suggests that variants of these genes contribute largely to AD pathogenesis.展开更多
文摘目的比较异种胶原蛋白基质(XCM)和自体结缔组织移植瓣(CTG)用于牙周软组织增量的效果。方法检索PubMed、Web of Science、EMBASE、Cochrane、CNKI、CBM、万方数据库、中文科技期刊全文数据库,查找利用XCM和CTG进行牙周软组织增量效果的临床随机对照研究。利用RevMan 5.3软件分析、比较两者牙周软组织增量的效果,包括角化龈宽度增量、角化龈厚度增量、平均根面覆盖率和手术时间。结果共纳入10篇临床随机对照研究。Meta分析结果显示,两组患者在术后6个月时角化龈宽度增量及根面覆盖率方面效果的差异无统计学意义(P>0.05),术后12个月时XCM效果不如CTG(P<0.05);术后12个月XCM的角化龈厚度增量效果不如CTG(P<0.05);XCM的手术时间短于CTG(P<0.05)。结论有限的证据表明,在增加角化龈宽度和提高根面覆盖率方面,XCM与CTG无差异;在增加角化龈厚度方面,无足够证据表明XCM不如CTG;但XCM的手术时间显著短于CTG。尚需随访时间更长的、多中心、大样本、前瞻性随机对照临床研究来进一步验证该问题。
基金supported by the National Natural Science Foundation of China(91439203)National Key Basic Research Program of China(2012CB518004,2012CB517801)
文摘Aortic dissection （AD） is a devastating, heterogeneous condition of aorta. The homeostasis between collagens and matrix metalloproteases （MMPs）/tissue inhibitors of MMPs （TIMPs） system in the extracellular matrix plays an important role for structure and functions of aorta. However, our knowledge on association between variants of genes in this system and pathogenesis of AD is very limited. We analyzed all yet known coding human genes of collagens （45 genes）, MMPs/TIMPs （27 genes） in 702 sporadic AD patients and in 163 matched healthy controls, by using massively targeted next-generation and Sanger sequencing. To define the pathogenesis of potential disease-causing candidate genes, we performed transcriptome sequencing and pedigree co-segregation analysis in some genes and generated Col5a2 knockout rats. We identified 257 pathogenic or likely pathogenic variants which involved 88.89% （64/72） genes in collagens-MMPs/TIMPs system and accounted for 31.05% （218/702） sporadic AD patients. In them, 84.86% patients （185/218） carried one variant, 12.84% two variants and 2.30% more than two variants. Importantly, we identified 52 novel probablY pathogenic loss-of-function （LOF） variants （20 nonsense, 16 frameshift, 14 splice sites, one stop-loss, one initiation codon） in 11.06% （50/452） AD patients, which were absent in 163 controls （P=2.5-10-5）. Transcriptome sequencing revealed that identified variants induced dyshomeostasis in expression of collagens-TIMPs/MMPs systems. The Col5a2-/- rats manifested growth retardation and aortic dysplasia. Our study provides a first comprehensive map of genetic alterations in collagens-MMPs/TIMPs system in sporadic AD patients and suggests that variants of these genes contribute largely to AD pathogenesis.
