Strategy of newly treatment for periodontal disease using the pathogenic bacterial genome information

分析TDC 60基因组信息有望为牙周炎发病和进展的机制提供新的见解。因此，我们使用全基因组序列在TDC 60株中寻找特异性毒力因子，并使用2-DE和MALD-TOF质谱法发现与W83株相比，具有更高水平的脂肪肽酶PepD-2，一种小分子酶-1（Mfa 1），一种胶原溶解相关的肽酶Dap 2。PepD的晶体结构显示为整体折叠和二聚体结构。Bestatin具有剂量依赖性地抑制牙龈卟啉单胞菌生长的能力。在牙龈卟啉单胞菌的蛋白质降解过程中，二肽酶在其他肽酶产生的肽片段的最终断裂中起着普遍的作用。

Analyzing the genomic informationfor TDC60 is expected to provide new insights into the mechanisms underlying the onset and progression of periodontitis. For that reason, we searched for the specific virulence factor in the TDC60 strain using the complete genome sequence s,and found higher levels of adipeptidasePepD-2,a minorfibire-1(Mfa1),a collagenolysis-related peptidase Dap2 comparedto the W83 strain using 2-DE and MALD -TOF mass spectrometry. The crystal structure of PepD showed that the overall flding and dimeric organization. Bestatin has the ability to dose-dependentlyinhi it the P. gingivalis growth. Dipeptidases play a generalrole in the final break own of peptide fragments produced by other peptidases during the protein degradation process in P. gingivalis.