Disequilibrium of plasma protease/anti-protease due to severe periodontal disease contributes to human subarachnoid hemorrhage
Disequilibrium of plasma protease/anti-protease due to severe periodontal disease contributes to human subarachnoid hemorrhage
复制标题
严重牙周病导致血浆蛋白酶/抗蛋白酶失衡导致人类蛛网膜下腔出血
DOI：
10.1093/neuopn/okaa007
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Takagi Y
中科院分区：
文献类型：
--
作者：
Yoshioka S;Miyamoto T;Satomi J;Tada Y;Yagi K;Shimada K;Naruishi K;Shikata E;Yamaguchi I;Yamaguchi1 T;Korai M;Okayama Y;Harada M;Kitazato K;Kanematsu Y;Nagahiro S;Takagi Y
背景颅内动脉瘤破裂引起的蛛网膜下腔出血的病理生理机制尚不清楚。虽然SAHS和牙周病（PD）之间的关系已被建议，机制需要澄清。EQUITIVETo评估PD和SAHS之间的关系，并确定牙周病原体与SAHs. METHODS相关的这一前瞻性研究包括连续患者破裂（n= 11）和未破裂（n= 14）IA和健康对照组（n= 8）。由牙医使用社区牙周病治疗需求指数（CPITN）评估PD患者的血浆和菌斑龈下细菌脱氧核糖核酸（DNA）水平。分析血浆基质金属蛋白酶（MMP-9）、基质金属蛋白酶组织抑制剂（TIMP-2）和前胶原I的水平，发现颅内动脉瘤破裂患者的CPITN评分显著高于对照组，提示颅内动脉瘤破裂与严重PD相关。虽然没有发现破裂特异性细菌，但重度PD患者的菌斑龈下细菌DNA阳性率明显高于非重度PD患者。多变量逻辑回归分析表明，探诊出血（BOP）与颅内动脉瘤破裂相关（比值比，1.10; 95%置信区间1.04-1.20; P=. 0001）。BOP与血浆MMP-9水平呈正相关，MMP-9/TIMP 2比值失衡。BOP与血浆Ⅰ型前胶原水平呈负相关（P<. 05、每个人）。这表明，局部炎症与严重的PD可能有全身性的影响，并导致破裂IAs.CONCLUSIONDisequilibrium血浆蛋白酶/抗蛋白酶相关的BOP率高，在严重的PD可能是由于IA破裂。
BACKGROUNDThe pathophysiology of subarachnoid hemorrhages (SAHs) due to ruptured intracranial aneurysms (IAs) remains unclear. Although a relationship between SAHs and periodontal disease (PD) has been suggested, the mechanism requires clarification.OBJECTIVETo evaluate the relationship between PD and SAHs and to identify periodontal pathogens associated with SAHs.METHODSThis prospective study included consecutive patients with ruptured (n= 11) and unruptured (n= 14) IAs and healthy controls (n= 8). The plasma and plaque subgingival bacterial deoxyribonucleic acid (DNA) levels in PD were evaluated by a dentist using the Community Periodontal Index of Treatment Needs (CPITN). Plasma levels of matrix metalloproteinase (MMP-9), tissue inhibitors of matrix metalloproteinase (TIMP2), and procollagen I were analyzed.RESULTSPatients with ruptured IAs, had significantly higher CPITN scores than the controls, suggesting that ruptured IAs were associated with severe PD. Although no rupture-specific bacteria were identified, the positive rate of plaque subgingival bacterial DNA was significantly higher in patients with severe PD than in those without severe PD. Multivariate logistic regression analysis indicated that bleeding on probing (BOP) was associated with ruptured IAs (odds ratio, 1.10; 95% confidence interval 1.04–1.20; P=. 0001). BOP was positively associated with plasma MMP-9 levels and a disequilibrium in the MMP-9/TIMP2 ratio. BOP was negatively correlated with plasma procollagen I levels (P<. 05, for each). This suggested that local inflammation with severe PD might have systemic effects and lead to ruptured IAs.CONCLUSIONDisequilibrium of plasma protease/anti-protease associated with a high BOP rate in severe PD may be attributable to IA rupture.