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치수 치근단 병소의 전구 위험요인으로서의 제 2 형 당뇨의 역할에 관한 소고
김진희,배광식,서덕규,홍성태,이윤,홍삼표,금기연 大韓齒科保存學會 2009 Restorative Dentistry & Endodontics Vol.34 No.3
Diabetes Mellitus (DM) is a syndrome accompanied with the abnormal secretion or function of insulin, a hormone that plays a vital role in controlling the blood glucose level (BGL). Type 1 and 2 DM are most common form and the prevalence of the latter is recently increasing. The aim of this article was to assess whet her Type 2 DM could act as a predisposing risk factor on the pulpo-periapical pathogenesis. Previous literature on the pathologic changes of blood vessels in DM was thoroughly reviewed. Furthermore, a histopathologic analysis of artificially-induced periapical specimens obtained from Type 2 diabetic and DM-resistant rats was compared. Histopathologic results demonstrate that the size of periapical bone destruction was larger and the degree of pulpal inflammation was more severe in diabetic rats, indicating that Type 2 DM itself can be a predisposing risk factor that makes the host more susceptible to pulpal infection. The possible reasons may be that in diabetic state the lumen of pulpal blood vessels are thickened by atheromatous deposits, and microcirculation is hindered. The function of polymorphonuclear leukocyte is also impaired and the migration of immune cells is blocked. leading to increased chance of pulpal infection. Also, lack of collateral circulation of pulpal blood vessels makes the pulp more susceptible to infection. These decrease the regeneration capacity of pulpal cells or tissues, delaying the healing process. Therefore, when restorative treatment is needed in Type 2 DM patients, dentists should minimize irritation to the pulpal tissue under control of BGL. 당뇨(Diabetes Mellitus)란 혈당을 조절하는 인슐린의 분비나 기능에 장애를 야기하는 질환으로 인슐린 의존성 여부에 따라 제 1 형과 제 2 형으로 분류된다. 본 종설은 최근 증가 추세에 있는 제 2 형 당뇨가 치수 치근단 병소의 병인 과정에 전구 위험 요인으로 작용할 수 있는지를 평가 하고자 문헌고찰을 통해 당뇨의 병인 과정에서 특징적으로 나타나는 혈관 합병증에 관해 알아보고, 부가적으로 제 2 형 당뇨 쥐 모델에서 인위적인 치수감염 후 얻은 치근단 조직의 조직병리학적 분석을 시행하였다. 조직학적 관찰 결과 제 2 형 당뇨 쥐에서 대조군에 비해 치수 치근단 병소의 크기가 증가하였고, 치수 염증 반응도 심하게 나타난 것으로 보아 당뇨 자체가 숙주를 감염에 취약한 상태로 만드는 전구 위험요소로 작용하였음을 알 수 있었다. 이러한 이유로는 첫째, 당뇨 시 전반적으로 나타나는 혈관 내 죽상 침착(atheromatous deposits)에 의해 혈관 내벽의 두께가 두꺼워져 미세 순환의 장애는 물론 탐식 세포의 기능 저하, 면역 세포의 혈류 이동이 차단되어 치수 감염 시 쉽게 치근단 병소로 이환될 가능성이 높고, 둘째 치수 혈관에서 특징인 측부 순환(collateral circulation)의 부재에 따른 살균성 다형핵 백혈구의 활동 억제를 포함한 미세 혈관계의 취약성으로 인해 치수 조직의 재생능이 저하되어 추가적인 감염원의 공격에 대한 방어 및 치유 저하를 더욱 심화시키기 때문인 것으로 사료된다. 따라서 제 2 형 당뇨 환자의 수복치료 시 치과의사는 당뇨 조절 하에서 치수 조직의 자극을 최소화하기 위한 세심한 처치가 필요하다.
Kim, Hyun Soo,Woo, Jong Shin,Kim, Bu Yong,Jang, Hyun Hee,Hwang, Seung Joon,Kwon, Sung Jin,Choi, Eun Young,Kim, Jin Bae,Cheng, Xianwu,Jin, Enze,Kim, Woo Shik,Kim, Kwon Sam,Kim, Weon Elsevier 2014 Atherosclerosis Vol.233 No.2
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD).</P> <P><B>Methods</B></P> <P>Patients with stable CAD were screened by conventional carotid ultrasound and patients with carotid plaque thickness more than 2 mm were performed by CEUS for the presence of IPN. Plasma levels of biomarkers and clinical outcomes were evaluated.</P> <P><B>Results</B></P> <P>Among consecutive 89 patients fulfilled the inclusion criteria, 30 patients without IPN (group 1) and 59 patients with IPN (group 2) were analyzed. There were no significant difference in baseline characteristics except for mean age (62.9 ± 10.1 yrs versus 68.4 ± 9.6 yrs, <I>p</I> = 0.015). On multivariate analysis, only MMP-9 (<I>p</I> = 0.021, 95% CI 1.002–1.027) showed a significant association with IPN. But patients with IPN showed only trend for a history of cardiovascular disease (CVD) (44% versus 30%, <I>p</I> = 0.19) and one-year cardiovascular events (CVE) (6.8% versus 3.3%, <I>p</I> = 0.50) compared to group 1. Maximum plaque thickness (<I>p</I> = 0.04, 95% CI 1.230–6.322) showed a significant correlation with the clinical outcome including CVD or CVE.</P> <P><B>Conclusion</B></P> <P>MMP-9 correlated with IPN on CEUS. For clinical implication, however, large prospective studies are needed.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We examine intraplaque neovascularization using contrast enhanced ultrasound. </LI> <LI> We model correlation between intraplaque neovascularization with biomarkers. </LI> <LI> The factors to affect clinical outcomes would be examined including intraplaque neovascularization. </LI> <LI> Only MMP-9 showed a significant association with intraplaque neovascularization. </LI> <LI> Maximum plaque thickness showed a significant correlation with the clinical outcome. </LI> </UL> </P>
Chung Hyemoon,Kim Bu Yong,Kim Hyun Soo,Kim Hyung Oh,Lee Jung Myung,Woo Jong Shin,Kim Jin Bae,Kim Woo-Shik,Kim Kwon Sam,Kim Weon 대한영상의학회 2020 Korean Journal of Radiology Vol.21 No.7
Objective: To investigate the predictive value of intraplaque neovascularization (IPN) for cardiovascular outcomes. Materials and Methods: We evaluated 217 patients with coronary artery disease (CAD) (158 men; mean age, 68 ± 10 years) with a maximal carotid plaque thickness ≥ 1.5 mm for the presence of IPN using contrast-enhanced ultrasonography. We compared patients with (n = 116) and without (n = 101) IPN during the follow-up period and investigated the predictors of major adverse cardiovascular events (MACE), including cardiac death, myocardial infarction, coronary artery revascularization, and transient ischemic accident/stroke. Results: During the mean follow-up period of 995 ± 610 days, the MACE rate was 6% (13/217). Patients with IPN had a higher maximal thickness than those without IPN (2.86 ± 1.01 vs. 2.61 ± 0.84 mm, p = 0.046). Common carotid artery-peak systolic velocity, left ventricular mass index (LVMI), and ventricular-vascular coupling index were significantly correlated with MACE. However, on multivariate Cox regression analysis, increased LVMI was independently related to MACE (p < 0.05). The presence of IPN could not predict MACE. Conclusion: The presence of IPN was related to a higher plaque thickness but could not predict cardiovascular outcomes better than conventional clinical factors in patients with CAD.
Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice
Kim, Hyo-Yeon,Kim, Joon-Ki,Choi, Jun-Ho,Jung, Joo-Yeon,Oh, Woo-Yong,Kim, Dong Chun,Lee, Hee Sang,Kim, Yeong Shik,Kang, Sam Sik,Lee, Seung-Ho,Lee, Sun-Mee The Japanese Pharmacological Society 2010 JOURNAL OF PHARMACOLOGICAL SCIENCES Vol.112 No.1
<P><I>Forsythiae Fructus</I> is known to have diuretic, anti-bacterial, and anti-inflammatory activities. This study examined the hepatoprotective effects of pinoresinol, a lignan isolated from <I>Forsythiae Fructus,</I> against carbon tetrachloride (CCl<SUB>4</SUB>)–induced liver injury. Mice were treated intraperitoneally with vehicle or pinoresinol (25, 50, 100, and 200 mg/kg) 30 min before and 2 h after CCl<SUB>4</SUB> (20 <I>μ</I>l/kg) injection. In the vehicle-treated CCl<SUB>4 </SUB>group, serum aminotransferase activities were significantly increased 24 h after CCl<SUB>4</SUB> injection, and these increases were attenuated by pinoresinol at all doses. Hepatic glutathione contents were significantly decreased and lipid peroxidation was increased after CCl<SUB>4</SUB> treatment. These changes were attenuated by 50 and 100 mg/kg of pinoresinol. The levels of protein and mRNA expression of inflammatory mediators, including tumor necrosis factor-<I>α</I>, inducible nitric oxide synthase, and cyclooxygenase-2, were significantly increased after CCl<SUB>4</SUB> injection; and these increases were attenuated by pinoresinol. Nuclear translocation of nuclear factor-<I>κ</I>B (NF-<I>κ</I>B) and phosphorylation of c-Jun, one of the components of activating protein 1 (AP-1), were inhibited by pinoresinol. Our results suggest that pinoresinol ameliorates CCl<SUB>4</SUB>-induced acute liver injury, and this protection is likely due to anti-oxidative activity and down-regulation of inflammatory mediators through inhibition of NF-<I>κ</I>B and AP-1.</P>