牙周干预对伴冠心病牙周炎患者血清炎性因子和脂联素的影响

目的分析冠心病伴牙周炎患者牙周干预治疗前、后血清中炎性因子和脂联素水平的变化,探讨慢性牙周炎与冠心病的关系及牙周干预治疗对冠心病伴牙周炎患者的重要性。方法本研究包括冠心病伴牙周炎患者56例和单纯冠心病不伴牙周炎患者42例。冠心病伴牙周炎患者给予牙周干预治疗,对冠心病组及冠心病伴牙周炎组干预前、后的牙周临床指标及血清炎性因子（CRP、TNF-α、IL-6）和脂联素水平进行比较分析。结果冠心病伴牙周炎组牙周干预后牙周临床指数比干预前明显好转。冠心病伴牙周炎组干预前与冠心病组相比,所有血清炎性因子（CRP、TNF-α、IL-6）水平升高;干预3个月后明显降低（P〈0.05）。冠心病伴牙周炎组干预前水平有所降低的脂联素在干预3个月后明显升高（P〈0.05）。结论慢性牙周炎可增加冠心病的发病风险,牙周干预治疗可降低血清中炎性因子水平,提高血管保护因子水平,对冠心病病程的发展有改善作用。     

C反应蛋白基因多态性与慢性牙周炎的相关性研究

目的 研究中国汉族人群中C反应蛋白(C-reactive protein,CRP)+1444C/T、CRP+1059G/C两种基因多态性与慢性牙周炎的关系,为进一步探讨CRP在牙周炎与冠状动脉粥样硬化性心脏病相关性中的作用和意义提供依据.方法 检测126例慢性牙周炎患者(CP组)和113名牙周健康或龈炎者(对照组)的牙周临床指数(附着丧失、探诊深度和探诊出血)、CRP水平及CRP+1059G/C、CRP+1444C/T基因多态性分布情况.结果 CP组中CRP+1059C等位基因的频率为6.7%(17/252);对照组4.9%(11/226),CP组与对照组之间的基因型分布和等位基因频率的分布差异均无统计学意义(0.250.5).结论 CRP+1059G/C、+1444C/T基因可能是CRP的功能性基因,尽管牙周炎与心血管疾病显著相关且CRP+1059G/C、+1444C/T与心血管疾病有相关性,但是这两个基因位点可能对中国汉族人群牙周炎患者的血清CRP水平影响不显著.     

伴冠心病牙周炎患者牙周基础治疗的临床疗效观察

目的 观察伴有冠状动脉粥样硬化性心脏病(以下简称冠心病)的牙周炎患者牙周基础治疗后临床指标的变化,并评价其治疗效果.方法 32例伴有冠心病的牙周炎患者,在1个月内完成口腔卫生指导、洁治、刮治和根面平整术,治疗后6周复查,进行牙周维护,在治疗前和治疗后3个月时记录全口牙周情况:菌斑指数(plaque index,PLI)、探诊深度(probing depth,PD)、附着丧失(attachment loss,AL)、牙龈出血指数(bleeding index,BI),并进行血清超敏C-反应蛋白(high-sensitivity C-reactive,hs-CRP)、总胆固醇、甘油三酯、高密度脂蛋白胆固醇(high-density lipoprotein,HDL)、低密度脂蛋白胆固醇(low-density lipoprotein,LDL)及血糖的检测.结果 牙周治疗后3个月患者的临床指标显著改善,平均PD由(3.95±0.15)mm减少至(2.93±0.21)mm,平均AL由(3.08±0.43)mm降至(2.43±0.37)mm,PD≥5 mm的位点百分比由(22.37±6.88)%降至(3.00±1.80)%,差异均有统计学意义(P＜0.01).牙周治疗后3个月患者的hs-CRP水平显著降低,由(2.71±2.69)mg/L降至(1.99±2.14)mg/L,差异有统计学意义(P＜0.01);总胆固醇,甘油三酯、HDL、LDL及血糖的测定值与治疗前相比差异均无统计学意义(P＞0.05).结论 在本研究范围内,对于伴有冠心病的牙周炎患者,牙周基础治疗取得良好的治疗效果,患者的牙周临床指标改善,血清hs-CRP水平降低.     

牙周炎症对冠心病患者CRP水平影响的初探

目的通过横向研究初步探讨牙周炎症对冠心病患者CRP水平的影响。方法受检者共60人,包括冠心病＋牙周炎组、单纯牙周炎组和健康对照组,每组20人。检测超敏C反应蛋白（hs—CRP）,牙周临床指标包括牙周探诊深度、附着丧失、出血指数、菌斑指数,并检测血脂水平（HDL、LDL、TG、CHO）和白细胞计数。采用ANOVA法分析以上指标在各组间的差别,Pearson法分析hs—CRP与牙周指标间的相关性。结果牙周炎＋冠心病组hs．CRP显著高于单纯牙周炎组和健康组（P〈0．05）,单纯牙周炎组的hs—CRP水平又显著高于健康组（P〈0．05）。牙周炎＋冠心病组牙周指标均高于单纯牙周炎组和健康组。受检者的血清hs—CRP水平与牙周指数显著相关（P〈0．05）。结论牙周感染和炎症可能是牙周炎＋冠心病患者hs—CRP水平升高的原因之一。     

Release of cytokines by stimulated peripheral blood mononuclear cells in chronic periodontitis

Objective

The emergence of periodontal medicine increased interest in defining the behaviour of peripheral blood cells in periodontitis subjects in comparison with healthy group. The aim of this study was to evaluate the levels of interleukin (IL)-8, tumour necrosis factor-α (TNF-α), IL-6 and IL-10 released by Escherichia coli lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMC) obtained from the peripheral blood of chronic periodontitis subjects.

Design

PBMC samples were isolated from 19 systemically healthy donors, divided into generalized chronic periodontitis (n = 10) and healthy (n = 9) subjects. Cells were incubated for 24–48 h in 500 μL wells containing RPMI 1640 and stimulated with 1.0 ng/mL of E. coli LPS. Supernatants were used to quantify the amounts of IL-8, TNF-α, IL-6 and IL-10 released using enzyme-linked immunosorbent assay (ELISA).

Results

PBMC cells from periodontitis subjects released higher levels of TNF-α and IL-6 than those from healthy subjects (P < 0.05). Conversely, the supernatants of the stimulated PBMC cells obtained from healthy subjects presented higher amounts of IL-8 than those from periodontitis (P < 0.05). No differences were observed in the levels of IL-10 (P > 0.05) between groups.

Conclusion

In conclusion, the results of the present study showed that E. coli LPS-stimulated PBMC from subjects with periodontitis present a different pattern of cytokine release when compared to PBMC from healthy subjects. This phenomenon could have implications locally, in periodontitis, as well as in systemic diseases.     

慢性牙周炎合并冠心病患者牙周基础治疗对细胞因子水平的影响

目的研究牙周基础治疗对重度慢性牙周炎合并冠心病患者牙周临床指标、外周血细胞因子和C反应蛋白水平的影响。方法筛选重度慢性牙周炎合并稳定型冠心病患者32例,采用非手术牙周基础治疗方法,治疗前及治疗后4周测量牙周探诊深度（probingdepth,PD）、附着丧失（attachment loss,AL）和探诊出血指数（bleed—ing压计index,BI）,许采集外周静脉血,采用放射免疫法和免疫比浊分析法分别检测白细胞介索-1β（interleukin-1β,1L-1β）、门细胞介素-2（interleukin-2,IL-2）、白细胞介素-6（interleukin-6,IL-6）、肿瘤坏死因子-α（tumor necrosis fac—for-α,TNF—α）和C反应蛋白（C—reactive pmtein,CRP）含量。结果牙周基础治疗4周后,PD由（5．35±0．97）mm减至（2.72±0．65）mm,AL由（5．83±1．12）mm减至（3．24±0．79）mm,BI由3．45±0．83降至0．80±0．77,差砰均有统计学意义（P〈0．05）。外周血IL-1β、IL-2和IL-6水平均有所下降,TNF—α及CRP水平均数略有升高,其中IL-1β由（0．184±0．045）ng/mL降至（0．145±0．039）ng／mL,TNF—α由（1．082±0．206）ng/mL升高至（1．182±0．154）ng/mL,治疗前后IL-1β及TNF-α水平的差异有统计学意义（P〈0．05）.结论 重度慢性牙周炎合并冠心病的患者,牙周基础治疗可显著改善牙周临床指标,降低外周血IL-1β水平,升高TNF-α水平,     

延续性口腔健康教育在双波长激光治疗老年慢性牙周炎患者中的效果评价

目的 探讨对双波长激光治疗的老年慢性牙周炎患者应用延续性口腔健康教育的临床效果。方法 选择2016年3月—2018年3月接受双波长激光治疗的150例老年慢性牙周炎患者,随机分为2组。将75例应用常规诊间口腔卫生宣教的患者设为对照组,75例应用延续性口腔健康教育的患者设为实验组。采用SPSS21.0软件包对所得数据进行统计学分析,比较2组的口腔行为、牙龈指数、菌斑指数变化。结果 实验组正确刷牙、定期口腔检查与维护、口腔良好习惯所占比例分别为97.33%、93.33%、92.00%,均显著高于对照组（P<0.05）;实验组干预3个月和6个月后,牙龈指数和菌斑指数分别为1.24±0.14、1.08±0.10和1.50±0.10、1.69±0.26,均显著低于对照组（P<0.05）。结论 对双波长激光治疗的老年慢性牙周炎患者应用延续性口腔健康教育,可改善其口腔行为和牙周状况,值得推广应用。     

牙周炎和慢性阻塞性肺疾病动物模型的建立及其相关性分析

目的 应用SD大鼠建立慢性牙周炎(chronic periodontitis,CP)和慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)动物模型,探讨CP和COPD的相关机制.方法 将40只SD大鼠按随机数字法分为4组:A组:正常对照组;B组:CP组;C组:COPD组;D组:CP+COPD组,每组10只.各组按实验设计施加相应建模因素,于实验10周末处死动物.分别检查各组大鼠的牙周指标及肺功能状况,并观察牙周和肺部的组织病理学改变,酶联免疫吸附法检测血清中肿瘤坏死因子(TNF)-α水平,并行统计学分析.结果 A、C组出血指数分别为(0.25±0.04)、(1.30±0.25),附着丧失分别为(0.43±0.02)、(0.51±0.02)mm,与A、C组相比,B、D组大鼠的出血指数[分别为(3.85±0.34)、(4.01±0.44)]、附着丧失[分别为(0.90±0.27)、(0.98±0.18)mm]均明显升高(P＜0.05);与A组0.2 s末用力呼气量与用力肺活最比值(forced expiratory volume in 0.2 second toforced vital capital ratio,FEV0. 2/FVC值)(65.34±2.63)相比,B、C、D组大鼠FEV0 2/FVC值[分别为(57.49±6.77)、(58.10±2.40)、(49.53±2.86)]明显降低,表明动物模型建造成功.其中D组肺功能与病理学改变均较C组更大,各实验组与正常对照组TNF-α比较差异均有统计学意义(P＜0.05),D组TNF-α含量[(23.422±2.815)μg/L]升高最为明显.结论 在CP和COPD相关关系大鼠动物模型中,CP可能对COPD具有促进和诱发作用.     

慢性牙周炎合并慢性阻塞性肺疾病患者牙龈卟啉单胞菌rag位点基因分析

目的:分析不同rag基因型牙龈卟啉单胞菌在慢性牙周炎合并慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者中的分布状况.方法:选择慢性牙周炎及合并COPD的慢性牙周炎患者各30例,收集唾液样本,采用16S rDNA聚合酶链反应(PCR)法检测牙龈卟啉单胞菌的检出...     

不同程度慢性牙周炎患者病情的二年自然进展

目的　观察不同程度慢性牙周炎的自然进展规律。方法　纵向观察 16 9例轻、中、重度慢性牙周炎患者在 2年中的疾病自然进展 ,检查除第三磨牙外的全口牙 ,每颗牙 6个位点 ,以探诊深度、附着丧失为指标 ,两次检查之间附着丧失加重≥ 3mm的牙位定为活动性进展。结果　活动性发生率依基线时疾病的轻、中、重程度而逐渐增高 ,按位点活动性的发生率分别为 0 14 %、0 39%及0 73% ,按个体活动性的发生率分别为 15 5 6 %、2 9 89%及 4 3 2 4 % ,差异有统计学意义。结论　重度牙周炎患者是牙周破坏活动性进展的高危人群。     

Quantification of tryptase-TIM-3 double-positive mast cells in human chronic periodontitis

ObjectivesMast cells (MCs) are implicated in the pathogenesis of allergic reactions and inflammatory conditions through the release of inflammatory mediators. So far limited attention has been given to the role of MCs in periodontitis. T cell immunoglobulin mucin domain (TIM)-3 is an immunomodulatory molecule and influences MC function. However, whether TIM-3 is expressed on MCs in the process of human periodontal disease has not been reported. Therefore, we identified MCs by toluidine blue staining and examined the expression of TIM-3 on tryptase-positive MCs in different severities of human chronic periodontitis using double-immunofluorescence staining in this study.Material and methodsA total of 83 human periodontal specimens were involved in this study, including healthy control tissues (n = 25), chronic moderate periodontitis (n = 28), and chronic severe periodontitis (n = 30). The gingival specimens were fixed in 10% buffered formalin, stained with haematoxylin and eosin for histopathology, with toluidine blue for MCs, and with double-immunofluorescence for identification of tryptase-TIM-3 double-positive MCs in gingival tissues.ResultsCompared with healthy controls, the score of gingival tissue inflammation was significantly increased in the chronic moderate periodontitis (P = 0.013) and chronic severe periodontitis (P < 0.0001), and the densities (cells/mm²) of tryptase-TIM-3 double-positive MCs were significantly increased in both the chronic moderate (P = 0.011) and severe periodontitis groups (P < 0.0001). However, compared with the chronic moderate periodontitis group, both the score of gingival tissue inflammation (P = 0.012) and the density of tryptase-TIM-3 double-positive MCs (P = 0.011) in gingival tissue were significantly increased in the severe periodontitis groups.ConclusionSignificantly increased number of tryptase-TIM-3 double-positive MCs had the similar tendency as the severity of periodontitis inflammation in human chronic periodontitis. Our data suggest that TIM-3 may have a role on MCs in human chronic periodontitis.     

中、重度牙周炎与冠心病患者C反应蛋白及血脂水平的比较

目的 研究汉族人群中、重度牙周炎与冠心病的相关性并初步探讨C反应蛋白在二者相关性中的可能作用.方法 检测和分析40名健康者(健康组)、40例中、重度牙周炎患者(牙周炎组)、28例冠状动脉粥样硬化性心脏病(简称冠心病)患者(冠心病组)及47例同时患冠心病及中、重度牙周炎的患者(冠心病+牙周炎组)血清C反应蛋白水平、血脂水平(血清低密度脂蛋白、高密度脂蛋白胆固醇、总胆固醇和甘油三酯)和牙周临床指数(附着丧失、探诊深度和探诊出血).结果 单因素方差分析结果显示,健康组、牙周炎组、冠心病组及牙周炎+冠心病组的血清C反应蛋白水平分别为(1.30±0.15)、(2.44±0.18)、(5.99±0.82)和(6.88±0.71)mg/L,各组血清C反应蛋白水平间的差异具有统计学意义(P<0.001),且经协方差分析校正年龄、受教育状况、血压和体重指数后显示,各组血清C反应蛋白水平间的差异仍具有统计学意义(P<0.001).多元Logistic回归分析结果显示,中、重度牙周炎患者发生冠心病的可能性高于牙周健康者,其发生冠心病的相对风险率比值比为2.417(P=0.039;95%CI:1.126～6.659).经协方差分析校正年龄、受教育状况、血压和体重指数后,各组血清总胆固醇水平间差异仍具有统计学意义(P=0.017).结论 严重的牙周感染可能通过改变血清C反应蛋自水平继而影响全身炎症反应和冠心病的发生及发展,可能是冠心病事件的危险因素之一.     

Oxidative damage of rat liver induced by ligature-induced periodontitis and chronic ethanol consumption

Objective

Oxidative stress plays a central role in the initiation and progression of liver disease. Chronic ethanol consumption induces oxidative damage of the liver. Using a rat model, we previously showed that chronic administration of lipopolysaccharide and proteases to gingival sulcus induced both periodontal inflammation and liver injury. Periodontitis and ethanol consumption may have an additional effect on hepatic oxidative damage. The present study investigated the effects of periodontitis on ethanol-induced oxidative damage of the liver using a rat model.

Design

Male Wistar rats were divided into four groups (six rats/group). During the experimental period of eight weeks, two groups were fed an ethanol-containing liquid diet, and two groups were on a pair-fed control diet. Four weeks prior to the end of the experimental period, one group from each dietary treatment was ligated to induce periodontitis, while the other group was left unligated. In order to evaluate hepatic oxidative damage, the level of hexanoyl-lysine and the ratio of reduced form glutathione/oxidized form glutathione (GSH/GSSG) was determined. The concentration of blood hexanoyl-lysine was also measured as an index of circulating lipid peroxide.

Results

Ligature-induced periodontitis increased plasma levels of hexanoyl-lysine. In the liver, periodontitis decreased the GSH/GSSG ratio, and the combination of periodontitis and ethanol consumption induced a significant increase in hexanoyl-lysine level compared to ethanol consumption alone.

Conclusion

In the rat model, ligature-induced periodontitis increased plasma lipid peroxide, decreased the hepatic GSH/GSSG ratio and augmented ethanol-induced lipid peroxidation in the liver.     

Identification of periodontal pathogens and severity of periodontitis in patients with and without chronic kidney disease

Objective

In this study of patients with chronic periodontitis (CP), the severity of the disease and the main periodontal pathogens identified in patients with chronic kidney disease (CKD) were compared with those detected in individuals without systemic disease.

Design

Nineteen patients with CP without evidence of systemic disease (control group), 25 patients with CP and CKD who were in the pre-dialysis stages (pre-dialysis group), and 22 patients with CP and CKD who were on renal replacement therapy (RRT group) were examined. The severity of CP was based on the investigation of probing depth (PD) and clinical attachment level (CAL). The definition and stage of CKD were based on the criteria proposed by the Kidney Disease Outcomes Quality Initiative of the National Kidney Foundation. Glomerular filtration rate (GFR) was estimated using the equation of Modification of Diet in Renal Disease and the identification of microorganisms in subgingival plaque was performed using polymerase chain reaction (PCR).

Results

Candida albicans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola were more common in patients who were on RRT and pre-dialysis than in control subjects. CP was more severe in patients with CKD. A strong association was observed between the frequency of C. albicans (P = 0.056), P.gingivalis (P = 0.008), T. denticola (P = 0.013) and CAL, when CKD patients were compared with the control group.

Conclusion

CP is more severe and is associated with increased frequency of C. albicans, P. gingivalis, T. forsythia, and T. denticola in patients with CKD.     

Association between periodontitis and chronic obstructive pulmonary disease in a chinese population

Background: A relationship between periodontitis and chronic respiratory disease has been suggested by recent studies. The aim of this study is to explore the association between periodontitis and chronic obstructive pulmonary disease (COPD) in a Chinese population. Methods: We conducted a case-control study of 581 COPD cases and 438 non-COPD controls. Lung function examination, a 6-minute walk test, and the British Medical Research Council questionnaire were performed. Periodontal clinical examination index included probing depth (PD), attachment loss (AL), bleeding index (BI), plaque index (PI), and alveolar bone loss. A validated index for predicting COPD prognosis, the body mass index, airflow obstruction, dyspnea, and exercise capacity (BODE) index, was also calculated. Results: Participants with more severe COPD were more likely to have severe periodontal disease. PD, AL, PI, alveolar bone loss, and the number of teeth were significantly associated with all stages of COPD (all P <0.001). When compared to controls (BODE = 0), participants with higher BODE scores had significantly higher AL (P <0.001), BI (P = 0.027), PI (P <0.001), alveolar bone loss (P <0.001), and the number of teeth (P <0.001). PI appeared to be the main periodontal health-related factor for COPD, with an odds ratio (OR) = 9.01 (95% CI = 3.98 to 20.4) in the entire study population OR = 8.28 (95% CI = 2.36 to 29.0), OR = 5.89 (95% CI = 2.64 to 13.1), and OR = 2.46 (95% CI = 1.47 to 4.10) for current, smokers, and non-smokers, respectively. Conclusion: Our study found a strong association between periodontitis and COPD, and PI seemed to be a major periodontal factor for predicting COPD among Chinese adults.     

牙周炎及胃病患者牙菌斑中的幽门螺杆菌

目的 明确牙周炎及胃病患者的牙菌斑中是否存在幽门螺杆菌（Ｈｐ）及Ｈｐ是否为细胞毒素相关基因Ａ阳性。方法 利用尿素酶Ｃ基因和ｃａｇＡ设计引物,通过聚合酶链反应（ＰＣＲ）检测口腔中的Ｈｐ。选择１３例胃病及１０例牙周炎患者,每例患者选６个有牙龈炎症的牙位取龈上、龈下菌斑,共计２７６份样本用于ＰＣＲ检测。结果 胃病组１１例患者和牙周炎组全部病例均少有１份菌斑样本检出Ｈｐ,其中尿素酶Ｃ基因在胃病组的阳性率为     

Periodontal therapy reduces arginase activity in saliva of patients with chronic periodontitis

This present study evaluated the salivary arginase activity (SAA) in patients with chronic periodontitis and the effect of periodontal therapy on the activity of such enzyme. Thirty-six patients (mean age, 45.97 ± 14.52), 18 chronic periodontitis subjects (test group), and 18 periodontally healthy individuals (control group) participated in the study. Clinical periodontal examinations included measurements of probing pocket depth (PD), clinical attachment level (CAL), plaque (PI), and gingival (GI) indexes. The test group received periodontal therapy according to individual needs. The saliva sample was collected from all study population at baseline (both groups) and 30 days after periodontal therapy (test group). SAA was determined by measuring the l-ornithine formation from l-arginine and was expressed as mU/ml. The results showed that the mean values of SAA were statistically different between control and test groups. SAA was about 2.5 times higher in test than control groups. Thirty days after periodontal therapy, enzyme levels were 1.56 times lower than before periodontal therapy. We concluded that SAA is increased in chronic periodontitis subjects when compared to periodontally healthy individuals and that periodontal therapy significantly reduced SAA levels. It was suggested that in the near future, SAA may be used as a salivary marker of periodontal status.     

慢性牙周炎患者龈沟液中有机酸的分析研究

目的研究慢性牙周炎患者龈沟液中有机酸的种类,分析其与牙周组织炎症状况间的关系。方法应用毛细管电泳技术检测37例慢性牙周炎患者和16名牙周健康者龈沟液中的有机酸成分;比较分析慢性牙周炎患者不同探诊深度(probingdepth,PD)的龈沟液中有机酸成分。结果慢性牙周炎患者龈沟液中琥珀酸、丁酸和戊酸的检出率及检出浓度均显著高于牙周健康对照组,差异有统计学意义(P<0.05);丙酸在两组间的检出率差异无统计学意义,但在炎症组中的检出浓度明显高于对照组(P<0.05);琥珀酸、丙酸与丁酸在炎症组A组(PD=4mm)与B组(4mm6mm)龈沟液中的差异有统计学意义(P<0.05)。结论龈沟液中琥珀酸、丙酸、丁酸和戊酸与慢性牙周炎的关系较为密切,其中琥珀酸、丙酸和丁酸的表达与牙周袋深度相关。     

Serum leveis of inflammatory markers in type 2 diabetes patients with chronic periodontitis

Diabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear.

Objective

This study aimed to evaluate serum leveis of inflammatory markers, IL-8, IL-6 and monocyte chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis.

Material and Methods

Forty two individuals were enrolled in this study and assigned to one of five groups: diabetes mellitus with inadequate glycemic control and periodontitis (DMI+P, n = 10), diabetes mellitus with adequate glycemic control and periodontitis (DMA+P, n = 10), diabetes mellitus without periodontitis (DM, n = 10), periodontitis without diabetes (P, n=6), and neither diabetes nor periodontitis (H, n = 6). Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbAlc). Inflammatory serum markers IL-8, IL-6 and (MCP-1) were measured by ELISA.

Results

DMI+P and DMA+P groups presented higher PD (p=0.025) and AL (p=0.003) values when compared to the P group. There were no significant differences among groups for IL-6, IL-8 and MCP-1 serum levels.

Conclusions

Although periodontitis was more severe in diabetic patients, the serum levels of the investigated inflammatory markers did not differ among the groups.