Hyperlipidemia in patients with periodontitis

BACKGROUND: Periodontitis is a bacterial infection, which has been classified as a local chronic inflammation. This, as well as cardiovascular disease, may share common risk factors such as smoking, diabetes, behavioral factors, aging, and male gender. The aim of this study was to evaluate the association between hyperlipidemia and periodontitis. MATERIALS AND METHODS: The levels of plasma lipids in 40 subjects with periodontitis (CPITN score III or IV, pocket depth 4 mm) with mean age 32.3 +/-1.2 years were measured and compared with those obtained from 40 age and sex matched controls. Both groups were systemically healthy according to their medical history. RESULTS: Total cholesterol (CHL) and triglycerides (TG) were significantly higher in the case group (P=0.045 and P=0.016, respectively). HDL and LDL cholesterols were higher in patients but did not have any significant differences with controls. The frequency of persons with pathologic values of TG and CHL were significantly higher in cases compared with controls. CONCLUSIONS: These results showed hyperlipidemia may be associated with periodontitis in healthy people. However, it is unclear whether periodontitis causes an increase in levels of serum lipids or hyperlipidemia is a risk factor for both periodontitis and cardiovascular disease.     

Periodontal infections contribute to elevated systemic C-reactive protein level

BACKGROUND: Periodontitis is a local inflammatory process mediating destruction of periodontal tissues triggered by bacterial insult. However, this disease is also characterized by systemic inflammatory host responses that may contribute, in part, to the recently reported higher risk for cardiovascular disease (CVD) among patients with periodontitis. Moderate elevation of C-reactive protein (CRP) has been found to be a predictor of increased risk for CVD. Elevated CRP levels in periodontal patients have been reported by several groups. In this study, we examined whether CRP plasma levels are increased in periodontitis and if there is a relation to severity of periodontal disease and to the periodontal microflora. METHODS: CRP serum levels were assessed using radial immunodiffusion assay in 174 subjects, 59 with moderate mean clinical attachment loss (AL) (2.39+/-0.29 mm) and 50 with high AL (3.79+/-0.86 mm) as compared to 65 periodontally healthy controls (AL, 1.74+/-0.18 mm). Clinical attachment loss, probing depths, and percentage of periodontal pocket sites > or =5 mm were measured. The presence of periodontal pathogens Porphyromonas gingivalis (P.g.), Prevotella intermedia (P.i.), Campylobacter recta (C.r.), and Bacteroides forsythus (B.f.) in subgingival plaque samples was measured by immunofluorescence microscopy. RESULTS: Statistically significant increases in CRP levels were observed in subjects with periodontal disease when compared to healthy controls (P= 0.036). Subjects with high levels of mean clinical attachment loss had significantly higher mean CRP levels (4.06+/-5.55 mg/l) than controls (1.70+/-1.91 mg/l), P= 0.011. The CRP levels were adjusted for factors known to be associated with elevated CRP, including age, smoking, body mass index (BMI), triglycerides, and cholesterol. Age and BMI were found to be significant covariates. The reported range for CRP as a risk factor for CVD, peripheral vascular diseases, or stroke is 1.34 mg/l to 6.45 mg/l and the mean of this range is 3 mg/l. The percentage of subjects with elevated levels of CRP > or = 3 mm was significantly higher in the high clinical AL group (38%; 95% Cl: 26.7%, 49.3%) when compared to the control group (16.9%; 95% CI: 9.25%, 24.5%), P= 0.011. The presence of periodontal pathogens P.g., P.i., C.r., and B.f. in subgingival samples was positively associated with elevated CRP levels (P= 0.029). CONCLUSIONS: The extent of increase in CRP levels in periodontitis patients depends on the severity of the disease after adjusting for age, smoking, body mass index, triglycerides, and cholesterol. Also, there are elevated levels of CRP associated with infection with subgingival organisms often associated with periodontal disease, including P.g., P.i., C.r., and B.f. Recent investigations emphasized the role of moderate elevated CRP plasma levels as a risk factor for CVD. The positive correlation between CRP and periodontal disease might be a possible underlying pathway in the association between periodontal disease and the observed higher risk for CVD in these patients.     

Risk factors for atherosclerosis in cases with severe periodontitis

Aim: Studies have reported on an association between cardiovascular disease (CVD) and periodontitis. The purpose of this case–control study was to provide an insight into this association by determining the plasma levels of some risk markers for CVD in cases with periodontitis.
Materials and Methods: Sixty-eight cases with periodontitis, mean age 53.9 (SD 7.9) years, and 48 randomly selected healthy controls, mean age 53.1 (SD 7.9) years, were investigated. Fasting blood plasma was analysed for glucose, lipids, markers systemic inflammation, cytokines and antibodies against heat shock proteins (Hsp). The associations between periodontitis and the various substances analysed in plasma were calculated using a multivariate logistic regression model, which compensated for age, gender, smoking and body mass index.
Results: The regression analyses revealed a significant association between periodontitis and high levels of C-reactive protein (CRP) [odds ratio (OR) 4.0, confidence interval (CI) 1.4–11.4] and fibrinogen (OR 8.7, CI 2.6–28.4), IL-18 (OR 6.5, CI 2.2–19.5), and decreased levels of IL-4 (OR 0.12, CI 0.0–0.5). The study showed increased levels of antibodies against Hsp65 (OR 2.8, CI 1–7.6) and 70 (OR 2.9, CI 1.1–7.8) and decreased levels of antibodies against Hsp60 (OR 0.3, CI 0.1–0.8).
Conclusions: Periodontitis was associated with increased levels of CRP, glucose, fibrinogen and IL-18, and with decreased levels of IL-4.     

Compromised GCF total antioxidant capacity in periodontitis: cause or effect?

BACKGROUND: Oxidative stress is implicated in the pathogenesis of periodontitis. The total antioxidant capacity (TAOC) of gingival crevicular fluid volume (GCF) and plasma appears compromised in periodontitis, but it is unclear whether this predisposes to, or results from the inflammatory process. AIM: To investigate longitudinal changes in GCF and plasma TAOC following reductions in periodontal inflammation with successful non-surgical therapy. MATERIALS AND METHODS: Two longitudinal studies were run in series on non-smokers with chronic periodontitis (CP). Study-1 (n=17) assessed index sites with mild disease; Study-2 (n=18) investigated deep sites. GCF sampling and clinical measures were performed at baseline and 3 months post-therapy. Plasma and GCF TAOC was determined by enhanced chemiluminescence and 32 age/sex-matched periodontally healthy controls were used. RESULTS: Therapy improved clinical outcomes consistent with the literature. There were no differences in plasma TAOC between periodontitis patients (507+/-92 microMTeq) and controls (520+/-100 microMTeq; p=0.57) at baseline, but GCF TAOC was lower (p<0.0001) in CP patients (680+/-371 microMTeq) than controls (1129+/-722 microMTeq). Successful periodontal therapy did not alter plasma TAOC (p=0.56), but GCF TAOC increased (by 449+/-722 microMTeq, p<0.001) to control subject levels (p=0.47) CONCLUSIONS: Local total antioxidant capacity in CP appears to reflect increased oxygen radical activity during periodontal inflammation and can be restored to control subject levels by successful non-surgical therapy.     

"益肾清火"方对大鼠牙周炎症和免疫功能的影响

目的观察中药“益肾清火”方对大鼠牙周炎症和免疫功能的影响。方法选择12个月龄SD大鼠,分为A、B、C、D共4组。A组为空白对照组,B组为牙周炎造模组,C组为造模后灌服中药高剂量组,D组为造模后灌服中药等效剂量组。牙周炎造模成功后,A、B组动物灌喂生理盐水,C、D组动物灌喂中药3个月。分别采用脱钙骨切片、流式细胞术及ELISA法测定用药前后动物牙周组织、外周血中T细胞的分类及比值、IL-2和IL-1β水平的变化,并采用SAS6.04软件包对数据进行单因素方差分析。结果牙周炎大鼠灌服“益肾清火”方3个月后,与B组相比,C、D组的牙周组织炎症明显改善;各组外周血中CD4 T/CD8 T的比值分别为3.55±0.94、2.42±0.75、3.23±1.14和3.29±0.83,B组比其余3组低(P<0.05);IL-2与IL-1β分别为(36.03±2.63/179.04±17.29)pg/ml、(25.18±3.08/306.09±13.38)pg/ml、(38.44±2.58/176.33±45.38)pg/ml和(36.81±2.45/182.13±43.97)pg/ml。与其余3组相比,B组IL-2水平显著下降,IL-1β显著升高(P<0.01),但以上指标在两用药组之间无显著差别(P>0.05)。结论中药“益肾清火”方能改善实验性牙周炎动物的牙周炎症,对动物机体免疫有一定的调节作用。     

Periodontitis is characterized by elevated PAI-1 activity

OBJECTIVES: Periodontitis is a chronic infectious disease and has been associated with cardiovascular diseases (CVD). We investigated whether plasma levels of markers of a prothrombotic state were elevated in patients with periodontitis in comparison with healthy controls. MATERIALS AND METHODS: Untreated patients with moderate (n=53) and severe periodontitis (n=38) and healthy controls (n=39) were recruited. Levels of von Willebrand factor (vWF), prothrombin fragment 1+2 (F1+2), plasminogen activator inhibitor-1 (PAI-1) activity and D-dimer were measured as markers of a prothrombotic state. RESULTS: The erythrocyte sedimentation rate (ESR), plasma C-reactive protein (CRP) and leucocyte counts (WBC) were significantly higher in patients with periodontitis. No statistically significant difference was found among the three groups for vWF (p=0.264), F1+2 (p=0.295) and D-dimer (p=0.572). However, PAI-1 was clearly elevated in the severe periodontitis group (p=0.001), even after adjusting for potential confounding factors (p(adj)=0.004). Moreover, more patients than controls were having vWF and PAI-1 levels above the respective population medians. CONCLUSIONS: In periodontitis, elevated levels of PAI-1 activity are observed compared with healthy controls. This may increase the potential for impaired fibrinolysis, a condition that results in a prothrombotic state. We suggest that this state, if left untreated, may contribute to an increased risk for CVD.     

Matrix metalloproteinase-2 may be involved with increased bone loss associated with experimental periodontitis and smoking: a study in rats

BACKGROUND: Smoking has been associated with periodontitis severity and is considered a risk factor for its development. It has been reported that matrix metalloproteinase (MMP) produced by host cells plays a major role in periodontal tissue destruction. Thus, the present study tested, in rats, the hypothesis that local increased levels of MMP-2 would be associated with the enhanced periodontitis-related bone loss after intermittent cigarette smoke inhalation (CSI). METHODS: Twenty-seven adult male Wistar rats were used. A ligature was placed around one of the mandibular first molars of each animal and they were randomly assigned to the following control (N = 13) or CSI (N = 14) group. Sixty days later, the animals were sacrificed, the gingival tissues harvested, and the specimens processed for decalcified sections. Extracts from the gingival tissues were prepared and assayed for MMP-2 expression. RESULTS: Intergroup comparisons (unligated sites) showed that CSI might directly affect alveolar bone (0.16 +/- 0.03 mm2 versus 0.24 +/- 0.09 mm2 for non-smokers and smokers, respectively; P = 0.001). Moreover, CSI significantly enhanced bone loss resulting from experimental periodontitis (0.64 +/- 0.36 mm2 versus 1.50 +/- 0.50 mm2 for non-smokers and smokers, respectively; P<0.05). In addition, zymography demonstrated that CSI also enhanced both MMP-2 levels and activity in the gingival tissues around ligated teeth. CONCLUSION: Within the limits of the present investigation, it can be assumed that the effect of CSI on MMP-2 levels and activity may account for the increased periodontitis progression rate observed in smokers.     

Correlation between levels of fibrinogen, beta455 g/A fibrinogen gene polymorphism and chronic periodontitis]

OBJECTIVE: To investigate the relationship between plasma levels of fibrinogen, the-beta455 G/A fibrinogen gene polymorphism and the severity of periodontal inflammation and to explore the possible role of fibrinogen in the association of periodontitis with coronary heart disease (CHD). METHODS: A total of 121 patients with moderate to severe periodontitis and periodontally healthy and gingivitis controls were enrolled in the study. Peripheral blood samples were collected and the plasma fibrinogen levels were determined by the clotting method of Clauss. Polymerase chain reaction and restriction fragment length polymorphism analysis with Hae III were used to examine the -beta455 G/A fibrinogen gene polymorphism. RESULTS: Fibrinogen levels were significantly higher in moderately or severely chronic periodontitis patients [(3.45 +/- 0.68) g/L] than periodontally healthy and gingivitis controls [(2.47 +/- 0.42) g/L, P < 0.001]. The carrier status of the A allele at position -455 in the beta fibrinogen gene was associated with elevated fibrinogen levels and the frequency of the-A455 allele in the beta fibrinogen gene in the patient group was significantly higher than in the control group (P = 0.032). Carriers of the -A455 allele were about 3-fold more likely to have moderate or severe periodontitis as compare to individuals without the -A455 allele( OR = 3. =135, P= 0.008). CONCLUSIONS: Fg-beta455 G/A polymorphism may contribute to the elevated plasma fibrinogen levels and put individuals at higher risk of having severe periodontitis. As the independent risk factor of CHD, fibrinogen levels and Fg-beta455 G/A polymorphism may play a role in the pathogenesis of periodontitis.     

Gingival crevicular fluid inflammatory mediators and bacteriology of gingivitis in nonhuman primates related to susceptibility to periodontitis

The hypothesis to be tested was that the microbiota and resulting local host inflammatory response characteristics in oral conditions of high levels of chronic gingival inflammation increases susceptibility to progressing periodontitis. This study used cynomolgus monkeys, Macaca fascicularis (nonhuman primates), with high and low levels of long-standing gingival inflammation to define the profiles of gingival crevicular fluid mediators, cytokines and immunoglobulins; describe the subgingival microbiota; and evaluate their susceptibility to ligature-induced periodontitis. Sixteen nonhuman primates were stratified into two groups (HI, LO) based upon Bleeding Index as a measure of the natural level of inflammation (HI = 1.26 +/- 0.45; LO = 0.22 +/- 0.16). The host mediator levels, subgingival microbiota, and clinical characteristics of the LO and HI groups were compared after 30 days of oral hygiene, during a 30 day experimental gingivitis (7, 14, and 30 days), and during periodontitis (30, 60, and 90 days). The results demonstrated that nonhuman primates with high levels of long-standing gingival inflammation when compared to those nonhuman primates with low inflammation show: 1) different inflammatory mediator profiles in gingival crevicular fluid (particularly for immunoglobulin A (IgA) and IgG levels), 2) a different quantitative and qualitative subgingival microbiota; and 3) a similar progression of periodontitis. Thus, while variations in host inflammatory responses to local factors exist in the nonhuman primates, an extensive subgingival challenge (such as ligation) may negate these individual differences.     

Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study

BACKGROUND AND AIM: A cluster of metabolic factors defines a syndrome that predisposes to diabetes and cardiovascular disease. Chronic infections such as periodontitis might alter these individual metabolic factors and the systemic inflammatory burden. The aim of this study was to investigate the association between severe periodontitis and increase in inflammatory and metabolic risk factors for cardiovascular disease. MATERIALS AND METHODS: We examined 302 patients with severe periodontitis and 183 healthy controls, and we collected a blood sample from each subject in order to investigate differences in inflammatory (leukocyte numbers and differential counts) and metabolic markers (lipids and glucose). RESULTS: After correcting for differences in age, gender, smoking and ethnicity, periodontitis subjects exhibited a low-grade systemic inflammation (increased white cell counts, 1.10+/-1.02 x 10(9)/l, 95%CI 1.05-1.15, p=0.0001), dyslipidemia [lower high-density lipoprotein cholesterol, 1.14+/-1.03 mmol/l, 95%CI 1.08-1.20, p<0.0001 and higher low-density lipoprotein cholesterol, 1.12+/-1.03, 95%CI 1.05-1.19, p<0.0001) and increased non-fasting serum glucose levels (1.04+/-1.01 mmol/l, 95%CI 1.02-1.06, p=0.01) when compared with controls. The associations were confirmed in a subpopulation of Caucasian non-smokers. A trend for a dose dependent effect of the number of periodontal pockets on the tested inflammatory and metabolic markers was observed. Conclusions: These data suggest a possible link between severe generalized periodontitis, systemic inflammation and a dysmetabolic state in otherwise healthy individuals.     

Periodontitis as a Novel Contributor of Adipose Tissue Inflammation Promotes Insulin Resistance in a Rat Model

Background: Recent studies have indicated that the chronic low‐grade inflammation induced by periodontitis is related to obesity and type 2 diabetes mellitus. The purpose of this study is to investigate the effects of periodontitis on obesity‐related adipose tissue inflammation and subsequent systemic insulin resistance in a rat model. Methods: Thirty‐two rats were divided into four groups of eight: 1) obese rats with periodontitis (combination group); 2) obese rats without periodontitis (obesity group); 3) normal rats with periodontitis (periodontitis group); and 4) normal rats without periodontitis (control group). Monosodium glutamate was used to induce obesity during the early postnatal period. Periodontitis was induced by ligatures for 8 weeks. Morphologic features of white adipose tissue (WAT) and islets were observed, and fasting plasma glucose and insulin concentrations and homeostasis model assessment for insulin (HOMA‐IR) were measured at 5 months. Differences among groups were compared with the Fisher post hoc least significant difference test. Results: A slight increase of stromal vascular fractions (SVFs) and macrophage infiltration in the WAT of the periodontitis group was observed. Significant proliferation of SVFs and macrophage infiltration were induced in the combination group. HOMA‐IR scores in the combination and periodontitis groups were higher than in the obesity and control groups, respectively. The disturbance of islet architecture was consistent with a high HOMA‐IR score in the combination group. Conclusions: Periodontitis induced initial stages of WAT inflammation and acted as a contributing factor to exacerbate proinflammatory phenotype of WAT and promote the development of insulin resistance in the obese rat model.     

Histological characteristics associated with suppurating periodontal pockets

The purpose of this study was to characterize histologically the gingival lesion associated with suppuration in advanced periodontitis. Thirty-three bleeding, suppurating (S) and 23 bleeding, nonsuppurating (NS) interproximal biopsies were obtained from nine patients and processed for light microscopy. Pocket depths (mean +/- SD) were 6.7 +/- 1.6 mm (S) and 5.4 +/- 2.2 mm (NS). Six-micron serial sections were stained with (1) hematoxylin/eosin and (2) van Gieson. Quantitative cell types were determined by a grid intersection counting technique at x 1000. Volumetric analysis of collagen-poor (inflammation) areas was conducted using a computer biometric system that revealed three histologic patterns: Type I sites showed mild to moderate inflammation (less than 50% infiltrate, S = 15, NS = 20); Type II sites showed intense inflammation (greater than 50% infiltrate, S = 17, NS = 3); and only one (S) site had a large connective tissue abscess (Type III). The mean percentage of collagen-poor area was significantly larger in suppurating (42.1 +/- 25.5%) versus nonsuppurating (27.7 +/- 20.4%) sites (P = 0.02). In both S and NS sites, plasma cells (means = 66%) and lymphocytes (means = 27%) predominated in the inflammatory infiltrates. Histologically, suppuration appeared to be associated with increased gingival inflammation and a slight increase in connective tissue neutrophils.     

Low- and high-yield cigarette smoke inhalation potentiates bone loss during ligature-induced periodontitis

BACKGROUND: It is well recognized that cigarette consumption is a strong risk factor for periodontitis. Tobacco companies have developed a cigarette with low levels of toxic compounds; however, its effect on periodontium has not been investigated. The aim of this study was to verify the impact of smoke produced by low- and high-yield cigarettes on bone loss resulting from ligature-induced periodontitis. METHODS: A total of 36 male Wistar rats were used in the study. A ligature was placed around one of the mandibular first molars (ligated teeth) of each animal, and they were assigned randomly to one of three groups: group 1: control (N = 10), group 2: 30 days' inhalation of smoke produced by high-yield cigarettes (N = 13), and group 3: 30 days' inhalation of smoke produced by low-yield cigarettes (N = 13). The animals were sacrificed 30 days after ligature placement, and the specimens were processed for decalcified sections. RESULTS: Intergroup analysis of unligated teeth (without periodontal disease) did not show a significant difference regarding periodontal ligament area (2.40 +/- 0.5 mm(2), 2.72 +/- 0.7 mm(2), and 2.61 +/- 0.4 mm(2) for groups 1, 2, and 3, respectively; P >0.05). Conversely, significant differences were noted in ligated teeth (with periodontitis); bone loss was directly proportional to the level of toxic compounds in the cigarettes (5.74 +/- 0.5 mm(2), 7.40 +/- 0.50 mm(2), and 6.51 +/- 0.50 mm(2) for groups 1, 2, and 3, respectively; P <0.05). CONCLUSION: Low- and high-yield cigarettes potentiated bone loss during experimental periodontitis in a directly proportional fashion.     

Periodontitis and risk for atherosclerosis: an update on intervention trials

Aims: Periodontitis has been associated with an increased risk of cardiovascular events. The nature of the association is unclear because both periodontitis and cardiovascular disease (CVD) share a host of risk factors. Intervention trials are critical to explore the relationship. If the association were causal, successful periodontal therapy will lead to an attenuation of the effect – CVD.
Material and Methods: The paper reviewed the design and the results of intervention trials aimed at improving systemic inflammation, endothelial dysfunction, carotid atherosclerosis and cardiovascular events.
Results: Early systematic reviews and a definitive controlled clinical trial indicate that intensive periodontal therapy results in a decrease in systemic inflammation and an improvement of endothelial dysfunction in systemically healthy subjects. A pilot trial has indicated the feasibility to assess the impact of periodontal therapy on carotid atherosclerosis in a primary cardiac prevention design.
Conclusions: Efforts to test causality in the relationship between periodontitis and CVD are ongoing. Evidence to date is consistent with the notion that severe generalized periodontitis causes systemic inflammation and endothelial dysfunction. Periodontitis has effects that go beyond the oral cavity and its treatment and prevention may contribute to the prevention of atherosclerosis.     

冠心病伴牙周炎病人血清中Lp-PLA2的研究

目的:通过观察冠心病伴中重度牙周炎、单纯冠心病、单纯中重度牙周炎及健康对照组间血浆中脂蛋白相关磷脂酶A2(1ipoprotein-associated phospholipase A2,Lp-PLA2)及其与临床牙周指标的相关性,探讨牙周炎与心血管疾病的相互关系。方法:选取经冠状动脉造影确诊为冠心病且伴有中重度牙周炎的病人24名(C+P组),单纯冠心病病人36名(C组),单纯中重度牙周炎病人32名(P组)及健康对照组(H组)28名。对所有受检者进行口腔检查,记录其基本资料及相关牙周指标,并收集血液标本,采用ELISA检测血浆中Lp-PLA2水平。结果:C+P组、C组、P组的Lp-PLA2水平高于H组,差异有统计学意义(P<0.05),相关性分析结果显示P组血浆中Lp-PLA2水平与牙周袋深度、附着丧失呈显著正相关,且具有统计学意义(P<0.05)。结论:牙周炎能引起血浆中Lp-PLA2的升高,提示牙周炎作为感染因素可能是心血管疾病的又一危险因素。     

Do patients with aggressive periodontitis have evidence of diabetes? A pilot study

Davies RC, Jaedicke KM, Barksby HE, Jitprasertwong P, Al‐Shahwani RM, Taylor JJ, Preshaw PM. Do patients with aggressive periodontitis have evidence of diabetes? A pilot study. J Periodont Res 2011; 46: 663–672. © 2011 John Wiley & Sons A/S Background and Objective: Complex relationships exist between diabetes and periodontal disease. Diabetes is accepted as a risk factor for periodontal disease, and recent evidence supports the existence of a bidirectional relationship between these two diseases. It has been hypothesized that inflammation, lipids and adipokines may mediate these relationships. However, research regarding the above relationships with respect to aggressive periodontitis is very limited. This pilot study aimed to investigate whether patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes and have altered serum levels of inflammatory mediators, lipids and adipokines. Material and Methods: Glycaemic control markers (random plasma glucose and glycated haemoglobin), inflammatory mediators (high‐sensitivity C‐reactive protein, tumour necrosis factor‐α, interleukin‐1β, interleukin‐6, interferon‐γ and interleukin‐18), lipids (triglycerides, total cholesterol and high‐density lipoprotein‐cholesterol) and adipokines (leptin, adiponectin and resistin) were measured in serum samples from 30 patients with aggressive periodontitis and 30 age‐ and sex‐matched periodontally healthy control subjects, none of whom had a previous diagnosis of diabetes. Results: Levels of glycaemic control markers, inflammatory mediators, lipids and adipokines were not significantly different (p > 0.05) between the aggressive periodontitis patients and healthy subjects for unadjusted and adjusted analyses (adjusting for body mass index, smoking, ethnicity, age and sex). The p‐value for the adjusted analysis of adiponectin in female aggressive periodontitis patients compared with the female control subjects reached 0.064, the mean adiponectin level being lower in the female aggressive periodontitis patients (4.94 vs. 5.97 μg/mL). Conclusion: This pilot study provided no evidence to suggest that patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes or altered serum levels of inflammatory mediators, lipids and adipokines.     

The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease

Epidemiological studies have implicated periodontitis (PD) as a risk factor for development of cardiovascular disease (CVD). Persistent infections such as periodontitis induce inflammatory and immune responses which may contribute to coronary atherogenesis, and, in conjunction with other risk factors, may lead to coronary heart disease (CHD). In this review, mechanisms are described that may help explain the association between periodontal infections and CHD. Periodontal diseases are bacterial infections associated with bacteremia, inflammation, and a strong immune response, all of which may represent significant risk factors for the development of atherogenesis, CHD, and myocardial infarction (MI). Several mechanisms may participate in this association, including those induced by oral organisms, and those associated with host response factors. This review will focus on host factors. Oral pathogens and inflammatory mediators (such as interleukin [IL]-1 and tumor necrosis factor [TNF]-alpha) from periodontal lesions intermittently reach the bloodstream inducing systemic inflammatory reactants such as acute-phase proteins, and immune effectors including systemic antibodies to periodontal bacteria. This review will describe the potential role of various inflammatory as well as immunologic factors that may play a role in periodontitis as a possible risk factor for CHD.     

血脂水平与牙周炎发病相关性及牙周基础治疗对血脂的影响

目的探究血脂水平与牙周炎发病的相关性及牙周基础治疗对血脂水平的影响。 方法选取2018年3月至2019年3月深圳市龙华区中心医院口腔科收治的118例慢性牙周炎患者，根据牙周炎严重程度分为轻度组（36例）、中度组（52例）、重度组（30例），另取同期30例牙周健康且无全身系统疾病的体检者为对照组，应用t检验比较牙周炎患者和对照组之间、牙周基础治疗前后血清三酰甘油（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）水平，单因素方差分析比较轻度组、中度组、重度组的TG、TC、HDL-C、LDL-C水平，应用采用Logistic回归分析血脂与牙周炎发病的相关性，并观察牙周基础治疗后血脂水平变化。 结果118例慢性牙周炎患者牙周基础治疗前血清TG、TC、HDL-C和LDL-C水平分别为（2.2 ± 0.8）、（5.3 ± 1.0）、（1.3 ± 0.3）和（2.8 ± 0.6）mmol/L，与对照组[（1.5 ± 0.7）、（4.4 ± 0.9）、（1.9 ± 0.3）和（1.8 ± 0.5）mmol/L]相比，差异均有统计学意义（t_TG = 4.306，P_TG = 0.036；t_TC = 6.781，P_TC = 0.028；t_HDL-C = 5.023，P_HDL-C = 0.031；t_LDL-C = 4.974，P_LDL-C = 0.034）。并且，随着牙周炎程度加重，HDL-C水平逐渐降低，差异无统计学意义（F = 0.933，P = 0.192），而TG、TC和LDL-C水平及高脂血症占比逐渐升高，差异有统计学意义（F_TG = 5.762，P_TG = 0.033；F_TC = 6.237，P_TC = 0.029；F_LDL-C = 6.685，P_LDL-C = 0.024；χ²_{高脂血症占比} = 4.513，P_{高脂血症占比} = 0.039）。Logistic回归分析显示，牙周炎是导致TG、TC、LDL-C升高的独立性危险因素（OR_TG = 3.264，95% CI_TG = 1.733 ~ 5.934；OR_TC = 2.937，95% CI_TC = 1.342 ~ 4.926；OR_LDL-C = 2.427，95% CI_LDL-C = 1.256 ~ 3.125）。牙周基础治疗后，轻中度患者血清TG、TC、LDL-C水平较治疗前降低，HDL-C水平较治疗前升高，差异有统计学意义。 结论牙周炎是TG、TC、LDL-C升高的独立性危险因素，牙周基础治疗可有助改善血脂水平，降低动脉粥样硬化、心血管疾病发生风险。     

IL-6 levels in gingival crevicular fluid (GCF) from patients with non-insulin dependent diabetes mellitus (NIDDM), adult periodontitis and healthy subjects

Cytokines play an important role in the pathology associated with chronic inflammatory diseases. One of these cytokines, interleukin 6 (IL-6) is a major mediator of the host response to tissue injury, infection and bone resorption. In the present study, gingival crevicular fluid (GCF) level of IL-6 was determined in patients with non-insulin dependent diabetes mellitus (NIDDM) with periodontitis, adult periodontitis, and healthy controls by use of an enzyme linked immunosorbent assay (ELISA). Twenty-four NIDDM patients with periodontitis, twenty-four adult periodontitis and twenty-four healthy controls were selected for the study. GCF sampling was performed on the vestibular aspects of maxillary incisors and canine teeth. Plaque index (PI), gingival index (GI), gingival bleeding time index (GBTI), probing depth (PD) and probing attachment levels (PAL) were recorded from each sampling area and also the entire dentition. NIDDM and adult periodontitis patients had numerous sites with radiographic evidence of alveolar bone resorption, loss of attachment and pocket depth greater than 3 mm. The mean GCF IL-6 level was 2.43 +/- 0.97 ng/ml in NIDDM patients, 1.31 +/- 0.92 ng/ml in adult periodontitis and 0.62 +/- 0.58 ng/ml in healthy subjects, respectively (p < 0.05). GCF IL-6 levels were markedly higher in NIDDM and adult periodontitis groups compared to the healthy controls. No correlation was found between GCF IL-6 levels and all clinical parameters. These findings suggested that GCF IL-6 levels were significantly higher in the area of inflammation and periodontal destruction locally. The high IL-6 levels in NIDDM patients might be due to different microbial flora in periodontal pockets and altered immune system. Future studies are needed to evaluate the complex interaction among IL-6 GCF levels, host response and local microbial environment in the NIDDM patients.     

Periodontal Status Affects C‐Reactive Protein and Lipids in Patients With Stable Heart Disease From a Tertiary Care Cardiovascular Clinic

Background: There are scarce data on the impact of the periodontal condition in the control of biomarkers in patients with cardiovascular disease (CVD). The aim of this study is to assess whether periodontal inflammation and tissue breakdown are associated with C‐reactive protein (CRP) and lipids in patients with stable heart disease. Methods: This cross‐sectional study included 93 patients with stable coronary artery disease (57 males; mean age: 63.5 ± 9.8 years) who were in outpatient care for at least 6 months. After applying a structured questionnaire, periodontal examinations were performed by two calibrated periodontists in six sites per tooth at all teeth. Blood samples were collected from patients on the day of periodontal examination to determine levels of CRP, lipids, and glycated hemoglobin. Multiple linear regression models were fitted to evaluate the association among different periodontal and blood parameters controlling for sex, body mass index, glycated hemoglobin, use of oral hypoglycemic drugs, and smoking. Results: Overall, the sample presented high levels of periodontal inflammation and tissue breakdown. Unadjusted mean concentrations of triglycerides (TGs), very‐low‐density lipoprotein cholesterol, and glucose were significantly higher in individuals with severe periodontitis. When multiple linear regression models were applied, number of teeth with clinical attachment loss ≥6 mm and presence of severe periodontitis were significantly associated with higher CRP concentrations. Bleeding on probing was significantly associated with TGs, total cholesterol, and non‐high‐density lipoprotein cholesterol. Conclusion: In this sample of patients with stable CVD, current periodontal inflammation and tissue breakdown are associated with cardiovascular inflammatory markers, such as CRP and lipid profile.