侵袭性牙周炎龈沟液中硫化物的检测

目的:检测侵袭性牙周炎(AgP)龈沟液中硫化物浓度水平变化并探讨其与牙周临床指标的关系。方法:采用金刚牙周诊断仪进行龈沟液硫化物和牙周临床指标测定。选定实验组(T)16例侵袭性牙周炎病人,56个牙,共336个位点。其中健康牙(T1)16个,位点96个;炎症牙(T2)40个,位点240。对照组(C):全身、牙周健康者10例,20个牙,共120个位点。测定所选位点龈沟液(gingival crevicu lar flu id,GCF)中硫化物水平(su lcus su lph ide level,SUL),牙周袋探诊深度(pocket prob ing depth,PPD),牙周临床附着丧失水平(c lin i-cal attachm ent level,CAL),龈沟出血指数(su lcus b leed ing index,SB I)。结果:①3组受检牙龈沟液中硫化物浓度不同。侵袭性牙周炎炎症牙位组GCF中硫化物浓度(0.2210±0.0415)×10-6mol/L高于健康牙位组(P<0.05)、正常对照组;健康牙位组GCF中硫化物浓度(0.1025±0.0198)×10-6mol/L高于正常对照组(0.0523±0.0044)×10-6mol/L。②经相关性分析,侵袭性牙周炎炎症牙位组(T1)GCF中硫化物的浓度均值与PD、SB I和CAL均呈正相关关系,健康牙位组(T1)、正常对照组(C)GCF中硫化物浓度均值与PD、SB I及CAL无相关性。结论:侵袭性牙周炎病人龈沟液中的硫化物是参与牙周炎症反应的重要调节因子,其水平变化可反映牙周组织的炎症状态。     

吸烟和非吸烟慢性牙周炎患者基础治疗后龈沟液肝细胞生长因子水平的变化

目的研究吸烟和非吸烟的慢性牙周炎患者牙周基础治疗前后龈沟液（GCF）中肝细胞生长因子（HGF）的水平变化。了解吸烟和基础治疗对GCF中HGF的水平的影响。方法将研究对象分为吸烟慢性牙周炎组和非吸烟慢性牙周炎组,每组患者各15例,实验牙各30颗,用滤纸条法在龈沟袋内获取牙周基础治疗前后的GCF样本．采用酶联免疫吸附试验（ELISA）测定其中的HGF水平。结果基础治疗后慢性牙周炎患者非吸烟组与吸烟组相比,GCF中HGF水平降低更明显（P〈0．01）。结论吸烟和GCF中HGF水平变化有关系。     

维族绝经妇女龈沟液IL-6、血清雌二醇水平与牙周炎的关系

目的:探讨维吾尔族绝经早期的牙周炎患者龈沟液IL-6及血清雌二醇(E2)水平与牙周炎的关系。方法:共79例绝经年限均≤5a的妇女纳入本研究。采集30颗牙周健康牙和49颗牙周炎患牙的龈沟液(GCF),记录牙周临床观察指标。采集慢性牙周炎患者的血样本。应用放射免疫分析法检测GCF中IL-6和血清中E2的浓度。结果:牙周健康组GCF中IL-6浓度为(1088.10±102.33)pg/ml;慢性牙周炎组GCF中IL-6浓度明显高于牙周健康牙组(P<0.005);慢性牙周炎患牙GCF中IL-6浓度与GI、PPD、CAL均呈正相关(r=0.564,P<0.005;r=0.335,P<0.05;r=0.324,P<0.05)。血清E2≤30pg/ml组的妇女牙周炎患牙牙周临床指标、GCFIL-6浓度与E2>30pg/ml组无显著差异(P>0.05)。结论:健康牙GCF中含有微量IL-6。牙周炎患牙GCF中IL-6的水平反映了牙周炎症的严重程度,可以尝试作为判断维族妇女牙周病变程度的一个指标。绝经早期患慢性牙周炎的维族妇女,血清E2水平与牙周炎患牙的病变程度及GCF中IL-6的水平无关。     

生物活性玻璃植入前后龈沟液量及弹性蛋白酶水平的研究

目的　观察生物活性玻璃 (bioactiveglass,BAG)植入后龈沟液量和弹性蛋白酶水平的变化情况 ,以判断牙周组织的炎症反应。方法　用翻瓣术加BAG移植治疗 13处牙周骨下袋 ,用单纯翻瓣术治疗 7处骨下袋。测定术前及术后 1、2、3、4、6、8、10、12周的龈沟液 (gingivalcrevicularfluid ,GCF)量及GCF中弹性蛋白酶 (elastase ,EA)水平。结果　两组GCF量的变化相似 ,术后 1周GCF量明显升高 ,术后 3周至术前水平 ,6周左右达最低值。BAG组的BCF -EA水平在术后各时间点均较术前明显降低 ;翻瓣组GCF -EA水平在术后 1个月内明显低于术前 ,随后有逐渐回升趋势。术后 12周时 ,BAG组的GCF -EA水平明显低于翻瓣组 (P <0 .0 5 )。结论　BAG可能有助于减轻牙周组织的炎症。     

吸烟对慢性牙周炎患者龈沟液及牙龈组织中β防御素2、3的影响

目的 探讨吸烟对慢性牙周炎患者龈沟液（gingival crevicular fluid,GCF）及牙龈组织中β防御素(human beta def-ensin,hBD)2、3表达的影响。方法 将研究对象分为吸烟慢性牙周炎组和非吸烟慢性牙周炎组。采用酶联免疫吸附法（Elisa）检测hBD2、3的浓度;反转录多聚合酶链反应(RT-PCR)检测hBD2、3mRNA的表达,并做半定量分析。相关数据采用SPSS 17．0软件包进行统计学分析。结果 在GCF中,hBD2、3在吸烟组的水平表达均低于非吸烟组;hBD2、3在2组牙龈组织样本中均有mRNA表达,其中吸烟组较非吸烟组mRNA表达水平减弱。结论 吸烟可使GCF及牙龈组织中hBD2、3的表达发生改变,提示吸烟可对牙周宿主免疫防御系统产生消极影响。     

吸烟对牙周炎患者龈沟液中弹性蛋白酶水平的影响

目的比较吸烟与非吸烟牙周炎患者和健康人龈沟液中细胞外弹性蛋白酶EA-s和细胞内弹性蛋白酶(EA-p)水平的变化。方法选择慢性牙周炎患者41例,共146个探诊出血(BOP)、牙周袋探诊深度(PD)≥4mm、附着丧失(AL)≥2mm的牙周炎位点,将其分为吸烟组79个,非吸烟组67个。同时选择牙周健康者31人作为对照,共85个探诊不出血,牙龈指数(GI)≤1,PD≤3mm,AL≤1mm的位点,同样分为2组,吸烟组45个,非吸烟组40个。观察牙周治疗前、后牙周临床指标菌斑指数(PLI),GI,PD,AL,BOP和龈沟液中EA-s、EA-p水平的变化。结果牙周炎患者中,吸烟组的GI,AL和EA-s水平低于非吸烟组(P<0.05),其余指标差异无显著性(P>0.05),健康者的各项指标差异均无显著性(P>0.05)。无论是吸烟组还是不吸烟组,牙周炎患者的EA-s,EA-p水平均高于健康者(P<0.05)。结论吸烟会降低牙周炎患者龈沟液中EA-s水平,但对EA-p水平影响不大。吸烟对健康人EA水平无显著影响。     

吸烟对牙周基础治疗效果影响的研究

目的评价吸烟与非吸烟慢性牙周炎患者牙周基础治疗1个月后的疗效差异。方法选择36例慢性牙周炎患者,吸烟组20例,非吸烟组16例,基线时两组牙周炎病情相似。从牙列的4个象限选取探诊深度在5～9mm范围的位点1～2个,吸烟组108个位点,非吸烟组88个位点,观察这些位点在牙周基础治疗前、治疗后1个月临床指标的变化,包括菌斑指数(PLI),牙龈出血指数(BI),牙周袋探诊深度(PPD)和附着丧失(AL);在作临床观察的同时,对治疗前后龈沟液白介素(IL)-1β进行检测。结果治疗前(基线时)两组PLI、BI、PPD、AL以及IL-1β差异不显著,牙周基础治疗1个月后,两组的各项指标均有明显的改善,但吸烟组改善程度明显低于非吸烟组(P<0.05)。结论慢性牙周炎患者,吸烟者牙周基础治疗的效果差于     

慢性牙周炎治疗前后龈沟液中PGE2、IL-6、IL-8的变化

目的检测慢性牙周炎患牙龈沟液(GCF)中PGE2、IL-6、IL-8在治疗前后的浓度,探讨评价牙周治疗效果的指标.方法选择20例牙周炎患牙,用超声波治疗仪进行龈下刮治,检查治疗前、治疗后4周龈沟出血指数(SBI),并收集治疗前后的GCF,用ELISA检测其中PGE2、IL-6、IL-8的浓度.结果治疗前后SBI分别为2.87±0.52和1.32±0.28,P＜0.01;PGE2 浓度为254.86±123.60和157.78±129.06 (ng/ml),P＜0.05;而IL-6、IL-8的浓度没有显著性差异.结论经过彻底的牙周治疗后,GCF中PGE2浓度明显降低,IL-6、IL-8降低没有统计学意义,提示作为牙周治疗效果评价的指标,PGE2较IL-6、IL-8等更为敏感.     

牙周炎治疗对患者龈沟液IL-8水平的影响

目的　研究牙周炎基础治疗前后IL 8水平的变化。方法　采用双抗夹心ABC ELISA法测定成人牙周炎患者 (AP)、健康对照以及牙周炎治疗前后患者的龈沟液中IL 8浓度和总量。结果　在疾病组和健康组之间以及牙周病治疗前后对照 ,IL 8浓度无统计学差异 (P >0 0 5 ) ,而IL 8总量、GCF量均存在着统计学差异 (P <0 0 5 ,P <0 0 0 1) ,并且发现治疗对IL 8水平有着明显影响。结论　IL 8总量在成人牙周炎病程中显示动态性改变 ,检验GCF中IL 8的水平对评价牙周炎的治疗是有价值的。?     

吸烟对牙周炎治疗前后龈沟液中弹性蛋白酶水平变化的影响

目的:比较吸烟和不吸烟的牙周炎患者治疗前后龈沟液中细胞外弹性蛋白酶EA-s和细胞内弹性蛋白酶EA-p水平的变化。方法:选取慢性牙周炎患者41人,共146个探诊出血,PD≥4 mm,CAL≥2 mm的牙周炎位点,将其分为吸烟组79个,非吸烟组67个。观察牙周治疗前后牙周临床指标PLI、G I、PD、CAL、BOP和龈沟液EA-s、EA-p水平的变化。结果:治疗前,吸烟组的G I和EA-s水平低于非吸烟组(P<0.05)。治疗后,两组各临床指标,EA-s、EA-p水平均有不同程度下降。两组间,PLI、G I、BOP等临床指标无显著差异(P>0.05),非吸烟组EA-s、EA-p水平均较低(P<0.05)。结论:吸烟的牙周炎患者龈沟液中EA-s水平较低,但EA-p水平与非吸烟者差别不大。治疗后,非吸烟者龈沟液EA-s,EA-p水平更低,可能与吸烟者牙周治疗效果不佳有关。     

Tobacco smoking and gingival neutrophil activity in young adults

Abstract . The influence of smoking on the activity of the gingival neutrophils in young periodontally healthy adults was studied. The neutrophil activity was measured in terms of the gingival crevicular fluid (GCF) levels of elastase, lactoferrin (LF), a-1-antitrypsin (a-1-AT), α-2-macroglobulin (α-2 MG) and protein. 30 healthy dental students with no clinical signs of periodontitis, 15 smokers (8 women and 7 men) aged 20–32 years and 15 non-smokers (7 women and 8 men) aged 22–31 years, volunteered to take part in the investigation. The gingival inflammation was registered at 6 sites and the GCF volume was collected from the same sites. The GCF volume was measured with a Periotron 6000®. The elastase activity was measured with a chromogenic low molecular substrate and the LF, α-1-AT, α-2-MG levels were determined with ELISA. The protein concentration was measured by the Bradford method.The results showed a statistically significantly lower GCF volume among smokers as compared to non-smokers. No significant difference was found in the elastase activity/μl of the GCF supernatant between smokers and non-smokers but there was a large inter-individual variation. Nor did the concentrations of LF, α-1-AT, 7alpha;-2-MG and protein per μl GCF differ significantly between the 2 groups. The results suggest that the influence of smoking on the examined factors associated with neutrophil activity is limited under healthy or slightly inflamed gingival conditions giving only small amounts of GCF.     

Elastase in gingival crevicular fluid from smokers and non-smokers with chronic inflammatory periodontal disease

OBJECTIVE: To compare elastase concentrations in gingival crevicular fluid (GCF) from individual sites of smokers and non-smokers.
MATERIALS AND METHODS: Twelve pairs of smokers and non-smokers with untreated, moderate to advanced chronic inflammatory periodontal disease were matched for gender, age, ethnicity and the clinical and radio-graphic extent of disease. Durapore filter strip samples were collected over 30 s from two mesiopalatal sites on upper left posterior teeth. Samples were analysed for: I) polymorphonuclear neutrophil leucocyte (PMNL) cell counts; 2) PMNL elastase-αI-antitrypsin complex in the GCF supernatant by ELISA; and 3) functional elastase, free or bound to α2-macroglobulin, estimated from activity against N-tert-butoxycarbonyI-alanyl-prolyl-nor-valylg-chlorothiobenzyl ester in supernatant and lysates of GCF PMNLs.
RESULTS: There were no differences in disease parameters between groups except that bleeding on probing was less extensive in smokers (P< 0.001). Cell counts and elastase content of crevicular PMNLs showed no differences between groups. Lower concentrations of elastase were found in GCF supernatants from smokers than non-smokers. This difference was observed for functional elastase (mean [s.d.] = 30.21 [17.60] against 73.77 [75.26] ng μI^-1, P <0.05) and elastase complexed with αl-antitrypsin (8.97 [6.54] ng μl^-1 against 25.71 [22.07] ng μI^-1, P < 0.001).
CONCLUSIONS: Smokers have lower elastase concentrations in GCF than non-smokers. Further investigation is required to elucidate the underlying cause and its relationship with periodontal disease.     

Granulocyte elastase,matrix metalloproteinase-8 and prostaglandin E2 in gingival crevicular fluid in matched clinical sites in smokers and non-smokers with persistent periodontitis

BACKGROUND/AIMS: Smokers with persistent periodontitis may have granulocytes with impaired function. This study aimed to determine the levels of granulocyte elastase, matrix metalloproteinase-8 (MMP-8) and prostaglandin E2 (PGE2) in gingival crevicular fluid (GCF) in smokers and non-smokers with persistent periodontitis. METHODS: We analyzed GCF from 70 matched sites in 29 periodontitis and 6 gingivitis sites in 34 subjects, 17 smokers, and 17 non-smokers. We also analyzed separately GCF from 28 of these subjects, 14 smokers and 14 non-smokers in 14 matched periodontitis sites. The following measurements were made: elastase complexed to alpha1-antitrypsin (EA-alpha1AT) and MMP-8 with ELISA, functional elastase with a chromogenic substrate, and PGE2 with radioimmunoassay (125I RIA). The significance of the findings was determined with Mann-Whitney test. RESULTS: In the 29 matched periodontitis sites, smokers had significantly more functional elastase (p<0.005) and more EA-alpha1AT (p<0.05) than non-smokers. In the 14 matched periodontitis sites in 14 smokers and 14 non-smokers, the former had significantly more functional elastase than the latter (p<0.001). A significant correlation was found between EA-alpha1AT and MMP-8 in smokers (p<0.05) and non-smokers (p<0.001) and a positive correlation between levels of functional elastase and MMP-8 in non-smokers (r2=0.98; p<0.001). CONCLUSIONS: Granulocyte function seems to be impaired in smokers with persistent periodontitis. The cells react to the bacterial challenge by releasing serine proteases, which reflect the degradation of connective tissue. The risk of progression of the disease is therefore higher in smokers with persistent periodontitis than in non-smokers.     

Effects of smoking on clinical parameters and the gingival crevicular fluid levels of IL-6 and TNF-alpha in patients with chronic periodontitis

OBJECTIVE: Smoking is an important environmental risk factor for the initiation and progression of periodontal diseases. The aim of this study was to evaluate the effects of smoking on clinical parameters and the gingival crevicular fluid (GCF) contents of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels in patients with chronic periodontitis. MATERIAL AND METHODS: The study base consisted of 41 patients including 22 volunteer current smokers with an age range of 32-59 (44.41+/-7.88) years and 19 volunteer non-smokers with an age range of 36-59 (46.94+/-6.07) years. The first month after non-surgical periodontal therapy was accepted as the baseline of the study. The clinical parameters including plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing depth (PD), clinical attachment loss (CAL) were recorded and GCF samples were collected for analysis of GCF contents of IL-6 and TNF-alpha levels. At the 3rd and 6th months, all of these procedures were repeated. RESULTS: In smokers, only CAL was significantly higher at the 3rd month compared with non-smokers (p<0.05). GI and BOP were higher in non-smokers than smokers in both periods (p<0.05). PI showed increases from the initial to the 6th month in smokers (p<0.05). Although the differences between two groups with regard to IL-6 and TNF-alpha were not significant (p>0.05), the total amount of TNF-alpha in GCF decreased from the initial to the 6th month in smokers (p<0.05). There were no significant correlations between the mean total amount of IL-6 and TNF-alpha in GCF and clinical parameters in both evaluation periods in smokers (p>0.05). CONCLUSION: The present study demonstrated that cigarette smoking increases the amount of dental plaque over time in smokers and does not influence GCF contents of IL-6 and TNF-alpha.     

The effect of different cigarette smoking levels on gingival crevicular fluid volume and periodontal clinical parameters in Saudi Arabia

IntroductionPeriodontal disease is a chronic inflammatory condition of the periodontium. It is the main cause of tooth loss and is considered one of the biggest threats to the oral cavity. Tobacco smoking has long been associated with increased risk for periodontal, peri-implant, and other medical diseases.ObjectiveTo evaluate the effect of smoking and its level on periodontal clinical parameters (probing depth (PD), plaque index (PI), gingival index (GI), clinical attachment level (CAL), bleeding on probing (BOP), and the volume of gingival crevicular fluid (GCF)) in healthy and chronic periodontitis individuals.Material and MethodA total of 160 participants were recruited in the present study, who were equally divided into the following five groups: healthy controls (C), healthy smokers (HS), nonsmokers with periodontitis (PNS), light smokers with periodontitis (PLS), and heavy smokers with periodontitis (PHS). GCF volume and periodontal clinical parameters (PD, PI, GI, CAL, and BOP) were assessed for each participant and compared between the study groups.ResultThere was a statistically significant difference in PD, PI, GI, CAL, and BOP between healthy and periodontitis patients (p < 0.001). The mean PI, PD, and CAL were considerably higher in heavy smokers than light smokers and non-smokers (P < 0.001). In contrast, the mean GI and BOP were significantly lower in heavy smokers than in light smokers and non-smokers. There was a statistically significant difference in GCF between healthy and periodontitis patients (p < 0.001). The mean GCF readings were higher in heavy smokers than light smokers or non-smokers (P < 0.001).ConclusionThe present study confirms the influence of smoking on periodontal clinical parameters. Smoking was associated with increased PD, PI, CAL, and GCF readings; however, GI and BOP were decreased in smokers. The number of cigarettes played a key role in the volume of GCF and periodontal clinical parameters.     

Plasminogen activator system in smokers and non-smokers with and without periodontal disease

BACKGROUND: The present study assessed levels of plasminogen activator (PA) system proteins in gingival crevicular fluid (GCF) and serum of chronic gingivitis, chronic periodontitis patients and periodontally healthy subjects and evaluated how smoking influenced these levels. METHODS: Twenty chronic gingivitis; 20 chronic periodontitis patients and 20 periodontally healthy volunteers were consecutively recruited according to the inclusion criteria so that exactly half of the subjects in each category were smokers. GCF samples from four sites together with serum samples were obtained from each subject. GCF levels of tissue type PA (t-PA), urokinase type PA (u-PA), PA inhibitor-1 (PAI-1) and PA inhibitor-2 (PAI-2) and serum concentrations of cotinine, u-PA and PAI-1 were analysed by enzyme-linked immunosorbent assay. RESULTS: The only statistically significant difference between smokers and non-smokers was a lower GCF PAI-2 concentrations in healthy smokers compared with healthy non-smokers (p<0.01). Gingivitis and periodontitis patients had higher GCF concentrations of PAI-2 than healthy subjects (p<0.002 and p<0.02 respectively). The ratio of u-PA:PAI-1 and t-PA:PAI-1 were significantly higher in GCF of smokers with periodontitis compared with "healthy" smokers, whereas the ratio of t-PA:PAI-2 was significantly lower in smokers with periodontal disease (p<0.05). CONCLUSIONS: GCF levels of the PA system proteins are increased in chronic gingivitis and periodontitis compared with healthy gingiva. Smoking had only subtle effects on the GCF PA system proteins with the exception of PAI-2, and the balance of activators and inhibitors. These findings suggest one mechanism whereby smoking may exert detrimental effects on the periodontal tissues.     

GCF MMP-8 levels in smokers and non-smokers with chronic periodontitis following scaling and root planing accompanied by systemic use of flurbiprofen

BACKGROUND: Cigarette smoking has been identified as an important risk factor for the initiation and progression of chronic periodontitis (CP). The aim of this study was to investigate the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on matrix metalloproteinase (MMP)-8 levels in gingival crevicular fluid (GCF) samples from smoking and non-smoking patients with CP. METHODS: Twenty-nine non-smoking and 29 smoking patients with CP were divided into four groups according to periodontal treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 x 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 x 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded; GCF samples were collected from each sampling area at baseline and after the 10-day period of drug intake by a single examiner who was unaware of the treatment modality. Assays for GCF MMP-8 were carried out by an enzyme-linked immunosorbent assay. RESULTS: All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment (P < 0.05), but no statistical differences were observed in PD and CAL scores after therapy. In all groups, the reduction of GCF MMP-8 levels after therapy was statistically significant compared to baseline levels (P < 0.001). When groups 1 and 3 and 2 and 4 were compared according to GCF MMP-8 levels after the therapy, no statistically significant differences were observed (P = 0.117 and P = 0.485, respectively). CONCLUSION: Flurbiprofen administration had no additional inhibitory effect over SRP alone on GCF levels of MMP-8 in smokers compared to non-smokers with CP.     

Tobacco smoking and neutrophil activity in patients with periodontal disease

BACKGROUND: Tobacco smoking has considerable negative effects on periodontal health. The mechanisms behind these effects are incompletely understood but may be related to the host response. The aim of the present study was to investigate the influence of tobacco smoking on the gingival crevicular fluid (GCF) levels of elastase, lactoferrin (LF), alpha-1-antitrypsin (alpha-1-AT), and alpha-2-macroglobulin (alpha-2-MG) under periodontally diseased conditions. METHODS: The study population included 15 smokers (5 women and 10 men) aged 34 to 69 years and 17 non-smokers (5 women and 12 men) aged 31 to 81 years. Clinical registration of gingival index (GI), plaque index (PI), probing depth, as well as sampling of GCF were made at 3 sites with severe lesions and 3 sites with moderate lesions in each individual. The elastase activity was measured with a chromogenic low molecular substrate and the LF, alpha-1-AT, and alpha-2-MG concentrations with ELISA. RESULTS: The results showed that, with regard to severe lesions, smokers had a significantly lower concentration of alpha-2-MG as well as significantly lower total amounts of alpha-2-MG and alpha-1-AT than non-smokers. With regard to moderate lesions, smokers tended to exhibit a lower concentration of alpha-2-MG, but the difference was not statistically significant. Comparing moderate and severe lesions, smokers exhibited no gradual increase with disease severity in contrast to non-smokers, who showed significantly or almost significantly increased levels of LF and alpha-2-MG in severe as compared to moderate lesions. CONCLUSIONS: The present results indicate that the levels of alpha-2-MG and alpha-1-AT are suppressed in smokers with periodontitis, suggesting that smoking interferes with these protease inhibitors. This may be one mechanism by which smoking affects the inflammatory response.     

Gingival crevicular fluid leptin levels in periodontitis patients with long-term and heavy smoking

BACKGROUND: The aim of the present study was to evaluate gingival crevicular fluid (GCF) leptin levels and the influence of long-term and heavy smoking on GCF leptin levels in patients with chronic periodontitis. METHODS: In this study, 143 individuals were divided into three groups: non-smokers (NS), smokers (S), and control (C). Three subgroups of NS and S were grouped as follows: a) probing depth (PD) 5 mm. For each patient, PD, gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), and clinical attachment level (CAL) values were recorded. The GCF leptin levels obtained from sampling sites were determined by using enzyme-linked immunosorbent assay kits. RESULTS: The GCF leptin levels were found significantly lower in the a and b subgroups in the S group than those in the NS group (P <0.05). The inflammatory markers GI and GBTI showed significant correlations with leptin in NS (P <0.05). CONCLUSIONS: Our results suggest that higher leptin GCF levels in healthy sites in periodontitis patients may play a protective role in periodontal disease. Further studies are needed to determine the cellular origin of the leptin in the gingiva and the effect of plasma leptin levels on GCF leptin concentrations.