Cigarette smoking in patients referred for periodontal treatment

Abstract — 369 adult patients with moderate to severe periodontitis were compared with a survey sample from the population of Stockholm regarding smoking habits. The results showed that the frequency of daily cigarette smokers was significantly greater in the periodontitis sample. The odds ratio for a smoker to appear among periodontitis patients was more than doubled as compared to the population at large. In addition, the periodontal variables of PII, GI, probing depth and the patient's experience of gingival bleeding were recorded and compared between smoking and non-smoking patients. PII was found to be similar in smokers and non-smokers. Signs and symptoms of gingivitis as evidenced by the patients' experience of gingival bleeding and by GI were less pronounced in patients who smoke. Only 25% of smokers reported bleeding gingiva as compared to 51 % of non-smokers. No differences were observed regarding probing depth except for lingual pockets of the maxilla where a significantly greater probing depth was observed in smokers. It was concluded that smokers may run an increased risk for periodontitis. Furthermore, gingival inflammatory symptoms seem to be suppressed in patients who smoke.     

Oral melanin pigmentation related to smoking in a Turkish population

OBJECTIVE: Besides genetic factors, tobacco smoking has been found to be the major cause of oral melanin pigmentation. The purpose of the present study was to evaluate the frequency of oral melanin pigmentation in a Turkish population and to present its correlation with clinical parameters relevant to periodontal status in current smokers, non-smokers, former smokers. METHOD: A sample of 496 patients was randomly selected. The subjects were interviewed regarding their smoking habits. They were clinically examined by a single examiner for the presence of oral melanin pigmentation in different oral mucosal regions. The same examiner recorded the clinical parameters including GI (gingival index), PI (plaque index), BOP (bleeding on probing), PD (probing depth) and GR (gingival recession). Examiner 2 completed a questionnaire concerning skin color and smoking habits. RESULTS: In the study group, 41% were current smokers, 46% nonsmokers and 13% former smokers. The frequencies of pigmented areas were significantly higher in current smokers than in those without any smoking habits. The clinical parameters revealed similar findings for all groups. Low GI and BOP values were observed for current smokers when compared with non-smokers and former smokers, respectively. GI values were significantly associated with the pigmentations in gingiva. CONCLUSIONS: The results of our study show that smokers in a Turkish population had significantly more pigmented oral surfaces than nonsmokers.     

Periodontitis lesions in smokers and non-smokers

Differences in the progression of periodontitis have been observed between smokers and non-smokers. The aim of the present study was to compare vascular and inflammatory cell densities in periodontitis lesions from smokers and non-smokers to gain further understanding of the influence of smoking on histopathological characteristics of the disease. Two groups of patients with generalized severe periodontitis were recruited. One group consisted of 25 current smokers, aged 33–69 yr, while the second group comprised 21 non-smokers, aged 35–76 yr. From each patient, gingival biopsies were harvested from one periodontitis site (probing pocket depth ≥6 mm and bleeding on probing) and one site without clinical signs of gingival inflammation (reference site). Immunohistochemical analyses were performed to assess the density of vessels and inflammatory cells. Small differences existed between smokers and non-smokers regarding the size, proportion, number, and density of cells in periodontitis lesions. However, the vascular density in periodontitis lesions was significantly higher in non-smokers than in smokers. In clinically healthy reference sites, lesions were considerably smaller than in periodontitis sites and presented with similar vascular densities in smokers and non-smokers.     

Smoking modulates interferon-gamma expression in the gingival tissue of patients with chronic periodontitis

Although interferon-gamma (IFN-gamma) plays a critical role in periodontitis, no information is available regarding the effect of smoking on this cytokine in the periodontium. Therefore, this study aimed to evaluate the effect of smoking on the IFN-gamma levels in gingival tissue from patients with chronic periodontitis. Sixty-two patients were assigned to three groups: healthy [non-smoking and periodontally healthy individuals (probing depth or= 5 mm and bleeding on probing; n = 25)]; and smoking [smokers (>or= 1 pack/day for at least 10 yr) diagnosed with chronic periodontitis (n = 25)]. Gingival biopsies were analyzed by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Regardless of smoking status, diseased patients presented higher levels of IFN-gamma than peridontally healthy patients. In sites with comparable types of periodontitis, smoking increased both protein and mRNA levels of IFN-gamma in gingival tissue. Within the limits of this study, it can be concluded that modulation of periodontal tissue destruction by smoking may involve its effect on IFN-gamma production.     

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.     

EVALUATION OF CLINICAL PERIODONTAL CONDITIONS IN SMOKERS AND NON-SMOKERS

Given that tobacco smoking habit is a risk factor for periodontal diseases, the aim of this study was to compare clinical periodontal aspects between smokers and non-smokers. The clinical status were assessed in 55 patients, 29 smokers and 26 non-smokers, aged 30 to 50 years, with mean age of 40. The clinical parameters used were: probing depth (PD), plaque index (PI), gingival index (GI), clinical attachment level (CAL), gingival recession (GR) and gingival bleeding index (GBI) for arches (upper and lower) and teeth (anterior and posterior). Tooth loss was also evaluated in both groups. Multiple regression analysis showed: tendency of greater probing depth and clinical attachment level means for smokers; greater amount of plaque in smokers in all regions; greater gingival index means for non-smokers with clinical significance (p<0.05) in all regions. Although, without statistical significance, the analysis showed greater gingival bleeding index means almost always for non-smokers; similar gingival recession means in both groups and tendency of upper tooth loss in smokers and lower tooth loss in non-smokers. The findings of this study showed that clinical periodontal parameters may be different in smokers when compared to non-smokers and that masking of some periodontal signs can be a result of nicotine''s vasoconstrictor effect.     

Effect of smoking on gingival crevicular fluid cytokine profile during experimental gingivitis

BACKGROUND: Cigarette smoking is a significant risk factor in the pathogenesis of periodontal disease, able to influence both the subgingival microbiota and host responses. AIM: The aim of the present study was to determine the influence of smoking on the amount of IL-1beta, IL-4 and IL-8 in gingival crevicular fluid (GCF) during experimental gingivitis in humans. MATERIAL AND METHODS: Twenty-two healthy subjects, 10 smokers and 12 non-smokers, participated in the study. After professional cleaning, they performed optimal hygiene to reach perfect clinical gingival health. Oral hygiene measures were ceased for a period of 10 days. Clinical indices, including plaque index (PI), gingival index (GI), probing pocket depth (PPD) and bleeding on probing (BOP), were assessed 2 days before (day -2), at the beginning (day 0) and at the end of the experimental gingivitis period (day 10). At the same time, GCF was collected from 12 sites in each patient, by means of durapore filter membranes. Total amounts of IL-1beta, IL-4 and IL-8 were determined by enzyme-linked immunoadsorbent assay. RESULTS: Clinical data revealed that both smokers and non-smokers showed an increase in PI, GI and BOP scores during the experiment. Although no differences were noted with regard to PI at day 10, the GI and BOP were significantly less pronounced in smokers than non-smokers (p < 0.005). Non-smokers showed higher total amounts of IL-4 but lower amounts of IL-8 than smokers, throughout the experiment. Total amounts of IL-1beta and IL-8 increased significantly during plaque accumulation in both groups. IL-4 remained stable for the smoker group and decreased for the non-smoker group. CONCLUSIONS: The present results indicate that smoking interferes with cytokine production. When performing studies regarding the pathogenesis of periodontitis, the smoking status of the participants needs to be taken into consideration.     

米诺环素对慢性牙周炎辅助治疗的疗效观察

目的 评价牙周袋局部应用米诺环素软膏联合刮治和根面平整治疗慢性牙周炎的疗效。方法 64名患中到重度慢性牙周炎的男性吸烟者随机分成SRP和SRP+M两组。对SRP组患者施行刮治和根面平整,对SRP+M组患者在刮治和根面平整的基础上,牙周袋局部应用米诺环素软膏。记录两组患者在基线、3个月和6个月时的菌斑指数（PlI）、牙龈指数（GI）、探诊出血（BOP）、探诊深度（PD）及附着丧失（AL）的变化并进行统计学分析。结果 治疗过程中有6例患者被排除,有效病例数为58例,每组29例。牙周治疗3个月和6个月后,两组患者的PlI、GI和BOP均无统计学差异（P>0.05）,但PD和AL有统计学差异（P<0.05）。治疗后3个月SRP组PD下降1.32 mm,AL减轻1.14 mm;而SRP+M组PD下降1.98 mm,AL减轻1.87 mm。对于基线检查PD≥7 mm的深牙周袋,治疗后3个月SRP组PD下降2.21 mm,AL减轻1.23 mm;而SRP+M组PD下降3.48 mm,AL减轻2.62 mm。治疗后6个月PD和AL状况与3个月相比变化不大。与SRP组相比,SRP+M组临床症状改善更明显。结论 龈下局部应用米诺环素软膏辅助治疗慢性牙周炎可取得较好的疗效,特别是对于有深牙周袋、吸烟的牙周炎患者,机械治疗联合局部应用缓释抗菌素较单纯机械治疗的疗效更好。     

Relationship between smoking and folic acid, vitamin B12 and some haematological variables in patients with chronic periodontal disease

AIM: The purpose of this study was to investigate the relationship between cigarette smoking and the serum levels of folic acid, vitamin B(12) and some haematological variables in patients with periodontal disease. PATIENTS AND METHODS: The study base consisted of 88 volunteer patients with periodontal disease, including 45 current smokers in the age range 31-68 years and 43 non-smokers in the range 32-66 years. The clinical parameters included plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (CAL). Folic acid, vitamin B(12) and haematological variables were determined from peripheral blood samples. RESULTS: PI, PD and CAL means were significantly higher in smokers than non-smokers (p<0.05). The serum folic acid concentration of smokers was lower than that of non-smokers (p<0.05), whereas the white blood cell count was higher in smokers than in non-smokers (p<0.05). CONCLUSION: The results of this study suggest that among patients with periodontal disease the serum folic acid concentration is lower in smokers compared with 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.     

Laser doppler estimation of the influence of tobacco-smoking on the blood microcirculation in the periodont at the patients with the different stages of periodontal diseases

Smoking appears to be one of the most significant risk factors in the development and progression of periodontal disease. Smoking is also a risk factor in the development of peripheral vascular diseases. Blood vessels in smokers are fewer and are subjected to stenosis. Clinically, it is well known that bleeding on probing, gingival exudates and redness and swelling in gingival sites of smokers are less than in non-smokers. According to previous studies, there is a relative increase in gingival blood flow immediately after smoking, while gingival blood flow itself is considerably decreased in healthy smokers in comparison with non-smokers. In this investigation, we used laser Doppler flowmetry to study gingival microcirculation in smokers with light, moderate and heavy periodontitis in comparison with non-smokers with the same diseases. Our results show, that smoking decreases gingival blood flow in smokers with periodontitis comparing to non-smokers with periodontitis. Immediately after smoking there is an increase in gingival microcirculation. In 30 minutes we observed a marked decrease in gingival blood flow in all groups, followed by gradual restoration of blood flow rate, registered before smoking. This restoration took 1.5-2 hrs in group with light periodontitis, 2 hrs in group with moderate periodontitis and more than 2 hrs in group with heavy periodontitis. We suppose, that constant changes in blood supply of periodontal tissue caused by smoking may contribute to higher prevalence and faster progression of inflammatory periodontal diseases in smokers.     

Comparison of the validity of periodontal probing measurements in smokers and non-smokers

AIM: To determine whether the reduced inflammation and bleeding and increased fibrosis reported in tobacco smokers affect the validity of clinical probing measurements by altering probe tip penetration. METHOD: A constant force probe was used to measure probing depths and sound bone levels at six sites on 64 molar teeth (384 sites) in 20 smoking and 20 non-smoking patients from grooves made with a bur at the gingival margin prior to extraction. Connective tissue attachment levels were measured from the grooves with a dissecting microscope following extraction. Data were analysed using robust regression with sites clustered within subjects. RESULTS: Sites in smokers showed more calculus but less bleeding than sites in non-smokers (p<0.05). The mean clinical probing depth was not significantly different (smokers: 5.54 mm, confidence intervals=4.81 to 6.28; non-smokers: 6.05 mm, ci=5.38 to 6.72). The corresponding post-extraction pocket depth measurements (smokers: 4.95 mm, ci=4.30 to 5.61; non-smokers: 5.23 mm, ci=4.49 to 5.96) were less than clinical probing depth in sites from both smokers and non-smokers (p<0.01). However, the proportional difference was less in smokers (p<0.05), particularly in deeper pockets, indicating that clinical probe tip penetration of tissue was greater in non-smokers. Regression analysis indicated that the presence of calculus and bleeding also influenced the difference in clinical probe penetration (p<0.05). CONCLUSION: Clinical probing depth at molar sites exaggerates pocket depth, but the probe tip may be closer to the actual attachment level in smokers due to less penetration of tissue. This may be partly explained by the reduced inflammation and width of supra-bony connective tissue in smokers. These findings have clinical relevance to the successful management of periodontal patients who smoke.     

Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss

BACKGROUND: Our purpose was to test the hypotheses that cigar and pipe smoking have significant associations with periodontal disease and cigar, pipe, and cigarette smoking is associated with tooth loss. We also investigated whether a history of smoking habits cessation may affect the risk of periodontal disease and tooth loss. METHODS: A group of 705 individuals (21 to 92 years-old) who were among volunteer participants in the ongoing Baltimore Longitudinal Study of Aging were examined clinically to assess their periodontal status and tooth loss. A structured interview was used to assess the participants' smoking behaviors with regard to cigarettes, cigar, and pipe smoking status. For a given tobacco product, current smokers were defined as individuals who at the time of examination continued to smoke daily. Former heavy smokers were defined as individuals who have smoked daily for 10 or more years and who had quit smoking. Non-smokers included individuals with a previous history of smoking for less than 10 years or no history of smoking. RESULTS: Cigarette and cigar/pipe smokers had a higher prevalence of moderate and severe periodontitis and higher prevalence and extent of attachment loss and gingival recession than non-smokers, suggesting poorer periodontal health in smokers. In addition, smokers had less gingival bleeding and higher number of missing teeth than non-smokers. Current cigarette smokers had the highest prevalence of moderate and severe periodontitis (25.7%) compared to former cigarette smokers (20.2%), and non-smokers (13.1%). The estimated prevalence of moderate and severe periodontitis in current or former cigar/pipe smokers was 17.6%. A similar pattern was seen for other periodontal measurements including the percentages of teeth with > or = 5 mm attachment loss and probing depth, > or = 3 mm gingival recession, and dental calculus. Current, former, and non- cigarette smokers had 5.1, 3.9, and 2.8 missing teeth, respectively. Cigar/pipe smokers had on average 4 missing teeth. Multiple regression analysis also showed that current tobacco smokers may have increased risks of having moderate and severe periodontitis than former smokers. However, smoking behaviors explained only small percentages (<5%) of the variances in the multivariate models. CONCLUSION: The results suggest that cigar and pipe smoking may have similar adverse effects on periodontal health and tooth loss as cigarette smoking. Smoking cessation efforts should be considered as a means of improving periodontal health and reducing tooth loss in heavy smokers of cigarettes, cigars, and pipes with periodontal disease.     

Tobacco smoking and periodontal health in a Saudi Arabian population

BACKGROUND: The objective of this study was to examine the association between tobacco smoking, in particular water pipe smoking, and periodontal health. METHODS: A total of 262 citizens of Jeddah, Saudi Arabia in the age range from 17 to 60 years volunteered to participate in the study. The clinical examinations were carried out at King Faisal Specialty Hospital and Research Center in Jeddah and included assessments of oral hygiene, gingival inflammation, and probing depth. Smoking behavior was registered through a questionnaire and confirmed by an interview. Participants were stratified into water pipe smokers (31%), cigarette smokers (19%), mixed smokers (20%), and non-smokers (30%). RESULTS: The mean probing depth per person was 3.1 mm for water pipe smokers, 3.0 mm for cigarette smokers, 2.8 mm for mixed smokers, and 2.3 mm for non-smokers. The association between smoking and probing depth was statistically significant controlling for age (P <0.001). The association between lifetime smoking exposure and mean probing depth was statistically significant in water pipe as well as cigarette smokers controlling for age (P <0.001). Using multivariate analysis, besides smoking, the gingival and plaque indexes were associated with increased probing depth. The prevalence of periodontal disease defined as a minimum of 10 sites with a probing depth > or =5 mm was 19.5% in the total population, 30% in water pipe smokers, 24% in cigarette smokers, and 8% in non-smokers. The prevalence was significantly greater in water pipe and cigarette smokers compared to non-smokers (P <0.001). The relative risk for periodontal disease increased by 5.1- and 3.8-fold in water pipe and cigarette smokers, respectively, compared to non-smokers (P <0.001 and P <0.05, respectively). CONCLUSIONS: An association was observed between water pipe smoking and periodontal disease manifestations in terms of probing depth measurements. The impact of water pipe smoking was of largely the same magnitude as that of cigarette smoking.     

吸烟对牙周炎患者龈下刮治和根面平整术疗效影响的研究

[摘要] 目的 比较吸烟与不吸烟牙周炎患者实施龈下刮治和根面平整治疗术(scaling and root planning,SRP)时,对探诊深度(probing depth,PD)和临床附着水平(clinical attachment level,CAL)的影响。方法 选择临床上中到重度的牙周炎患者,其中53例吸烟患者,56例非吸烟患者,局麻下行龈下刮治和根面平整术(SRP)后,局部龈下放置25%的甲硝唑膜。由同一位检查者分别于初诊及6个月复诊时用牙周探针检查记录探诊深度(PD)和临床附着水平(CAL)。结果 治疗后6个月复诊时,吸烟组PD减小量和CAL增加量均小于不吸烟组(P<0.05),螺旋体比例降低量吸烟组亦较小(P<0.05)。结论 吸烟患者对SRP治疗的反应性较差,且对于局部抗生素治疗的敏感性亦较低。     

The effect of cigarette smoking on the severity of periodontal disease among older Thai adults

BACKGROUND: The aim of this study is to determine the effect of cigarette smoking on the severity of periodontitis in a cross-sectional study of older Thai adults. METHODS: The study population consisted of 1,960 subjects (age 50 to 73 years old). All subjects received both medical and dental examinations. Periodontal examinations, including plaque score, probing depth, and clinical attachment level, were done on all teeth present in two diagonal quadrants. Sociodemographic characteristics and smoking status were obtained by questionnaires. Multinomial logistic regression was used to address the association between cigarette consumption and mean clinical attachment level. RESULTS: In this study population, 48.7% were non-smokers, 14.4% were current smokers, and 36.9% were former smokers. Current smokers had higher percentage of sites with plaque, deeper mean probing depth, and greater mean clinical attachment level than former smokers and non-smokers. The odds of having moderate and severe periodontitis for current smokers were 1.7 and 4.8 times greater than non-smokers, respectively. Former smokers were 1.8 times more likely than non-smokers to have severe periodontitis. Quitting smoking reduced the odds of having periodontitis. For light smokers (<15 packyear), the odds for severe periodontitis reverted to the level of non-smokers when they had quit smoking for > or =10 years. For moderate and heavy smokers (> or =15 packyear), the odds of having severe periodontitis did not differ from those of non-smokers when they had quit smoking for > or =20 years. CONCLUSIONS: There was a strong association between cigarette smoking and the risk of periodontitis among older Thai adults. Quitting smoking appears to be beneficial to periodontal health.     

Periodontitis in smokers and non-smokers: intra-oral distribution of pockets

AIM: The purpose of the present study was to establish retrospectively whether the disease severity differs between smokers and non-smokers. METHODS: The study population consisted of 183 periodontitis patients, 79 smokers and 104 non-smokers. These subjects had been referred by general dentists to the Clinic for Periodontology, Utrecht, because of periodontal problems and were selected on the basis of the clinical diagnosis: adult periodontitis. The proportion of bleeding sites and the intra-oral distribution of probing pocket depth was evaluated. RESULTS: No statistically-significant differences between smokers (SM) and non-smokers (NSM) were found regarding the mean % of sites that bled upon probing (SM=76%, NSM=72%). Overall differences in the prevalence of probing depths > or =5 mm between smokers and non-smokers were found (SM=44%, NSM=34%). The proportion of sites with a probing pocket depth of > or =5 mm was consistently higher in smokers in the anterior, premolar and molar regions. The data also show that in the upper jaw at the anterior and premolar teeth, the largest differences are found between smokers and non-smokers. Smokers have more sites with a pocket depth > or =5 mm, especially on the lingual surfaces of these teeth. CONCLUSIONS: The present study indicates that cigarette smoking is a factor associated with deeper periodontal pockets and an intra-oral distribution that is suggestive of a local effect.     

Effects of smoking on periodontal tissues

BACKGROUND/AIMS: Most studies about the association between tobacco and periodontal disease have shown that tobacco negatively affects periodontal tissues, although some authors have failed to demonstrate such association. Very few studies have tried to find out whether the effect of tobacco on periodontal tissues was similar for women and men. The aims of this investigation were to confirm the possible relationship between tobacco consumption and periodontitis, to study the correlation between intensity of smoking and disease severity, and to investigate any differences between genders related to the effects of tobacco consumption in periodontal health. MATERIAL AND METHODS: In this case-control study, 240 dental patients were selected according to previously defined criteria and were divided in two groups according to their periodontal status. Patients with established periodontitis constituted the case group. The remaining patients constituted the control group. Smoking status, probing depth, gingival recession, clinical attachment level, tooth mobility, periodontal bleeding index and plaque index were determined for each participant. Generated data were processed for statistical analysis using multiple comparisons, covariance analysis and logistic regression analysis. RESULTS: Logistic regression analysis showed that smokers had 2.7 times and former smokers 2.3 times greater probabilities to have established periodontal disease than non-smokers, independent of age, sex and plaque index. Among cases, probing depth, gingival recession and clinical attachment level were greater in smokers than in former smokers or non-smokers, whereas plaque index did not show differences. Bleeding on probing was less evident in smokers than in non-smokers. There was a dose-effect relationship between cigarette consumption and the probability of having advanced periodontal disease. The association between tobacco smoking and periodontal disease was more evident after 10 years of smoking, independent of age, gender and plaque index. Finally, it was observed that tobacco affected periodontal tissues more severely in men than in women. CONCLUSIONS: Smoking is a risk factor strongly associated with periodontitis. The effects of smoking on periodontal tissues depend on the number of cigarettes smoked daily and the duration of the habit. The effect of tobacco on periodontal tissues seems to be more pronounced in men than in women.     

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     

Serum IgA and IgG antibodies to Treponema vincentii and Treponema denticola in adult periodontitis, juvenile periodontitis and periodontally healthy subjects

13 patients with untreated adult periodontitis (AP) were compared to 8 subjects free of periodontal disease (H) with respect to plaque index (PlI), gingival index (GI), probing depth (PD) and differential counts of subgingival bacterial morphotypes from a pooled sample of 6 surfaces with the greatest probing depth. Serum antibody levels to T. vincentii and T. denticola strains were also determined in these subjects as well as in the sera from 5 subjects with localized juvenile periodontitis (LJP). Subjects with AP had significantly elevated proportions of spirochetes and motile rods and lower proportions of coccoid cells than H subjects. They also exhibited significantly higher PlI and GI scores and greater probing depths. Antibody levels were normalized against a standard serum and expressed as ELISA units (EU). IgA and IgG antibody levels to all tested spirochete strains were significantly elevated in AP subjects as compared to subjects in group H or subjects with LJP. No significant differences in antibody titers were detectable between the H and LJP groups with respect to any of the tested strains. No significant correlation could be demonstrated between serum antibody titers to any of the oral spirochete strains tested and the proportions of oral spirochetes determined microscopically.