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.     

Gingival blood flow in periodontitis patients before and after periodontal surgery assessed in smokers and non-smokers

BACKGROUND: The aim of this study was to evaluate the gingival blood flow of smokers and non-smokers with periodontal disease before and after surgical periodontal treatment. METHODS: Nine smokers and six non-smokers with at least two periodontal lesions were included in the study. Laser Doppler flowmetry was used to measure blood flow in two gingival sites and two skin sites. Two intrabony defects were treated surgically at the same time; enamel matrix derivative was applied at random to one of the sites, whereas the other site received a placebo gel. We measured resting gingival blood flow (GBF) and responses to cold pressor test (CPT) and to smoking and made continuous measurements of blood pressure (BP). Resting GBF levels of 26 young healthy subjects were used as a reference value. RESULTS: Resting GBF was significantly lower for the periodontitis patients compared to the reference subjects, regardless of smoking habits. GBF and gingival vascular conductance (VC) decreased significantly pre- and postoperatively in response to smoking. CPT evoked significant decreases in VC in smokers and non-smokers. Skin blood flow decreased significantly in response to CPT, more so in the non-smokers. BP was significantly higher in the non-smokers. CONCLUSIONS: Resting GBF of periodontitis patients was not lower in smokers than in non-smokers, but it was significantly lower than in the younger reference subjects. In contrast to our earlier findings in healthy subjects, smoking one cigarette may cause a decrease in GBF and VC in periodontitis patients. These observations suggested the existence of a dysfunction in the gingival vasculature in smokers and non-smokers with periodontitis.     

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.     

The effect of smoking on epithelial proliferation in healthy and periodontally diseased marginal gingival epithelium

BACKGROUND: Smoking causes an increase in the thickness of gingival epithelium, which is the outcome of increased keratinocyte proliferation or loss. Smoking-related changes in the proliferative activity of the gingival epithelium are largely uncharacterized for periodontal diseases. The aim of the present study was to determine the effects of smoking on the proliferation of the epithelium in periodontally diseased marginal gingiva by comparing the expression patterns of two different proliferation markers. METHODS: Gingival biopsies (N=60) were obtained from smokers who had clinically healthy gingiva (n=10), smokers with gingivitis (n=10), smokers with periodontitis (n=10), non-smokers with clinically healthy gingiva (n=10), non-smokers with gingivitis (n=10), and non-smokers with periodontitis (n=10). The quantitative measurement of maximum epithelial thickness was performed on hematoxylin and eosin-stained sections. The expression patterns for proliferating cell nuclear antigen (PCNA) and Ki67 were evaluated immunohistochemically. RESULTS: The percentage of PCNA-positive cells was higher than the percentage of Ki67-positive cells in all groups (P<0.001). When the mean values of PCNA and Ki67 were compared in each group, a statistically significant difference was observed only in the healthy smoker group (P=0.003). Significant differences in PCNA proliferation indices were only found between the smoker group and the non-smoker healthy group (P=0.015). CONCLUSIONS: Smoking had an affect on the proliferation of cells in the oral gingival epithelium, regardless of periodontal status. The increase in thickness of the epithelium was not associated with smoking; periodontal status and inflammation seemed to be more important factors. Smoking induced the replication activity of gingival epithelium and induced DNA repair.     

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.     

Potential mechanisms of susceptibility to periodontitis in tobacco smokers

Tobacco smoking is probably the most important, controllable environmental risk factor in periodontitis. It results in changes in the vascular, inflammatory, immune and healing responses. The degree of exposure to tobacco smoking can be measured in pack years or by measuring serum cotinine and nicotine levels. In a previous paper we reported elevated levels of serum soluble intercellular adhesion molecule-1 (sICAM-1) in smokers, regardless of periodontal status. Elevated sICAM-1 has been found to be a risk marker for cardiovascular disease. In the present paper we report the short-term effects of an episode of smoking on blood flow and levels of sICAM-1. Human volunteers included non-smokers, light smokers and heavy smokers. Relative blood flow was monitored in the gingivae and forehead skin using a laser Doppler flowmeter and serum levels of sICAM-1, cotinine and nicotine measured before during and up to 60 min following an episode of smoking. We could not provide evidence to support the theory that there is localized vasoconstriction within the gingival tissues. In contrast, there was a significant increase in blood flow in the forehead skin of light smokers which was not observed in non-smoking controls or in heavy smokers, suggesting a long-term tolerance in this latter group. The level of sICAM-1 remained unchanged during this episode, further suggesting a long-term effect. In a parallel group of subjects, we were able to demonstrate a direct significant correlation between sICAM and serum cotinine levels. These observations may be relevant to aetiological mechanisms in periodontitis and other smoking-associated diseases.     

Smoking-attributable periodontal disease in the Australian adult population

Background: The extent to which periodontitis is attributable to smoking in Australia has not been examined. Objectives: To investigate the smoking–periodontitis relationship and to estimate the public health impact of smoking on periodontitis in Australia. Material and Methods: The National Survey of Adult Oral Health 2004–2006 collected nationally representative oral epidemiologic data for the Australian adult population. Examiners measured probing pocket depth (PPD) and gingival recession at three sites per tooth to compute clinical attachment level (CAL). Moderate‐severe cases were defined as having: 2 interproximal sites (not on same tooth) with 4 mm CAL or with 5 mm PPD. Smoking status was defined as never‐, former‐ or current‐smoker. Current‐smokers were further classified into light‐, moderate‐ or heavy‐smoker using calculated pack‐years. Age, sex and socioeconomic position were examined as potential confounders. Results: Twenty‐three per cent were former‐smokers and 15% were current‐smokers. Prevalence of periodontitis was 23%. In unadjusted analyses, former‐ and current‐smokers had significantly higher periodontitis prevalence than never‐smokers. Relative to non‐smokers, adjusted prevalence ratios (95% confidence interval) for periodontitis were as follows: former‐smokers: 1.22 (1.03–1.46), moderate‐smokers: 1.63 (1.16–2.30); and heavy‐smokers: 1.64 (1.27–2.12). The population attributable fraction of smoking for moderate‐severe periodontitis was 32% (equivalent to 700,000 adults). Conclusion: Smoking has a significant impact on periodontal health of the Australian adults.     

吸烟对慢性牙周炎牙龈微循环影响的初步研究

目的 从牙龈微循环方面探讨吸烟促进慢性牙周炎的机制。方法 试验一选取慢性牙周炎吸烟患者（A组）、慢性牙周炎不吸烟患者（B组）、牙周健康不吸烟志愿者（C组）上前牙各102颗,应用激光多普勒血流仪进行上前牙区牙龈血流量（GBF）检测。试验二根据是否吸烟将牙周翻瓣术中取材牙龈分为吸烟组（A’组）和不吸烟组（B’组）,并将牙周健康不吸烟者行牙冠延长术或埋伏阻生智齿拔除术中取材牙龈作为对照组（C’组）,通过组织切片进行3组牙龈组织微血管密度（MVD）计数。采用SPSS 22.0软件包进行数据统计分析。结果 B组与C组相比,各牙位GBF均有增加,其中12牙、21牙、23牙差异有统计学意义（P<0.05）。B’组MVD高于C’组（P<0.05）;A’组与B’组MVD间差异无统计学意义（P>0.05）。结论 牙周炎症会引起GBF、牙龈MVD的增高,但吸烟并不会引起牙龈微循环（GBF、MVD）的显著变化,尚不支持吸烟通过影响牙龈微循环促进慢性牙周炎发生发展这一机制。     

吸烟对慢性牙周炎牙龈微循环影响的初步研究

目的 从牙龈微循环方面探讨吸烟促进慢性牙周炎的机制。方法 试验一选取慢性牙周炎吸烟患者（A组）、慢性牙周炎不吸烟患者（B组）、牙周健康不吸烟志愿者（C组）上前牙各102颗,应用激光多普勒血流仪进行上前牙区牙龈血流量（GBF）检测。试验二根据是否吸烟将牙周翻瓣术中取材牙龈分为吸烟组（A’组）和不吸烟组（B’组）,并将牙周健康不吸烟者行牙冠延长术或埋伏阻生智齿拔除术中取材牙龈作为对照组（C’组）,通过组织切片进行3组牙龈组织微血管密度（MVD）计数。采用SPSS 22.0软件包进行数据统计分析。结果 B组与C组相比,各牙位GBF均有增加,其中12牙、21牙、23牙差异有统计学意义（P<0.05）。B’组MVD高于C’组（P<0.05）;A’组与B’组MVD间差异无统计学意义（P>0.05）。结论 牙周炎症会引起GBF、牙龈MVD的增高,但吸烟并不会引起牙龈微循环（GBF、MVD）的显著变化,尚不支持吸烟通过影响牙龈微循环促进慢性牙周炎发生发展这一机制。     

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     

Cigarette smoking in patients referred for periodontal treatment

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 PlI, GI, probing depth and the patient's experience of gingival bleeding were recorded and compared between smoking and non-smoking patients. PlI 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.     

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.     

Smoking as a risk factor for periodontitis

Smokers have a higher susceptibility for periodontitis than non-smokers. Smoking is associated with more loss of attachment, progressive periodontal breakdown and also with a poor response to periodontal treatment. This is caused by the direct effect of nicotine on several factors that play a bacterial attack. These factors include the gingival vascularization and cellular defense mechanisms. The periodontal status of former smokers is intermediate to that of those who have never smoked and current smokers. Smoking cessation seems to have a beneficial effect on periodontal health.     

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.     

Smoking and crevicular fluid levels of IL-6 and TNF-a in periodontal disease

Smoking is a well-documented risk factor for periodontal disease, although the mechanisms of its negative influence are not well understood. In the present study, the influence of smoking on the gingival crevicular fluid (GCF) content of the pro-inflammatory cytokines IL-6 and TNF-alpha was investigated in patients with moderate to severe forms of the disease. The study base consisted of 108 patients including 45 current smokers, 28 former smokers and 35 non-smokers. The median GCF sample levels of IL-6 and TNF-alpha were 5.0 pg/ml and 61.0 pg/ml, respectively, for current smokers, 13.0 pg/ml and 51.0 pg/ml, respectively, for former smokers, and 10.0 pg/ml and 12.0 pg/ml, respectively, for non-smokers. The differences between smoking groups with regard to IL-6 were not significant suggesting that the IL-6 content was not influenced by smoking. In contrast, the TNF-alpha content was significantly increased in current smokers as compared to non-smokers confirming our previous observations. The present results in patients with moderate to severe periodontal disease may indicate different mediator functions of IL-6 and TNF-alpha in response to smoking.     

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.     

吸烟对牙周炎患者牙龈组织中成纤维细胞及胶原纤维的影响

目的研究吸烟对牙龈成纤维细胞和胶原纤维的影响.方法分别选取12例吸烟和10例不吸烟中重度牙周炎患者以及5例牙周健康者的牙龈组织标本,分为吸烟组、不吸烟组和对照组.通过Masson染色,光镜观察成纤维细胞和胶原纤维的形态及牙龈组织内胶原纤维相对面积的改变;另每组各选取3例标本,在透射电镜下观察牙龈成纤维细胞及胶原纤维的超微结构.结果吸烟牙周炎患者牙龈内胶原纤维破坏程度重于不吸烟组,新生胶原纤维少.吸烟组胶原纤维面积较不吸烟组无显著性差异(P＞0.05);在超微结构上,吸烟与不吸烟牙周炎患者牙龈成纤维细胞均存在明显的变性,吸烟组重于不吸烟组.结论吸烟可能通过对牙龈成纤维细胞和胶原纤维的损伤,降低牙周组织的修复能力.     

Laser Doppler flowmeter measurement of relative gingival and forehead skin blood flow in light and heavy smokers during and after smoking

AIM: To determine the effect of the smoking experience on relative blood flow in gingiva and to compare this to skin. METHOD: A laser Doppler flowmeter was used to record relative blood flow to healthy gingiva and to forehead skin in smokers and non-smoking controls. Smoking status was verified by quantitative analysis of serum cotinine. Continuous measurements were made over sequential periods with the subject at rest, during a sham smoking exercise, during smoking of a standard research cigarette (2R1, University of Kentucky) for 5 min and throughout a subsequent recovery period. Non-smoking controls sham smoked during the equivalent 5 minute smoking period. RESULTS: No significant differences with respect to the proportional changes of relative gingival blood flow between time points were observed between the groups. However, between-group comparisons of relative blood flow revealed a significant increase in the relative blood flow to the forehead skin of light smokers (serum cotinine < or =60 ng/ml; n=6), when compared to heavy smokers (serum cotinine > or = 100 ng/ml; n=9) or to non-smokers (serum cotinine < or = 10 ng/ml; n=6), 2 min following the smoking experience (p = 0.007). CONCLUSION: The results do not seem to support the theory that tobacco smoking causes localised vasoconstriction in the periodontal tissues in humans. These data show that smoking causes an acute increase in relative blood flow in forehead skin in light smokers compared to heavy smokers, suggesting a potential induction of tolerance in regular users of tobacco.     

吸烟对牙周基础治疗前后龈沟液量和弹性蛋白酶水平的影响

目的　评价吸烟是否影响牙周炎基础治疗前、后龈沟液 (gingivalcrevicularfluid ,GCF)量和龈沟液中弹性蛋白酶 (elastase ,EA)的水平。方法　将 37例男性慢性牙周炎患者分为吸烟组 (2 2例 ,12 2个牙位点 ,每日吸烟≥ 2 0支 )和非吸烟组 (15例 ,90个牙位点 )。牙周炎基础治疗前、后用滤纸条法收集GCF ,用Periotron 6 0 0 0龈沟液测量仪测定GCF量。对吸烟组 92个位点和非吸烟组 6 0个位点GCF样本 ,用底物分解法检测EA水平。结果　治疗前吸烟组GCF量 (139 2± 33 4 )U和EA水平(0 6 34± 0 5 87)明显低于非吸烟组 [GCF量 :(15 5 4± 39 7)U ,EA水平 :0 835± 0 5 72 ],P <0 0 1。治疗后 ,两组GCF量和EA水平均显著降低 (P <0 0 0 1)。但吸烟组 91个位点 (74 6 % )GCF和 70个位点(76 1% )的EA水平治疗后有改善 ;而非吸烟组高达 88个位点 (97 8% )GCF和 5 6个位点 (93 3% )的EA水平有改善 (P <0 0 1)。结论　治疗前探诊深度相同的情况下 ,吸烟组GCF量和EA水平均低于非吸烟组 ,治疗后吸烟组的GCF和EA的减少程度不如非吸烟组明显。     

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.