Exposure to tobacco smoking and periodontal health

BACKGROUND: The influence of smoking behavior on the periodontal health condition was clinically and radiographically studied in 257 dentally aware adults in the age range 20-69 years, including 50 current smokers, 61 former smokers and 133 non-smokers. AIMS: The clinical variables to be investigated were frequency of diseased sites > or =4 mm, frequency of gingival bleeding sites and plaque index. In addition, the periodontal bone height was radiographically assessed as a % of the dental root length. METHODS: All variables were based on full-mouth examinations including all teeth and periodontia. RESULTS: The observations indicated an inferior periodontal health condition associated with smoking. This was evidenced by a significantly greater frequency of diseased sites and a significantly greater reduction of periodontal bone height in current smokers as compared to non-smokers. The condition of former smokers was intermediate between current smokers and non-smokers, suggesting that former smokers who have quit smoking have a better periodontal health condition than current smokers, although worse than that of non-smokers. The finding that former smokers exhibited less disease than current smokers suggests that smoking cessation may be beneficial and mitigate the untoward effects inflicted by smoking, allowing a normalization towards non-smoker conditions. Heavy exposure was consistently associated with more severe a condition than light exposure, suggesting that the relationship between smoking exposure and periodontal morbidity is dose-dependent. CONCLUSIONS: Altogether, the present observations identify a negative impact from smoking on periodontal health and provide further evidence that tobacco smoking is an avoidable risk for periodontal disease.     

Influence of tobacco smoking on periodontal bone height. Long-term observations and a hypothesis

AIM: The aim of the investigation was to estimate the magnitude of the long-term influence of chronic smoking on the periodontal bone height. METHODS: The study population included 19 continuous smokers, 28 former smokers and 44 non-smokers in the age range 20-60 years at baseline. The participants were examined at two points in time with an interval of 10 years. The height of the periodontal bone was determined from bite-wing radiographs of the first and second premolars of the maxilla and the mandible and measured from the cemento-enamel junction (CEJ) to the periodontal bone crest (PBC) mesially and distally to the preselected teeth. RESULTS: The mean (SD) CEJ-PBC distance at baseline was 1.82 (1.01) mm for smokers, 1.65 (0.81) mm for former smokers, and 1.16 (0.59) mm for non-smokers (p=0.016). The mean (SD) 10-year bone height reduction was 0.74 (0.59) mm for smokers as against 0.26 (0.31) mm for former smokers and 0.27 (0.29) mm for non-smokers. Controlling for age and baseline bone height level, the magnitude of the reduction was significantly dependent of smoking (p=0.000). The widening gap between smokers and non-smokers over time suggested that the bone height reduction of smokers took place at an accelerated rate. CONCLUSION: On the basis of the observations it is hypothesized that smoking induces an acceleration of the periodontal bone height reduction rate and that smoking cessation results in a return towards non-smoker rate.     

Long-term effect of smoking on vertical periodontal bone loss

OBJECTIVES: The objective of the present study was to investigate the influence of smoking on vertical periodontal bone loss over 10 years. MATERIAL AND METHODS: The study base consisted of a population that was examined on two occasions with a 10-year interval, including 91 individuals, 24 smokers, 24 former smokers, and 43 non-smokers. The assessment of vertical bone loss was based on full sets of intra-oral radiographs from both time points. The severity of vertical bone loss was expressed as the proportion of proximal sites with vertical defects per person. RESULTS: The 10-year increase in the proportion of vertical defects was statistically significant in all groups (p<0.001) and, in addition, significantly associated with smoking (p<0.05). In particular, the difference between smokers and non-smokers was significant (p<0.01) whereas former smokers did not differ from non-smokers. Moreover, the 10-year vertical bone loss was significantly greater in heavy exposure smokers than in light exposure smokers suggesting an exposure-response effect (p<0.01). Compared with non-smokers the unadjusted 10-year relative risk was 2.3-fold increased in light exposure smokers and 5.3-fold increased in heavy exposure smokers (p<0.05). CONCLUSIONS: The present observations indicate a significant long-term influence of smoking on vertical periodontal bone loss, yielding additional evidence that smoking is a risk factor for periodontal bone loss.     

Tobacco smoking and periodontal bone height in a Saudi Arabian population

AIM: To study the association between tobacco smoking, in particular water pipe smoking, and periodontal bone height. METHODS: A study sample of 355 individuals in the age range 17-60 years was recruited from Jeddah, Saudi Arabia. The smoking behavior was registered through a questionnaire during interview. Participants were stratified into water pipe smokers (33%), cigarette smokers (20%), mixed smokers (19%) and non-smokers (28%). The periodontal bone height was measured from digital panoramic radiographs mesially and distally to each tooth and expressed as a percentage of the root length. RESULTS: The mean periodontal bone height was 76.2% for water pipe smokers, 75.8% for cigarette smokers, 80.2% for mixed smokers and 80.9% for non-smokers. The association between smoking and mean bone height was statistically significant controlling for age (p<0.001). The association between life-time smoking exposure and mean bone height controlling for age was statistically significant in water pipe smokers and cigarette smokers (p<0.01). The prevalence of bone loss in excess of 30% of the bone height was 27% in water pipe smokers, 24% in cigarette smokers, 9% in mixed smokers and 6% in non-smokers. The prevalence was significantly greater in water pipe smokers and cigarette smokers compared with non-smokers (p<0.001). The relative risk of periodontal bone loss associated with water pipe and cigarette smoking after adjustment for age was 3.5-fold and 4.3-fold elevated, respectively, compared with non-smoking (p<0.01). CONCLUSION: An association between tobacco smoking and periodontal bone height reduction is observed. The impact of water pipe smoking is of the same magnitude as that of cigarette smoking.     

Cigarette smoking and periodontal bone loss

The association between smoking and loss of periodontal bone height was investigated in Swedish dental hygienists. The study group included 210 subjects: 24 to 60 years of age, 30% smokers, 32% former smokers, and 38% non-smokers. The study was based on bite-wing radiographs, where loss of the interproximal bone height was measured as the distance from the cemento-enamel junction (CEJ) to the interdental septum (IS). The magnitude of the CEJ-IS distance was read at 12 sites, representing 3 maxillary and 3 mandibular bone septa in each subject. The CEJ-IS distance was significantly greater for smokers when compared to non-smokers, mean +/- SEM 1.71 +/- 0.08 mm and 1.45 +/- 0.04 mm, respectively. The mean +/- SEM for former smokers was 1.55 +/- 0.05 mm. In smokers, the CEJ-IS distance increased with increased smoking exposure. The results, based on adults with good oral hygiene, suggest that loss of periodontal bone is related to smoking. The smoking related bone loss is not correlated with plaque infection.     

Interleukin-1 genetic association with periodontitis in clinical practice

BACKGROUND: Periodontitis is a bacterial disease modified by multiple risk factors. The pro-inflammatory cytokine interleukin- (IL-1) is a key regulator of the host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. It has been reported that variations in the IL-1 gene cluster on chromosome 2 are associated with increased susceptibility to severe adult periodontitis. METHODS: The present study evaluated the association between a composite IL-1 genotype, including allele 2 at each of two loci (IL-1A +4845 plus IL- B +3954), and a broad spectrum of periodontally healthy to diseased patients in a population that is typically encountered in a dental practice setting. Ninety patients, non-smokers or former smokers with less than 10 pack-year (pk/yr) history, were recruited from a private dental practice. The major outcome variable was bone loss determined by computerized linear measurements of radiographs. Genotypes were analyzed from finger-stick blood samples using previously reported methods. RESULTS: Multivariate logistic regression models demonstrated that patient age, former smoking history, and the IL-1 genotype were significantly associated with severity of adult periodontitis. For non-smokers or former light smokers (<5 pk/yr), IL-1 genotype positives were at increased odds ratio of having moderate to severe periodontal disease of 3.75 (95% CI: 1.04-13.50) to 5.27 (95% CI: 1.23-22.70), depending on ethnicity, compared to IL-1 genotype negatives. Former moderate smokers (>5 pk/yr and <10 pk/yr) who were IL-1 genotype negative were at increased odds ratio of having moderate to severe periodontal disease of 7.43 (95% CI: 1.20-46.20) compared to non-smokers or former light smokers who were IL-1 genotype negative. In addition, past smoking history was also a significant effect modifier as demonstrated by the statistically significant interaction between past smoking history status and IL-1 genotype status. CONCLUSIONS: This study demonstrates that the composite IL-1 genotype is significantly associated with the severity of adult periodontitis. It also confirmed that both IL-1 genotyping and smoking history provide objective risk factors for periodontal disease in a private practice environment.     

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.     

Cigarette smoking and alveolar bone height in subjects with a high standard of oral hygiene

Smokers and non-smokers were compared with respect to alveolar bone height. The study covered 235 subjects aged 21-60 years, 72 of whom were smokers. Oral hygiene status and dental care habits were above average and of equal standard in both groups (PlI = 0.9). Alveolar bone height was assessed on radiographs and expressed as % of the root length. Alveolar bone height was significantly reduced in smokers as compared to non-smokers, the mean +/- SEM being 77.9 +/- 1.3% and 82.8 +/- 0.6%, respectively (P less than 0.001). Regression analysis suggested that periodontal breakdown judged from loss of alveolar bone over time was more accelerated in smokers than non-smokers. The lower bone height in smokers remained when age and oral hygiene were allowed for. It is concluded that smoking is a risk factor for periodontal health.     

The association of cigarette smoking with alveolar bone loss in postmenopausal females

BACKGROUND, AIMS: The purpose of this 2-year longitudinal clinical study was to determine the impact of smoking on alveolar bone height and density changes in postmenopausal females. METHODS: 59 postmenopausal women completed this study, including 38 non-smokers and 21 smokers. All subjects had a history of periodontitis, participated in 3- to 4-month periodontal maintenance programs and were within 5 years of menopause at the study outset. 4 vertical bite-wing radiographs of posterior sextants were taken at baseline and 2-year visits. Radiographs were evaluated using computer-assisted densitometric image analysis (CADIA); changes in interproximal alveolar bone density and changes in alveolar bone height were determined. Relative clinical attachment levels (RCAL) and presence/absence of plaque and bleeding on probing were recorded. RESULTS: Smokers exhibited a higher frequency of alveolar bone height loss (p<0.05) and crestal (p<0.03) and subcrestal (p<0.02) density loss relative to non-smokers. Smokers exhibited a trend (p<0.08) toward a higher frequency of > or =2.0 mm RCAL loss over the 2-year period. Plaque and bleeding on probing did not differ between smokers and non-smokers. A significant interaction, determined by repeated measures ANOVA, was noted between systemic bone mineral density (BMD) at the lumbar spine and smoking on alveolar bone density change (p<0.05). Only non-smoking patients with normal BMD realized a mean net gain in alveolar bone density; osteoporotic/osteopenic subjects (n=25) and smokers lost alveolar bone density. CONCLUSION: Postmenopausal female smokers were more likely to lose alveolar bone height and density than non-smokers with a similar periodontitis, plaque and gingival bleeding experience. In addition, both smoking and osteoporosis/osteopenia provided a negative influence on alveolar bone.     

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 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.     

Tobacco smoking and periodontal health in a Saudi Arabian population

BACKGROUND & AIM: Tobacco smoking exerts a harmful effect on the periodontal tissues manifested by periodontal pockets, attachment loss and periodontal bone loss. Current evidences on the effects of tobacco on periodontal health mainly concern cigarette smoking. In view of the increasing popularity of water pipe smoking in Arabian countries and reports confirming that water pipe smoking has health effects similar to those of cigarette smoking, there is a need for a better understanding of the potential harm of this smoking habit. The present thesis was carried out in order to explore whether water pipe smoking is associated with periodontal health in a manner similar to cigarette smoking. MATERIAL & METHODS: Residents in Jeddah City, Saudi Arabia, were invited to participate in the study by means of announcements in two daily newspapers. 355 individuals, 100 women and 255 men (17-60 years) responded to a standardized questionnaire and digital panoramic dental radiographs were taken. The questionnaire included information about oral hygiene practices, dental care and smoking habits. Of these subjects, 262 (73%) also volunteered for clinical examination, including assessments of oral hygiene, gingival inflammation and probing depth. Subgingival microbial test was carried out in 198 individuals for the detection of 12 different bacterial species most commonly associated with periodontal disease using the checkerboard DNA-DNA hybridization technique. Participants were stratified into water pipe smokers 33%, cigarette smokers 20%, smokers of both water pipe and cigarettes (mixed smokers 19%) and non-smokers 28%. RESULTS: Tobacco smoking is associated with a suppression of the gingival bleeding response to plaque accumulation. A suppressive effect was observed in both cigarette and water pipe smokers compared to non-smokers (Study I). Both cigarette and water pipe smoking were associated with the presence of more than 10 pockets of > or = 5 mm probing depth. The relative risk for periodontal disease was 5.1-fold and 3.8-fold increased in water pipe and cigarette smokers, respectively, compared to non-smokers (p < 0.01). The relative risk associated with heavy smoking was about 8-fold elevated in water pipe smokers and 5-fold elevated in cigarette smokers, suggesting an exposure-response effect (Study II). Tobacco smoking was associated with a reduction of the periodontal bone height. The reduction was of similar magnitude in water pipe smokers and cigarette smokers. The relative risk of periodontal bone loss of more than 30% of the root length was 3.5-fold and 4.3-fold elevated in water pipe and cigarette smokers, respectively, compared to non-smokers (p < 0.01). The relative risk associated with heavy smoking was 7.5-fold elevated in water pipe smokers and 6.3-fold elevated cigarette smokers (Study III). Further more, cigarette smokers, water pipe smokers and non-smokers exhibited similar periodontal microflora (Study IV). CONCLUSION: Tobacco smoking is associated with inferior periodontal health. The impact of water pipe smoking is of largely the same magnitude as that of cigarette smoking. The association between tobacco smoking and an inferior periodontal health seems to be independent of the subgingival microflora. Water pipe smoking habit should be considered in periodontal health.     

Production of volatile sulphur compounds in diseased periodontal pockets is significantly increased in smokers

OBJECTIVE: This study was undertaken in order to test the hypothesis that the consequences of tobacco smoking may include increased synthesis of toxic volatile sulphur compounds in diseased periodontal pockets. DESIGN: A cross-sectional, parallel study comparing groups of smokers and non-smokers with periodontitis and the level of volatile sulphur compounds in the gingival sulci of these subjects. PATIENTS AND METHODS: Levels of volatile sulphur compounds were measured in diseased periodontal sites of 12 smokers and 11 non-smokers using a portable sulphide monitor. Anaerobic and aerobic counts of the total cultivable subgingival microflora of both groups were also determined. RESULTS: The percentage of sites per subject with high levels of sulphides (> or = 10 units) detected in moderate (4-6 mm) and deep (> or = 7 mm) periodontal pockets was found to be significantly higher in smokers, compared to non-smokers (P = 0.040 and P = 0.005, respectively). No significant difference in the microbiological parameters tested were observed between the two groups. CONCLUSIONS: Increased production of volatile sulphur compounds may represent a further mechanism of increased susceptibility to periodontitis in smokers and also help to explain the reported association between smoking and halitosis.     

Some risk factors for periodontal bone loss in 50-year-old individuals. A 10-year cohort study

Objective: The aim of this 10-year prospective study of 50-year-old individuals was to analyze the incidence of periodontal bone loss and potential risk factors for periodontal bone loss. Methods: The subject sample was generated from an epidemiological survey performed in 1988 of subjects living in the County of Värmland, Sweden. A randomized sample of 15% of the 50-year-old inhabitants in the county was drawn. At the 10-year follow-up in 1998, 320 (75%) of the 449 individuals examined at baseline were available for re-examination, out of which 4 had become edentulous. Full-mouth clinical and radiographic examinations and questionnaire surveys were performed in 1988 and 1998. Two hundred and ninety-five individuals (69%) had complete data for inclusion in the analysis of radiographic bone changes over 10 years. Non-parametric tests, correlations and stepwise multiple regression models were used for statistical analysis of the data. Results: The mean alveolar bone level (ABL) in 1988 was 2.2 mm (0.05) and a further 0.4 mm (0.57) (p=0.000) was lost over the 10 years. Eight percent of the subject sample showed no loss, while 5% experienced a mean bone loss of 1 mm. Smoking was found to be the strongest individual risk predictor (RR=3.2; 95% CI 2.03–5.15). When including as smokers only those individuals who had continued with the habit during the entire 10-year follow-up period, the relative risk was slightly increased (3.6; 95% CI 2.32–5.57). Subjects who had quit smoking before the baseline examination did not demonstrate a significantly increased risk for disease progression (RR=1.3; 95% CI 0.57–2.96). Stepwise multiple regression analysis revealed that smoking, % approximal sites with probing pocket depth 4 mm, number of teeth and systemic disease were significant explanatory factors for 10-year ABL loss (R²=0.12). For never smokers, statistically significant predictors were number of teeth, mean ABL, % periodontally healthy approximal sites and educational level (R²=0.20). Conclusion: The inclusion of smokers in risk analysis for periodontal diseases may obstruct the possibility to detect other true risk factors and risk indicators.     

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.     

Cytokine profile in gingival crevicular fluid of aggressive periodontitis: influence of smoking and stress

BACKGROUND: Cigarette smoking and stress are considered risk factors that have been associated with periodontal disease progression. Conflicting results have been reported concerning the direct influence of smoking on the subgingival microbiota of periodontitis patients. Cytokine production may also be influenced by smoking and stress leading to an imbalance that disturbs the host-parasite relationship. AIM: The objective of the present study was to evaluate the influence of cigarette smoking on the gingival crevicular fluid (GCF) levels of interleukin (IL)-1beta, IL-4, IL-6 and IL-8 in aggressive or early onset periodontitis (EOP) patients and in healthy controls (H), psychosocial stress being considered as modifying factor. MATERIAL AND METHODS: Sixty-five EOP and 35 periodontally healthy individuals participated in this cross-sectional study. All the participants were interviewed about their smoking habits and their stressful social events. Clinical examination included the assessment of plaque index (PI), bleeding on probing (BOP), clinical attachment level (CAL) and probing pocket depth (PPD). GCF was collected using durapore strips, from four sites per patient, randomly selected in each quadrant. The total amounts of IL-1beta, IL-4, IL-6 and IL-8 were measured in a total of 400 samples using commercially available enzyme-linked immunosorbent assays. RESULTS: All clinical parameters were significantly higher in the EOP group compared to the H group. There were no significant differences between EOP smokers and EOP non-smokers with regard to plaque accumulation, CAL and PPD of the sampling sites, whereas mean CAL and PPD of the diseased sites were greater in EOP smokers than in EOP non-smokers. In addition, EOP smokers seemed to have significantly less BOP and greater bone loss compared to EOP non-smokers. Significant interactions between "EOP" and "smoking" were present for total amounts of IL-1beta and IL-4. IL-1beta, IL-6 and IL-8 showed significant main effects with healthy smokers and healthy non-smokers, respectively. For IL-8, stress presented a statistically significant interaction with smoking status and EOP (F=4.742, p=0.030). More specifically EOP smokers were statistically affected by stress. CONCLUSIONS: Smoking influences host-related factors including cytokine network. The relative importance of smoking and stress-related alterations and their precise mode of action in increasing the risk of aggressive periodontitis remains to be elucidated.     

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.     

Clinical expression of TNF-α in smoking-associated periodontal disease

Abstract. The level of TNF-α in gingival crevicular fluid (GCF) was analyzed with respect to smoking in patients with untreated moderate to severe periodontal disease including 30 current smokers, 19 former smokers and 29 non-smokers, in the age range 31–79 years, Concomitantly the occurrence of the periopathogens Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg) and Prevotella intermedia (Pi) and the GCF levels of albumin, IgA and IgG were analyzed. With regard to clinical characteristics, there were no statistically significant differences between smoking groups. The occurrence of patients positive for the periopathogens Aa, Pg and Pi was 28.2%, 41.0% and 91.0%, respectively. There were no statistically significant differences between smoking groups with regard to occurrence or relative frequency of these periopathogens. An exception was a significantly lower occurrence of Aa in former smokers as compared to non-smokers. The chief novelty of the study was the observation of a clearly increased level of TNF-α in GCF associated with smoking. Both current and former smokers exhibited significantly higher levels of TNF-α in comparison to non-smokers, whereas the levels of albumin, IgA and IgG were the same irrespective of smoking. In conclusion, the present observations in patients with moderate to severe periodontal disease suggest that smoking is associated with elevated GCF levels of the cytokine TNF-α.     

Influence of smoking on the outcome of periodontal surgery

Abstract. The 5-year outcome following periodontal surgery was evaluated in 57 patients that had received regular maintenance care throughout the follow-up period. The study population included 20 smokers, 20 former smokers and 17 non-smokers in the age range 37–77 years. The clinical characteristics evaluated were supragingival plaque, gingival bleeding and pocket probing depth. The region assigned for surgery was, in addition, radiographically evaluated in terms of periodontal bone height. Furthermore, the occurrence of the periopathogens Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg) and Prevotella intermedia (Pi) and the gingival crevicular fluid (GCF) levels of tumor necrosis factor alpha (TNF-α) were assessed at follow-up. Plaque index was 28.5% at baseline and 32.9% at follow-up, indicating a good standard of oral hygiene, and gingival bleeding 31.7% and 24.9%, respectively, suggesting a low to moderate level of gingival inflammation. In regions assigned for surgery, pocket probing depth decreased significantly from on average 5.6 mm to 4.3 mm ( p <0.0001) and periodontal bone height increased significantly from on average 62.5% to 67.5% ( p <0.0001). In terms of bone height, the outcome was less favorable among smokers compared with non-smokers. There was a predominance of smokers among patients exhibiting loss of bone height after the 5 years of maintenance. No significant associations were found between the therapeutical outcome and supragingival plaque or subgingival occurrence of periopathogens. The associations between GCF levels of TNF-α and probing depth and bone height were unclear, whereas the level of TNF-α was significantly elevated in smokers.     

Noxious effect of cigarette smoking on periodontal health

Periodontal probing depth, furcation involvement and tooth mobility were compared in smokers and non-smokers. The study covered 242 subjects aged 21–60 yr, 76 of whom were smokers. Oral hygiene status and dental care habits were above average and of similar standard in both groups (Pll = 0.9). Probing depth was measured at 6 sites around all teeth and sites with a depth of 4 mm or more were regarded as diseased. Both number and probing depth of pockets were significantly greater in smokers than in non-smokers. On average, smokers exhibited 36.0 sites with a probing depth of 4 mm or more, in contrast to 21.8 sites in non-smokers. Probing depth was 2.59 ± 0.06 (mean ± SEM) and 2.36 ± 0.03 in smokers and non-smokers, respectively. The relatively greater occurrence of pockets in smokers remained even when allowance was made for age and oral hygiene. There were also significantly increased numbers of teeth with furcation involvement, pocket involvement and hypermobility in smokers. It is concluded that smoking is associated with a deterioration in periodontal health and that the influence of smoking may be independent of plaque exposure.