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.     

A 10-year prospective study of tobacco smoking and periodontal health

BACKGROUND: To date only a few studies have evaluated the long-term influence of smoking and smoking cessation on periodontal health. The present study, therefore, was undertaken with the aim to prospectively investigate the influence of smoking exposure over time on the periodontal health condition in a targeted population before and after a follow-up interval of 10 years. METHODS: The primary study base consisted of a population of occupational musicians that was investigated the first time in 1982 and scheduled for reinvestigation in 1992 and 2002. The 1992 investigation included 101 individuals from the baseline study constituting a prospective cohort including 16 smokers, who had continued to smoke throughout the entire length of the 10-year period; 28 former smokers who had ceased smoking an average of approximately 9 years before the commencement of the baseline study; 40 non-smokers, who denied ever having smoked tobacco; and 17 individuals whose smoking pattern changed or for whom incomplete data were available. The clinical and radiographic variables used for the assessment of the periodontal health condition of the individual were frequency of periodontally diseased sites (probing depth > or =4 mm), gingival bleeding (%), and periodontal bone height (%). The oral hygiene standard was evaluated by means of a standard plaque index. RESULTS: The changes over the 10 years with respect to frequency of diseased sites indicated an increased frequency in continuous smokers versus decreased frequencies in former smokers and non-smokers. Controlling for age and frequency of diseased sites at baseline, the 10-year change was significantly associated with smoking (P <0.001). The differences between current smokers and non-smokers, and between current and former smokers, respectively, were statistically significant (P<0.001). Moreover, the 10-year change increased significantly with increasing smoking exposure controlling for age (P= 0.01). In terms of periodontal bone height, the 10-year changes implied statistically significant reductions within current as well as former smokers (P <0.001 and P <0.05, respectively), but not within non-smokers. The overall change was significantly associated with smoking controlling for age and bone height level at baseline (P<0.01), including statistically significant differences between current smokers and non-smokers and between current and former smokers, respectively (P<0.05). Moreover, the 10-year bone height reduction increased significantly with increasing smoking exposure controlling for age (P <0.05). With regard to gingival bleeding, the 10-year differences between smoking groups were not statistically significant. Plaque index remained low throughout in all smoking groups at an overall average level of about 0.8. CONCLUSIONS: The results suggest that periodontal health is compromised by chronic smoking as evidenced by an increase of periodontally diseased sites concomitant with loss of periodontal bone height, as compared to non-smokers whose periodontal health condition remained unaltered throughout the 10-year period of investigation. The periodontal health condition in former smokers, similar to that of non-smokers, remained stable, suggesting that smoking cessation is beneficial to periodontal health.     

Risk indicators for periodontal disease in a remote Canadian community--a dental practice-based study

OBJECTIVES: The purpose of this cross-sectional study was to identify risk markers and risk indicators for periodontal attachment loss in a remote Canadian community. Of special interest was the association between smoking and periodontal disease experience. METHODS: Data were collected from a convenience sample of 187 adult patients attending a dental office in a rural community located in Northern Ontario. Information was obtained via a questionnaire and a periodontal examination. The questionnaire included the use of dental services, self-care behaviors, general health status, smoking, and personal characteristics. Periodontal health was assessed using the mean periodontal attachment loss (MPAL), measured at two sites on all remaining teeth and the proportions of sites examined with loss of 2 mm or more and 5 mm or more. Plaque scores and measures of the number of missing teeth also were obtained. The relationships between mean periodontal attachment loss, the proportion of sites with 5 mm or more of loss and independent variables such as age, sex, current smoking status, mean tooth plaque scores, flossing frequency, and regularity of preventive dental visits were examined in bivariate and multivariate analyses. RESULTS: The data revealed a mean periodontal attachment loss of 3.9 mm (SD=1.5). The mean proportion of sites examined with loss of 2 mm or more was 0.89 and the mean proportion with loss of 5 mm or more was 0.35. In linear regression analysis, plaque scores, the number of missing teeth, age, current smoking status, regularity of dental visits, and flossing frequency had statistically significant independent effects and explained 60.0 percent of the variance in mean periodontal attachment loss. Just over 30 percent of subjects had severe periodontal disease, defined as 50 percent or more of sites examined with loss of 5 mm or more. In logistic regression analysis, missing teeth, dental visiting, smoking status, age, and flossing frequency had significant independent effects. The strongest association observed was with smoking, which had an odds ratio of 6.3. The logistic regression model correctly predicted 64.3 percent of cases with severe disease. CONCLUSIONS: The data indicate that the periodontal health of these patients is poor. Risk indicators or markers of poor periodontal health in the population studied included missing teeth, plaque scores, age, current smoking status, regularity of dental visits, and flossing frequency. This supports previous findings that behavioral factors play an important role in periodontal disease.     

Relationship of cigarette smoking to attachment level profiles

OBJECTIVES: The present investigation examined clinical features of periodontal disease and patterns of attachment loss in adult periodontitis subjects who were current, past or never smokers. MATERIAL AND METHODS: 289 adult periodontitis subjects ranging in age from 20-86 years with at least 20 teeth and at least 4 sites with pocket depth and/or attachment level >4 mm were recruited. Smoking history was obtained using a questionnaire. Measures of plaque accumulation, overt gingivitis, bleeding on probing, suppuration, probing pocket depth and probing attachment level were taken at 6 sites per tooth at all teeth excluding 3rd molars at a baseline visit. Subjects were subset according to smoking history into never, past and current smokers and for certain analyses into age categories <41, 41-49, >49. Uni- and multi-variate analyses examined associations between smoking category, age and clinical parameters. RESULTS: Current smokers had significantly more attachment loss, missing teeth, deeper pockets and fewer sites exhibiting bleeding on probing than past or never smokers. Current smokers had greater attachment loss than past or never smokers whether the subjects had mild, moderate or severe initial attachment loss. Increasing age and smoking status were independently significantly related to mean attachment level and the effect of these parameters was additive. Mean attachment level in non smokers <41 years and current smokers >49 years was 2.49 and 4.10 mm respectively. Stepwise multiple linear regression indicated that age, pack years and being a current smoker were strongly associated with mean attachment level. Full mouth attachment level profiles indicated that smokers had more attachment loss than never smokers particularly at maxillary lingual sites and at lower anterior teeth. CONCLUSIONS: In accord with other studies, smokers had evidence of more severe periodontal disease than past or never smokers. At all levels of mean attachment loss, smokers exhibited more disease than never smokers. Difference in mean attachment level between smokers and never smokers at individual sites was not uniform. Significantly more loss was observed at maxillary lingual sites and lower anterior teeth suggesting the possibility of a local effect of cigarette smoking.     

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.     

Effect of cigarette smoking on human PDL fibroblasts attachment to periodontally involved root surfaces in vitro

BACKGROUND/AIM: Cigarette smoking is one of the most significant risk factors in the development and further advancement of inflammatory periodontal disease. However, no study has been performed to investigate the effect of smoking on the attachment of human periodontal ligament fibroblasts to either periodontally diseased or healthy roots. The present study was conducted to evaluate the attachment of fibroblasts derived from healthy human periodontal ligament (PDL) to periodontally diseased root surfaces of smokers. METHOD: The subjects included 14 smokers and seven nonsmokers with at least a single periodontally involved anterior tooth planned for extraction. In addition, seven impacted third molars, which had been removed from nonsmoking adolescents, were used as a healthy control. The smoking status of each patient was determined by classifying the volunteers into four groups according to their level of cigarette consumption at the initial examination (seven patients each). Nonsmoking subjects who had never smoked cigarettes and had healthy periodontium were called healthy control (G1). In subjects with periodontal diseases, nonsmoking subjects who had never regularly smoked cigarettes (< 2 cigarettes/week) were called positive control (G2), smokers consuming or=20 cigarettes/day were located in group G4. To exclude the effects of all local irritants except for the adsorbed tobacco products, all teeth were subjected to thorough scaling and root planing 1 week before extraction. After 1 week of meticulous home care and continued smoking experience, teeth were extracted and the periodontally involved test areas were prepared for PDL culturing. PDL cells were cultured on root segments for 24 h. Samples were prepared for SEM viewing, photographing and counting at x750 in a standard area. RESULTS: The results of this study indicated that smokers' data (G3, G4) revealed a significant reduction of attached PDL cells when compared to that of nonsmokers' healthy and positive controls (G1, G2). No significant difference in the mean number of attached cells was found between data derived from smokers' groups (G3 vs. G4). The attached cells in all groups varied in shape; they were flatter in the control groups, while they were round in smokers' groups, with no dose-dependent effect. CONCLUSION: The present results suggest that cigarette smoking compromises PDL cell adhesion to root planed surfaces, which might affect periodontal regeneration following therapy.     

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.     

Isolation and characterization of subgingival staphylococci from periodontitis patients and controls

OBJECTIVES: To isolate and characterize subgingival staphylococci from patients with periodontal disease and from periodontally healthy controls, to evaluate the periodontal environment as a potential source for systemic staphylococcal infections. METHODS: Periopaper strips were used to isolate subgingival staphylococci from 28 patients with chronic periodontitis and 28 periodontally healthy age and sex-matched controls. Staphylococci were identified by microbiological methods and antibiotic resistance profiles determined. RESULTS: Staphylococci were isolated from 54% diseased subgingival and 43% healthy subgingival sites in over 50% periodontitis patients and from 29% healthy subgingival sites in 54% controls. No significant differences in the frequency of isolation or numbers of staphylococci isolated from diseased and healthy sites were noted. Staphylococcus epidermidis was the predominant oral species. Seventy per cent (115 of 165) of all isolates were penicillin-resistant. CONCLUSIONS: Subgingival staphylococci are present in both periodontitis patients and controls. In periodontitis there is an increased risk of bacteraemia because of the increased dentogingival surface area. The dental and periodontal health of patients at risk from haematogenous infections should therefore be maintained at a high level. Antibiotic resistance profiles of the oral staphylococcal isolates suggest that amoxicillin may no longer be a suitable antibiotic for prophylaxis against systemic infections such as prosthetic valve endocarditis.     

PRESENCE OF BACTERIA IN DENTINAL TUBULES

This study demonstrated that a significant number of bacteria is present in the radicular dentinal tubules of periodontally diseased human teeth. Ten periodontally diseased teeth were prepared and stained by Brown and Brenn technique for histological examination. Bacteria were detected in all teeth. It is suggested that bacteria may invade dentinal tubules exposed to periodontal pocket and are very hard to be eliminated by conventional mechanical and chemical periodontal therapy. Contaminated dentinal tubules of periodontally diseased teeth can thus act as active bacterial reservoirs to promote recolonization of mechanically treated root surfaces, which could interfere with the periodontal healing and progression of the 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.     

Periodontal disease in mothers indicates risk in their children

Introduction.  It is well established that severe periodontitis clusters in families, but there are no data about the relationship between mothers with chronic periodontitis and their children's periodontal status.
Objective.  To evaluate a risk for periodontal diseases in children of periodontally diseased and healthy mothers.
Methods.  Four study groups were included: (I) 20 female patients with untreated generalized severe chronic periodontitis, (II) their children (34), (III) 13 periodontally healthy mothers and (IV) their children (13). Material was collected from years 2004–2006. The clinical examination included registration of visible plaque index, modified gingival index and, bleeding sites on probing. Periodontal microbiological samples were obtained from all study subjects and the isolates were identified according to morphology and biochemical profiles; similar interfamilial pathogens were compared by PCR-technique.
Results.  The children of diseased mothers more frequently had periodontal diseases, especially gingivitis. In addition, clinical parameters of gingival inflammation were more expressed and oral hygiene was worse in this group of children. VPI and VPI% of the diseased and healthy mothers differed significantly. The most common oral pathogens were P. intermedia/nigrescens and A. actinomycetemcomitans . The children of healthy mothers harboured pathogens less frequently than the children of diseased mothers. The sharing of P. intermedia/nigrescens was more frequent (5 families) than A. actinomycetemcomitans (2 families).
Conclusion.  Maternal indicators, such as periodontitis, hygiene habits, and periodontal microflora are risk factors for childhood periodontal diseases, and might be predictive of future childhood and adolescent periodontitis.     

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.     

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.     

DNA probe analysis in smoker and non smoker rapidly progressive periodontitis patients--a pilot study.

Smoking is one of the most significant risk factors in the development and further advancement of inflammatory periodontal disease. The bacteria A. actinomycetemcomitans, P. gingivalis and P. intermedius as indicated as the potential pathogens associated with periodontal disease. Since the bacteria mentioned as well as smoking are factors associated with periodontitis it is of importance to elucidate the interrelationship between these factors. The purpose of this study was to investigate the prevalence of A. actinomycetemcomitans, P. gingivalis and P. intermedius in subgingival plaque samples obtained form healthy and diseased sites of patients with rapidly progressive periodontitis who were smokers and non smokers along with other clinical parameters.     

Prevalence of chronic periodontal disease using probing depth as a diagnostic test

The prevalence of chronic periodontal disease was investigated using the occurrence of diseased pocket sites as the diagnostic criterion. The study group comprised 250 dentally aware subjects aged 21-60 years, with a high number of teeth remaining in all age groups. The % of sites with a probing depth of greater than or equal to 4 mm was 16% for the total sample. Most diseased sites (69%) were in the 4-mm class, with only 4% at depths greater than or equal to 7 mm. 82% on the subjects had 1 or more sites greater than or equal to 4 mm. With probing depth as the sole criterion for diagnosis of chronic periodontal disease, prevalence in a sample is heavily dependent on the critical levels selected for probing depth and cut-off point. With critical levels of 4 mm for probing depth and 1 diseased site for the cutoff point, prevalence was 49% in the 21-30 year age group and 95% in the 51-60 year age group. A shift in cutoff point to 40 diseased sites gave a prevalence of 2% and 41%, respectively, in the 2 age groups. For a critical depth of 7 mm and a cutoff point of 1 diseased site, the prevalence was 2% and 43% for the 2 age groups, respectively. Aspects of importance for the decision-making process on disease are discussed.     

Progression of periodontal disease in a maintenance population of smokers and non-smokers: a 3-year longitudinal study

BACKGROUND: Cigarette smoking is accepted as an important factor that increases the risk for the initiation and progress of chronic periodontitis. However, the effect of cigarette smoking on the recurrence of disease in patients undergoing regular maintenance therapy is less understood. Therefore, we set out to assess disease progression longitudinally in smoking and non-smoking subjects with chronic periodontitis undergoing periodontal maintenance therapy every 3 to 4 months. METHODS: A total of 108 subjects undergoing regular maintenance therapy for chronic periodontitis were followed over a 3-year period. Self-reports of smoking status were confirmed by analysis of exhaled carbon monoxide concentrations. Clinical parameters (plaque index [PI], bleeding on probing [BOP], clinical attachment loss [CAL], probing depth [PD], and tooth loss) were recorded at yearly reevaluation visits. The study was carried out in a university hospital setting. RESULTS: Longitudinal measurements were obtained from 81 (75%) subjects. There were no differences in inflammatory indices at baseline or over time (PI and BOP; both P >0.05) between smokers (N = 16; age: 54 +/- 6 years) and non-smokers (N = 65; age: 59 +/- 14 years). Likewise, there was no difference between the smoking groups with respect to disease progression (measured as changes in prevalence [number] and proportion [percentage] of progressing sites and as mean CAL, PD, and tooth loss; all P >0.05). CONCLUSION: In this small population, regular maintenance treatment in a cross-section of highly motivated subjects with chronic periodontitis seemed to be equally successful in preventing progressive periodontal tissue destruction in current smokers and current non-smokers.     

Smoking and GCF levels of IL-1beta and IL-1ra in periodontal disease

AIMS: GCF levels of the cytokine IL-1beta and its receptor antagonist IL-1ra were analyzed with respect to smoking in patients with moderate to severe periodontal disease. The study population included 22 smokers and 18 non-smokers in the age range 32-86 years. Concomitantly, the GCF levels of IgA, IgG, albumin and total protein were analyzed. METHOD: Samples of GCF were obtained from 2 diseased sites in each patient by means of an aspiration method. IL-1beta, IL-1ra, IgA and IgG were determined with immunoelectrophoresis. Total protein was determined by the BCA method. RESULTS: The clinical characteristics in terms of probing depth and frequency of diseased sites and supragingival plaque did not differ between smokers and non-smokers. Gingival bleeding, however, was significantly depressed in smokers. IL-1beta was detected in GCF of 95% of both smokers and non-smokers and IL-1ra in all patients. The GCF level of IL-1ra was approximately 1,000-fold that of IL-1beta. The GCF levels of IL-1beta and IL-1ra were high in comparison with those of TNF-alpha and IL-6 determined by the same method in our earlier studies. CONCLUSION: Our observations did not reveal any influence of smoking on the levels of IL-1beta and IL-1ra in GCF.     

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.     

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.