Evaluation of 2 methods to assess gingival bleeding in smokers and non-smokers in natural and experimental gingivitis

Abstract. The purpose of the present study was to compare the bleeding tendency as elicited by probing the marginal gingiva (BOMP) and probing to the bottom of the pocket (BOPP) in smokers and non-smokers in natural gingivitis and during experimental gingivitis, 11 smokers (sm) and 14 non-smokers (nsm) were recruited. When they had less than 20% approximal bleeding sites, they entered a 14-day trial period of experimental gingivitis'. Subjects returned 30 days later, after resuming normal oral hygiene procedures, for a final gingival assessment. A split-mouth design was chosen using 2 contra-lateral quadrants for each index (being either BOMP or BOPP). A consistently higher bleeding score of approximately 10% was observed by probing to the bottom of the pocket. At day 14 with both indices, a significant difference between smokers and non-smokers was detected (BOMP: sm=15%, nsm = 30%; BOPP: sm = 27%, nsm=44%). The increment between gingival health and experimental gingivitis was significantly higher in non-smokers than in smokers but comparable for both indices (BOMP: sm=8%, nsm = 23%; BOPP: sm=9%, nsm=26%). Probing to the bottom of the pocket results in significantly more bleeding in gingival health and gingivitis as compared to probing of the marginal gingiva. This shows that evaluation of the gingival condition with BOMP, the method of choice with respect to gingivitis, can be used as a parameter for inflammation when comparing smokers and nonsmokers. The suppressed inflammatory response to plaque accumulation, as observed in smokers, indicates that they should be identified as a separate group when they participate as panellists in (experimentally induced) gingivitis     

Gingival recession in smokers and non-smokers with minimal periodontal disease

BACKGROUND/AIMS: Smoking is a major risk factor for destructive periodontal disease. There is limited information with regard to effects of smoking in subjects with minimal periodontal destruction. The aim of the present investigation was to assess the development of gingival recession in young adult smokers and non-smokers. METHODS: 61 systemically healthy young adults, 19 to 30 years of age completed the final examination. 30 volunteers smoked at least 20 cigarettes per day, whereas 31 subjects were non-smokers. Clinical periodontal conditions were assessed 4x within a time period of 6 months. Site-specific analyses considering the correlated structure of data were performed. RESULTS: At the outset, 50% of subjects presented with gingival recession at 1 or more sites. There was no significant difference in the prevalence of gingival recession between non-smokers and smokers. Severe recession in excess of 2 mm affected about 23% non-smokers but only 7% smokers. Some further gingival recession developed during the 6-month observation period. In a multivariate logistic regression analysis, the risk for recession development appeared not to be influenced by smoking status after adjusting for periodontal probing depth, recession at baseline, tooth brushing frequency, gender, jaw, tooth type and site. CONCLUSIONS: Present data did not support the hypothesis that smokers are at an increased risk for the development of gingival recession.     

Parotid salivary S-IgA antibodies during experimental gingivitis in smokers and non-smokers

Persons who smoke display a less pronounced increase of gingival bleeding in the experimental gingivitis model as compared with non-smokers. The aim of the present study was to investigate whether this could partly be explained by differences in levels of parotid total secretory IgA (S-IgA) or parotid S-IgA reactive with selected oral microorganisms. Parotid saliva samples were obtained from 11 smoking and 14 non-smoking volunteers, at baseline, after 5 and 14 days of full mouth experimental gingivitis. Output levels of total S-IgA and of specific S-IgA reactive with cell extracts from Actinobacillus actinomycetemcomitans, Actinomyces naeslundii, Campylobacter rectus, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus micros, Streptococcus gordonii and Streptococcus mutans were determined in the samples by means of ELISA. Smokers and non-smokers were found to have similar output levels (microg/min) of total S-IgA, and the values did not significantly change during the experimental gingivitis trial. Parotid salivary outputs (units/min) of the bacteria-specific S-IgA at baseline and at days 5 and 14, were not different between smokers and non-smokers; no changes were observed during the experimental gingivitis trial. The present observations indicate that total S-IgA and bacteria-specific S-IgA in saliva are not main factors that can explain the less pronounced increase of gingival bleeding in the experimental gingivitis model in smokers as compared with non-smokers.     

Salivary cystatin activity and cystatin C in natural and experimental gingivitis in smokers and non-smokers

Background: Recent studies show that subjects with natural gingivitis or periodontitis have elevated levels of salivary cystatins compared to periodontally healthy individuals. Increased glandular output of cystatins in inflammatory conditions suggests an active, most likely protective, rôle for these proteins in inflammatory processes. Furthermore, it has been shown that the development of gingival inflammation is suppressed in smokers during experimental gingivitis. Aims: The purpose of the present study was to investigate whether (i) the levels of salivary cystatins in natural gingivitis are related to smoking status, and (ii) to study whether experimentally induced gingivitis is associated with changes in salivary cystatin levels, in both smokers and non‐smokers. Material and Methods: Whole saliva samples were taken in relation to natural gingivitis, gingival health and 14‐day experimental gingivitis in 25 non‐dental students (14 non‐smokers and 11 smokers). The salivary flowrate was determined. Samples were analyzed for levels of protein, cystatin and cystatin‐C. Results: Salivary flow and protein concentrations in cleared human whole saliva samples of non‐smokers and smokers were not different from each other at any timepoint during the trial. With regard to cystatins, the results showed that in the state of natural gingivitis cystatin activity is lower in smokers as compared to non‐smokers. In smokers, the resolution of natural gingivitis to the state of gingival health did not result in a change of cystatin activity and levels of cystatin C. At the end of the 14‐day experimental gingivitis period, smokers showed a decrease in cystatin activity and cystatin C as well as lower outputs of cystatin activity and cystatin C. Conclusion: Smoking is associated with lower cystatin activity and output of cystatin C during gingival inflammation.     

The association between neutrophil numbers and interleukin-1alpha concentrations in gingival crevicular fluid of smokers and non-smokers with periodontal disease

OBJECTIVES: To test whether neutrophil numbers are directly correlated with interleukin-1alpha (IL-1alpha) concentrations in gingival crevicular fluid (GCF) of patients with periodontitis, and to investigate the effects of smoking on these parameters. MATERIALS AND METHODS: A total of 99 GCF samples from 33 patients (14 smokers) suffering from severe chronic periodontitis were collected using Durapore filter strips. Polymorphonuclear leucocyte (PMN) numbers were counted using a Coulter cell counter and IL-1alpha levels were determined by ELISA. Total GCF protein was measured by Bio-Rad assay as a surrogate measure of GCF volume. RESULTS: Mean IL-1alpha concentrations were significantly reduced in smokers compared with non-smokers (non-smokers: 3.29+/-2.02 pg/microg protein, smokers 1.59+/-1.13 pg/microg protein). There was no association between PMN numbers and IL-1alpha concentrations found when analysed either by site or by patient. PMN numbers were not significantly different between the two groups (non-smokers: 1.16 x 10(6)+/-1.04 x 10(6); smokers: 7.30 x 10(5)+/-8.07 x 10(5)). Smoking did not affect mean total protein concentration of samples. CONCLUSIONS: Smoking significantly decreased IL-1alpha concentrations in GCF without affecting GCF volume sampled. The lack of association between IL-1alpha concentration and neutrophil numbers suggests that the reduced IL-1alpha concentrations seen in smokers is independent of any possible effect of smoking on neutrophil chemotaxis, and further suggests that smoking may directly inhibit IL-1alpha production.     

Effect of non-surgical treatment on gingival bleeding in smokers and non-smokers

According to previous findings, gingival bleeding seems to be reduced under the influence of cigarette smoking. The present study deals with the effect of non-surgical therapy on gingival bleeding in smokers and non-smokers. The underlying hypothesis was that the therapeutic effect in terms of reduction of gingival bleeding might differ in smokers and non-smokers. Twenty patients with moderate to severe periodontitis, 10 smokers and 10 non-smokers, took part in the study. Gingival bleeding was assessed by probing under a standardized pressure (60 g), and measurements were performed before and 1 month after the completion of active treatment. The active treatment included debridement of supra- and sub-gingival deposits by means of hand instrumentation. The treatment caused a reduction in plaque index and gingival bleeding both in smokers and in non-smokers. The plaque reduction was significantly greater in smokers. Nevertheless, the reduction in gingival bleeding was significantly less pronounced than that attained in non-smokers. The findings suggest that the gingival bleeding response to treatment is reduced in smokers. It would seem that in response to a given amount of plaque reduction the changes in gingival bleeding will be less apparent under the influence of smoking.     

Association between smoking,betel chewing and gingival bleeding in rural Sri Lanka

OBJECTIVE: To ascertain the association between tobacco use and gingival bleeding in a rural community in Sri Lanka. MATERIAL AND METHODS: A cross-sectional field-based study was carried out in 2178 rural males aged 20-60 years, employing a multistage cluster sampling technique. The levels of plaque and gingivitis were recorded on four sites of all teeth present excluding third molars, using the plaque index (PLI) and gingival index (GI). Information pertaining to sociodemographic variables, oral hygiene practices and tobacco consumption habits was obtained from all subjects. RESULTS: One-way anova combined with the Bonferroni test disclosed that betel chewers had a significantly higher mean number of sites with gingival bleeding (22.6+/-21.8) than smokers (10.8+/-11.2) and nontobacco users (8.7+/-6.8) (p<0.0001). A higher proportion of betel chewers (55.1%) showed > or =12 bleeding sites compared to smokers (27.6%). Logistic regression analysis revealed that the association between betel chewing and gingival bleeding was positive (OR=2.41; p<0.0001) whereas that of smoking and gingival bleeding was negative (OR=0.75; p<0.05). Oral hygiene had the strongest relationship with gingival bleeding (OR=18.11). CONCLUSION: While confirming the masking effect of smoking on gingival bleeding, these findings indicate that betel chewing might significantly enhance gingival bleeding in the population studied.     

Toothbrushing efficiency in smokers and non-smokers

The present study was conducted to determine whether smokers have more plaque than non-smokers, and whether higher plaque scores subsequently found in smokers could be explained by differences in toothbrushing time, efficiency and frequency. Plaque was scored from photographs, before and after toothbrushing, in 64 smokers and 64 non-smokers, aged 20-40 years, matched for age and sex. The results showed that in both sexes smokers had more plaque than non-smokers. Male smokers brushed for a shorter time, and had more plaque after toothbrushing, than male non-smokers. A similar, though non-significant trend was found in females. There was no association between tobacco consumption and frequency of toothbrushing. It was concluded that the poorer oral cleanliness found in smokers both before and after toothbrushing may be explained, in part at least, by their shorter toothbrushing time.     

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

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

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

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

Oral microbiota in smokers and non-smokers in natural and experimentally-induced gingivitis

Abstract. The present study primarily aimed at investigating the oral microbiota in smokers and non-smokers with established gingivitis and monitoring its composition during experimental gingivitis. Secondly, it aimed at examining whether the composition of the microbiota is associated with different levels of gingival inflammation during this experimental gingivitis trial. For this purpose, 25 non-dental university students with gingivitis were recruited. 11 subjects were smokers and 14 were non-smokers. After achieving gingival health, they entered a 14-day experimental gingivitis trial. Plaque and bleeding were assessed before entering into the study (intake), at day 0. day 5 and at day 14 of the experiment. Microbiological samples from mucosal sites and dental plaque (taken at intake, day 0, and day 14) were analysed for the presence of Actinomyces species. Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros. Porphyromonas gingivalis, Prevotella intermedia and Streptococcus species. At day 14 of the experimental period, the level of plaque formation was not different between smokers and nonsmokers, but bleeding scores were lower in smokers than in non-smokers (15% and 30%) respectively, p= 0.01). The change from natural gingivitis to a state of gingival health and a subsequent change from gingival health to experimentally induced gingivitis was accompanied by quantitative alterations in the cultivable microbiota in both groups. Changes were most prominent in the transition from gingival health to experimental gingivitis and were found in dental plaque for Actinomyces species, C. rectus, F. nucleatum, and P. intermedia. Within the group of non-smokers, a distinction was made between subjects with a‘weak’or 'strong’inflammatory response. No relationship with a single bacterial species could be established which would likely explain the differences in levels of inflammation. It is concluded that differences in response to experimental gingivitis are not caused by major differences in the composition of the oral microbiota.     

Interleukin 1 and receptor antagonist levels in gingival crevicular fluid in heavy smokers versus non-smokers

BACKGROUND/AIMS: This study aimed to investigate the concentration of the cytokine interleukin (IL)-1beta and its receptor antagonist IL-1ra in gingival crevicular fluid (GCF) in patients with adult periodontitis who were heavy smokers compared with non-smokers. METHOD: GCF samples were collected from two groups of subjects: smokers and non-smokers. Thirty-nine GCF samples were harvested from 13 subjects with moderate to severe adult periodontitis who were heavy smokers. A further 30 GCF samples were harvested from 10 subjects with moderate to severe adult periodontitis who were non-smokers. Subjects were selected from both genders and none had any relevant systemic illness, were pregnant, had recent medication or had received any periodontal therapy in the preceding 3 months. One deep bleeding site, one deep non-bleeding site and one healthy site were investigated in each subject. Clinical measurements were recorded for each site, after obtaining a GCF sample using a Periopaper strip. IL-1beta and IL-1ra were quantified using new commercially available ELISA kits (Quantikine), and could be detected in all samples. RESULTS: For smokers, the mean concentrations for IL-1beta were 2714.5 (SD 4416.2) pg/ micro L for healthy sites, 37.0 (SD 57.2) pg/ micro L for non-bleeding periodontitis sites and 24.5 (SD 29.2) pg/ micro L for bleeding periodontitis sites. The concentrations of IL-1beta for non-smokers for the same category of sites were 393.8 (SD 867.1), 74.2 (SD 107.0) and 73.1 (SD 61.0) pg/ micro L, respectively. The mean concentrations of IL-1ra for smokers were 5.8 x 10(5) (SD 9.7) pg/ micro L for healthy sites, 2.2 x 10(5) (SD 0.15) pg/ micro L for deep non-bleeding sites and 0.19 x 10(5) (SD 0.07) pg/ micro L for deep bleeding sites. The concentrations for non-smokers were: 4.1 x 10(10) (SD 3.8), 18.1 x 10(5) (SD 20.4) and 3.2 x 10(5) (SD 2.3) pg/ micro L, respectively. Significance levels of P < 0.05 were found for comparisons of healthy vs. deep bleeding and deep non-bleeding sites for IL-1beta and IL-1ra in smokers, before adjustments for multiple testing. However, none of these comparisons reached statistical significance following adjustments for multiple testing. P < 0.05 for the correlation between IL-1beta and IL-1ra at healthy sites in smokers only. Differences in GCF concentrations for IL-1beta in smokers vs. non-smokers were significant for deep bleeding sites only (P < 0.05), the mean concentration of IL-1beta being lower in GCF from smokers vs. non-smokers. All differences in GCF concentrations of IL-1ra reached statistical significance for smokers vs. non-smokers. The mean concentrations of IL-1ra in GCF were lower in smokers compared with non-smokers for all categories of sites. CONCLUSIONS: A decreased concentration of IL-1beta and also IL-1ra was found in GCF from periodontitis sites compared to healthy sites in smokers and in non-smokers, although this did not reach statistical significance following adjustments for multiple testing. For comparisons between heavy smokers and non-smokers, statistically significant differences were found in the GCF concentrations of IL-1beta from deep bleeding sites only. Statistically significant differences were found in the IL-1ra concentrations for smokers vs. non-smokers for all categories of sites.     

Anxiety, gingival inflammation and periodontal disease in non-smokers and smokers - an epidemiological study

OBJECTIVES: The aim of the present study was to investigate the influence of anxiety, measured by one single question, on gingival inflammation and periodontal disease in non-smokers and smokers. MATERIAL AND METHODS: The participants were 144 subjects with untreated periodontal disease 30-40 years of age, and 26 healthy controls, 30-40 years of age. All subjects were clinically examined and answered an uncomplicated question regarding anxiety in every day life, as well as smoking habits. The periodontitis subjects were divided into; an aggressive periodontitis (AP)-group and a chronic periodontitis (CP)-group. Fisher's exact probability t-test, analysis of variance (anova), Mann-Whitney U-test and analysis of covariance (ancova) were used as statistical methods. RESULTS: Anxious subjects had a significantly higher gingival index than non-anxious subjects, when controlling for smoking (p<0.01). The healthy anxious non-smokers had an average score of GI 1.6 (+/-0.4 SD) compared with 1.2 (+/-0.4 SD), p<0.05 for the non-anxious non-smokers. Anxious smokers with periodontits (AP-/CP-group) had significantly more sites with pockets >/=5 mm, compared with non-anxious smokers, (p<0.05). CONCLUSIONS: The results of the present study, suggest that self-reported anxiety was associated with an adverse affect on the gingiva. Anxiety seemed to be associated with increased severity of periodontal disease in smokers.     

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.     

Healing response of gingival recession defects following guided tissue regeneration procedures in smokers and non-smokers

Abstract This retrospective study evaluated healing response in gingival recession defects following guided tissue regeneration (GTR) in smokers. 22 systemically healthy patients who had been treated for deep (4 mm), buccal. Miller's class I or II gingival recession defects with ePTFE membranes were included. Patients were regarded as smokers if they smoked more than 10 cigarettes/day at the time of surgical procedure. Occasional and former smokers were excluded. 9 patients (6 male, mean age 29 years) were smokers, while 13 patients (4 male, mean age 35 years) were non smokers. Clinical parameters, recorded pre surgery and at 6 months post surgery. included defect-specific plaque (DPI) and bleeding on probing (BoP) scores, recession depth (RD). probing depth (PD). clinical attachment level (CAL). and keratinized tissue width (KG). Extent of membrane exposure (ME) and newly formed tissue (NFT) gain were assessed at membrane removal. Statistical analysis revealed no significant differences between smokers and non-smokers in demographic and pre surgery defect characteristics. DPI and BoP scores were similar pre surgery and remained almost unchanged thorough out the observation interval in both groups. ME was significantly greater in smokers (2.6±1.4 mm) than in non smokers (1.3±0.6 mm). NFT gain was 2.8±1.0 mm in smokers and 3.6±1.4 mm in non-smokers, the difference being not statistically significant. Smokers showed significantly less RD reduction and root coverage (2.5±1.2 mm and 57%, respectively) compared to non-smokers (3.6±1.1 mm and 78%, respectively). In conclusion, the results indicate that treatment outcome following GTR in gingival recession defects is impaired in cigarette smokers.     

Subgingival temperature in smokers and non-smokers with periodontal disease

Abstract The purpose of this study was to compare subgingival temperature in a group of smokers to that of a group of non-smokers with similar levels of periodontal disease. 40 adult subjects. 20 cigarette smokers and 20 non-smokers with evidence of adult periodontitis were examined. Subgingival temperature was measured at 6 sites around each of 4 maxillary anterior teeth. Probing depth, and the presence or absence of bleeding was also recorded. In addition, the sublingual temperature was recorded. All sites were classified as diseased or healthy. Healthy sites did not bleed and had a probing depth of ≥ 4mm. diseased sites were any site which had a probing depth ≥ 5 mm. or which bled on probing. Mean sublingual and site temperatures were calculated for smokers and non-smokers. Mean temperature differentials (ΔT) between the sublingual temperature and the site temperature were calculated for each site. Smokers had a warmer mean sublingual temperature than non-smokers. A significant difference in subgingival site temperature was demonstrated between the smokers and non-smokers, with the mean site temperature being 0.4°C warmer in smokers (p < 0.01). When healthy or diseased sites were compared between smokers and non-smokers, smokers also had warmer mean site temperatures than non-smokers for both healthy and diseased sites (p < 0.01). When the mean temperature differentials (ΔT) between healthy and diseased sites were compared across each group, significant differences were also found. For healthy sites, the smokers had a mean ΔT 0.2°C lower (p < 0.01) than the non-smokers, representing warmer sites. In diseased sites however. ΔT was 0.3°C higher (p < 0.01) in smokers, representing cooler sites.     

Oral hygiene compliance and gingivitis expression in cigarette smokers

Abstract – The compliance with an oral hygiene intervention program and its effect on oral cleanliness and gingivitis was studied in smokers and non-smokers. The study group represented patients with regular dental attendance. It comprised 68 patients 21-60 yr of age, including 28 habitual smokers. The program included toothbrushing with an electric toothbrush for 12 months. Oral cleanliness was evaluated according to a percentage plaque index and gingivitis according to the percentage of bleeding sites. The compliance with the oral hygiene program was very high among smokers and non-smokers. Plaque index at baseline was very similar in smokers and non-smokers and remained so during the course of the investigation. Following the introduction of the oral hygiene program, plaque index decreased in both groups, and there were no statistically significant differences between the two groups. In spite of the similarity in plaque index, gingival bleeding was significantly lower in smokers than non-smokers. The results suggest that smokers and non-smokers do not differ with respect to habitual oral hygiene or compliance with hygiene programs. In smokers, however, the clinical gingivitis expression in response to plaque is suppressed.     

Investigation of periodontal destruction patterns in smokers and non-smokers

BACKGROUND: Previous work has suggested that tobacco smoking has a local as well as a systemic effect on the severity of periodontal disease. Objective: To test the hypothesis that smokers have more disease in the upper anterior region. METHODS: A retrospective stratified random sample of 49 non-smokers and 39 heavy smokers (>or=20 cigarettes/day) was obtained from a total of 3678 referred patients with adult periodontitis. Probing depth data were collected from clinical records and radiographic measurements were carried out on existing dental panoramic tomographs to assess the inter-proximal bone levels. RESULTS: The proportion of sites with "bone loss" 4.5 mm or greater was higher in smokers, the greatest difference being observed in upper anterior sites (smokers: 73.3+/-25.5%, non-smokers: 48.3+/-31.2%, p<0.001). A difference was also observed when the number of palatal sites probing 4 mm or greater in the upper anterior region was expressed as a proportion of all such sites in the mouth (smokers: 12.3+/-6.8%, non-smokers: 9.8+/-8.8%; p=0.050). CONCLUSION: The overall pattern of tissue destruction was consistent with a systemic effect of smoking. The suggestion of a marginal local effect of the smoking habit in maxillary anterior palatal sites requires further investigation.