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.     

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

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

Expression of ICAM-1 and E-selectin in gingival tissues of smokers and non-smokers with periodontitis.

BACKGROUND: Tobacco smoking affects systemic concentrations of soluble intercellular adhesion molecule (ICAM)-1, but its effect on local expression of adhesion molecules in gingival tissue has not been studied previously. METHODS: E-selectin and ICAM-1 expression on small blood vessel endothelia in gingival biopsies obtained from smokers (n=17) and non-smokers (n=17) with periodontitis was examined with immunohistochemistry. Blood vessels were identified with monoclonal antibody for von Willebrand's factor. RESULTS: A significantly larger number of vessels were observed in inflamed tissues of non-smokers than smokers (P<0.05). The number and proportion of vessels expressing both ICAM-1 and E-selectin was greater in sites with inflammation compared to non-inflamed sites in both smokers and non-smokers (P<0.05). The proportion of the total number of vessels expressing ICAM-1 in non-inflamed sites was greater in non-smokers compared with smokers (P<0.05). CONCLUSIONS: These results suggest that the inflammatory response in smokers with periodontitis may not be accompanied by an equivalent increase in vascularity. Reduced ICAM-1 expression in non-inflamed areas of smokers could reflect a systemic effect of tobacco smoking on ICAM-1 independent of inflammation.     

Clinical and microbiological effect of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients

OBJECTIVES: To compare the effects of scaling and root planing (SRP) on clinical and microbiological parameters at selected sites in smoker and non-smoker chronic and generalized aggressive periodontitis patients. MATERIALS AND METHODS: Clinical parameters including probing depth (PD), relative attachment level (RAL), and bleeding upon probing (BOP), and subgingival plaque samples were taken from four sites in 28 chronic periodontitis (CP) and 17 generalized aggressive periodontitis (GAgP) patients before and after SRP. Polymerase chain reaction assays were used to determine the presence of A. actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, Prevotella intermedia and Treponema denticola. RESULTS: Both CP and GAgP non-smokers had significantly greater reduction in pocket depth (1.0+/-1.3 mm in CP smokers versus 1.7+/-1.4 mm in non-smokers, p=0.007 and 1.3+/-1.0 in GAgP smokers versus 2.4+/-1.2 mm in GAgP non-smokers, p<0.001) than respective non-smokers, with a significant decrease in Tannerella forsythensis in CP sites (smokers 25% increase and non-smokers 36.3% decrease, p<0.001) and Prevotella intermedia at GAgP sites (smokers 25% reduction versus 46.9% in non-smokers, p=0.028). CONCLUSION: SRP was effective in reducing clinical parameters in both groups. The inferior improvement in PD following therapy for smokers may reflect the systemic effects of smoking on the host response and the healing process. The lesser reduction in microflora and greater post-therapy prevalence of organisms may reflect the deeper pockets seen in smokers and poorer clearance of the organisms. These detrimental consequences for smokers appear consistent in both aggressive and CP.     

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.     

Association between cigarette smoking and the intraoral distribution of periodontal disease in Thai men over 50 years of age

Aim: This study aimed to investigate the effects of cigarette smoking on periodontal conditions in specific tooth regions of older Thai men. Methods: There were 272 current smokers, 714 former smokers, and 477 non‐smokers enrolled in the present study. Differences between groups in the mean probing depth or attachment loss were compared using ancova . The relationship between smoking exposure or cessation duration and periodontal conditions was examined using linear trend analysis. Results: Smokers had deeper pockets and attachment loss than non‐smokers. The greatest differences between smokers and non‐smokers were observed in the maxillary posterior palatal region, where current smokers had 0.88 mm greater attachment loss than non‐smokers, compared to 0.36–0.60 mm observed in other tooth regions. Among the current smokers, there was a trend towards an increase in attachment loss with increasing smoking exposure in the maxillary posterior regions. However, it was not statistically significant. Among the former smokers, a better periodontal condition was observed, depending on the length of time since smoking cessation; this was most pronounced in the maxillary posterior palatal region. Conclusions: The palatal site of maxillary posterior teeth was the area most affected by cigarette smoke. The results suggest a possible local effect of smoking in addition to its systemic effects.     

Effect of periodontal therapy in smokers and non-smokers with advanced periodontal disease: results after maintenance therapy for a minimum of 5 years

BACKGROUND: Longitudinal clinical studies show smoking is a risk factor for periodontal disease progression. It has also been documented that smoking impairs healing after periodontal therapy. However, the longitudinal effect of smoking on treatment results in patients who undergo long-term maintenance therapy has not been extensively investigated. This study clinically and radiographically compared smoking and non-smoking patients who had been treated for advanced periodontal disease and who received maintenance therapy for a minimum of 5 years. METHODS: Twenty-nine patients were selected over a 6-month period when they presented for a regularly scheduled visit in a private office. Patients were selected on the basis of initially having lost 50% of bone support on 50% of their teeth; had received follow-up therapy for at least 5 years; were compliant at 75% of the appointments; and had plaque scores < 20% in 75% of the visits. All patients had received non-surgical and surgical therapy as required for pocket elimination. Fourteen were active smokers during the entire maintenance period. Clinical measurements of probing depths and presence of plaque and gingivitis and a new set of standardized radiographs were taken. RESULTS: Smokers had higher mean radiographic bone loss values prior to treatment (7.52 +/- 1.39 versus 6.65 +/- 1.39) and at the final examination (7.32 +/- 1.42 versus 6.29 +/- 1.29) mean radiographic bone loss as well as initial, immediate post-therapy, and final percent of pockets > or = 6 mm (1.42% +/- 1.87% versus 0.60% +/- 1.11%). Differences were not statistically significant. Over 5 to 8 years, seven sites in four non-smokers and 11 sites in six smokers exhibited radiographic bone loss > or = 2 mm. One tooth in a non-smoker and three teeth in two smokers were lost. In a logistic regression analysis, smoking increased the odds ratio 10.7 times of having > or = 1 site with bone loss > or = 2 mm. CONCLUSION: The present study on a small group of patients treated for advanced periodontal disease and well maintained over 5 to 8 years showed no statistically significant differences between smokers and non-smokers in clinical probing depth and radiographic bone loss measurements.     

Smoking influences decision making in periodontal therapy: a retrospective clinical study.

BACKGROUND: Mechanical periodontal therapy consists of a non-surgical course, followed by surgical treatment to eliminate or reduce remaining pathological pockets. Only if diligent mechanical therapy fails are additional measures considered. It has been documented that smoking interferes with the host defense mechanisms. This study addresses the question is meticulous non-surgical periodontal therapy equally successful in smokers and non-smokers? If not, is a thorough and cumbersome non-surgical approach in smokers worth undertaking? METHODS: Thirty-five smokers and 35 non-smokers were selected retrospectively from a pool of 306 patients treated in a private practice over a 17-month period. All had at least 14 teeth present with 8 presenting with gingival pockets > or =6 mm. Non-surgical treatment was performed in 6 to 10 appointments and results were evaluated 6 to 12 weeks after therapy. Bleeding on probing sites with probing depths > or =5 mm were then considered for surgical treatment. RESULTS: Before treatment smokers had statistically significantly higher mean percent of pockets 4 to 5 mm and > or =6 mm (40.36+/-10.65 and 26.51+/-11.95, respectively, compared to 30.38+/-7.57 and 20.42+/-10.03 for non-smokers) and showed significantly lower proportional reduction of these parameters with treatment (50.80+/-33.76 and 81.36+/-19.82 for pocket 4 to 5 mm and 6 mm, compared to 68.43+/-21.23 and 91.7+/-8.92 for nonsmokers). A multivariate analysis gave smoking, plaque control, and initial percent of sites > or =6 mm to be significant predictors of the percent of teeth in need of further therapy. In non-smokers, treatment was apparently successful in all tooth types with the exception of upper first and second molars (28.5% failure) and lower second molar (20% failure). In smokers, rates of further treatment needs were particularly high in the premolar-molar area in both jaws, ranging from 31.4% to 48.5% for an individual tooth type; 42.8% of smokers and 11.5% of non-smokers needed further treatment in 16% of their teeth (pretest probability). A decision analysis showed that for smokers with at least 1 of 5 sites > or =6 mm, one should initiate surgical treatment, rather than first treat non-surgically. If the point of indifference that the decision is correctly set at 95%, the pretest probability should be >12%. There is a higher risk that non-surgical therapy will fail, for instance if we lower the point of indifference to 60%, the pretest probability should be >31%. CONCLUSIONS: It is concluded that smoking impairs healing after nonsurgical periodontal therapy. The decision analysis of this study questions the need for a thorough course of non-surgical treatment in smokers with advanced periodontal disease.     

吸烟对牙周基础治疗前后龈沟液量和弹性蛋白酶水平的影响

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

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.     

Cigarette smoking negatively affects healing response following flap debridement surgery

BACKGROUND: The purpose of the present parallel design, controlled clinical trial was to evaluate the treatment outcome following flap debridement surgery (FDS) in cigarette smokers compared to non-smokers. METHODS: After initial therapy, 57 systemically healthy subjects with moderate to advanced periodontitis who presented with one area (at least 3 teeth) where surgery was required were selected. Twenty-eight patients (mean age: 39.6 years, 20 males) were smokers (> or = 10 cigarettes/day); 29 patients (mean age: 43.9 years, 7 males) were non-smokers. Full-mouth plaque (FMP) and bleeding on probing (BOP) scores, probing depth (PD), clinical attachment level (CAL), and recession depth (RD) were assessed immediately before and 6 months following surgery. Only sites with presurgery PD > or = 4 mm were used for statistical analysis. RESULTS: Presurgery FMP and BOP were similar in smokers and non-smokers and significantly decreased postsurgery in both groups. Overall, PD reduction and CAL gain were greater, although not significantly, in non-smokers (2.4 +/- 0.9 mm and 1.6 +/- 0.7 mm, respectively) than in smokers (1.9 +/- 0.7 mm and 1.2 +/- 0.7 mm, respectively). For moderate sites (PD 4 to 6 mm), no significant differences in PD and CAL changes were found between groups. For deep sites (PD > or = 7 mm), PD reduction was 3.0 +/- 1.0 mm in smokers and 4.0 +/- 0.8 mm in non-smokers, and CAL gain amounted to 1.8 +/- 1.1 mm in smokers and 2.8 +/- 1.0 mm in non-smokers (P = 0.0477). In smokers, 16% of deep sites healed to postsurgery PD values < or = 3 mm as compared to 47% in non-smokers (P = 0.0000); 58% of deep sites in smokers showed a CAL gain > or = 2 mm, as compared to 82% in non-smokers (P = 0.0000). CONCLUSIONS: Results of the study indicated that: 1) FDS determined a statistically significant PD reduction and CAL gain in patients with moderate to advanced periodontitis; 2) smokers exhibited a trend towards less favorable healing response following FDS compared to non-smokers, both in terms of PD reduction and CAL gain; and 3) this trend reached clinical and statistical significance at sites with initial deep PD.     

Coronally positioned flap for root coverage in smokers and non-smokers: stability of outcomes between 6 months and 2 years

BACKGROUND: Smoking adversely affects the short-term outcomes of coronally positioned flap (CPF) root coverage procedures, but the long-term stability of this procedure in smokers has not been studied. The objective of this study was to evaluate the effect of smoking on the long-term outcomes of CPF in recession treatment. METHODS: CPF was used to treat a Miller Class I defect in a maxillary canine or premolar in 10 current smokers (> or =10 cigarettes daily for > or =5 years) and 10 non-smokers (never smokers). At baseline and 6, 12, and 24 months, clinical parameters, including probing depth (PD), clinical attachment level (CAL), recession depth (RD), and width of keratinized tissue (KT), were determined. RESULTS: Intragroup analysis showed that CPF failed to maintain the gingival margin at the initially achieved position. RD significantly increased in smokers (from 0.84 +/- 0.49 to 1.28 +/- 0.58 mm) and in non-smokers (from 0.22 +/- 0.29 to 0.50 +/- 0.41 mm) between 6 and 24 months. Further analysis showed that 50% of smokers and 10% of non-smokers lost between 0.5 and 1.0 mm of root coverage in the same period. Intergroup analysis showed that smokers had significantly greater residual recession (P = 0.001) at 24 months. Both smokers and non-smokers lost CAL and experienced decreases in KT. CONCLUSIONS: The long-term stability of CPF outcomes is less than desirable, particularly in smokers. Two years after a CPF procedure, smokers have significantly greater residual recession compared to non-smokers both statistically and clinically.     

Quantitative evaluation of the vasculature and fibronectin localization in gingival connective tissue of smokers and non-smokers

BACKGROUND: It has been shown that tobacco is a significant risk factor for periodontal disease. The reason for decreased gingival bleeding in smokers is not known. The aim of the present study was to demonstrate the localization of fibronectin in the extracellular matrix of the inflamed gingiva of smokers and non-smokers and to evaluate the chronic effect of smoking on the gingival microvessel number (NVES) and vascular surface density (VSD). METHODS: Seventy-four (74) adult patients with periodontitis were included in this investigation. Of these patients, 38 were smokers and 36 were non-smokers. Probing depths (PD), papillary bleeding index (PBI) of both groups, and the smoking habits of the smokers were recorded. Biopsy specimens obtained during periodontal surgery were prepared to evaluate fibronectin distribution and to quantitate the vasculature. RESULTS: The mean VSD values of smokers and non-smokers were 6.721 +/- 1.845 and 5.721 +/- 3.118 (mean +/- SD), and the mean NVES of smokers and non-smokers was 31.582 +/- 11.810 and 30.145 +/- 15.442, respectively. The difference between the mean PD and PBI values of the 2 groups was not statistically significant. The location of the biopsy specimen, whether in the anterior or posterior area of the mouth, did not lead to any statistically significant differences between the groups. In addition, the number of years smoked and the tobacco brand used did not result in statistically significant differences. The most intense staining of fibronectin was observed beneath the epithelium around the blood vessels of the uppermost region of the connective tissue, showing a fibrillar and diffuse distribution; however, there was no significant difference between smokers and non-smokers. CONCLUSION: The results of the present study indicate that smoking does not affect the vascular surface density, number of vessels per mm2 stroma, or fibronectin distribution in subepithelial gingival connective tissue.     

Non-surgical periodontal treatment with and without adjunctive metronidazole in smokers and non-smokers

AIM: To determine whether adjunctive metronidazole therapy would compensate for the poorer treatment response to scaling and root planing reported in smokers. METHOD: A single-blind, randomised clinical trial of 28 smokers and 56 non-smokers, stratified for periodontitis disease severity and randomly allocated to 3 treatment groups: (1) Scaling and root planing using an ultrasonic scaler with local anaesthesia (SRP), (2) SRP+ metronidazole tabs 200 mg tds for 7 days, (3) SRP + 2 subgingival applications of 25% metronidazole gel. Probing depths (PD) and attachment levels (AL) were recorded with a Florida probe at baseline, 2 months and 6 months post treatment by a single examiner who was unaware of the treatment modality. Results were analysed for all sites with baseline probing depths equal to or greater than Florida probe recordings of 4.6 mm using analysis of variance. RESULTS: Reductions in probing depth at 6 months were significantly less (p < 0.001) in the smokers (mean 1.23 mm, 95% confidence intervals = 1.05 to 1.40 mm) than in the non-smokers (1.92, 1.75 to 2.09 mm). Attachment level gains were approximately 0.55 mm and there was no statistically significant difference between smokers and non-smokers. There were no differences in any clinical measure in response to the three treatment regimens at 2 or 6 months for either smokers or non-smokers. A reduction in the proportion of spirochaetes was observed at 6 months which was less in smokers than in non-smokers (p = 0.034). Multiple linear regression analysis on probing depth at 6 months demonstrated that smoking was a significant explanatory factor (p < 0.001) for poor treatment outcome, whilst the presence or absence of adjunctive metronidazole was not (p = 0.620). CONCLUSION: This study confirms that smokers have a poorer treatment response to SRP, regardless of the application of either systemic or locally applied adjunctive metronidazole.     

Impact of smoking on marginal bone loss

PURPOSE: To compare marginal implant bone loss (MBL), survival, and radiographic evidence of success of dental implants among smokers and nonsmokers. MATERIALS AND METHODS: Consecutive records of 161 patients (aged 23 to 89 years, mean 57 years) treated with a total of 646 implants between the years 1995 and 1998 were examined. Patients were divided into 3 groups: nonsmokers, moderate smokers, and heavy smokers. Tobacco exposure was calculated by cigarettes per day and by pack-years. Follow-up ranged from 1 to 7 years (mean 3.8 years). Postoperative panoramic radiographs obtained before implant exposure and annually thereafter were analyzed for MBL changes. The influence of smoking and other variables on MBL was analyzed at all implant sites. RESULTS: Generally, smokers had more MBL than nonsmokers (0.153 +/- 0.092 mm and 0.047 +/- 0.048 mm, respectively; P < .001). When each jaw was examined separately, smoking had a greater effect on MBL in the maxilla than in the mandible (0.158 +/- 0.171 mm versus 0.146 +/- 0.158 mm, respectively; P < .001). Furthermore, in the maxilla, heavy smokers had the greatest amount of MBL (0.1897 +/- 0.1825 mm), followed by moderate smokers (0.123 +/- 0.156 mm) and nonsmokers (0.0460 +/- 0.070 mm) (P < .001). In the mandible, there was no distinction between heavy and moderate smokers, and both had greater MBL than nonsmokers (P < .001). Only 3 of the 646 implants failed; the cumulative survival rate was 99.5%. Overall radiographic success rate was 93.2%. Nonsmokers had a higher radiographic success rate (97.1%) than smokers (87.8%) (P < .001). CONCLUSIONS: This study demonstrated a relationship between MBL and smoking habits. A higher incidence of MBL was found in the smoking group, and this was more pronounced in the maxilla.     

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.     

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.     

Impaired healing response of periodontal furcation defects following flap debridement surgery in smokers. A controlled clinical trial

OBJECTIVES: The purpose of the present parallel-design, controlled clinical trial was to evaluate the treatment outcome of periodontal furcation defects following flap debridement surgery (FDS) procedure in cigarette smokers compared to non-smokers. MATERIALS AND METHODS: After initial therapy, 31 systemically healthy subjects with moderate to advanced periodontitis, who presented at least one Class I or II molar furcation defect, were selected. Nineteen patients (mean age: 40.3 years, 15 males) were smokers (>or=10 cigarettes/day) and 12 patients (mean age: 44.8 years, 3 males) were non-smokers. Full-mouth plaque score (FMPS) and full-mouth bleeding score (FMBS), probing pocket depth (PPD), vertical clinical attachment level (v-CAL), and horizontal clinical attachment level (h-CAL) were assessed immediately before and 6 months following surgery. RESULTS: Overall, statistically significant v-CAL gain was observed in smokers (1.0 +/- 1.3 mm) and non-smokers (1.3+/-1.1 mm), the difference between groups being statistically significant (p=0.0003). In proximal furcation defects, v-CAL gain amounted to 2.3+/-0.7 mm in non-smokers as compared to 1.0+/-1.1 mm in smokers (p=0.0013). At 6 months postsurgery, non-smokers presented a greater h-CAL gain (1.3+/-1.1 mm) than smokers (0.6+/-1.0 mm), with a statistically significant difference between groups (p=0.0089). This trend was confirmed in both facial/lingual (1.4+/-1.0 versus 0.8+/-0.8 mm) and proximal furcation defects (1.2+/-1.3 versus 0.5+/-1.2 mm). The proportion of Class II furcations showing improvement to postsurgery Class I was 27.6% in smokers and 38.5% in non-smokers. After 6 months, 3.4% of presurgery Class I furcation defects in smokers showed complete closure, as compared to 27.8% in non-smokers. CONCLUSIONS: The results of the present study indicated that (1) FDS produced clinically and statistically significant PPD reduction, v-CAL gain, and h-CAL gain in Class I/II molar furcation defects, and (2) cigarette smokers exhibited a less favorable healing outcome following surgery in terms of both v-CAL and h-CAL gain.     

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.     

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.