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.     

Salivary calcium reflects skeletal bone density of heavy smokers

OBJECTIVE: Our recent studies suggest, that elevated calcium concentration of saliva is characteristic of periodontitis. In this study we analyzed the effect of smoking on salivary calcium and bone density by comparing the level of salivary calcium and the ultrasound scale of bone density of heavy smokers to those of non-smokers. DESIGN: Salivary samples were collected from 603 women (50-62 years) participating in a pre-screen referral program for osteoporosis. Out of this group a total of 577 were accepted for the present study. General health, medications and tobacco smoking were recorded. The group included 487 non-smokers, 37 moderate smokers (1-10 cigarettes per day) and 53 heavy smokers (>10 cigarettes per day). Bone density was measured at the right heel by the quantitative ultrasound technique. Calcium and phosphate concentrations of saliva were measured and expressed as microg/ml of saliva. RESULTS: The ultrasonographic variables of the heel, broadband ultrasound attenuation (BUA), speed of sound (SOS) and T-score (a standard deviation unit from mean values of healthy young adults) of heavy smokers were significantly lower than those of women who did not smoke (P = 0.007, 0.014 and 0.011, respectively). Salivary calcium concentration of heavy smokers 70.5 (14.6) microg/ml was higher than that of non-smokers 64.0 (14.1) microg/ml (P = 0.001). There were no significant differences in salivary phosphate level or in the salivary flow rate between heavy smokers and non-smokers. Conclusions: Heavy smokers seem to have lower bone mineral density and higher salivary calcium than their non-smoking counterparts. We suggest that the high salivary calcium concentration of smokers is in connection with skeletal calcium disturbances.     

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.     

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.     

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。     

Subepithelial connective tissue graft for root coverage in smokers and non-smokers: a clinical and histologic controlled study in humans

BACKGROUND: The aim of this study was to evaluate root coverage of gingival recessions and to compare graft vascularization in smokers and non-smokers. METHODS: Thirty subjects, 15 smokers and 15 non-smokers, were selected. Each subject had one Miller Class I or II recession in a non-molar tooth. Clinical measurements of probing depth (PD), relative clinical attachment level (CAL), gingival recession (GR), and width of keratinized tissue (KT) were determined at baseline and 3 and 6 months after surgery. The recessions were treated surgically with a coronally positioned flap associated with a subepithelial connective tissue graft. A small portion of this graft was prepared for immunohistochemistry. Blood vessels were identified and counted by expression of factor VIII-related antigen-stained endothelial cells. RESULTS: Intragroup analysis showed that after 6 months there a was gain in CAL, a decrease in GR, and an increase in KT for both groups (P <0.05), whereas changes in PD were not statistically significant. Smokers had less root coverage than non-smokers (58.02% +/- 19.75% versus 83.35% +/- 18.53%; P <0.05). Furthermore, the smokers had more GR (1.48 +/- 0.79 mm versus 0.52 +/- 0.60 mm) than the non-smokers (P <0.05). Histomorphometry of the donor tissue revealed a blood vessel density of 49.01 +/- 11.91 vessels/200x field for non-smokers and 36.53 +/- 10.23 vessels/200x field for smokers (P <0.05). CONCLUSION: Root coverage with subepithelial connective tissue graft was negatively affected by smoking, which limited and jeopardized treatment results.     

Effect of cigarette smoking on periodontal status of healthy young adults

BACKGROUND: It has been shown that tobacco is a significant risk factor for periodontal disease; however, there have been few studies on young populations where problems of general health can be discounted. The purpose of this study was to examine the influence of tobacco consumption on the periodontal condition of a young, healthy population. METHODS: The study population consisted of 304 young Caucasian males (average age 19.38 +/- 0.72 years) entering the Armed Forces. All the subjects completed a self-administered questionnaire on age, oral hygiene habits, previous dental examinations, and quantity and length of tobacco use. The periodontal examination consisted of the plaque index (PI); periodontal bleeding index (PBI); probing depth (PD); and clinical attachment level (CAL). One- and 2-way ANOVA was used to compare data recorded between smokers and non-smokers. RESULTS: Forty-six percent of subjects reported that they brushed their teeth at least once a day, but only 13% visited a dentist at least once a year. Over half (53%) were habitual smokers, 43% smoking between 5 and 20 cigarettes per day; 39% of the smokers had been smoking for less than 5 years. Mean PI was 31.24 +/- 14.88 (27.19 +/- 15.93 for smokers and 35.78 +/- 12.17 for non-smokers), with significant differences between non-smokers and those who smoked 5 to 20 cigarettes per day (26.85 +/- 16.11, P<0.0001). Mean PBI was 42.29 +/- 8.43 (non-smokers 44.67 +/- 6.53 and smokers 40.17 +/- 9.46). Significant differences were found between the PBI of the non-smokers and of those who smoked 5 to 20 cigarettes per day (39.90 +/- 9.64, P <0.0001). There were also differences in the PBI between those who brushed their teeth once (40.53 +/- 9.61) and twice (44.86 +/- 5.9) a day (P<0.0001). Mean PD was 1.62 +/- 0.43 mm (non-smokers 1.56 +/- 0.36 and smokers 1.68 +/- 0.49). Deeper probing depths were recorded among smokers than among non-smokers, with statistically significant differences (P<0.049); statistically significant differences were also found between those who attended (1.49 +/- 0.50) and those who did not attend (1.65 +/- 0.42) regular dental check-ups (P<0.031). Mean CAL 1.75 +/- 0.41 (non-smokers 1.64 +/- 0.32 and smokers 1.82 +/- 0.44). CONCLUSIONS: It may be concluded that, even at such an early age, tobacco consumption affects the periodontal health. It is necessary to inform young smokers of the risk of tobacco use regarding periodontal health.     

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.     

The effects of nicotine and age on replication and viability of human gingival fibroblasts in vitro

The aim of the present study was to examine: (1) the effects of nicotine on human gingival fibroblasts (HGF); (2) differences between smokers (> or = 10 cigarettes/day at least for 5 years) and non-smokers; (3) differences between patients of different age. HGF were obtained, through biopsies during periodontal surgical procedures, from 15 patients which were divided in 4 groups: 4 patients, smokers aged < or = 25 years; 4 patients, non-smokers aged < or = 25 years; 3 patients, smokers aged > or = 40 years; 4 patients, non-smokers aged > or = 40 years. Nicotine has been tested in 3 different concentrations: 6 microg/ml; 60 microg/ml; 600 microg/ml. To assess cells viability, the neutral red (NR) test was used; to evaluate cell proliferation, the Hoechst test was employed. After 48 h of nicotine exposure, it was found that 600 microg/ml nicotine was strongly cytotoxic to HGF of all groups, with a significant reduction of both proliferation and viability of cells versus control. Comparison between groups of the same age: when comparing untreated HGF (i.e., control values) of smokers < or = 25 years versus non-smokers < or = 25 years, cell proliferation, but not viability, was found to be increased in smokers. Both viability and proliferation of control cells of smokers > or = 40 years were increased versus non-smokers > or = 40 years. HGF of non-smokers < or = 25 years, when exposed to nicotine 600 microg/ml, have less viability and proliferation than HGF of smokers of the same age. Comparison between groups of different age: In the smoker group, untreated HGF (i.e., control values) had similar viability and proliferation, irrespective of age, but nicotine 600 microg/ml kills more HGF in smokers < or = 25 years than in smokers > or = 40 years. In non-smokers, untreated HGF < or = 25 years replicate less, but are not less viable than HGF > or = 40 years. When challenged with nicotine 600 microg/ml, HGF < or = 25 years were less viable than HGF > or = 40 years. From this study, it appears that the smoking history and the patient age could be relevant for final evaluation of the results, since HGF from smokers are less sensitive to nicotine than HGF from non-smokers, and cells from older donors are more resistant to nicotine than cells from younger donors.     

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.     

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.     

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.     

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.     

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.     

Grapefruit consumption improves vitamin C status in periodontitis patients

OBJECTIVE: Previous studies demonstrate a relationship between a lack of vitamin C and increased risk of periodontal disease. In the present study we examine the vitamin C plasma levels and inflammatory measures in periodontitis patients before and after the consumption of grapefruit. SUBJECTS AND METHODS: Fifty-eight patients with chronic periodontitis were assigned to the test group (non-smokers n=21, smokers n=17) and a diseased control group (non-smokers n=11, smokers n=9). Furthermore, 22 healthy subjects were recruited to compare vitamin C plasma levels between periodontally diseased and healthy subjects. Clinical evaluations, including plaque index (PI), sulcus bleeding index (SBI), probing pocket depths (PPD) and plasma vitamin C levels, were performed at baseline, and after two weeks of grapefruit consumption. RESULTS: At baseline, we observed significantly reduced plasma vitamin C levels in the test group and diseased controls in comparison with the healthy controls. On principle, smokers showed lower levels of vitamin C (mean 0.39 +/- 0.17 mg dl(-1)) than non-smokers (mean 0.56+/-0.29 mg dl(-1)). After grapefruit consumption, the mean plasma vitamin C levels rose significantly in the test group compared to the diseased controls (non-smokers: 0.87+/-0.39 mg dl(-1), smokers: 0.74+/-0.30 mg dl(-1)). Furthermore the SBI was reduced in the test group (non-smokers: from 1.68+/-0.6 to 1.05+/-0.6, p<0.001), whereas PI and PPD were unaffected. CONCLUSION: The present results show that periodontitis patients are characterised by plasma vitamin C levels below the normal range, especially in smokers. The intake of grapefruit leads to an increase in plasma vitamin C levels and improves sulcus bleeding scores. Longer term studies are necessary to determine whether other periodontal outcomes improve with such supplementation especially in smokers.     

The effect of smoking and periodontal treatment on salivary composition in patients with established periodontitis.

BACKGROUND: The purpose of this study was to evaluate the effect of smoking on the periodontal status and the salivary composition in subjects with established periodontitis before and after periodontal therapy. METHODS: Our study group included 26 healthy subjects, 12 smokers and 14 non-smokers with established periodontitis. Clinical measurements and non-stimulated whole saliva were obtained and analyzed at baseline and after scaling and root planing. Smokers presented at baseline with significantly greater probing depth (4.16+/-0.26) compared to non-smokers (3.52+/-0.32) which was statistically significant (P = 0.0268); likewise, baseline clinical attachment level was greater in smokers (4.49+/-0.31 compared to non-smokers 3.87+/-0.13; P = 0.0620). Mean plaque index was also greater in smokers compared to non-smokers (0.86 and 0.65, respectively; P = 0.0834). Baseline pretreatment sodium values were significantly greater in non-smokers (14.36 mEq/l compared to 9.31 mEq/l in smokers; P = 0.0662); likewise non-smokers exhibited 50% greater salivary calcium levels (6.04 mg/100 ml compared to 4.32 mg/100 ml in smokers; P = 0.0133). RESULTS: Post-treatment probing depth and clinical attachment level were not different between smokers and non-smokers; this in spite of significant difference in plaque index in smokers (0.35 compared to 0.13 in non-smokers; P = 0.0135). Post-treatment, smokers had reduced calcium concentration (3.58 mg/100 ml compared to 5.11 mg/100 ml in non-smokers; P = 0.0438). Treatment affected albumin level in smokers only, consequently non-smokers had significantly greater salivary albumin concentration (1.1 mg/100 ml compared to 0.38 mg/100 ml in smokers; P = 0.0274). CONCLUSIONS: Subjects with established periodontitis exhibited elevated concentrations of salivary electrolytes and proteins. Within this study group, smokers exhibited greater disease level but reduced sodium, calcium, and magnesium concentrations. Smokers responded favorably to treatment. The clinical improvement eliminated the differences in salivary composition.     

Plasma levels of mannan-binding lectin in relation to periodontitis and smoking

BACKGROUND: Mannan-binding lectin (MBL) is an important molecule of innate immunity; it acts as an opsonin and stimulates the classical complement pathway. Moreover, it has been suggested that MBL acts as a weak acute phase protein. We investigated whether MBL levels are increased in periodontitis, and we tested whether individuals deficient for MBL are more susceptible to periodontitis. METHODS: A total of 219 subjects participated in the study. Plasma samples from 115 periodontitis patients and 104 healthy controls were taken, and the MBL levels were measured by enzyme-linked immunosorbent assay (ELISA). MBL levels were analyzed in relation to periodontitis, taking into consideration age, gender, ethnic and educational background, and smoking status. In some analyses, subjects with MBL plasma levels <0.8 microg/ml were considered MBL deficient. RESULTS: MBL plasma concentrations were not significantly different in moderate and severe periodontitis compared to controls (1.6, 1.4, and 1.6 microg/ml, respectively). Also, the prevalence of MBL deficiency was not found to be different between controls and moderate and severe periodontitis (45%, 37%, and 36%). However, among all subjects and among the non-deficient subjects, MBL levels were markedly increased in heavy smokers (>10 cigarettes per day), irrespective of periodontal disease status, in comparison to non-smokers and light smokers. MBL plasma levels did not show a correlation with plasma C-reactive protein (CRP) and were also not related to the prevalence of specific periodontal pathogens. CONCLUSIONS: MBL levels were not elevated in periodontitis, and MBL deficiency was not related to susceptibility for periodontitis. The fact that MBL levels were higher among heavy smokers is the subject of further investigation.     

Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss

BACKGROUND: Our purpose was to test the hypotheses that cigar and pipe smoking have significant associations with periodontal disease and cigar, pipe, and cigarette smoking is associated with tooth loss. We also investigated whether a history of smoking habits cessation may affect the risk of periodontal disease and tooth loss. METHODS: A group of 705 individuals (21 to 92 years-old) who were among volunteer participants in the ongoing Baltimore Longitudinal Study of Aging were examined clinically to assess their periodontal status and tooth loss. A structured interview was used to assess the participants' smoking behaviors with regard to cigarettes, cigar, and pipe smoking status. For a given tobacco product, current smokers were defined as individuals who at the time of examination continued to smoke daily. Former heavy smokers were defined as individuals who have smoked daily for 10 or more years and who had quit smoking. Non-smokers included individuals with a previous history of smoking for less than 10 years or no history of smoking. RESULTS: Cigarette and cigar/pipe smokers had a higher prevalence of moderate and severe periodontitis and higher prevalence and extent of attachment loss and gingival recession than non-smokers, suggesting poorer periodontal health in smokers. In addition, smokers had less gingival bleeding and higher number of missing teeth than non-smokers. Current cigarette smokers had the highest prevalence of moderate and severe periodontitis (25.7%) compared to former cigarette smokers (20.2%), and non-smokers (13.1%). The estimated prevalence of moderate and severe periodontitis in current or former cigar/pipe smokers was 17.6%. A similar pattern was seen for other periodontal measurements including the percentages of teeth with > or = 5 mm attachment loss and probing depth, > or = 3 mm gingival recession, and dental calculus. Current, former, and non- cigarette smokers had 5.1, 3.9, and 2.8 missing teeth, respectively. Cigar/pipe smokers had on average 4 missing teeth. Multiple regression analysis also showed that current tobacco smokers may have increased risks of having moderate and severe periodontitis than former smokers. However, smoking behaviors explained only small percentages (<5%) of the variances in the multivariate models. CONCLUSION: The results suggest that cigar and pipe smoking may have similar adverse effects on periodontal health and tooth loss as cigarette smoking. Smoking cessation efforts should be considered as a means of improving periodontal health and reducing tooth loss in heavy smokers of cigarettes, cigars, and pipes with periodontal disease.     

Tobacco as a risk factor for survival of dental implants

BACKGROUND: It has been shown that smoking habits represent an increased risk for impaired bone healing and implant failure. This study aimed to evaluate the implant survival rates among non-smokers (NS) and different kinds of smokers (S). METHODS: A retrospective analysis was made over a 5-year period of the clinical and radiographic findings corresponding to 66 consecutive patients who had received a total of 165 dental implants. Patients were divided into two groups: S, 40 patients (95 implants; 58% of the sample); and NS, 26 patients (70 implants; 42% of the sample). Also, S and NS were classified into four different categories according to daily tobacco use: NS, 26 patients and 70 implants; light smokers (LS), 23 patients and 44 implants; moderate smokers (MS), 11 patients and 25 implants; and heavy smokers (HS), six patients and 26 implants. RESULTS: Sixteen implants (9.7%) failed and had to be removed. Group S showed 15 failures and a success rate of 84.2%. Group NS had only one failure, giving a success rate of 98.6%. The risk of implant failure was approximately 31% in those who smoked more than 20 cigarettes per day. HS showed statistical differences from NS or LS. However, they did not show any differences from MS. CONCLUSIONS: Within the limits of the present study, the use of tobacco involves a 15.8% risk of implant failure, with a 13.1 odds ratio. LS or MS tobacco use involves a 10.1% relative risk of implant loss, whereas the consumption of >20 cigarettes per day increases this risk to 30.8%.     

The effect of sanguinarine on human peripheral blood neutrophil viability and functions

Human polymorphonuclear cell (PMN) viability, morphology, adherence, chemotaxis, oxidative metabolism, degranulation and phagocytosis were evaluated following treatment with sanguinarine (SANG). SANG was noncytotoxic to PMNs at all concentrations tested (0.31-200 microM). SANG entered the PMNs rapidly without altering the membrane fluidity and localized in the nuclear matrix. SANG (1.56-6.21 microM) inhibited chemotaxis, chemokinesis and adhesion in a dose-dependent manner, with a complete inhibition at 6.2 microM concentration. Concentrations of SANG up to 1.56 microM did not affect PMN oxidative burst; however, higher concentrations were found to inhibit basal as well as PMA-induced superoxide anion generation. The effect of SANG was time- and dose-dependent, and could be reversed if the PMNs were exposed to 12.5 microM or lower concentrations of SANG for less than 5 min. Autologous serum increased the tolerance of PMNs to SANG. Exogenous Ca2+ or Mg2+ did not alter the SANG-mediated inhibition of PMN functions. Treatment of PMNs with 3.12 microM or higher concentrations of SANG also resulted in inhibition of PMN degranulation and phagocytosis. The results suggest that SANG-mediated inhibition of PMN functions, without cytolysis or resultant release of inflammatory mediators, may have clinical implications.