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.     

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.     

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.     

Effects of cigarette smoking on the rate of plaque formation

In 2 separate studies, plaque was harvested (i) from 15 smokers and 15 non-smokers after a 48-h period without oral hygiene, and (ii) from 15 smokers and 12 non-smokers after a 48 h hygiene-free period following complete plaque removal by toothbrushing. No significant association emerged between wet weight of accumulated plaque and cigarette smoking, in either study. In the second study, the mean plaque calcium concentration was raised in smokers compared with non-smokers, and significantly raised in 7 heavy smokers relative to non-smokers. In both instances, calcium concentration was significantly raised relative to (total) phosphorus concentration, which may indicate that the additional calcium was not in mineral deposits. These results may reflect an association between calcium concentration of plaque and tobacco consumption.     

Effects of smoking on periodontal tissues

BACKGROUND/AIMS: Most studies about the association between tobacco and periodontal disease have shown that tobacco negatively affects periodontal tissues, although some authors have failed to demonstrate such association. Very few studies have tried to find out whether the effect of tobacco on periodontal tissues was similar for women and men. The aims of this investigation were to confirm the possible relationship between tobacco consumption and periodontitis, to study the correlation between intensity of smoking and disease severity, and to investigate any differences between genders related to the effects of tobacco consumption in periodontal health. MATERIAL AND METHODS: In this case-control study, 240 dental patients were selected according to previously defined criteria and were divided in two groups according to their periodontal status. Patients with established periodontitis constituted the case group. The remaining patients constituted the control group. Smoking status, probing depth, gingival recession, clinical attachment level, tooth mobility, periodontal bleeding index and plaque index were determined for each participant. Generated data were processed for statistical analysis using multiple comparisons, covariance analysis and logistic regression analysis. RESULTS: Logistic regression analysis showed that smokers had 2.7 times and former smokers 2.3 times greater probabilities to have established periodontal disease than non-smokers, independent of age, sex and plaque index. Among cases, probing depth, gingival recession and clinical attachment level were greater in smokers than in former smokers or non-smokers, whereas plaque index did not show differences. Bleeding on probing was less evident in smokers than in non-smokers. There was a dose-effect relationship between cigarette consumption and the probability of having advanced periodontal disease. The association between tobacco smoking and periodontal disease was more evident after 10 years of smoking, independent of age, gender and plaque index. Finally, it was observed that tobacco affected periodontal tissues more severely in men than in women. CONCLUSIONS: Smoking is a risk factor strongly associated with periodontitis. The effects of smoking on periodontal tissues depend on the number of cigarettes smoked daily and the duration of the habit. The effect of tobacco on periodontal tissues seems to be more pronounced in men than in women.     

Calcium and phosphate concentrations and precipitate formation in whole saliva from smokers and non-smokers

Previous reports in the literature indicate that smoking is associated with increased plaque accumulation and/or mineralization. This might be due to an effect of tobacco smoke on properties of saliva. The present study examined the stability of components in fresh and incubated saliva in smokers and non-smokers. Saliva from smokers, collected immediately after smoking a cigarette, did not differ significantly from that of non-smokers in the turbidity developing after incubation (24 h, 37°C), which may reflect aggregation of salivary components by mechanisms analogous to those involved in plaque formation. This finding is in agreement with our previous result (Macgregor. Edgar & Greenwood 1985) which showed that the rate of plaque formation did not differ between smokers and non-smokers. Although an intimation of higher initial calcium concentrations, greater precipitation of calcium and development of more turbidity during incubation was observed in the salivas of smokers than those of non-smokers, the major reason for the greater plaque accumulation and calculus in smokers is probably inadequate oral hygiene.     

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

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

The Effect of Tobacco Smoking on Salivation

Aim

The purpose of this study was to examine the detrimental effect of smoking on the function of the salivary glands.

Material and Methods

The study was conducted on 60 patients who were divided into two groups: a test group which included smokers and control group represented by non-smokers. Each group included 30 patients. General information was collected from all the respondents via a questionnaire as well as the data on the duration of smoking and number of cigarettes smoked per day. Saliva was collected by spitting method in a graduated tube and the amount of unstimulated and stimulated saliva was measured and recorded in ml per minute. Stimulated saliva was collected immediately after rinsing the mouth with a 2% aqueous solution of citric acid which is carried salivary stimulation. The presence of pigmentation on the teeth and coated tongue were recorded during clinical examination. The degree of oral hygiene was determined by plaque index. All the obtained data were statistically analyzed with significance level p <0.05.

Results

The results showed no significant differences in the amount of saliva between smokers and non-smokers, however, the amount of saliva decreases significantly with the duration of smoking and increasing age of smokers. Also proven was the difference in the quality of saliva: smokers have thick saliva and nonsmokers predominantly serous. In addition, smokers have poorer oral hygiene status than non-smokers, and demonstrated a positive correlation between the level of oral hygiene and length of smoking tobacco.

Conclusion

This study has proven that smoking adversely affects salivation: long-term smoking reduces the secretion of saliva and changes its quality.Key words: Smoking, Tobacco Use Disorder, Saliva, Salivation, Xerostomia     

The effect of different cigarette smoking levels on gingival crevicular fluid volume and periodontal clinical parameters in Saudi Arabia

IntroductionPeriodontal disease is a chronic inflammatory condition of the periodontium. It is the main cause of tooth loss and is considered one of the biggest threats to the oral cavity. Tobacco smoking has long been associated with increased risk for periodontal, peri-implant, and other medical diseases.ObjectiveTo evaluate the effect of smoking and its level on periodontal clinical parameters (probing depth (PD), plaque index (PI), gingival index (GI), clinical attachment level (CAL), bleeding on probing (BOP), and the volume of gingival crevicular fluid (GCF)) in healthy and chronic periodontitis individuals.Material and MethodA total of 160 participants were recruited in the present study, who were equally divided into the following five groups: healthy controls (C), healthy smokers (HS), nonsmokers with periodontitis (PNS), light smokers with periodontitis (PLS), and heavy smokers with periodontitis (PHS). GCF volume and periodontal clinical parameters (PD, PI, GI, CAL, and BOP) were assessed for each participant and compared between the study groups.ResultThere was a statistically significant difference in PD, PI, GI, CAL, and BOP between healthy and periodontitis patients (p < 0.001). The mean PI, PD, and CAL were considerably higher in heavy smokers than light smokers and non-smokers (P < 0.001). In contrast, the mean GI and BOP were significantly lower in heavy smokers than in light smokers and non-smokers. There was a statistically significant difference in GCF between healthy and periodontitis patients (p < 0.001). The mean GCF readings were higher in heavy smokers than light smokers or non-smokers (P < 0.001).ConclusionThe present study confirms the influence of smoking on periodontal clinical parameters. Smoking was associated with increased PD, PI, CAL, and GCF readings; however, GI and BOP were decreased in smokers. The number of cigarettes played a key role in the volume of GCF and periodontal clinical parameters.     

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.     

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.     

Effect of smoking on crevicular polymorphonuclear neutrophil function in periodontally healthy subjects

BACKGROUND: Polymorphonuclear neutrophils (PMNs) represent the first line of cellular defences in the gingival crevice. Smoking, as probably the most important environmental risk factor for periodontitis, has been shown to adversely affect many neutrophil functions. OBJECTIVE: The aim of this study was to investigate the influence of smoking on PMN numbers and function in periodontally healthy smokers and non-smokers. METHODS: Sixty subjects were recruited: 15 non-smokers, 15 light smokers (< 5 cigarettes/day), 15 moderate smokers (5-15 cigarettes/day) and 15 heavy smokers (> 15 cigarettes/day). Full mouth plaque index, sulcus bleeding index and probing depths were measured. Crevicular washings were obtained from all subjects to harvest PMNs. Numbers of PMNs, percentage viability, and percentage phagocytosis of opsonized Candida albicans were recorded. RESULTS: Mean plaque scores and probing depths were (non-significantly) increased in smokers compared to non-smokers. Mean sulcus bleeding index scores were significantly lower in moderate (0.10 +/- 0.10) and heavy (0.07 +/- 0.11) smokers compared to non-smokers (0.14 +/- 0.13) (p < 0.05). Compared to non-smokers (1.73 +/- 1.08 x 10(6)/ml), the numbers of PMNs were higher in light (1.98 +/- 0.96 x 10(6)/ml) and moderate (2.03 +/- 1.43 x 10(6)/ml) smokers and were lower in heavy smokers (1.68 +/- 1.18 x 10(6)/ml), though there were no significant differences in PMN counts between the groups (p > 0.05). Percentage viability of PMNs was significantly lower in light (77.6 +/- 7.8%), moderate (76.5 +/- 8.2%) and heavy (75.0 +/- 6.5%) smokers compared to non-smokers (85.5 +/- 6.0%) (p < 0.05). Furthermore, the ability of PMNs to phagocytose was significantly impaired in light (58.3 +/- 4.1%), moderate (51.9 +/- 2.33%) and heavy (40.9 +/- 3.5%) smokers compared to non-smokers (74.1 +/- 4.1%) (p < 0.05), with evidence of a dose-response effect. CONCLUSION: Cigarette smoking adversely affected PMN viability and function in this periodontally healthy population.     

EVALUATION OF CLINICAL PERIODONTAL CONDITIONS IN SMOKERS AND NON-SMOKERS

Given that tobacco smoking habit is a risk factor for periodontal diseases, the aim of this study was to compare clinical periodontal aspects between smokers and non-smokers. The clinical status were assessed in 55 patients, 29 smokers and 26 non-smokers, aged 30 to 50 years, with mean age of 40. The clinical parameters used were: probing depth (PD), plaque index (PI), gingival index (GI), clinical attachment level (CAL), gingival recession (GR) and gingival bleeding index (GBI) for arches (upper and lower) and teeth (anterior and posterior). Tooth loss was also evaluated in both groups. Multiple regression analysis showed: tendency of greater probing depth and clinical attachment level means for smokers; greater amount of plaque in smokers in all regions; greater gingival index means for non-smokers with clinical significance (p<0.05) in all regions. Although, without statistical significance, the analysis showed greater gingival bleeding index means almost always for non-smokers; similar gingival recession means in both groups and tendency of upper tooth loss in smokers and lower tooth loss in non-smokers. The findings of this study showed that clinical periodontal parameters may be different in smokers when compared to non-smokers and that masking of some periodontal signs can be a result of nicotine''s vasoconstrictor effect.     

Oral hygiene compliance and gingivitis expression in cigarette smokers

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.     

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.     

Smoking affects the subgingival microflora in periodontitis

BACKGROUND: Tobacco smoking has been identified as one major risk factor for destructive periodontal disease. Scaling and root planing have been shown to be less effective in smokers with periodontitis. The aim of the present study was to compare the subgingival microbial flora of treated and untreated smokers and non-smokers. METHODS: Four independent adult patient groups with periodontitis were included in this investigation: 88 untreated smokers (U-S); 90 untreated non-smokers (U-NS); 119 treated non-smokers (T-NS); and 171 treated smokers (T-S). Clinical variables included cumulative plaque index (CPI), probing depth (PD), clinical attachment level (CAL), cumulative bleeding index (CBI), and cumulative suppuration index (CSI). Paper point samples from the deepest bleeding pocket in each quadrant of the dentition were analyzed for the presence and levels of 6 periodontal bacterial pathogens using anaerobic culture techniques. RESULTS: U-S showed a higher mean cumulative plaque index than U-NS (3.5 versus 2.7). Mean PD and mean CAL were higher in the T-S in comparison to the T-NS group (7.0 versus 6.6 mm and 5.6 versus 4.7 mm, respectively). Microbiological characteristics of U-S were a higher prevalence of Prevotella intermedia/nigrescens and higher mean levels of Peptostreptococcus micros (Pm) and Fusobacterium nucleatum (Fn). T-S patients were characterized by higher prevalence of Bacteroides forsythus (Bf), Pm, and Campylobacter rectus (Cr) and higher mean levels of Pm and Fn. The mean percentage of B. forsythus tended to be higher in the T-S group than in the T-NS group (6.9% versus 5.6%). The relative risk to be infected with Bf, Pm, and Cr was statistically higher in smokers (odds ratios: 1.9, 1.9, and 1.6, respectively). The chance to find > or =10% of Bf, Pm, and/or Fn was 3.3 higher in smokers when A. actinomycetemcomitans and P gingivalis were absent. Detection of > or =20% Pm/Fn in treated patients was strongly associated with smoking (odds ratio 13.8, P= 0.002). CONCLUSIONS: Smoking is a determining factor for the composition of the subgingival microflora in adult patients with periodontitis and may select for a specific cluster of periodontal pathogens, notably Bf, Pm, Fn, and Cr. On the basis of these observations, smoking, among other criteria, may be one parameter to use in deciding to treat refractory periodontitis in smokers with a systemic antibiotic therapy directed against smoking-associated periodontal bacteria.     

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

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

Effect of cigarette smoking on the transition dynamics in experimental gingivitis

This paper reports the findings of an experimental gingivitis study conducted in smokers and non-smokers. 33 volunteers were examined and underwent prophylaxis during a period of 4 weeks. 28 subjects who showed a plaque index less than 0.20 on all prophylaxis occasions were permitted to continue in the study. Subjects then had their gingival status recorded, had their teeth polished and were requested to abstain from all oral hygiene measures for the following 21 days. After 5 days, 10 days and 21 days, plaque and gingival status were recorded using the criteria of the plaque index and gingival index. After the examination on day 21, the teeth were polished and oral hygiene was re-instituted. Following 2 weeks of supervised oral hygiene, recordings of plaque and gingival status were performed. At the initial examination, there was no difference between the clinical assessment of plaque and gingival status in smokers and non-smokers. Similar amounts of plaque accumulated in the 2 groups during the period of no oral hygiene, but smokers exhibited less gingival inflammation assessed clinically than non-smokers. This difference occurred as a result of an apparently lowered incidence rate and a markedly higher recovery rate in smokers compared to non-smokers. These findings may indicate that smokers for reasons yet unknown have a reduced capacity to mount and maintain an effective defense reaction to a given plaque challenge.     

Correlation in inorganic ion concentration between saliva and plaque fluid

The composition and the concentration of inorganic ions in dental plaque significantly influence the initiation and the development of dental caries through altering the degree of saturation of the aqueous phase surrounding the dental enamel. In order to know how plaque is affected by saliva, the composition and the concentration of inorganic ions in saliva and plaque fluid were investigated. The ionic concentrations of sodium and chlorine had similar values between plaque fluid and saliva. However, the concentrations of the inorganic ions such as ammonium, potassium, magnesium, calcium, and phosphate were significantly different between plaque fluid and saliva. This meant that the saliva and plaque fluid were different in its inorganic composition presumably reflected by the metabolic activity of bacteria in the plaque. On the other hand, as for the correlation coefficients between plaque fluid and saliva composition, statistically significant correlation was observed in ions such as sodium, ammonium, potassium, magnesium, and chlorine but not in calcium, phosphate, or in pH values. This was possibly due to the fact that saliva was the main source of supply of these ions. However as for calcium and phosphate, no close correlation was found possibly because they could be supplied also through tooth enamel dissolution. The discrepancy of the results with former studies on this point was speculatively explained by,the difference of the plaque age used. It was considered reasonable that the pH value was independent, as it is mainly decided by the activity of the bacteria in the plaque.     

Bone height changes in individuals with periodontal disease: a 17-year prospective longitudinal study

OBJECTIVE: The aim of this study was to analyse changes in bone height after 17 years in smokers and non-smokers with periodontal disease, and to compare these with clinical assessment outcome. MATERIAL AND METHODS: Participants comprised 50 adults with periodontitis and 18 healthy controls from a randomly selected epidemiological sample. Their mean age at the end of the study was 54.2 (SD+/-3.09) years. The study included radiographic analysis compared with clinical data. RESULTS: The periodontitis group had significantly (p<0.001) higher values than their healthy counterparts for plaque index (PLI), gingival index (GI), calculus index (CI), and bleeding on probing (BOP) at baseline and after 17 years. At the end of the follow-up, never-smokers with periodontitis had higher values for PLI (p<0.05) and ex-smokers and smokers had higher GI and BOP (p<0.001) than the controls. In all individuals with periodontitis, maxillary molars were most affected. Smokers had more severe marginal bone loss over time. Vertical bone defects were more often seen on the mesial side of teeth (p<0.05). CONCLUSION: Marginal bone level in this prospective study did reveal tooth groups at higher risk for progression of periodontal disease.