Periodontitis and smoking: an evidence-based appraisal.
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Biomedical subjects
Publications and source records attributed to Jan Bergström.
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OBJECTIVE: The aim of the present cross-sectional study was to investigate a possible association between the use of Swedish moist snuff and periodontal bone loss. MATERIAL AND METHODS: The study was carried out on 84 apparently healthy men in the age range 26-54 years, 25 current snuff users, 21 former snuff users, and 38 never-users. The periodontal bone height was evaluated from bitewing radiographs measuring the distance from the cement-enamel junction (CEJ) to the periodontal bone crest (PBC) at pre-molars and molars in each quadrant of the dentition. RESULTS: The mean (95% confidence interval (95% CI)) CEJ-PBC distance was 1.00 (0.87-1.13), 1.12 (0.97-1.26), and 1.06 (0.95-1.16) mm for current users, former users, and never-users, respectively. The association between snuff use and bone height level controlling for age was not statistically significant (anovaF = 0.3, p > 0.05). There was, further, no statistically significant difference between light and heavy exposure users controlling for age (anovaF = 1.0, p > 0.05). CONCLUSION: Our observations suggest that the use of Swedish moist snuff is not associated with periodontal bone loss.
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OBJECTIVE: A radiographic investigation into the relationship between tobacco smoking and subgingival dental calculus was conducted in an adult population, including 48 current smokers, 57 former smokers, and 125 non-smokers. MATERIAL AND METHODS: Assessment of subgingival calculus was based on a full set of radiographs. Mesial and distal root surfaces were assessed as to presence or absence of radiopaque deposits apical to the cemento-enamel junction. The severity of subgingival calculus deposition, labeled subgingival calculus load, was estimated from both the total number and the proportion of proximal sites affected. RESULTS: The overall prevalence of individuals exhibiting at least one subgingival calculus positive site was 43%, ranging from 15% in age stratum 20-34 years to 72% in age stratum 50-69 years. The prevalence among current smokers, former smokers, and non-smokers was 71%, 53%, and 28%, respectively. The differences between smoking groups were statistically significant (p<0.001). The mean subgingival calculus load of current smokers, former smokers, and non-smokers was 3.4, 1.2, and 0.6 affected sites per person, respectively, or expressed as mean proportions, 6.2%, 2.4%, and 1.1%, respectively. The association between smoking and subgingival calculus load was statistically significant (p<0.001). The subgingival calculus load increased with increasing smoking exposure, suggesting a dose-response relationship. CONCLUSION: The present observations in dentally aware adults indicate a strong and independent impact of tobacco smoking on subgingival calculus deposition.
OBJECTIVES: To explore the subgingival periodontal microflora in a Saudi Arabian population with a special focus on its relationship with various smoking habits. MATERIAL AND METHODS: A total of 198 individuals in the age range 17-60 years were included in the study. 29% were water-pipe smokers, 18% cigarette smokers, 13% smokers of both water pipe and cigarettes (mixed smokers) and 40% non-smokers. For each individual, a subgingival plaque sample from the deepest site in each quadrant was obtained. The checkerboard DNA-DNA hybridization technology was used to determine the presence of Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Tannerella forsythensis, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Treponoma denticola, Peptostreptococcus micros, Campylobacter rectus, Eikenella corrodens, Selenomonas noxia and Streptococcus intermedius. Two cut-off levels for detection were used, score 1(10(5) bacteria) and score 3 (10(6) bacteria). RESULTS: The prevalence of individuals positive for the different microorganisms at score 1 cut-off varied from 7% to 95%. At score 3 cut-off the prevalence varied from 0% to 30%. The depth of sample site was a key factor for detection. When the depth of sample site was taken into account, no statistically significant differences were observed between cigarette smokers, water-pipe smokers, and non-smokers with regard to occurrence of the microorganisms studied. CONCLUSIONS: No major differences were observed between cigarette smokers, water-pipe smokers, and non-smokers regarding the occurrence of the periodontal microorganisms studied suggesting that this portion of the subgingival periodontal microflora is independent of tobacco smoking.
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.
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.
BACKGROUND: Major depression can be treated by means of cognitive-behavioural therapy, but as skilled therapists are in short supply there is a need for self-help approaches. Many individuals with depression use the internet for discussion of symptoms and to share their experience. AIMS: To investigate the effects of an internet-administered self-help programme including participation in a monitored, web-based discussion group, compared with participation in web-based discussion group only. METHOD: A randomised controlled trial was conducted to compare the effects of internet-based cognitive-behavioural therapy with minimal therapist contact (plus participation in a discussion group) with the effects of participation in a discussion group only. RESULTS: Internet-based therapy with minimal therapist contact, combined with activity in a discussion group, resulted in greater reductions of depressive symptoms compared with activity in a discussion group only (waiting-list control group). At 6 months' follow-up, improvement was maintained to a large extent. CONCLUSIONS: Internet-delivered cognitive cognitive-behavioural therapy should be pursued further as a complement or treatment alternative for mild-to-moderate depression.
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.
PURPOSE: To investigate the relationship between water pipe and cigarette smoking and the prevalence and severity of vertical periodontal bone defects. MATERIAL AND METHODS: A study sample of 355 individuals in the age range 17 to 60 years was recruited from Jeddah, Saudi Arabia. Full sets of intra-oral radiographs for each individual were assessed with regard to the presence or absence of vertical bone defects. A vertical defect was defined as an angular resorption of the interdental marginal bone of 2 mm or more at either the mesial or distal aspect of the root. RESULTS: The overall prevalence of vertical defects was 39%, with a specific prevalence of 47% in water pipe smokers, 54% in cigarette smokers, and 23% in non-smokers. The prevalence was significantly elevated in both types of smokers compared with non-smokers (p < 0.001). Expressed as the proportion of sites with vertical defects per person, the severity was 2.6% for water pipe smokers, 2.8% for cigarette smokers, and 1.3% for non-smokers. The association between smoking and severity of vertical defects was statistically significant (p < 0.001). The severity of vertical defects was significantly greater in heavy exposure compared to light exposure smokers in water pipe as well as cigarette smokers (p < 0.001). The relative risk associated with water pipe and cigarette smoking was 2.9-fold and 6.6-fold increased, respectively, compared to non-smoking. CONCLUSION: The present observations suggest that prevalence and severity of vertical periodontal bone defects are increased in tobacco smokers. The association of vertical bone loss with water pipe smoking is comparable to the association with cigarette smoking.
PURPOSE OF REVIEW: The aim of this article is to review the emerging literature on the use of the Internet in the treatment of anxiety disorders. The questions asked are: (1) are Internet-delivered treatments for anxiety disorders supported by the research literature? (2) what is the quality of the evidence as it stands? (3) is there any evidence to suggest that Internet interventions can be harmful? RECENT FINDINGS: Recent and ongoing trials on panic disorder show that Internet-based self-help with minimal therapist contact is a promising approach in the treatment of panic disorder. However, trials have been small and there is a need for large-scale trials and studies conducted in psychiatric settings as most studies have recruited patients via advertisement. There is no evidence in the literature that Internet intervention is harmful, but most likely a stepped-care approach would be feasible to handle cases who fail to respond. SUMMARY: Internet-delivered interventions for anxiety disorders, and in particular panic disorder, are promising. There is however a need for further research and evaluation and there is also a need to find a proper place for such interventions in the clinical management of anxiety disorders, preferably using a stepped-care approach.
Tobacco smoking is the main risk factor associated with chronic destructive periodontal disease. No other known factor can match the strength of smoking in causing harm to the periodontium. The harmful effects manifest themselves by interfering with vascular and immunologic reactions, as well as by undermining the supportive functions of the periodontal tissues. The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the ensuing clinical symptoms of bone loss, attachment loss, pocket formation, and eventually tooth loss. A review of the international literature that has accumulated over the past 20 years offers convincing evidence that smokers exhibit greater bone loss and attachment loss, as well as more pronounced frequencies of periodontal pockets, than non-smokers do. In addition, tooth loss is more extensive in smokers. Smoking, thus, considerably increases the risk for destructive periodontal disease. Depending on the definition of disease and the exposure to smoking, the risk is 5- to 20-fold elevated for a smoker compared to a never-smoker. For a smoker exposed to heavy long-life smoking, the risk of attracting destructive periodontal disease is equivalent to that of attracting lung cancer. The outcome of periodontal treatment is less favorable or even unfavorable in smokers. Although long-term studies are rare, available studies unanimously agree that treatment failures and relapse of disease are predominantly seen in smokers. This contention is valid irrespective of treatment modality, suggesting that smoking will interfere with an expected normal outcome following commonplace periodontal therapies. The majority of available studies agree that the subgingival microflora of smokers and non-smokers are no different given other conditions. As a consequence, the elevated morbidity in smokers does not depend on particular microflora. The mechanisms behind the destructive effects of smoking on the periodontal tissues, however, are not well understood. It has been speculated that interference with vascular and inflammatory phenomena may be one potential mechanism. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing. Smoking research over the past two decades has brought new knowledge into the domains of periodontology. Even more so, it has called into question the prevailing paradigm that the disease is primarily related to intraoral factors such as supra- and subgingival infection. Smoking research has revealed that environmental and lifestyle factors are involved in the onset and progression of the disease. Being the result of smoking, destructive periodontal disease shares a common feature with some 40 other diseases or disorders. As a consequence, periodontal disease should be regarded as a systemic disease in the same way as heart disease or lung disease. Thus, chronic destructive periodontal disease in smokers is initiated and driven by smoking. Its progression may or may not be amplified by unavoidable microbial colonization.
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.
The relation between smoking and apical periodontitis has been little studied to date. The aim of the present study was to investigate whether tobacco smoking might be associated with the prevalence or severity of periapical lesions. A total of 247 individuals, 81 current smokers, 63 former smokers, and 103 non-smokers participated in the study. The periapical condition was expressed as the number and percentage of radiographically detectable lesions and, in addition, as a severity index. The overall prevalence of apical periodontitis was 52% and the overall prevalence of endodontic treatment 58%. There was no significant influence of smoking on the prevalence of either apical periodontitis or endodontic treatment. The mean number (percentage) of periapical lesions per person was 1.9 (6%) in current smokers, 1.5 (4%) in former smokers, and 1.0 (3%) in non-smokers. Controlling for age, the association between smoking and periapical lesions was not statistically significant. The mean periapical severity index including all teeth, or teeth affected by periapical lesions alone, did not significantly differ between smoking groups. It is concluded that the present observations do not lend support to the assumption that tobacco smoking is associated with apical periodontitis.
OBJECTIVE: The magnitude of risk for periodontal disease associated with smoking was investigated by exploring the interrelationships between definition of disease, prevalence and relative risk in a population of dentally aware individuals. MATERIALS AND METHODS: A total of 133 smokers and 242 non-smokers in the age range 20-69 years served as the database. Criteria based on clinical probing of pocket depth and radiographic measurement of bone height were used for the purpose of disease definition. Various pocket frequency cutoff points for two probing depth levels, > or =5 and > or =6 mm, and, in addition, the 30th, 25th, and 20th percentiles of the bone height distribution were alternately selected as criteria. RESULTS: Disease definition had an impact on the prevalence, and the relative risk varied as a function of the prevalence. For a broad definition of disease such as 1% of pockets > or =5 mm, the prevalence for smokers was approximately twice the prevalence for non-smokers and the odds ratio (OR) was 3.0. A narrower definition such as 15% of pockets > or =5 mm resulted in decreased prevalences for both smokers and non-smokers and an OR of 12.1. Increasing exposures correlated with greater magnitudes of risk. Heavy exposure was associated with greater risk than light exposure. For the combination of a narrow disease definition and heavy exposure, the relative risk was considerable (OR 9.8-20.3). CONCLUSION: Smoking-associated relative risk is dependent on definition of disease and prevalence. Given other factors, a narrow definition will result in a low prevalence and a high risk and, vice versa, for a broader definition, prevalence will be high and the risk moderate.
BACKGROUND, AIMS: Over the past 10 years several studies have been published pointing towards a relationship between periodontal disease and various systemic disorders or diseases. The purpose of this retrospective study was to investigate the occurrence of self-reported systemic disorders in patients referred to a specialist clinic for periodontal treatment and to explore possible relationships between general health and periodontal disease severity in this population. MATERIAL AND METHODS: Data were collected from the dental records and the health questionnaires of 1006 subjects. Stepwise multiple linear regression analyses were adopted to calculate correlations between systemic disorders as independent variables and number of remaining teeth and the relative frequency of periodontal pockets of 5 mm or more, respectively, as the dependent variable. RESULTS: The number of remaining teeth was significantly and positively correlated to the presence of cardiovascular disease, diabetes and rheumatoid disease after adjustment for age, sex and smoking. The relative frequency of diseased sites, however, was not significantly correlated to any one of the investigated systemic health disorders. CONCLUSION: No significant associations between investigated systemic disorders and periodontal disease severity were found if the relative frequency of deep periodontal pockets was used as the clinical parameter for periodontal disease severity. However, cardiovascular disease, diabetes and rheumatoid disease were found to be significantly correlated to number of lost teeth, which may represent one aspect of periodontal health. This result held true in nonsmokers only.
BACKGROUND: Tobacco smoking has considerable negative effects on the outcome of periodontal treatment. The reason for the inferior therapeutical effect might be related to an altered neutrophil activity in terms of elastase and/or matrix metalloproteinase-8 (MMP-8), as well as in the protease inhibitor alpha-1-antitrypsin (alpha-AT) and alpha-2-macroglobulin (alpha-2-MG) activities. The aim of the present study, therefore, was to elucidate the effect of tobacco smoking on gingival crevicular fluid (GCF) levels of these substances following surgical treatment. METHODS: The study population included 15 smoking and 15 non-smoking patients with moderate to severe periodontitis receiving surgical treatment. Clinical examinations and collection of GCF were done prior to surgery and 1 and 5 weeks following treatment. The elastase activity was measured with a chromogenic low-molecular substrate and the levels of alpha-1-AT, alpha-2-MG, and MMP-8 with enzyme-linked immunosorbent assay. RESULTS: The results showed unaltered levels of alpha-1-AT, alpha-2-MG, and MMP-8 in smokers following surgery. In non-smokers, the levels of alpha-1-AT and alpha-2-MG increased, whereas MMP-8 levels decreased. The levels of elastase remained unaltered in both smokers and non-smokers. CONCLUSIONS: These results indicate that in the presence of smoking, the levels of alpha-1-AT, alpha-2-MG, and MMP-8 remained unaltered during the recovery period following surgical treatment. This is interpreted as a possible interference of smoking with the treatment response and may, in part, explain the clinical evidence of an inferior treatment outcome in smokers.