Cigarette smoking in patients referred for periodontal treatment

Preber, Hans; Bergström, Jan

doi:10.1111/j.1600-0722.1986.tb01372.x

Cited by 91 publications

(112 citation statements)

References 21 publications

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“…1984;Parvinen, 1984]. Smoking is also known to increase the prevalence of den tal plaque and the risk for development of periodontal dis ease [Preber and Bergstrom, 1986]. The present report is in accordance with our previous 12-year follow-up study | Ravald et al, in press], in which smokers also showed sig nificantly higher DFS scores than non-smokers.…”

Section: Discussionsupporting

confidence: 83%

Prediction of Root Caries in Periodontally Treated Patients Maintained with Different Fluoride Programmes

Ravald¹,

Birkhed²

1992

Caries Res

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The aims of the investigation were to evaluate the effect of diÿerent fluoride programmes, as adjuncts to professional plaque control every 3–4 months, on root caries incidence in periodontally treated patients and to identify risk factors for root caries development. Ninety-nine individuals, 33–76 years old, who had been treated for periodontal disease were subjected to one of three fluoride programmes during a 2-year period: (1) professional application, 3-4 times/year, of Duraphat® (n = 34) or (2) of a 0.4% stannous fluoride gel (n = 33), or (3) daily mouthrinsing with a 0.05% sodium fluoride solution (n = 32). A number of clinical recordings and laboratory tests, used as presumptive risk indicators for root caries, were carried out before and on three different occasions after the periodontal treatment. No statistically significant differences were found between the various fluoride programmes. During the 2-year period, a total of 246 new decayed or filled surfaces (DFS) were recorded, 72 (29.3%) of which were diagnosed as active and 124 (50.4%) as inactive root caries lesions; 50 (20.3%) of the surfaces had been restored. Individuals with ≥ 1 new root DFS during the 2 years (n = 50) differed significantly from those with 0 new root DFS (n = 49) as concerns salivary counts of mutans streptococci and lactobacilli, root plaque scores and percentage of exposed root surfaces. Baseline root caries prevalence (r = 0.43) and root plaque scores (r = 0.36) showed the highest correlations with new root DFS. By stepwise multiple regression analysis, it was shown that these two variables contributed significantly to the variance of root caries incidence (new DFS) during the 2-year period. Smokers had a significantly higher root caries prevalence at baseline and higher root caries incidence during the study than non-smokers.

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Section: Discussionsupporting

confidence: 83%

Prediction of Root Caries in Periodontally Treated Patients Maintained with Different Fluoride Programmes

Ravald¹,

Birkhed²

1992

Caries Res

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“…The tendency of an inadequate inflammatory response among smoker patients was first described in the early 1980s. [1][2][3][4] Studies during later years have confirmed these observations and contributed additional evidence that the gingival inflammatory response is altered by smoking. [5][6][7][8][9][10][11][12][13][14][15] The anti-hemorrhagic and anti-inflammatory effects imply that typical symptoms of inflammation, such as redness, bleeding, and edema appear comparably late in the disease process, if at all, in the average smoker patient.…”

Section: Smoking and Periodontal Inflammationsupporting

confidence: 56%

“…The concept of risk was introduced into periodontology several years ago 3 and has now been applied in several studies to estimate the risk associated with smoking.…”

Section: Smoking and Risk For Destructive Periodontal Diseasementioning

confidence: 99%

“…Almost all studies that have utilized pocket frequency or probing depth as a surrogate endpoint for destructive disease report a significantly greater pocket frequency and/or probing depth among smokers compared to non-smokers. 3,[26][27][28][29][30][31][32][33][34][35][36] Moreover, smokers suffer a greater rate of tooth loss than non-smokers. [37][38][39][40][41][42] Tooth loss can, indeed, be the result of other circumstances than periodontal disease.…”

Section: Smoking and Periodontal Inflammationmentioning

confidence: 99%

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Tobacco smoking and chronic destructive periodontal disease

2004

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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 unavoida...

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“…Isto pode ser explicado por uma maior busca de terapia periodontal por mulheres acarretando um número elevado de probandos do sexo feminino (HART et al, 1991). Todavia, este fato não é comprovado quando se analisam os descendentes diretos dos probandos, em que se verifica distribuição equivalente da doença periodontal entre indivíduos do sexo feminino e masculino (HART et al, 1991;BOUGHMAN et al, 1986 PREBER ;BERGSTRÖM, 1986;BECK;OFFENBACHER, 1995;GROSSI et al, 1994;RIVERA-HIDALGO, 2003 pertencentes ao mesmo grupo sócio-econômico foram comparados, não houve diferença quanto à susceptibilidade à destruição periodontal (GROSSI et al, 1994;GROSSI et al, 1995).…”

Section: Il-1rn (íNtron 2-vntr)unclassified

Avaliação da associação entre o polimorfismo dos genes IL-1A (-889), IL-1B (-511), IL-1B (+3954), IL-1RN (íntron2-VNTR) e TNFA (-308) e a periodontite agressiva

Freitas¹

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Cigarette smoking in patients referred for periodontal treatment

Cited by 91 publications

References 21 publications

Prediction of Root Caries in Periodontally Treated Patients Maintained with Different Fluoride Programmes

Prediction of Root Caries in Periodontally Treated Patients Maintained with Different Fluoride Programmes

Tobacco smoking and chronic destructive periodontal disease

Avaliação da associação entre o polimorfismo dos genes IL-1A (-889), IL-1B (-511), IL-1B (+3954), IL-1RN (íntron2-VNTR) e TNFA (-308) e a periodontite agressiva

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