Tobacco smoking and chronic destructive periodontal disease

Abstract

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...

Assessment of Some Biochemical Oxidative Stress Markers in Male Smokers with Chronic Periodontitis

“…The balance between destructive cytokines such as IL-1a, IL-1b, TNFa, IL6, IL8 and prostaglandins and protective cytokines such as TGF-b, IGF and interferons shifts more towards destructive profile in smokers. Also it has been speculated that the interference of smoking with inflammatory signs and symptoms is mediated by vasoconstructive effects of nicotine [2,3,[19][20][21]. The present study has observed that smokers with chronic periodontitis exhibit more clinical periodontal damage and relatively higher oxidative stress compared to non-smokers with chronic periodontitis.…”

“…Increased odds to develop oral cancer, caries, and periodontal disease and tooth loss have been reported [1]. Tobacco smoking is one of the main risk factor associated with chronic destructive periodontal disease and there is an emerging evidence to suggest that subgingival calculus formation is more prevalent and severe in smokers compared to the non-smokers [2]. Smokers are almost three times as likely to have severe periodontitis compared to the non-smokers [3].Smoking is associated with oxidative stress.…”

Sex difference in oral disease of millet agriculturalists from the Take-vatan lineage of the recent Bunun tribe of Taiwan

“…Smoking is clinically regarded as a strong risk factor for periodontal disease (e.g. Bergstrom, 2004). The smoking habit is widespread among the Bunun tribe: they cultivate tobacco themselves, the males and females generally begin to smoke at the age of 12 or 13 years, and they always carry a pipe with them (Yuasa, 2009).…”

Avaliação clínica e microbiológica em puérperas com doença periodontal e a sua relação com desfecho reprodutivo ruim.

“…Os fatores de risco, situação sócio-econômica, idade, etnia com associação na raça negra (Bosnjak et al, 2006;Henriques, 2003;Lieff et al, 2004) e também na raça branca (Pitiphat et al, 2008), parto pretermo prévio (Mokeem et al,2004), nível de escolaridade (Cruz et al, 2005), e tabagismo (Bergstrom, 1990(Bergstrom, , 1998(Bergstrom, , 2004Grossi et al, 1995;Holbrook et al, 2004;Jeffcoat et al, 2001aJeffcoat et al, , 2001bSwenson. 1979), também têm sido relacionados com os marcadores clínicos da doença periodontal e desfechos reprodutivos ruins (Kierse, 1989; Shah e Bracken, 2000; Shiono et al, 1986) nas gestantes.…”

“…Outro ponto crítico é a questão do impacto do tabagismo, um importante fator de risco para doença periodontal (Bergstrom, 1990(Bergstrom, , 2004Bergstrom et al, 1988;Grossi et al, 1995) e desfechos reprodutivos ruins (Kierse, 1989;Shah e Bracken, 2000;Shiono et al, 1986). Em nosso estudo apenas 7,6% de nossas amostras relataram que fumaram durante a gestação, mas não houve qualquer associação com doença periodontal ou com desfecho reprodutivo ruim, talvez em função deste baixo número, situação semelhante observada nos estudos de López et al (2002a) e Moore et al (2001).…”