DOI: 10.5958/j.2319-5886.2.2.

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International Journal of Medical Research & Health Sciences

www.ijmrhs.com
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Volume 2 Issue 2 April - June

Coden: IJMRHS
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Copyright @2013

ISSN: 2319-5886
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Received: 26 Feb 2013 Review article

Revised: 21 Mar 2013

Accepted: 24 Mar 2013

SMOKING-A TRUE PERIODONTAL HAZARD Mani Ameet M1, Mani Shubhangi A2, *Tejnani Avneesh H3, Gupta Ankit 4 Reader, 3Postgraduate student, Department of Periodontology, Rural Dental College, Pravara Institute of Medical Sciences, Loni, Maharashtra, India 2 Reader, Department of Orthodontics, Rural Dental College, Pravara Institute of Medical Sciences, Loni, Maharashtra, India 4 Senior Resident, General Medicine Department, Himalayan Institute of Medical Sciences, Jollygrant, Dehradun *Corresponding Author E-mail : avneesh316@yahoo.co.in,
ABSTRACT
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It is now well established that tobacco use in general and cigarette smoking in particular, is a major risk factor in the incidence and severity of several forms of periodontal diseases.A large number of studies have been published in the dental literature regarding this possible role. Much of the literature has also indicated that smokers affected with periodontitis respond less favourably to periodontal treatment be it non-surgical, surgical or regenerative. Numerous studies of the potential mechanisms whereby smoking tobacco may predispose to periodontal disease have been conducted, and it appears that smoking may affect the vasculature, the humoral immune system, and the cellular immune and inflammatory systems, and have effects throughout the cytokine and adhesion molecule network. The aim of this review is to consider the evidence for the association between smoking and periodontal diseases and to highlight the biological mechanisms whereby smoking may affect the periodontium. Keywords: Smoking, adverse effects, Chronic periodontitis, Neutrophils
INTRODUCTION

The role of tobacco and, more specifically, cigarette smoking as a public health problem has long been recognized. The magnitude of this problem was summarized in the 1989 Surgeon Generals Report, where it is stated that smoking is responsible for more than one of every six deaths in the United States. Dentistry has long been aware of the effects of tobacco on the soft tissues of oral cavity and the implications of this

in clinical practice. The effects of cigarette smoking on bone and connective tissues have been well documented in the medical literature.1 Tobacco smoking, mostly in the form of cigarette smoking, is recognized as the most important environmental risk factor in periodontitis, and, with respect to this, there is large number of supporting epidemiological studies. It has usually been necessary to rely on the vast body of medical literature that describes the noxious effects of smoking, and to apply this knowledge
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to the pathogenesis of periodontitis. Therefore, many of these mechanisms may be implied or speculative. This review will attempt to build on previous reviews in the periodontal literature and make attempts to primarily consider evidence that directly pertains to the periodontal tissues.2 Smoking and oral cleanliness: Sheiham (1971) evaluated a group of smokers and nonsmokers and found that the level of periodontal disease did not differ significantly when controlled for oral hygiene.3 Preber et al (1980), Feldman et al (1983) and Ismail and coworkers (1983) likewise observed smokers to have decreased levels of oral hygiene when compared to nonsmokers.4, 5, 6 Effect of smoking on plaque development; Early observational reports that smokers showed a higher prevalence of dental plaque than nonsmokers suggested that more severe periodontal disease in smokers might be because of greater accumulations of plaque.4 Studies in which the development of plaque and inflammation was observed in an experimental gingivitis model, showed that the rate of plaque formation was similar between smokers and non-smokers.7 Effect of smoking on the oral flora; The majority of studies have investigated the difference in the subgingival microflora between smoking and non-smoking subjects with periodontal disease. However, a study of the microbiota of the oral mucous membrane and saliva failed to establish a statistically significant trend for smokers to harbour greater proportions of putative periodontal pathogens.8 Similarly, an experimental gingivitis study showed no differences between smokers and non-smokers in the alterations to supra- and subgingival microflora.9 Effect of smoking on the subgingival microflora in periodontitis: A number of studies have indicated that smoking has little effect on the subgingival microflora. Preber et al (1992) compared the samples from smokers and non-smokers for the presence and proportion of A.a. comitans, Porphyromonas gingivalis and Prevotella intermedia and found no significant differences between the two groups.10 However,

recent studies have shown higher prevalence of potential periodontal pathogens in smokers than non-smokers.11,12,13 Effect of smoking on the prevalence and severity of periodontal disease:An association between smoking and acute necrotizing ulcerative gingivitis (ANUG) was demonstrated as early as 1946. Results from United States National Health And Nutrition Examination Survey (NHANES I) demonstrated that although current smokers had more plaque and periodontal destruction than former or never smokers, the association between periodontal disease and smoking remained, after adjusting for oral hygiene and other variables.6 Effect of smoking on gingival blood flow:There is little or no evidence that smoking induces gingival vasoconstriction. Early studies by Kardachi and Clarke (1974) hypothesized that nicotine induced vasoconstriction,14 but Baab and Oberg (1987) questioned the hypothesis.15 Later studies using Laser Doppler Flow demonstrated that the light smokers responded with a significant increase in blood flow, but heavy smokers showed no response, indicating a high level of tolerance. A more recent study showed that the gingival blood flow had significantly increased at 3 days following quitting smoking. This study provides important information on the recovery of healthy gingival tissue, post-quitting.16 Oxygen tension in the gingival tissues: Oxygen saturation of haemoglobin is affected and attempts have been made to measure this in the gingival tissue of smokers and non-smokers. Hanioka et al (2000) showed variable results. In healthy gingiva, smokers did appear to have lower oxygen saturation, whereas in the presence of inflammation, the converse was shown.17 The same group in another study showed that the pocket oxygen tension was significantly lower in smokers compared with nonsmokers.18 Gingival inflammation and bleeding: Some early studies suggested that smokers experienced less gingival bleeding than non-smokers.19 The reduced bleeding on probing was further
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demonstrated in a study by Bergstrom and Bostrom (2001). They were also able to show a dose-response effect.20 This reduced response in smokers has also been shown in studies using the experimental gingivitis model.21 The development of gingival redness and the volume of gingival crevicular fluid were also lower in smokers. The effect of smoking on gingival bleeding has also been studied in subjects who quit-smoking, where a relatively rapid recovery of the inflammatory response was seen.22 In a study the effect of cigarette smoking was evaluated in experimentally inducted gingivitis. The findings suggested that smokers have a reduced capacity to maintain an effective defense reaction to a given plaque challenge.23 The dose-dependent effect of cigarette smoking upon gingival bleeding on probing was investigated in a large representative sample of the US population (NHANES III). Results demonstrated that smoking had a strong suppressive effect on gingival bleeding. They concluded that smoking exerts a strong, chronic and dose-dependent suppressive effect on gingival bleeding on probing.24 Effect on the gingival vasculature:Smoking has a long-term chronic effect, impairing the vasculature of the periodontal tissues rather than a simple vasoconstructive effect following a smoking episode. The suppressive effect on the vasculature can be observed through less gingival redness, lower bleeding on probing and fewer vessels visible clinically and histologically. This may also have relevance to the healing response with impairment of revascularization.2 The hypothesis that cigarette smoking is causing vasoconstriction in the healthy human gingival was tested using laser Doppler flowmetry in healthy casual consumers of tobacco. Results revealed that cigarette smoking induced a modest hyperemic response in the gingiva. They concluded that though the gingival blood flow increased during smoking, small repeated vasoconstrictive attacks due to

cigarette smoking may in the long run contribute to gingival vascular dysfunction.25 Smoking and fibroblast function: The effects of nicotine and some other components of tobacco smoke have been tested in invitro studies on gingival and periodontal ligament fibroblasts. All published studies, with the exception of the study of Peacock et al. (1993) have demonstrated detrimental effects, which could have significant impact in the inflammatory destructive process and the healing response. However, most of these studies used concentrations of nicotine and cotinine that were far higher than those expected in plasma of smokers.2 Gingival fibroblasts:Peacock et al (1993) were the only researchers to show a positive effect of nicotine on the proliferation and attachment of gingival fibroblasts to plastic. Significant inhibition of proliferation of gingival fibroblasts at very high concentrations of nicotine was demonstrated by Tipton and Dabbous (1995), who also showed reduction in the production of type 1 collagen and fibronectine and an increase in the collagenase activity in culture media.2 Periodontal ligament fibroblasts: PDL fibroblast growth and attachment to tissue culture plates was inhibited by nicotine at high concentrations and no effects were seen at concentrations comparable with plasma levels in smokers in a study conducted by James et al (1999). Nicotine at high concentrations was also shown to be cytotoxic by Chang et al (2002). Gamal and Bayomy (2002) examined PDL fibroblast attachment to root surfaces and found that cell attachment was significantly less on root surfaces obtained from heavy smokers compared with non-smokers and healthy controls.2 Effect of smoking on the response to periodontal therapy: Smoking has been identified as one of the major predictive variables for response to periodontal therapy. In maintenance patients followed at least for 5 years, patients who smoked were twice as likely to lose teeth. The majority of studies involving nonsurgical therapy have shown less probing depth reduction and less attachment gain in
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smokers as compared to non-smokers. Among patients who have been surgically treated for periodontitis and then longitudinally followed, smokers exhibited less reduction in probing depths, less gain in clinical attachment levels, and less gain in bone height than non-smokers.1, 4 Smoking and neutrophil functions: Neutrophils are the predominant leukocytes in blood. It has become widely accepted that neutrophils defend periodontal tissues against infection by pathogens and subsequent tissue destruction. Neutrophils within the gingival crevice provide the first cellular host mechanism to control periodontal bacteria. On an average one million neutrophils per minute enter the oral cavity via the crevicular fluid. These cells protect the gingiva against microbial invasion by exhibiting a complex array of responses.1 Tobacco smoke exposure increases the number of neutrophils found in the systemic circulation and those exiting the pulmonary micro vasculature into the lungs. Despite inducing a significant systemic neutrophilia, tobacco smoking does not seem to affect the numbers of neutrophils entering the gingival sulcus and oral cavity. Indeed, limited evidence suggests that the number of neutrophils reaching the gingival sulcus in smokers may even be reduced. These findings imply that neutrophil transmigration across the periodontal microvasculature is impeded in tobacco smokers. Neutrophils are primary mediators of protection against periodontal plaque bacteria. However, neutrophil bactericidal activity involves multiple nonspecific mechanisms, and the inappropriate and/or continuous activation of periodontal neutrophils is thought to contribute to the degradation of gingival tissues and the progression of inflammatory periodontal disease. Neutrophils express functional receptor for several components and metabolites of tobacco smoke, such as nicotine, cotinine and aryl hydrocarbons. The numbers of nicotine receptors expressed by human neutrophils are increased in smokers and decline on cessation. Neutrophils also express several receptors for endogenous

factors such as interleukin-8, ICAM-1, TNF-. Thus, multiple receptor-agonist couples have been identified, suggesting that tobacco smoke is capable of affecting neutrophil function both directly and indirectly.2
CONCLUSION

From this discussion of the effects of tobacco smoking on the host response in periodontal diseases and its effect on periodontium, it is evident that these effects can occur throughout the periodontal tissues. Increasing evidence points to smoking as major risk factors for periodontitis, affecting the prevalence, extent & severity of disease. Also, one can make the general observation that the effects of tobacco smoking tip the balance towards periodontal destruction by stimulating destructive/ inflammatory responses and impairing protective/reparative responses. In addition smoking may influence the clinical outcome of non surgical & surgical therapy as well as the long term success of implant placement & it has become increasingly important to understand its impact on the initiation, progression & management of patients who smoke.
REFERENCES

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