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Periodontics

Dr. Sudheer S. Patil

(Prof. and Head, Department of Periodontics, Kothiwal Dental College and Research Centre, Moradabad, up, India).

CO- Author:


Dr. Nipun Dhalla

(B.D.S. , Final Year PG, Department of Periodontics, Kothiwal Dental College and Research Centre, Moradabad, up, India).)

Dr. Anand Pratap Singh
(B.D.S., P.G. Resident, Department of Oral Medicine & Radiology, Kothiwal Dental College and Research Centre, Moradabad, up, India).

Abstract

This concise review indicates the recent evidence that support smoking is the risk factor for periodontitis. Most findings support the fact that tobacco smoking modulates destruction of the periodontium through alteration in microcirculatory and host immune systems, connective tissue and bone metabolism. Researches on gingival crevicular fluid have demonstrated that there are lower levels of cytokines, enzymes and possibly polymorphonuclear cells in smokers. Tobacco smoking has widespread systemic effects, many of which may provide mechanisms for the increased susceptibility to periodontitis and the poorer response to treatment.

Introduction

Periodontal disease is an infectious, chronic, inflammatory disease characterized by the loss of connective tissue attachment and alveolar bone in association with the formation of the pocket and subsequent tooth loss. Current knowledge suggests that smoking is an important risk factor for the development of the periodontal disease, especially severe periodontitis.
Clinical, epidemiologic, and laboratory studies indicated an association between smoking and the prevalence and severity of periodontal disease and the majority of contemporary studies suggest that smoking increases the risk of periodontal diseases between two and six times.

In general therefore, there is substantial body of evidence to support the observation that the more a patient smokes, the greater the degree of periodontal disease.

So, this concise review describes smoking as a risk factors for periodontal disease under following different categories with supporting evidence.

  1. Epidemiological and clinical evidence
  2. Microbiological evidence
  3. Radiographical evidence
  4. Immunological evidence
  5. Genetic evidence
  6. Periodontal therapy
  • Epidemiological and clinical evidence:
  • Gingival bleeding

    1. According to Bergstrom et al (1988) the reduced inflammatory response is considered to be caused by lower increase in number of gingival blood vessels in smokers as compared to non smokers.
    2. Loesche (1994), Berstrom & Bostrom (2001) found that smoking leads to sustained peripheral vasoconstriction caused by chronic low doses of nicotine. This leads to reduced gingival bleeding. This effect can “mask” the presence of periodontal disease. The compromise gingival microvasculature could also lead to reduced oxygen tension that would allow periodontal anaerobes to prevail.
    3. The vasculature has also been examined in histological and immunocytochemical studies. In a very limited study of one histological section from three smokers and four non-smokers, Mirbod et al (2001) found that there were a high proportion of small vessels compared with large vessels in smokers compared with non-smokers, but no difference in the vascular density.

    Pocket depth and clinical attachment loss

    1. Cigarette smoking was associated mostly with a increase in probing depth and attachment loss, as well as greater tooth loss at an earlier age (Chen et al 2001).
    2. In periodontally involved sites the probe tip is generally located apical to the most coronal connective tissue fibers, but in health and gingivitis the probe tip falls short of the termination of the junctional epithelium. It is possible that the reduced inflammation and bleeding and increased fibrosis reported in smokers may affect clinical probing measurements because of less probe tip penetration.
    3. Cytotoxic substances such as nicotine and its major metabolic cotinine can be detected in the saliva, gingival crevicular fluid, serum, and urine demonstrating their systemic availability.
    4. Alavi et al (1995) conducted a study and seen that smoking reduces the absolute amount of GCF elastase in patients with established and untreated chronic periodontitis suggesting a compromised neutrophil response.
  • Microbiological evidence
    1. Some epidemiological studies have found that smokers exhibited higher accumulation of plaque and may harbor different or more putative periodontal pathogens.
    2. Higher level of calculus have been reported by some authors (Feldman,Bravacos and Rose , 1993, Lindin and Mullally,1994) but not by others (Bergstrom Eliasson and Preber,1991) thus possible higher accumulation of plaque and calculus among smokers may be owing to reasons other than smoking per se and may not be an explanation of the effects of tobacco on periodontium.
    3. Current smoker were 2.3 times more likely to be infected with B.forsythus and thus 3.1 times more likely to be infected with A.actinomycetemcomitans than their former and never smoking counterparts.
    1. Kazor et al. (1999), Zambon et al. (1996) found that smoking appears to select for specific periodontopathogens ( P. gingivalis, T. denticola and B. forsythus) thus increasing the risk of the development and progression of periodontal disease.
    1. Haffajee & Socransky (2001) found greater prevalence of orange and red complexes in smoker than in ex-smokers and never smokers: E. nodatum; F.nucleatum ss vincentii; P.intermedia; B. forsythus; P.gingivalis; T.denticola. This observation was seen in deep (>4mm) and shallow (<4mm) pockets.
  • Radiographical evidence
    1. The bone height reduction observed in smokers however was 2.7 times greater than that observed in non smoker suggesting on the average an almost 3 fold elevated bone height reduction rate under the influence of smoking.
    2. Tobacco smoking a well established risk factor for periodontal disease has negative effect on marginal bone. Bolin et al 1983 in their longitudinal study of marginal bone changes showed that the marginal bone was more affected in smokers than in non smokers.
    3. Vertical bone loss was influenced by smoking severity increase was significantly greater in smokers compared with non smokers. In addition the vertical bone loss increased comparably more in heavy exposure smokers than in light smokers. Smokers indicating an exposure response relation.
    4. It is possible that the effect of nicotine is related to vascular changes, resulting in insufficient vascular supply and indirectly leads to bone tissue breakdown and there is experimental evidence to suggest that nicotine as well as cigarette smoke have detrimental effects on bone cells and osteoprogenitor cells (Liu et al. 2001, 2003, Walker et al. 2001).
  • Immunological Evidence
    1. Tobacco smoking could interfere with the pathological chain of periodontitis through several mechanism. Smoking could impair the normal host response in bacterial clearance and the neutralizing of infection (Seymour,1991).
    2. The effect on cigarette smoking on total serum IgG, IgA and IgM classes are controversial with some reports, indicating suppression of total antibody titer levels and other studies. Therefore, one of the biological explanation for the epidemiologic associations between environmental factors, such as smoking and periodontitis, may be related to modification of antibody production and alteration of circulating immune complexes.
    3. In addition tobacco smoking may modify the production of proinflammatory cytokinines interleukin-1 (IL-1) and tumor necrosis factor α (TNF α) which are considered key regulators of host response of microbial challenge.
    1. Kamma et al (1999) reviewed some of the other factors that have been shown to differ among subjects with different smoking backgrounds. They have noted that smoking has been shown to reduce the functional activity of leukocytes and macrophages as well decreasing chemotaxis and phagocytosis of PMNs.
  • Genetic Evidence
    • Because one of the risk factor for periodontitis is tobacco use (Burgan, 1997) susceptibility to this disease may be linked to polymorphisms in gene coding for enzymes metabolizing tobacco derived-substances.
    • Recently, it has been reported that the slow acetylator genotype of NAT2 is associated with higher risk of periodontitis, particularly in smokers (Meisel et al, 2000; Kocher et al, 2002). Therefore polymorphism of other xenobiotics-metabolising enzymes, CYPs and GSTs, may also contribute to individual susceptibility to develop periodontitis.
    • The association between positive genotypes and the severity of periodontal disease was independent of smoking, suggesting no relationship between smoking and IL-1 genotypes; however relationships between IL-1 positive genotypes and smoking was evident.
    • Logistic regression analysis of periodontal disease with genotype-negative non-smokers as a reference group exhibited odds ratio of 0.98 for genotype-positive non-smokers, 2.37 for genotype-negative smokers, and 4.50 for genotype-positive smokers, thus suggesting synergism between IL-1 polymorphism and smoking.
  • Periodontal Therapy
    1. The effects of cigarette smoking may affect the outcomes of surgical as well as non-surgical periodontal therapy. Smoking also may contribute to implant failure (Bain & Moy, 1993; Gorman et al., 1994) whereas Weyant (1994) and Minsk et al., (1996) did not find statistically significant difference in the rate of implant failure in smokers and non-smokers.
    2. Some short-term follow-up studies after non-surgical therapy including scaling and root planning have shown poorer response to periodontal treatment among smokers compared with non smokers. The reduction in the number of sites with gingival bleeding was significantly less in smokers. (Preber & Bergstrom, 1985b). probing depth reduction (Preber & Bergstrom, 1985a) and attachment level gain (Grossi et al., 1996) were also lower among smokers.
    3. Arguments for a more profound action are recent observations suggesting association between smoking and lower level of elastase, proteolytic enzyme activity and MMP-8 in the oral cavity (Liede et al., 1999; Pauletto et al., 2000). This suggests that not only the inflammatory cell reactions but also other cell functions, e.g., regenerative cell functions may be suppressed by smoking.
    4. Thus, the smoking associated inadequate inflammatory response may be accompanied by an inadequate regenerative capacity of the periodontium. This may explain why healing following therapeutical intervention is retarded or impaired, and progression rate accelerated in smokers (Bergstrom et al., 2000).
    5. Smoking also impairs hard and soft tissue revascularization process, which may influence the repair of the periodontal tissues. As such, smoking could have a negative influence on periodontal surgical procedures. Some studies showed that cigarette smoking can affect flap debridement and regenerative and periodontal plastic surgeries.
    6. Root coverage following thick free gingival graft procedures is reportedly diminished by heavy cigarette smoking, and there are conflicting reports on smoking’s effect on the success of subepithelial connective tissue grafts. Clinical attachment gains are also less in smokers as compared to non-smokers following regenerative procedures.

    Periodontal healing

    1. There might be cytotoxic effects of substances such as nicotine and cotinine, which may adhere to root surfaces in smokers and alter the attachment properties of gingival fibroblast to root surfaces (Raulin et al. 1988, Mc Guire et al. 1989).
    2. An impaired healing might also be the result of interference of smoking with different PMN functions such as phagocytosis, chemotaxis and viability(Eichel and Sharik 1969, Kenney et al. 1977).
    3. Further, decreased level of other host factors such as serum IgG, IgA, IgM, but increased level of IgE in smokers might also contribute to impaired periodontal healing (Holt & Keast 1977, Johnson et al. 1990).

    Conclusions:

    While the precise mechanisms whereby cigarette smoking can exert an effect on periodontal tissues are not completely understood it is clear that it is still the most significant preventable risk factor for periodontitis.
    There is now considerable evidence for the role of smoking in the etiology of the periodontal disease and its adverse influence on the treatment of periodontitis, such that advising patients of the consequences of tobacco use is essential in the management of patients who smoke.

    Reference:

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    • Bergstrom J : Cigarette smoking as risk factor in chronic periodontal disease. Comniunity Dent Orol Epidemiol 1989; 17: 245-247.
    • Bergstrom J, Eliasson S, Preber H: Cigarette smoking and periodontal bone loss. J Periodontol 1991; 62:242-246.
    • Bergstrom J. & Bostrom L: Tobacco smoking and periodontal hemorrhagic responsiveness. Journal of Clinical Periodontology 2001; 28: 680–685.
    • Bergstrom, J. & Preber, H:Influence of cigarette smoking on the development of experimental gingivitis. Journal of Periodontal Research 1986; 21: 668–676.
    • Grossi SG, Genco RI, Machtei EE, Ho AW, Koch G, Dunford R : Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995; 66:23-29.
    • Holt PG : lmmune and inflammatory function in cigarette smokers. Thorax 1987;42:241-249.
    • Haffajee, A. D. & Socransky, S. S: Relationship of cigarette smoking to the subgingival microflora. Journal of Clinical Periodontology 2001; 28: 377–388.
    • Johnson, J. D., Houchens, D. P., Kluwe, W. M., Craig, D. K. & Fisher, G. L.: Effects of mainstream and environmental tobacco smoke on the immune system in animals and humans: a review. Critical Reviews in Toxicology 1990; 20: 369–395.
    • Kamma, J. J., Nakou, M. & Baehni, P. C. : Clinical and microbiological characteristics of smokers with early onset periodontitis. Journal of Periodontal Research1999; 34: 25–33.
    • Meisel P., Heins G., Carlsson L. E., Giebel J.,John U., Schwahn C. & Kocher T. : Impact of genetic polymorphisms on the smoking-related risk of periodontal disease: the population-based study SHIP. Tobacco Induced Diseases 2003; 1: 197–206.
    • Martinez-Canut P, Lorca A, Magan R: Smoking and periodontal disease severity. J Clin Periodontol 1995; 22:743-749.
    • Mirbod, S. M., Ahing, S. I. & Pruthi, V. K. : Immunohistochemical study of vestibular gingival blood vessel density and internal circumference in smokers and nonsmokers. Journal of Periodontology 2001; 72: 1318–1323.
    • CigaretteM. F., Loos, B. G., Van Steenbergen,Linden GJ, Mullally BH: Cigarette smoking and periodontal destruction in young adults. J Periodontol 1994;65:718-723.
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    • Pauletto, N. C., Liede, K., Nieminen, A., Larjava, H. & Uitto, V. J. :Effect of cigarette smoking on oral elastase activity in adult periodontitis patients. Journal of Periodontology 2000; 71:58–62.
    • Raulin LA, McPherson JC, McQuade MJ, Hanson BS: The effect of nicotine on the attachment of human fibroblasts to glass and human root surfaces in vitro. J Periodontol 1988; 59:318-325.
    • Zambon IJ, Grossi SG, Machtei EE, Ho AW, Dunford R, Genco RJ: Cigarette smoking increases the risk for subgingival infection with periodontal pathogens. J Periodontol 1996; 67:1050- 1054.

    Legends:-

    Clinical picture showing periodontitis.
    Clinical picture showing smoker’s melanosis
    OPG showing periodontitis.

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