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Complex Combination

The link is clear but new research continues to uncover clues on how tobacco use affects periodontal disease.

For several decades, scientific reports speculated about the relationship between tobacco use and periodontal disease.1,2 In 1996, the American Academy of Periodontology published a report asserting that a causal relationship exists between tobacco use and periodontal diseases.3

In studies that control for sex, age, race, and plaque levels, the detrimental effects of tobacco use on the periodontium persist.4,5 Studies indicate that tobacco is a key environmental risk factor for periodontal diseases.1,2,4,6 Depending on the extent of the habit and how disease is measured, tobacco users can be anywhere from 5 to 20 times at greater risk for a periodontal disease than their nonsmoking counterparts.1 In a large national study, approximately 75% of periodontal disease was attributable to tobacco use.7

A basic knowledge of the histological effects of tobacco use in the oral cavity helps dental hygienists understand what they see clinically. This information can also be transmitted to the patient. Although questions still remain concerning nicotine’s specific role and mechanism of action, certain effects are reported consistently. The periodontal literature repeatedly confirms that nicotine interferes with normal cellular functioning.1,2,8 Numerous studies have shown that nicotine interferes with wound healing, undermines the inflammatory process, and compromises the role of neutrophils, phagocytes, and macrophages.1,2,8,9,10 Nicotine also appears to interfere with the normal release of inflammatory cytokines, thereby prolonging tissue destruction.2,11


In the presence of nicotine, increased collagenase is produced while collagen production is impaired.12 Since connective tissue is being destroyed at a rate faster than it can be repaired, the rebuilding of connective tissue suffers. Other reports indicate that specific cellular proteins react negatively in the presence of nicotine. The negative reaction of these proteins can result in the disruption of fibroblastic binding, a process essential to healing.13 When fibroblasts are unable to bind to tooth surfaces and when cell-to-cell adhesion is compromised, the foundation for healing cannot be built.8

Nicotine requires oxygen to function. So on a cellular level, sources of oxygen needed for other necessary and normal metabolic activities are depleted. Without oxygen, expected cellular responses to inflammation are thwarted. The signaling systems of the inflammatory mediators are derailed so neutrophils do not respond to bacterial invasion in a systematic way.9 Cellular migration to the site of inflammation and the subsequent destruction of putative pathogens is disrupted so inflammation persists and tissue continues to be destroyed.3,9


Other variables that may affect the disease process are the types of subgingival microbiota present in the patient’s mouth. Periodontal pockets harbor more anaerobic bacteria than normal sulci. However, other differences may also exist.  Recently, subgingival microbiotic flora of chronically diseased smoking and nonsmoking periodontal patients were found to be significantly different. Smokers exhibited a higher prevalence of bacterial colonizations at pocket depths greater than 4 mm, with the greater differences in the maxilla than the mandible.14 Geographic location may even influence the types of subgingival microbiota found in periodontal patients with

For more information on tobacco cessation, visit the American Dental Hygienists’ Association’s website on its national Smoking Cessation Initiative at:

chronic periodontitis, although the evidence is inconclusive. Patients with tobacco use habits of longer duration and greater frequency most likely exhibit more extensive evidence of disease than the new or “less addicted” tobacco user. Thus, the relationship between oral health and tobacco use is often described as exposure dependent, ie, the greater the extent of the habit, the greater the extent of periodontal destruction.1 Clinically, patients who smoke often present with unexpected subgingival calculus in the maxillary anterior region.10


Adult smokers with chronic periodontal disease exhibit minimal bleeding in relationship to the extent of disease present.10 Gingival tissues subject to constant heat and chemical contact over time often appear dense, fibrotic and hyperplastic with a superimposed gray or whitish hue. Often the fibrotic nature of the tissue with its stippled appearance masquerades as healthy tissue. Probe readings, however, disprove the assumption of health. The chronic periodontal diseased patient who experiences a compromised immune response to bacterial invasion, impaired connective tissue rebuilding, and a diminished capacity to heal will appear clinically with greater attachment loss, decreased bone levels, more furcation involvement and a poor prognosis for the stability or improvement of the periodontal condition.1,2,4,6

Young adult smokers with aggressive periodontal disease most often exhibit some bleeding,10 possibly because their habit is newer than adult smokers’ and their tissue has not had as much exposure to the physical and chemical irritants present in tobacco and tobacco smoke. The bone loss found in young adult smokers is far greater than the extent found in their nonsmoking counterparts with generalized aggressive periodontal disease.10,17 The extent of attachment loss present in patients with localized aggressive periodontitis appears to be unaffected by tobacco use.15  This finding may be due to the intrinsically higher levels of IgG2 serum antibodies found in patients with localized aggressive periodontitis.15

Treatment planning can be challenging. First, the provider must realize that if the patient continues to use tobacco, little resolution can be expected.1,2,7,10 Smokers tend to exhibit different responses to treatment following scaling and root planing.1 The effectiveness (as measured by probing depths, attachment gains, and gingival height) of nonsurgical periodontal therapy in patients who use tobacco is compromised.1,2 This finding suggests that periodontally involved tobacco users should be seen more frequently for recare visits to compensate for destruction that is habit-related and to retard further damage. Tobacco-using patients also should adhere to diligent oral hygiene regimens. Effective toothbrushing and interdental plaque biofilm removal are essential. The use of antimicrobial rinses also may be indicated.

Subgingival pathogens are more difficult to eliminate in smokers following scaling and root planing and smokers are less responsive to surgical and nonsurgical therapies.1,2,4,5 Therefore, the use of adjunctive therapies in smokers is being examined. There is insufficient evidence to suggest that tobacco-using patients should receive adjunctive therapy or a particular adjunctive agent. Some success for tobacco users has been found in studies where locally delivered minocycline microspheres and adjunctive systemic amoxicillin and metronidazole were used.

Systemic doxycyline may also show some promise with patients presenting with severe periodontal disease. Further study is needed. Chronic periodontal patients who use tobacco often remain unresponsive.1,5 Prognosis is guarded unless abstinence from tobacco use is achieved.1,2,10 Without abstinence, periodontal destruction will continue, despite concerted efforts from patients and providers.1,2,10 Signs of periodontal destruction will remain and most likely worsen. Conversely, the former user will experience positive change. Initially, bleeding will increase.10 Patients need to be advised that this change is desirable and indicates health. Although bone cannot be regenerated without surgical interventions, the gingival anatomy and bone levels of the tobacco-free patient will stabilize.1,2,10 In time, the risk for periodontal disease between former smokers and never smokers converges and former smokers often can be placed on maintenance therapy.

When patients can see the oral effects of their habits, they are most open to tobacco cessation. Tissue color, consistency, anatomy, and pocket depths should be shown to the patient. The dental hygienist can also explain the past and present changes in radiographic bone levels and in pocket depths. This reality check often serves as a patient’s wake-up call to consider cessation. As pieces of this complex connection fall into place, dental hygiene interventions that provide more effective and cutting-edge care will make the most difference in the fight against tobacco use.


  1. Bergstrom J. Tobacco smoking and chronic destructive periodontal disease. Odontology. 2004;92(1):1-8.
  2. Johnson GK, Hill M. Cigarette smoking and the periodontal patient. J Periodontol. 2004;75:196-209.
  3. American Academy of Periodontology Position Paper : tobacco use and the periodontal patient. J Periodontol. 1996;67:51-56.
  4. Grossi SB, Genco RJ, Machtei EE, et al. Assessment of risk for periodontal disease II. risk indicators for alvelor bone loss. J Periodontol. 1995;66:23-29.
  5. Haber J, Kent R. Cigarette smoking in a periodontal practice. J Periodontol. 1992;63:100-106.
  6. Grossi SG, Zambon JJ, Ho AW, et al. Assessment of risk for periodontal diseaseI. risk indicators for attachment loss. J Periodontol. 1994;65:260-267.
  7. Tomar SL, Amsa S. Smoking attributable periodontitis in the United States: findings from NHANES III. J Periodontol. 2000;71:743-751.
  8. Austin GW, Cuenin MF, HockettSD , et al. Effect of nicotine on fibroblast B1 integrin expression and distribution in vitro. J Periodontol. 2001;72:438-444.
  9. McFarlane GD, Hertzberg MC, Wolff LF, Hardie NA. Refractory periodontitis associated with abnormal polymorphonuclear leukocyte phagocytosis and cigarette smoking. J Periodontol. 1992;63:908-913.
  10. Haber J. Cigarette smoking: a major risk factor for periodontitis. Compend Contin Educ Dent. 1994;15(8):1002, 1004-8.
  11. Meisel P, Schwahn C, Gesch D, et al. Dose effect relation of smoking and the Interlerkin-1 gene polymorphism in periodontal disease. J Periodontol. 2004;75:236-242.
  12. Baab DA, Oberg PA. The effect of cigarette smoking on gingival blood flow in humans. J Clin Perio. 1987;14:418-424.
  13. Mavropoulus A, Aars H, Brodin P. Hyperaemic response to cigarette smoking in healthy gingival. J Clin Periodontol. 2003;30:214-221.
  14. Haffajee AD, Socransky SS. Relationship of cigarette smoking to the subgingival microbiota. J Clin Periodontol. 2001;28:377-338.
  15. Schenkein HA, Gunsolley JC, Koertge TE, Schenkein JG, Tew JG. Smoking and its effects on early-onset periodontitis. J Amer Dent Assoc. 1995;126:1107-1113.

From Dimensions of Dental Hygiene. June 2005;3(6):16-17.

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