Smokers also present with increased radiographic bone loss compared with nonsmokers, and there is a dose-dependent relationship: The odds of heavy smokers having severe bone loss are higher (odds ratio [OR] 7.28) compared with light smokers (OR 3.25).9 These detrimental effects are also observed in populations that maintain good levels of oral hygiene. Cross-sectional studies demonstrated that smokers had significantly reduced bone levels compared with nonsmokers, with the observed amount of bone loss occurring in a shorter time frame in smokers.10 Similar conclusions were obtained when evaluating the bone levels of a different population (Swedish hygienists) through the assessment of bitewing radiographs. Smokers had the highest amount of radiographic bone loss compared with nonsmokers or former smokers.11
0Van Winkelhoff et al12 investigated the prevalence and levels of periodontal pathogens in both smokers and nonsmokers who were treated for periodontal disease as well as untreated populations. A higher prevalence of periodontal pathogens was noted in treated and untreated smokers in comparison with the respective nonsmoking populations. Based on these findings, the authors suggested integrating the use of systemic antibiotics in patients who do not exhibit a favorable response to initial treatment.12 Haffajee and Socransky13 performed a similar study, implementing DNA-DNA hybridization. Subjects were divided based on two criteria: (1) according to their smoking habits in current smokers, former smokers, and nonsmokers; (2) according to their periodontal status in periodontally healthy, well-maintained, and periodontitis patients. Current smokers had larger proportions of sites colonized by periodontal pathogens.13 Zambon et al14 came to similar conclusions after conducting a large cross-sectional study using immunofluorescence. Tannerella forsythia and Aggregatibacter actinomycemetcomitans were more likely to be identified in the subgingival microflora of smokers. Furthermore, there was a dose-dependent relationship between the risk of T forsythia infection and the number of pack-years.14
Systemic effects
Systemically, smoking can affect multiple components and mechanisms of the human immune response and subsequently the host response to periodontal pathogens. Smokers have been found to have a higher receptor activator of nuclear factor-κB ligand/osteoprotegerin (RANKL/OPG) ratio, which could partially explain the increased bone loss observed in smoking populations. This alteration in RANKL and OPG is observed not only in saliva15 but also in serum.16 Neutrophils constitute the first line of defense toward bacteria that accumulate in the gingival sulcus. Their function can be altered as a result of tobacco use.17 In later disease stages, antibody production also takes place. During that period, reduced levels of serum immunoglobulin G 2 (IgG2) are identified.18
Treatment outcomes
In the classic longitudinal studies performed at the University of Nebraska, periodontal patients were enrolled in a maintenance program and followed up for 6 years after receiving active treatment. Smokers demonstrated poorer response to surgical and nonsurgical treatment, having lower probing depth (PD) reduction and clinical attachment level (CAL) gain.19 When furcation sites were analyzed separately, smokers had 0.5 mm less CAL gain and 0.6 mm less PD reduction compared with nonsmokers.19 A noteworthy observation from a different publication by the same group is that smokers exhibited a similar percentage of sites with BOP as nonsmokers.20 Other studies reported smokers having higher percentages of sites with BOP than nonsmokers with similar levels of oral hygiene.21 The inferior response of smokers to nonsurgical periodontal treatment is also observed in cases where local delivery of antibiotics is used as an adjunct to scaling and root planing.22
As mentioned previously, smoking negatively affects the response to surgical as well as nonsurgical periodontal treatment.19,22,23 Guided tissue regeneration is negatively affected as well. Clinical studies performed in private practices in Italy concluded that smokers had approximately 3 mm less CAL gain 12 months postoperatively (2.1 ± 1.2 mm) compared with nonsmokers (5.2 ± 1.9 mm).24 When followed up for an extended period of 5 years, stable treatment outcomes were associated with patients who were not smokers, who maintained adequate oral hygiene, and who complied with supportive periodontal treatment.25 Similarly, soft tissue grafting procedures are negatively influenced by smoking habits.26
It should be noted that despite the fact that the treatment response following smoking cessation is comparable with nonsmokers, this does not reverse the detrimental effects of smoking that have already manifested.21,27 Tomar and Asma28 analyzed the data from the Third National Health and Nutrition Examination Survey (NHANES III). The sample consisted of more than 13,000 adults, and it was estimated that it is four times more likely for current smokers to have periodontitis compared with individuals who never smoked. When former smokers were analyzed separately, the ones who had quit smoking in the previous 2 years were more likely to be diagnosed with periodontitis, and this likelihood decreased gradually. Former smokers who quit smoking for at least 11 years were as likely to have periodontitis as those who had never smoked. According to this study, almost three-fourths of periodontitis cases in the United States (74.8%) are attributed to smoking.28
Ultimately, smoking increases the likelihood of tooth loss. McGuire and Nunn29 discussed the prognosis and prediction of tooth loss and followed up with periodontal maintenance patients for 14 years. They estimated the risk for tooth loss to be increased by 2.9 times for heavy smokers (Box 4-2).
BOX 4-2 Link between smoking and periodontal status
GTR, guided tissue regeneration; SRP, scaling and root planing.
DIABETES MELLITUS
According to the Centers for Disease Control and Prevention (CDC), an estimated 9.4% (30.3 million) of the U.S. population are diabetics, and almost 24% of this population (7.2 million) are undiagnosed.30 The American Diabetes Association classifies diabetes based on its pathophysiology into the following categories:
Type 1 (5% of diabetics): Caused by autoimmune destruction of the pancreatic β-cells. This results in inability of the pancreas to produce insulin.
Type 2 (90%–95% of diabetics): Characterized by insulin resistance, eventually leading to loss of β-cell insulin secretion.
Gestational (2%–10% of pregnancies): Onset usually during the second or third trimester of pregnancy. These individuals are more likely to develop Type 2 diabetes later in life.
Other: Examples include diseases of the exocrine pancreas, and drug- or chemical-induced syndromes.
Diabetes is considered another major risk factor for periodontal disease. The mechanisms that link diabetes to periodontal disease have been described as associated with the interaction of the advanced glycation end products (AGEs) with their receptor (RAGE). This interaction alters cell function, increases levels of reactive oxygen species, and increases the RANKL/OPG, therefore altering bone homeostasis and eventually leading to increased tissue destruction.31
Local effects
The composition of periodontal microbiota does not appear to be influenced by diabetes, according to the majority of the existing literature.31 Diabetics exhibit increased BOP, and this tendency increases as the level of diabetic control decreases.32 In a longitudinal study in Pima Indians, more than 2,200 subjects were enrolled and followed up for 2.5 years. The incidence of periodontitis was 2.6 times higher