Risk assessment is defined by numerous components.1,2 Risk is the probability that an individual will develop a specific disease in a given period. The risk of developing the disease will vary from individual to individual.
Risk factors may be environmental, behavioral, or biologic factors that, when present, increase the likelihood that an individual will develop the disease. Risk factors are identified through longitudinal studies of patients with the disease of interest. Exposure to a risk factor or factors may occur at a single point in time; over multiple, separate points in time; or continuously. However, to be identified as a risk factor, the exposure must occur before disease onset. Interventions often can be identified and when implemented, can help modify risk factors.
Box 32-1 lists elements of these categories of risk for periodontal disease.
Tobacco smoking is a well-established risk factor for periodontitis.1,3 A direct relationship exists between smoking and the prevalence of periodontal disease (see Chapter 10). This association is independent of other factors such as oral hygiene or age.4 Studies comparing the response to periodontal therapy in smokers, previous smokers, and nonsmokers have shown that smoking has a negative impact on the response to therapy. However, former smokers respond similarly to nonsmokers.5 These studies demonstrate the therapeutic impact of intervention strategies on patients who smoke (see Chapter 10).
Diabetes is a clear risk factor for periodontitis.1 Epidemiologic data demonstrate that the prevalence and severity of periodontitis are significantly higher in patients with type 1 or type 2 diabetes mellitus than in those without diabetes, and that the level of diabetic control is an important variable in this relationship (see Chapter 11).
It is well documented that accumulation of bacterial plaque at the gingival margin results in the development of gingivitis and that the gingivitis can be reversed with the implementation of oral hygiene measures.6 These studies demonstrate a causal relationship between accumulation of bacterial plaque and gingival inflammation. However, a causal relationship between plaque accumulation and periodontitis has been more difficult to establish. Often, patients with severe loss of attachment have minimal levels of bacterial plaque on the affected teeth, indicating that the quantity of plaque is not of major importance in the disease process. However, although quantity may not indicate risk, there is evidence that the composition, or quality, of the complex plaque biofilm is of importance.
In terms of quality of plaque, three specific bacteria have been identified as etiologic agents for periodontitis: Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, and Tannerella forsythia (formerly Bacteroides forsythus).7 Porphyromonas gingivalis and T. forsythia are often found in chronic periodontitis, whereas A. actinomycetemcomitans is often associated with aggressive periodontitis. Cross-sectional and longitudinal studies support the delineation of these three bacteria as risk factors for periodontal disease. Additional evidence that these organisms are causal agents includes the following8:
Although not completely supported by these criteria for causation, moderate evidence also suggests that Campylobacter rectus, Eubacterium nodatum, Fusobacterium nucleatum, Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus micros, Streptococcus intermedius, and Treponema denticola are etiologic factors in periodontitis.7
Anatomic factors, such as furcations, root concavities, developmental grooves, cervical enamel projections, enamel pearls, and bifurcation ridges, may predispose the periodontium to disease as a result of their potential to harbor bacterial plaque and present a challenge to the clinician during instrumentation. Similarly, the presence of subgingival and overhanging margins can result in increased plaque accumulation, increased inflammation, and increased bone loss. Although not clearly defined as risk factors for periodontitis, anatomic factors and restorative factors that influence plaque accumulation may play a role in disease susceptibility for specific teeth.9
The presence of calculus, which serves as a reservoir for bacterial plaque, has been suggested as a risk factor for periodontitis. Although the presence of some calculus in healthy individuals receiving routine dental care does not result in significant loss of attachment, the presence of calculus in other groups of patients, such as those not receiving regular care and patients with poorly controlled diabetes, can have a negative impact on periodontal health.2
Evidence indicates that genetic differences between individuals may explain why some patients develop periodontal disease and others do not. Studies conducted in twins have shown that genetic factors influence clinical measures of gingivitis, probing pocket depth, attachment loss, and interproximal bone height.10-12 The familial aggregation seen in localized and generalized aggressive periodontitis also is indicative of genetic involvement in these diseases (see Chapter 6).
Kornman et al13 demonstrated that alterations in specific genes encoding the inflammatory cytokines interleukin-1α (IL-1α) and interleukin-1β (IL-1β) were associated with severe chronic periodontitis in nonsmoking subjects.13 However, results of other studies have shown limited association between these altered genes and the presence of periodontitis. Overall, it appears that changes in the IL-1 genes may be only one of several genetic changes involved in the risk for chronic periodontitis. Therefore, although the alteration in the IL-1 genes may be a valid marker for periodontitis in defined populations, its usefulness as a genetic marker in the general population may be limited.14
Immunologic alterations, such as neutrophil abnormalities,15 monocytic hyperresponsiveness to lipopolysaccharide stimulation in patients with localized aggressive periodontitis,16 and alterations in the monocyte/macrophage receptors for the Fc portion of antibody,14,17 also appear to be under genetic control. In addition, genetics play a role in regulating the titer of the protective immunoglobulin G2 (IgG2) antibody response to A. actinomycetemcomitans in patients with aggressive periodontitis18 (see Chapter 25).
Both the prevalence and severity of periodontal disease increase with age.3,19,20 It is possible that degenerative changes related to aging may increase susceptibility to periodontitis. However, it also is possible that the attachment loss and bone loss seen in older individuals are the result of prolonged exposure to other risk factors over a person’s life, creating a cumulative effect over time. In support of this, studies have shown minimal loss of attachment in aging subjects enrolled in preventive programs throughout their lives.21,22 Therefore it is suggested that periodontal disease is not an inevitable consequence of the aging process and that aging alone does not increase disease susceptibility. However, it remains to be determined whether changes related to the aging process, such as intake of medications, decreased immune function, and altered nutritional status, interact with other well-defined risk factors to increase susceptibility to periodontitis.
Evidence of loss of attachment may have more consequences in younger patients. The younger the patient, the longer the patient has for exposure to causative factors. In addition, aggressive periodontitis in young individuals often is associated with an unmodifiable risk factor such as a genetic predisposition to disease.3