Diabetes

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).

Pathogenic Bacteria and Microbial Tooth Deposits

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

Therefore the quantity of plaque present may not be as important as the quality of the plaque in determining risk for periodontitis.

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

Age

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