Chronic periodontitis is the most prevalent form of periodontitis, and it generally demonstrates the characteristics of a slowly progressing inflammatory disease. However, systemic and environmental factors (e.g., diabetes mellitus, smoking) may modify the host’s immune response to the dental biofilm so that periodontal destruction becomes more progressive. Although chronic periodontitis is most frequently observed in adults, it can occur in children and adolescents in response to chronic plaque and calculus accumulation.
Chronic periodontitis has been defined as “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.”18 This definition outlines the major clinical and etiologic characteristics of the disease: (1) microbial biofilm formation (dental plaque); (2) periodontal inflammation (e.g., gingival swelling, bleeding on probing); and (3) attachment as well as alveolar bone loss.
In addition to the local immune response caused by the dental biofilm, periodontitis may also be associated with a number of systemic disorders and defined syndromes. In most cases, patients with systemic diseases that lead to impaired host immunity may also show periodontal destruction. Therefore, periodontitis is a disease that is not only limited to the area of the oral cavity; it is also associated with severe systemic diseases (e.g., cardiovascular disorders, diabetes mellitus).40
This chapter discusses clinical features that have been described for chronic periodontitis. In addition, the disease’s etiology is summarized with the use of categories that explain the known factors (i.e., microbiologic, immunologic, and genetic) involved in the pathology of chronic periodontitis.
Chronic periodontitis can be clinically revealed with periodontal screening and recording, which results in a periodontal screening index rating. The condition is diagnosed via the assessment of the clinical attachment level and the detection of inflammatory changes in the marginal gingiva (see Figure 23-1). Measurements of periodontal pocket depth in combination with the location of the marginal gingiva allow for conclusions to be drawn regarding the loss of clinical attachment (see Figures 23-2 and 23-6). Dental radiographs display the extent of bone loss, which is indicated by the distance between the cementoenamel junction and the alveolar bone crest (see Figure 23-3). The distinction between aggressive and chronic periodontitis is sometimes difficult, because the clinical features may be similar at the time of the first examination. At later time points during treatment, aggressive and chronic periodontitis may be differentiated by the rate of disease progression over time, the familial nature of aggressive disease, the disease’s resistance to periodontal anti-infective therapy, and the presence of local factors.
Chronic periodontitis is considered a site-specific disease. Local inflammation, pocket formation, attachment loss, and bone loss are the consequences of direct exposure to the subgingival plaque (biofilm). As a result of this local effect, pocket formation and attachment as well as bone loss may occur on one surface of a tooth, whereas other surfaces maintain normal attachment levels. As a result of the site-specific nature, the number of teeth with clinical attachment loss classifies chronic periodontitis into the following types:
During chronic periodontitis, the local inflammatory response may lead to different patterns of bone loss, including vertical (angular) and horizontal bone destruction. Although vertical bone loss is associated with intrabony pocket formation, horizontal bone loss is usually associated with suprabony (supra-alveolar) pockets.
The severity of periodontal destruction that occurs as a result of chronic periodontitis is generally considered a function of time in combination with systemic disorders that impair or enhance host immune responses. With increasing age, attachment loss and bone loss become more prevalent and more severe as a result of an accumulation of destruction. Disease severity may be described as mild, moderate, or severe (see Chapter 4):
Chronic periodontitis is commonly a slowly progressive disease that does not cause the affected individual to feel pain. Therefore, most patients are unaware that they have developed a chronic disease that is also associated with other systemic diseases (e.g., cardiovascular disease). For the majority of the patients, gingival bleeding during oral hygiene procedures or eating may be the first self-reported sign of disease occurrence. As a result of gingival recession, patients may notice black triangles between the teeth or tooth sensibility in response to temperature changes (i.e., cold and heat). In patients with advanced attachment and bone loss, tooth mobility, tooth movement, and, in rare occasions, tooth loss may be reported. In those individuals with advanced disease progression, areas of localized dull pain or pain sensations that radiate to other areas of the mouth or head may occur. The presence of areas of food impaction may add to the patient’s discomfort. Gingival tenderness or “itchiness” may also be found.
Patients appear to have the same susceptibility to plaque-induced chronic periodontitis throughout their lives. The rate of disease progression is usually slow, but it may be modified by systemic, environmental, and behavioral factors. The onset of chronic periodontitis can occur at any time, and the first signs may be detected during adolescence in the presence of chronic plaque and calculus accumulation. Because of its slow rate of progression, however, chronic periodontitis usually becomes clinically significant when a patient reaches his or her mid-30s or later.
Chronic periodontitis does not progress at an equal rate in all affected sites throughout the mouth. Some involved areas may remain static for long periods,33 whereas others may progress more rapidly. More rapidly progressive lesions occur most frequently in interproximal areas,32,34 and they may also be associated with areas of greater plaque accumulation and inaccessibility to plaque-control measures (e.g., furcation areas, overhanging margins of restorations, sites of malposed teeth, areas of food impaction).
Further factors that influence disease progression may be of systemic origin. Patients with poorly adjusted diabetes mellitus show a significantly higher risk of developing a severe progression of chronic periodontitis.43,61
Several models have been proposed to describe the rate of disease progression.57 In these models, progression is measured by determining the amount of attachment loss during a given period as follows:
• The random or episodic-burst model proposes that periodontal disease progresses by short bursts of destruction followed by periods of no destruction. This pattern of disease is random with respect to the tooth sites affected and the chronology of the disease process.
• The asynchronous, multiple-burst model of disease progression suggests that periodontal destruction occurs around affected teeth during defined periods of life and that these bursts of activity are interspersed with periods of inactivity or remission. The chronology of these bursts of disease is asynchronous for individual teeth or groups of teeth.
Chronic periodontitis increases in prevalence and severity with age, and it generally affects both genders equally. Periodontitis is an age-associated (not an age-related) disease. Nonetheless, the prevalence of periodontitis increases with age so that 40% of patients who are 50 years old or older and almost 50% of patients who are 65 years old or older show moderate periodontal destruction. The prevalence of severe forms of periodontitis also incr/>