Armitage, G. C. & Cullinan M. P. (2010). Comparison of the clinical features of chronic and aggressive periodontitis

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Armitage, G. C. & Cullinan M. P. (2010). Comparison of the clinical features of chronic and aggressive periodontitis. Journal of Periodontology 2000. Vol. 53, 12-27.

The authors at the beginning of their article came back to the historical perspective of chronic and aggressive periodontitis. In the late 1800s, chronic periodontitis “was clinically characterized as a slowly progressive destruction of the periodontium due to the accumulation of ‘lime deposits’ on the teeth, or ‘calcic inflammation of the peridental membrane’ and/or’serumal calculus.” Generalized aggressive periodontitis was not clearly described until the end of the 20th century. Some scientists described it as an “unusual form of periodontal disease that primarily affected some or all of permanent incisors and first molars of young individuals.” They believe that the cause of this disease is “defective deposition of cementum or ‘cementopathia’.” The disease was referred to as periodontosis. In 1966, the World Workshop in Periodontics decided to eliminate the term periodontosis from the periodontal nomenclature. Unfortunately, this term was retained, and periodontosis was a disease of the periodontium of healthy adolescents which was characterized by a rapid loss of alveolar bone. There were two forms of disease: in one form the affected teeth were first molars and incisors, in the second form most of the dentition was affected. The disease had its onset between age 11 and 13 years, was more common in females, and had a familial background. In the early 80s, scientists discovered the infectious etiology of the disease, and it could be treated effectively by therapy. Therefore, they replaced periodontosis to ‘juvenile periodontitis’. In 1999, the name of disease was changed to localized aggressive periodontitis.

According to the authors, chronic and aggressive periodontitis have many clinical features: infections occur in susceptible hosts, caused by biofilms on the tooth surfaces, and loss of periodontal attachment and alveolar bone. Chronic and aggressive periodontitis can affect the individuals that do not have general health conditions. According to the 1999 classification, if individuals have a systemic diseases, the resulting periodontitis should be classified as ‘periodontitis as a manifestation of systemic disease’. In this case, the systemic disease is an important component of successful treatment of the periodontal infection.

The authors state that the classification system for periodontitis is much better and more useful than diagnoses. Classification is a broad term and allows determining the amount and distribution of a disease in a population, investigating the causes of a disease, and applying this knowledge to the control of disease.

In spite of many shared clinical features, chronic and aggressive periodontitis have significant clinical differences: “age of onset, patterns of destruction, rates of progression, clinical signs of inflammation, and relative presence of plaque and calculus.” The combination of these clinical differences allows us to divide periodontitis into three major categories: chronic periodontitis, localized aggressive periodontitis, and generalized aggressive periodontitis. Localized and generalized chronic periodontitis are “two clinical expressions” of the same disease. The disease is characterized by signs of inflammation, such as redness, swelling, bleeding on proving, associated to moderate to heavy deposits of plaque and calculus. Chronic periodontitis usually progresses at a slow to moderate rate, and is also prevalent in similar populations and is “associated with similar genetic and environment risk factors.” Teeth with chronic periodontitis “usually have very complex and thick deposits of polymicrobial communities on affected root surfaces.” Localized and generalized aggressive periodontitis “can be considered to be different diseases.” Localized aggressive periodontitis is characterized by minimal signs of inflammation and small amount of plaque biofillm of “gram-negative coccoid and filamentous bacteria together with other microorganisms.” Also we can see small amount of calculus deposit. Generalized aggressive periodonititis differs in affecting most of the permanent dentition, very heavy plaque biofilm and calculus deposit, and “extremely intense gingival inflammation.”

The age of onset is an important characteristic to differ between chronic and aggressive forms of periodontitis. “Given similar amounts of periodontal damage (i.e. probing depths, attachment loss, and alveolar bone resorption), people with aggressive periodontitis are significantly younger than individuals with chronic periodontitis.” The authors state that it is not important for clinicians to know what the best age is (30 or 35 years) to distinguish between aggressive and chronic periodontitis, because the treatment is the same for a 30 or 35 years old person. Probably, it is for research purposes.

The rate of progression of disease is also an important characteristic to distinguish clinically chronic and aggressive periodontitis. Chronic periodontitis is a slowly progressing disease, and aggressive periodontitis has a rapid rate. The authors show the progression of bone loss over a nine-year period in a patient with chronic periodontitis in posterior regions of the mandible. Many factors influence the progression of periodontal diseases; these factors are the effectiveness of oral hygiene habits, access to dental care, genetically controlled susceptibility to periodontal infections, certain systemic diseases, smoking. According to authors, there is a tendency for increased progression of chronic periodontitis with age, and full mouth average rate of approximately 0.2 mm/year. An average rate of aggressive periodontitis is 0.46 mm/year. The radiographs appearances of patients with localized aggressive periodontitis show the relatively rapid progression of untreated localized aggressive periodontitis and treated localized aggressive periodontitis, but not respond to anti-infective therapy. The authors state that cross-sectional studies conclude “localized forms of the disease become generalized with increasing age.” Some cases demonstrate a family history of aggressive periodontitis.

The authors discuss a problem of pattern to the number and types of teeth involved in disease. According to the 1999 classification, the pattern of damage in generalized aggressive periodontitis includes “at least three permanent teeth other than first molars and incisors.” For localized aggressive periodontitis the pattern demonstrates all incisors and first molars. The authors are confused about term ‘localized’ and ‘generalized’. If a patient has only 28 teeth, and all incisors and first molars have the disease; according to the 1999 classification, this is localized aggressive periodontitis, but 12/28 is 42.9%, so this patient with localized aggressive periodontitis has generalized disease. The study suggested that patients with localized aggressive periodontitis have a number of affected teeth from 3 to 6, and patients with chronic periodontitis the number range from 18 to 28.

Clinical signs of inflammation are features of chronic and aggressive periodontitis. Localized aggressive periodontitis has low level of gingival inflammation (redness and swelling). According to authors, most patients with periodontitis “exhibit some clinical inflammation at affected sites, such as bleeding upon gentle probing along with redness and swelling of gingival margin.” Patients with generalized aggressive or chronic forms of periodontitis usually exhibit intense gingival inflammation.

The authors see a gap between diagnoses and classification. They conclude that “clinical distinction between chronic and aggressive periodontitis (especially generalized) is not clear cut.” But in their etiology and pathogenesis they have complete understanding.

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