Chronic vs. aggressive periodontitis

Aug. 1, 2010
Oh, the joys of periodontal disease assessment! I think I woke up on the wrong side of the bed one morning because I was looking for any excuse not to perform a comprehensive periodontal exam.

by Lynne H. Slim RDH, BSDH, MSDH
[email protected]

Oh, the joys of periodontal disease assessment! I think I woke up on the wrong side of the bed one morning because I was looking for any excuse not to perform a comprehensive periodontal exam. My stomach was growling (an embarrassing bodily noise), and my new young adult patient was 30 minutes late for his one-hour appointment. By the time the patient entered my operatory, I had only 15 minutes to take a digital panorex and perform an oral cancer and periodontal exam.

In some practices I would have been expected to squeeze in a prophylaxis too, but after viewing the digital panorex I quickly recognized generalized bone loss, and I knew I’d be spending a lot of time reviewing this patient’s medical history, medications, and family/social history. I ended up working through half of my lunch break so I could do a very thorough periodontal assessment.

Establishing a diagnosis based on disease type, extent, location, and severity is an essential first step in the treatment of gingival and periodontal diseases. What’s not often talked about in classifying periodontal diseases is the distinction between chronic and aggressive periodontitis. Both chronic and aggressive forms (localized and generalized) are complex infections that occur in susceptible hosts. The aforementioned patient had severe generalized bone loss, inflammation, and light calculus deposits. Upon disclosing, supragingival plaque biofilm was minimal. (I don’t use a plaque index but I always disclose.)

Some of the differences

I recently read a 2010 volume of Periodontology 2000 that discussed the comparative biology of chronic and aggressive periodontitis, and I thought I’d fill in my readers on some of what I learned. According to Armitage and Cullinan, chronic and aggressive periodontitis have a number of significant clinical differences. These include:

  • Age of onset. Individuals with aggressive periodontitis are significantly younger, but there are no fixed or arbitrary upper age limits.1
  • The loss of clinical attachment in patients with aggressive periodontitis is about three to four times faster. Chronic periodontitis progresses at an annual rate of about 0.2 to 0.25 mm, but rates are very difficult to estimate. There are many factors that influence how rapidly the periodontium is destroyed.1
  • In chronic periodontitis, there is no well-defined pattern of bone loss. In generalized aggressive periodontitis, most permanent teeth are affected. In localized aggressive periodontitis, there is no agreement on the number of teeth included, but in one case series, about three to six teeth were included. Teeth affected were molars and incisors.1
  • Patients with generalized aggressive periodontitis usually present with intense gingival inflammation, but that may or may not be the case with localized aggressive periodontitis. In addition, there appears to be no difference between chronic and aggressive periodontitis in terms of histopathology and immunopathology.2 For over 100 years, localized aggressive periodontitis in young people has been described as thin plaque biofilm and noticeably absent calculus.1
  • Plaque biofilm and calculus amounts seem to vary and there is no set pattern that distinguishes chronic from aggressive periodontitis.1
  • The global and national prevalence of aggressive periodontitis is much lower than chronic periodontitis, and seems to range from 1% to 15% in individuals younger than 35 years of age.3

Localized aggressive periodontitis debuts at puberty with attachment loss at the approximal surfaces of permanent incisors and first molars. It can appear in up to half of the children in an affected family.4 Slots reports that Epstein-Barr and cytomegalovirus (herpes viruses) are statistically associated with aggressive periodontitis, but these associations as “links” with progressive periodontitis may or may not be contributory causes. The concept of a herpes viral-bacterial coinfection requires more clarification and further study.

Both chronic and aggressive periodontitis share major environmental and genetic risk factors, and some clinicians find the differential diagnosis between these two diseases difficult and impossible. Smoking, oral hygiene, and psychological factors seem to play a role in both chronic and aggressive periodontitis. Knowledge regarding psychological issues such as stress is severely lacking.5

Treatment planning sequence for patients with chronic, localized, and generalized periodontitis varies from clinician to clinician, and there is no standardization, especially concerning the added value of systemic antibiotics as an adjunct to initial therapy.

Deas and Mealey recommend that a patient with generalized aggressive periodontitis should be referred for a complete blood count and either a casual or fasting blood glucose test. They also emphasize that standard brushing and flossing instructions are less likely to be adequate for aggressive disease, especially those patients with exposed furcations and root concavities.

Deas and Mealey also suggest SRP in combination with systemic antibiotics for patients with generalized aggressive periodontitis. The combination of metronidazole 500 mg three times a day, plus amoxicillin 500 mg three times a day, is perhaps the most popular antibiotic regimen in the periodontal literature. Initial use of antibiotic therapy is recommended 24 hours before SRP, and SRP should be performed over the short time period during which the antibiotic is prescribed.6

I will only work in dental practices where clinical excellence is encouraged. A specialist’s referral for cases of localized and generalized aggressive periodontitis is important in preventing poor hygiene practice.

My stomach growled even louder that day as I finished filling out the referral slip to the local periodontist. Lunch was delayed and my stomach talk was annoying, but I felt good about my clinical decision-making.


  1. Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontol 2000 2010: 53: 12-27.
  2. Smith M, Seymour GJ, Cullinan MP. Histopathological features of chronic and aggressive periodontitis. Periodontol 2000 2010: 53: 45-54.
  3. Demmer RT, Papapanou PN. Epidemiologic patterns of chronic and aggressive periodontitis. Periodontol 2000 2010: 53: 28-44.
  4. Slots J. Human viruses in periodontitis. Periodontol 2000 2010: 53: 89-105.
  5. Stabholz A, Soskolne WA, Shapira L. Genetic and environmental risk factors for chronic periodontitis and aggressive periodontitis. Periodontol 2000 2010: 53: 138-153.
  6. Deas D, Mealey BL. Response to chronic and aggressive periodontitis to treatment. Periodontol 2000 2010: 53: 154-165.

Lynne Slim, RDH, BSDH, MSDH, is an award-winning writer who has published extensively in dental/dental hygiene journals. Lynne is the CEO of Perio C Dent, a dental practice management company that specializes in the incorporation of conservative periodontal therapy into the hygiene department of dental practices. Lynne is also the owner and moderator of the periotherapist yahoo group: Lynne speaks on the topic of conservative periodontal therapy and other dental hygiene-related topics. She can be reached at [email protected] or

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