Gillian Air  /  Sanjay Bidichandani  /  Robert Broyles
  Paul DeAngelis  /  Jay Hanas  /  Martin Levine  /  Guangpu Li 

Jialing Lin  /  Hiroyuki Matsumoto  / Blaine Mooers /  Ann Louise Olson 

Karla Rodgers  /  Robert Steinberg  /  Leon Unger  /  Paul Weigel   /  Christopher West 

A new biochemical approach to understanding periodontal disease

The American Academy of Periodontology notes that intensive oral hygiene care and regular professional cleaning is the only way to control periodontal disease, inflammation of the gingiva (gingivitis) with loss of the periodontal attachment (periodontitis). A few adults (<0.5% of the population) are especially difficult to treat. If young adults with no periodontal disease stop tooth cleaning, most exhibit an increase in the indigenous microbiota (actinomyces, streptococci, Eikenella corrodens and capnocytophaga) at the gingival sulcus. A few days later, a ‘fuso-spirochetal’ microbiota appears and within 3 – 4 weeks, clinical signs of gingivitis. One possibility is that lysine decarboxylase from E. corrodens and capnocytophaga in the indigenous microbiota induces the GCF by depleting lysine to cadaverine, a non-metabolizable product. The depletion of lysine would inhibit the proliferation of dentally attached basal keratinocytes that make up the dental-epithelial attachment at the base of a gingival sulcus. Starved of the lysine from interstitial fluid, the DAT cells would release IL1, which induces the GCF and replenishes the lysine. However, the GCF provides proteins that enable the ‘fuso-spirochetal’ microbiota to grow in the sulcus and maintain the inflammation unless prevented by adequate oral hygiene. Recent studies supported by NIH-NIDCR and utilizing patients from Dr. Sig. Socransky’s periodontal clinic at the Forsyth Center, Boston, have confirmed that mild gingivitis, common in healthy and a few successfully treated periodontitis patients, is proportional to lysine decarboxylase activity, as measured from the cadaverine to lysine ratio in whole mouth biofilm samples. By contrast, many successfully treated periodontitis patients had moderate gingivitis unrelated to lysine decarboxylase activity. The findings suggest that lysine decarboxylase may initiate mild gingivitis but that differences in the host response or in the amount of residual ‘fuso-spirochetal’ microbiota explain the persistence of moderate gingivitis when periodontitis is easily controlled. By contrast, the change in the periodontal attachment level of ‘difficult-to-treat’ patients after therapy associated with the lysine decarboxylase activity of their biofilm. Whether this relationship was caused by or resulted from their ‘difficult-to-treat’ condition may be determined by treating such patients with lysine decarboxylase inhibitors (US Patents 6,103,220 and 6,187,296).

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