Purpose: Periodontal disease has traditionally been classified based upon history and clinical presentation, but considerable heterogeneity within each diagnostic category persists suggesting the need for improved periodontal classifications that better reflect the biology of the periodontal tissue-biofilm interface (PBI). The purpose of this study was to use biological parameters that are all influencing the local expression of disease at the PBI in combination with the clinical determinants of the periodontal tissue-biofilm interface to better understand the inflammatory and microbial phenotypes that may underlie clinical disease.
Materials and Methods: Data from an epidemiologic study that included full-mouth clinical periodontal measurements from 6793 community-dwelling subjects were analyzed to identify heterogeneity in disease presentation to create periodontal disease classifications based upon two measures more directly related to the PBI, probing depths (PD) and bleeding on probing (BOP) scores. This analysis ignored attachment loss measurements and focused on defining clinical disease based upon these two clinical measurements to describe the periodontal tissue biofilm interface. Four distinct PBI disease classifications emerged [Healthy (PBI-H), Gingivitis (PBI-G), moderate periodontitis (PBI-MP) and severe periodontitis (PBI-SP)]. The biological profile of these four disease groups was explored using serum antibody IgG levels, the level of periodontal organisms present and the gingival crevicular fluid (GCF) inflammatory mediator response.
Results: Subjects with PBI-H had lower levels of serum antibody, as compared to all diseased subjects. The level of organism present was similar for the healthy, gingivitis and moderate periodontitis subjects. PBI-G and PBI-MP had similar levels of serum antibody and microbes, but the PBI-SP group had higher levels of serum IgG and periodontal pathogens as well as elevated GCF levels of IL-1B, PGE2, MCP-1 and IL-6.
Conclusions: Severe periodontitis differs biologically from moderate periodontitis beyond severity in clinical presentation. PBISP is associated with an increase in microbial load, an enhanced antibody response and an increase in the innate inflammatory response.
Keywords: periodontal disease, diagnostics, gingival crevicular fluid