Development of a risk profile for periodontal disease: microbial and host response factors.
Advances in our understanding of the relationship between the microbial challenge and the host response in periodontal disease have led to the search for pathogenesis-based risk indicators or risk factors for disease progression. This evaluation is based on analysis of non-invasive or minimally invasive samples that allow measurement of the subgingival plaque microflora or the host response in gingival crevicular fluid (GCF), serum, or saliva. Studies conducted by us have indicated that in GCF, persistently elevated levels of beta-glucuronidase (beta G, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodontitis. This finding has been confirmed in a multicenter trial. We have also observed that a statistically significant positive correlation exists between beta G in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variations in the host response to the challenge. Furthermore, beta G levels in GCF were inversely correlated with the IgG serum antibody titer to a panel of periodontal pathogens, suggesting the essentially protective function of the systemic humoral response in periodontal disease. Data in the literature support this concept. In addition, recent studies of the relationship of antibody isotypes in GCF to progression of clinical attachment loss have suggested that IgA in GCF has a protective function. This may relate to the lack of complement activation by IgA. Alternately, the development of IgA antigen-specific responses are T-cell dependent, and reductions in local levels of IgA may indicate a decrease in T-helper cell function. These data have allowed development of strategies for identifying individual risk profiles for patients with periodontal disease based on the host response to the microbial challenge. With identification of these risk indicators/risk factors for active periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this approach to periodontal diagnosis. Improved patient management should result from the incorporation of these tests into clinical practice.
Lamster
I B
IB
Division of Periodontics, School of Dental and Oral Surgery, Columbia University, New York, NY.
Smith
Q T
QT
Celenti
R S
RS
Singer
R E
RE
Grbic
J T
JT
D018407:Bacterial Physiological Phenomena; D015415:Biomarkers; D005883:Gingival Crevicular Fluid / Q000201:enzymology / Q000276:immunology; D005966:Glucuronidase / Q000032:analysis; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology; D010510:Periodontal Diseases / Q000201:enzymology* / Q000276:immunology / Q000382:microbiology*; D010518:Periodontitis / Q000201:enzymology* / Q000276:immunology / Q000382:microbiology*; D012307:Risk Factors
D015415:Biomarkers; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D005966:Glucuronidase