DEVELOPMENT OF A RISK PROFILE FOR PERIODONTAL-DISEASE - MICROBIAL ANDHOST RESPONSE FACTORS

Citation
Ib. Lamster et al., DEVELOPMENT OF A RISK PROFILE FOR PERIODONTAL-DISEASE - MICROBIAL ANDHOST RESPONSE FACTORS, Journal of periodontology, 65(5), 1994, pp. 511-520
Citations number
37
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00223492
Volume
65
Issue
5
Year of publication
1994
Supplement
S
Pages
511 - 520
Database
ISI
SICI code
0022-3492(1994)65:5<511:DOARPF>2.0.ZU;2-G
Abstract
ADVANCES IN OUR UNDERSTANDING of the relationship between the microbia l challenge and the host response in periodontal disease have led to t he search for pathogenesis-based risk indicators or risk factors for d isease progression. This evaluation is based on analysis of non-invasi ve or minimally invasive samples that allow measurement of the subging ival plaque microflora or the host response in gingival crevicular flu id (GCF), serum, or saliva. Studies conducted by us have indicated tha t in GCF, persistently elevated levels of beta-glucuronidase (betaG, a marker for primary granule release from polymorphonuclear leukocytes) are associated with clinical attachment loss in patients with periodo ntitis. This finding has been confirmed in a multicenter trial. We hav e also observed that a statistically significant positive correlation exists between betaG in GCF and measures of the subgingival microbial challenge, but the correlation was less than 0.5, suggesting variation s in the host response to the challenge. Furthermore, betaG levels in GCF were inversely correlated with the IgG serum antibody titer to a p anel of periodontal pathogens, suggesting the essentially protective f unction 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 clinic al attachment loss have suggested that IgA in GCF has a protective fun ction. This may relate to the lack of complement activation by IgA. Al ternately, the development of IgA antigen-specific responses are T-cel l dependent, and reductions in local levels of IgA may indicate a decr ease 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 chall enge. With identification of these risk indicators/risk factors for ac tive periodontal disease, the next challenge is to provide clinicians with access to the tests and analyses that are required for this appro ach to periodontal diagnosis. Improved patient management should resul t from the incorporation of these tests into clinical practice.