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
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.