SERUM IGG ANTIBODY-RESPONSE TO ACTINOBACILLUS-ACTINOMYCETEMCOMITANS AND PORPHYROMONAS-GINGIVALIS - IMPLICATIONS FOR PERIODONTAL DIAGNOSIS

Citation
Ib. Lamster et al., SERUM IGG ANTIBODY-RESPONSE TO ACTINOBACILLUS-ACTINOMYCETEMCOMITANS AND PORPHYROMONAS-GINGIVALIS - IMPLICATIONS FOR PERIODONTAL DIAGNOSIS, Journal of clinical periodontology, 25(6), 1998, pp. 510-516
Citations number
25
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
ISSN journal
03036979
Volume
25
Issue
6
Year of publication
1998
Pages
510 - 516
Database
ISI
SICI code
0303-6979(1998)25:6<510:SIATAA>2.0.ZU;2-I
Abstract
The relationship of the serum antibody titer and avidity to the putati ve periodontal pathogens Actinobacillus actinomycetemcomitans (Aa) str ains Y4 and 29523 and Porphyromonas gingivalis (Pg) strain 381 were ex amined in relation to clinical parameters in 26 gingivitis and 28 peri odontitis patients. The relationship of antibody titer and avidity to infection with the homologous organism was also examined in a subset o f 30 patients. Antibody titer was determined by an enzyme-linked immun osorbent assay, and antibody avidity was assessed using a dissociation assay. Considering all patients, there was a significant negative cor relation between mean probing depth and antibody titer (r=-0.28) and a vidity (r=-0.28) to Aa Y4. There was a significant positive correlatio n of probing depth and antibody titer (r=0.46) and avidity (r=0.46) to Pg. The correlation of antibody titer and avidity to Aa and infection with Aa Y4 (r=-0.32, r=-0.21) and Aa 29523 (r=-0.35, r=-0.39) was neg ative, while the correlations of titer and avidity to Pg and presence of the organisms was strongly positive (r=0.40, r=0.35). These data in dicate that the relationship of serum antibody titer and avidity to cl inical parameters of periodontal disease severity and the level of inf ection with the homologous organism appears to be different for Aa and Pg. The development of an antibody response to Aa appears to protect the individual from infection with the organism. In contrast, the deve lopment of an antibody response to Pg was not able to eliminate the in fection. These results should be considered when developing a diagnost ic strategy for periodontal disease utilizing the humoral immune respo nse.