Humoral immune responses to Porphyromonas gingivalis before and following therapy in rapidly progressive periodontitis patients.
We have performed studies aimed at elucidating the nature of the humoral immune response in rapidly progressive periodontitis (RPP). We analyzed the sera of 36 periodontally normal subjects and 36 RPP patients for titers and avidities of IgG antibodies reactive with the antigens of Porphyromonas gingivalis using ELISA, prior to and following treatment. We used whole-cell sonicate, purified lipopolysaccharide (LPS), and total extractable protein as plate antigens. Twelve of the patients had antibody titers at least 2-fold greater than the median of the controls and were designated as seropositive. The remaining 24 patients had titers that did not exceed twice the median titer of the controls and were designated as seronegative. For both patient groups, antibody titers were highest when whole-cell antigen was used, intermediate for LPS, and lowest for the protein fraction. Following treatment, median titer for seropositive patients decreased from pretreatment values of 241.7 to 76.5, while median titer for seronegative patients increased from 39.5 to 80.1. Avidities of pretreatment sera from both patient groups for all 3 antigen preparations were lower than the median avidities of the control sera. Avidity significantly increased following treatment to levels greater than those for control sera in both patient groups. Thus, some young adults with severe periodontitis mount a humoral immune response and produce high levels of serum IgG antibodies reactive with antigens of P. gingivalis, while others do not. The antibodies produced are of relatively low avidity, and may therefore be relatively ineffective biologically. Therapy, which greatly reduces antigen load, appears to stimulate production of higher avidity IgG antibodies in both patient groups; in the seropositive group, low avidity antibodies appear to be replaced by antibodies of higher avidity. Both the purified LPS and protein fractions contain reactive antigen(s), although LPS binds more antibody. Our data are consistent with the idea that many RPP patients do not produce protective levels of biologically functional antibody during the course of their natural infection, but they may be stimulated to do so by treatment.
Chen
H A
HA
Research Center in Oral Biology, University of Washington, Seattle.
Johnson
B D
BD
Sims
T J
TJ
Darveau
R P
RP
Moncla
B J
BJ
Whitney
C W
CW
Engel
D
D
Page
R C
RC
D000328:Adult; D016301:Alveolar Bone Loss / Q000276:immunology / Q000382:microbiology / Q000628:therapy; D000907:Antibodies, Bacterial / Q000032:analysis / Q000096:biosynthesis* / Q000502:physiology; D000915:Antibody Affinity; D012534:Dental Scaling; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis / Q000502:physiology; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D010514:Periodontal Pocket / Q000276:immunology / Q000382:microbiology / Q000628:therapy; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology* / Q000628:therapy*; D016966:Porphyromonas gingivalis / Q000145:classification / Q000276:immunology*; D016745:Root Planing
D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D008070:Lipopolysaccharides