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Notes: Abstract 27 subjects with active destructive periodontal diseases were treated by modified Widman flap surgery and systemic tetracycline and divided into 4 groups based on pre- and post-therapy hazard rates (% of sites losing 〉 3 mm of attachment in 1 year). Pre- and post-therapy hazard rates were respectively: group T (3 subjects) 〈 4 and 〈 4; group II (8 subjects) 〉 4 and 〈 4; group III (3 subjects) 〈 4 and 〉 4; group IV (refractory group of 13 subjects) 〉 4 and 〉 4. Baseline mean pocket depths and attachment loss of groups 1 and II subjects were less than groups III and IV subjects and exhibited less suppuration. 6 group IV subjects lost a total of 38 teeth after therapy, in contrast to no tooth loss in subjects in the other 3 groups. Redness, bleeding on probing, plaque levels and age did not differ among groups. Subjects in the 4 groups differed in the subgingival species to which they showed elevated serum antibody responses. Group IV subjects showed elevated responses to a select range of gram-negative species, including A. actinomycetemcomitans strains Y4 or ATCC 29523, F. nucleatum and B. intermedius. No subject in any of the other groups exhibited an elevated response to B. intermedius. The mean % of each species in all sampled sites, both before and after therapy, was computed for each subject. Subjects in groups III and IV (high post-therapy hazard rates) exhibited elevated mean levels of B. forsythus, F. nucleatum, S. intermedius, E. corrodens, and B. gingivalis. Groups I and II subjects showed elevated mean levels of an unnamed Actinomyces species. Refractory subjects (group IV) did not constitute a homogeneous group. While subjects in this group had higher levels of pathogens, it appeared that they differed in the combinations of predominant species. 3 major microbial complexes were observed: (1) B. forsythus, F. nucleatum and W. recta (3 subjects); (2) S. intermedius, B. gingivalis and P. micros (3 subjects); (3) S. intermedius and F nucleatum (7 subjects) with or without B. gingivalis.

Notes: Abstract 76 subjects with prior evidence of destructive periodontal diseases were monitored clinically and immunologically every 2 months for up to 5 years. Clinical parameters measured included bleeding on probing, gingival redness. plaque accumulation, suppuration, pocket depth and attachment level. Blood samples were taken by venipuncture and serum antibody levels to a series of 18 subgingival species determined. 33 of these subjects showed evidence of active disease during the monitoring period, based on changes in attachment level measurements assessed using the tolerance method of analysis. Mean attachment loss in these 33 subjects varied from 1.4 mm to 9.0 (median value 3.4 mm) and subjects whose mean attachment level was above the median showed a higher % of pockets 〉 3 mm and more suppuration. Severity of gingival inflammation related poorly to mean attachment loss. Subgingival plaque samples were taken from the active site(s) and from control sites of equal pocket depth and attachment loss in the same active disease subjects, prior to therapy, for predominant cultivable microbiota studies. 50 randomly selected isolates were identified from each sample. Predominant cultivable species in 170 pretreatment active and inactive sites combined (8500 isolates) were enumerated. The most frequently detected species were F. nucleatum (112 sites) and S. intermedius (106 sites), although the predominant species in the samples from each subject differed. The distribution of putative pathogens differed among subjects. For example. A. actinomycetemcomitans was found in 21 samples in 11 subjects and B. forsythus was found in 18 samples from 10 individuals. Antibody response patterns to the 18 subgingival species also varied among subjects. More than 81% (26/32) of the subjects demonstrated a mean elevated serum antibody level to at least 1 micro-organism, while I subject showed an elevated response to 5 species. No pattern(s) of elevated antibody response(s) could be related to severity of attachment loss. Collectively, the data suggest that clinically, immunologically and microbiologically distinctive destructive periodontal diseases exist, and appropriate classifications could be devised.

Notes: Background/aims: Established periodontal diseases may be associated with antibody responses to periodontal pathogens, but it is not known at which stage of disease this antibody response is initiated. This study aimed to characterize the host systemic response in initial periodontitis, gingivitis, and periodontal health, to evaluate whether elevated serum antibodies to subgingival species could be detected in initial periodontitis.Method: Human systemic immune response were evaluated to 40 subgingival bacterial species in 16 healthy, 21 gingivitis, 11 initial periodontitis and 5 progressing recession adults. Subjects had minimal periodontal attachment level (AL) loss at baseline. Disease categories were determined after 12 months monitoring at three-month intervals. Increased AL loss 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:03036979:JCPE27007473:ges" location="ges.gif"/〉1.5 mm (disease activity) at interproximal sites defined initial periodontitis, recession was characterized by AL loss at buccal sites. Serum IgG antibodies were evaluated semi-quantitatively by immunoblot from blood taken at baseline, active and final visits.Results: No antibody was detected from 55% of reactions. When detected, levels were below those reported for advanced periodontitis subjects. There were no major differences in serum antibody levels between healthy, gingivitis and initial periodontitis subjects, despite differences in the subgingival microbiota. Serum antibodies for more species were detected in recession subjects, compared with the other study subjects. No changes in antibody levels were detected between baseline, active, and final visits. No systematic association between species colonization and presence of systemic antibody was observed.Conclusions: This study did not detect differential elevation of mean serum antibody levels in initial periodontitis subjects, suggesting that serum antibody levels are not sensitive risk markers for initial periodontitis.

Notes: The level and distribution of static crevicular fluid (SCF) antibody was studied in periodontal disease patients. Elevated levels of SCF antibody were demonstrated in approximately 9% of 1292 sites. The elevated responses were shown to be limited to particular bacterial specificities at any one site. Additional comparisons indicated that the frequency of elevated antibody levels in SCF were most closely related with responses to A. actinomycetemcomitans, B. gingivalis, and B. intermedius rather than clinical categorization.

Notes: Fifty-one subjects (16–61 years old) with evidence of prior destructive periodontal disease were monitored clinically and immunologically at bi-monthly intervals for up to 5 yr. Periodontal disease activity, determined as new attachment loss, was detected in 33 of these subjects. Only 4 of 51 subjects failed to show an elevated serum antibody level to any of the 18 subgingival species tested. The antibody level threshold established for periodontally healthy subjects was exceeded most often in diseased subjects with serum antibody to Actinobacillus sp., P. gingivalis, E. corrodens, C. concisus, F. nucleatum and P. intermedia in that order. In general, most serum antibody levels to subgingival species remained relatively consistent for periods as long as 5 yr. However, major increases and decreases in antibody could be detected to at most one or two species in individual subjects. In addition, prolonged, steady increases and decreases in antibody to specific species could be detected in certain subjects. These findings suggest that major changes occurring in serum antibody may reflect fluctuations in the nature of the infection. Differences were observed in the antibody level to specific species when subjects were divided into subsets on the basis of clinical criteria. These included high levels of antibody to A. actinomycetemcomitans Y4 in LJP and RPP subjects and to A. actinomycetemcomitans 29523 in LJP and GJP subjects.

Notes: Thirteen periodontally healthy subjects were monitored clinically for 6–12 months. Clinical measurements at 6-weekly intervals included duplicate PD measurements, presence of plaque, redness, and bleeding on probing. Baseline measurements consisted of 2 visits I wk apart. Microbial samples were taken from 11 of the subjects who had completed at least 8 months of monitoring. Levels of serum antibodies to 12 periodontal species were determined from 10 subjects. Standard deviations of replicate PD measurements, computed for each subject, ranged from 0.2–0.3 mm over the monitoring period. Plaque and redness increased during monitoring, and showed a weak association with PD change. Baseline and follow-up distributions of PD changes indicated that changes of 〉 1.5 mm could reasonably be considered to represent active sites. Five subjects demonstrated at least 1 site deepening by 1.5 mm over the period monitored, and these were considered putative active subjects. Sites from 2 subjects showed PD increases in the 6 wk just before sampling, and these were considered to represent active sites. Species associated with putative active subjects included Actinomyces naeslundii, Veillonella parvula, Selenomonas noxia and Prevotella nigrescens. Streptococcus sanguis, S. gordonii and Peptostreptococcus micros were associated with inactive subjects. S. gordonii and S. oralis were associated with health, whereas P. nigrescens was associated with gingivitis. Elevated serum antibodies were detected to A. actinomycetemcomitans in 4 subjects. The predominant microbiota of putative active subjects included some species previously associated with gingivitis, and some species previously associated with progressing periodontitis.

Notes: Experiments were performed to determine the effect of delayed-type hypersensitivity (DTH; cell mediated immunity) on subsequent periodontal bone loss in monoinfected (Actinobacillus actinomycetemcomitans [A actinomycetemcomitans]) gnotobiotic rats. Foot pad swelling reactions to A actinomycetemcomitans sonicate were used to monitor both immediate hypersensitivity and DTH. DTH was present in A actinomycetemcomitans immunized (I) animals when initially challenged with A actinomycetemcomitans. This DTH was maintained throughout the experimental period Sham-immunized (SI) animals did not show DTH until after 30 days of infection. The cellular infiltrate in the gingiva of immunized animals was relatively more mononuclear than the infiltrate of SI animals Serum IgG antibody to A actinomycetemcomitans was significantly elevated in I compared to SI animals. The relationship between the foot pad swelling and serum antibody levels suggested that an active Arthus type reaction was observed A actinomycetemcomitans injected rats demonstrated an Arthus-type reaction throughout the duration of the experiment SI animals only showed this reaction 30 days after immunization; the extent of swelling was always less than in the I group. Immunized rats demonstrated significantly elevated horizontal bone loss after infection for 90 days. The data suggest that a “mixed” hypersensitivity reaction to A actinomycetemcomitans occurs in presensitized rats and that the presence of this hypersensitivity can be associated with increased periodontal bone loss.