The purpose of this investigation was to use molecular and immunological techniques to determine whether oral Treponema infected the human brain. Pieces of frontal lobe cortex from 34 subjects were analyzed with species-specific PCR and monoclonal antibodies. PCR detected Treponema in 14/16 Alzheimer's disease (AD) and 4/18 non-AD donors (P < 0.001), and AD specimens had more Treponema species than controls (P < 0.001). PCR also detected Treponema in trigeminal ganglia from three AD and two control donors. Cortex from 15/16 AD subjects and 6/18 controls contained Treponema pectinovorum and/or Treponema socranskii species-specific antigens (P < 0.01). T. pectinovorum and/or T. socranskii antigens were also found in trigeminal ganglia and pons from four embalmed cadavers, and 2/4 cadavers also had Treponema in the hippocampus. These findings suggest that oral Treponema may infect the brain via branches of the trigeminal nerve.

Serum samples obtained from 59 persons who had acute necrotizing ulcerative gingivitis, periodontitis, syphilis, or Lyme disease were tested against Treponema phagedenis biotype Reiter, Treponema denticola, Treponema vincentii, and Treponema scoliodontum by indirect fluorescent-antibody staining methods. Although there were positive reactions for sera representing each of these study groups and for 20 (13%) of 156 samples collected from the general population (premarital screening for syphilis), titration endpoints were relatively low (.1:256). Serum samples from 18 persons who had gingivitis or periodontitis but no history of Lyme borreliosis were tested by enzyme-linked immunosorbent assay for antibodies to Borrelia burgdorferi. Of these, five (28%) had immunoglobulin M antibody and four (22%) contained immunoglobulin G antibodies to this spirochete. Adsorption with either sorbent commercially prepared from T. phagedenis biotype Reiter or with washed, whole cells of T. phagedenis biotype Reiter reduced cross-reactivity in the enzyme-linked immunosorbent assay for Lyme borreliosis.

It is generally recognized that bacteria in dental plaque at sites of periodontal diseases are not commonly found at sites of periodontal health. One hypothesis to explain the etiology of periodontitis is that pathogenic bacteria from diseased sites infect healthy sites. It has been suggested that gingival inflammation may predispose sites to colonization by bacteria associated with periodontal diseases. The purpose of this cross‐sectional study was to determine whether the detection frequency of selected bacteria at sites of periodontal health or gingivitis differed between subjects who were in good periodontal health, subjects who had gingivitis, or subjects with periodontitis. The clinical status of every tooth (except third molars) from 106 subjects was characterized by means of clinical attachment level, probing depth and by signs of inflammation. Subgingival plaque was collected from mesio‐facial and disto‐lingual surfaces. Specific monoclonal antibodies were used in an immunocytochemical assay to identify Campylobacter rectus, Eikenella corrodens, Porphyromonas gingivalis, pathogen‐related oral spirochetes (PROS, using Treponema pallidum subspecies pallidum monoclonal antibodies), T. denticola (serotypes A‐D), T. socranskii subspecies buccale and T. socranskii subspecies socranskii. Differences in detection of bacteria between groups of subjects were measured using odds ratios (OR). Results of this study indicate that PROS was the only identified bacterium at sites of both health and gingivitis that demonstrated a significant positive relationship with the presence of periodontitis. These findings do not prove that bacteria spread from periodontitis sites, nor do they imply that disease necessarily results from infection. However, these data do suggest that some bacteria associated with periodontitis are more likely than others to tolerate conditions at healthy sites and that the presence of periodontitis increases risk of infection at healthy sites. J Periodontol 1996;67:109–115.

The spirochetes found in dental plaque from patients with ulcerative gingivitis or chronic periodontitis have antigens that are thought to be unique to pathogenic treponemes. This close antigenic relation suggests that T. pallidum or a closely related organism may be involved in the pathogenesis of periodontal disease.

The purpose of this investigation was to determine whether monoclonal antibodies against pathogenrestricted antigens of Treponema pallidum subsp. pallidum could be used as probes for spirochetes in diseased gingival tissue from subjects with acute necrotizing ulcerative gingivitis. A biotin-streptavidin system was used to identify spirochetes bound by monoclonal antibodies in cryostat sections of tissue. Twelve of 16 tissue samples from diseased sites, but none of 8 tissue specimens from healthy sites, reacted with pathogen-restricted antibodies. Organisms were found in intact epithelium and connective tissues adjacent to ulcers. Staining intensity was often high in perivascular locations and around vesicular spaces. Monoclonal antibodies to Bacteroides gingivalis and Treponema denticola were each reactive with diseased gingival tissues, but staining was usually restricted to ulcerated areas. These studies extend recent observations that showed that subjects with acute necrotizing ulcerative gingivitis had both pathogen-related spirochetes in dental plaque and serum immunoglobulin G to pathogen-restricted antigens on T. pallidum subspecies, suggesting that pathogen-related spirochetes may be associated with the pathogenesis of certain periodontal diseases.