Bacteroides gingivalis, Bacteroides intermedius and Actinobacillus actinomycetemcomitans seem to be major pathogens in advancing periodontitis in man. First, these organisms are recovered in higher prevalence and proportions from progressive periodontitis lesions than from quiescent periodontal sites. Second, antibody levels against B. gingivalis and A. actinomycetemcomitans are markedly elevated in serum and gingival crevice fluid of periodontitis patients compared to normal controls. Third, B. gingivalis and B. intermedius elaborate potent proteases and A. actinomycetemcomitans various noxious substances which have the potential to perturb important host defenses and to disintegrate key constituents of the periodontal tissues. Monitoring these bacteria in advanced periodontal lesions may greatly assist the assessment of treatment efficacy and risk of further periodontal breakdown.

Samples of subgingival bacteria were collected with a clean curette from two relatively normal and two periodontally diseased sites in each of 12 patients with advanced periodontal disease. The samples were suspended in physiologic saline containing 1 % gelatin and examined within 1 hour by darkfield microscopy. From 100‐200 bacteria were classified on a percentage basis into one of the following categories: (1) coccoid cells, (2) straight rods, (3) filaments, (4) fusiforms, (5) curved rods, (6) small spirochetes, (7) medium‐sized spirochetes, (8) large spirochetes, and (9) motile rods. For each area sampled the following clinical criteria were also recorded: (1) Gingival Index, (2) Plaque Index, (3) probing depth and (4) gingival fluid flow. For each patient separate mean values were calculated for the normal and the diseased sites. The results indicated that significant differences existed in the microbial flora of clinically normal and diseased sites using a paired t‐test comparison (2α= 0.001), with coccoid cells more predominant at normal sites (74.3 % vs. 22.3 %), while at diseased sites motile rods were more frequent (12.7 % vs. 0.3 %), as well as curved rods (1.7 % vs. 0 %), small spirochetes (12.6 % vs. 1.1 %), medium‐sized spirochetes (18.5 % vs. 0.5 %) and large spirochetes (6.7 % vs. 0.2 %). The ratio of motile to non‐motile cells in the normal was 1:49, whereas at diseased sites the ratio was in the vicinity of 1:1. These results clearly show that a different flora is associated with healthy and periodontally diseased sites in the same patient population and that these differences can be detected by means of a technique which is simple and readily adaptable to a clinical setting. The data obtained in this fashion may be useful in monitoring the effect of various treatment modalities on the periodontal flora and possibly in determining the presence or absence of active disease.

Teeth slated for extraction were evaluated with respect to their periodontal status and classified accordingly into five categories; namely normal, gingivitis, periodontitis, periodontosis and postperiodontosis. After processing, one approximal surface of each tooth was sampled at various levels in an apico-occlusal direction for light and electron microscopic study of the associated bacterial flora. In normal samples, the flora consisted of a relatively thin, adherent bacterial layer confined to the enamel surface. The cells were predominantly coccoid in shape with cell wall features compatible with those of Gram-positive organisms. Isolated filamentous or branching forms and some Gram-negative bacteria were noted on the surface of the more apical portion of the bacterial layer. No flagellated cells or spirochetes were present. Gingivitis samples yielded a relatively more voluminous and complex supragingival flora with relatively more filamentous bacteria and more cells with a Gram-negative cell wall ultrastructure. These samples also contained corncob formations on the surface of supragingival deposits, and flagellated cells with spirochetes within the predominantly Gram-negative flora of the sulcus bottom. Supragingival bacterial deposits of periodontitis samples were similar to those observed in gingivitis. The subgingival flora consisted of relatively fewer cells adherent to the root surface with a concomitant increase in the population of Gram-negative and flagellated cells, as well as spirochetes. The tissue side of the subgingival flora generally exhibited a distinctive concentration of "test-tube brush" formations, spirochetes of predominantly medium size, and assorted cell types peculiar to this region. A transitional flora generally separated the supra- from the subgingival microbial population. Periodontosis samples had a relatively sparse, predominantly Gram-negative flora. A unique electron-dense, lobulated cuticular deposit covered the majority of the samples studied. Postperiodontosis samples were much more similar in their microbial flora to the periodontitis group. The results suggest that (1) a certain microbial flora may be compatible with a state of periodontal health; (2) a different flora is associated with varying degrees of periodontal disease; (3) the structure and composition of the supragingival flora differs markedly from that of the subgingival flora; (4) with the exception of periodontis, the alterations of the microbial flora as periodontal disease increases inseverity parallel the changes described previously in the microbial population collected on artificial crowns during experimentally induced gingivitis. The use of the expressions "microbial flora" or "microbial population" is considered preferable to the terms "plaque", "materia alba", or "debris" in reference to the microbiota of the gingival sulcus region.

Periodontitis is an inflammatory disease of the periodontium which is characterized by a progressive destruction of the tissues supporting the tooth. Its primary etiology is an ill-defined series of microbial infections which may be composed of only some of the more than 300 species of bacteria currently recognized in the oral cavity. The disease is currently considered to progress as periodic, relatively short episodes of rapid tissue destruction followed by some repair, and prolonged intervening periods of disease remission. Despite the apparent random distribution of episodes of disease activity, the resulting tissue breakdown exhibits a symmetrical pattern of alveolar bone loss and pocket formation which is common to several forms of periodontitis, although the distribution of the most affected teeth and surfaces may vary among diseases (e.g., juvenile periodontitis versus adult periodontitis or rapidly progressive periodontitis). Several reports have indicated that bacterial cells can be found in the pocket wall of periodontitis lesions. The translocation of bacteria into the tissues from the pocket environment is quite common, as evidenced by the common occurrence of bacteremias in patients with periodontitis following relatively minor events such as chewing and oral hygiene procedures. However, it is important to distinguish between the passive introduction of bacteria into periodontal tissues and frank invasion as might occur in an acute infection, since the pathological implications may be quite different.

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The subgingival occurrence of yeasts and species of Enterobacteriacae and Pseudomonas was studied in 500 adults with severe periodontitis. All subjects had sites non‐responding or “refractory” to conventional periodontal therapy. Most subjects had received one or more courses of broad‐spectrum systemic antibiotics. Subgingival microbial samples were collected with paper points and transported in VMGA III. The bacterial samples were plated on enriched brucella blood agar and incubated anaerobically, and on TSBV, TBC, and Sabouraud agar, which were incubated in 10% CO2. Yeasts were speciated using the API 20C micro‐method system and the germ tube test (for Candida albicans). Enteric organism's and pseudomonads were speciated with the API 20E kit system. Yeasts, enteric rods and pseudomonads were subjected to antibiotic susceptibility testing. The occurrence of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, and Bacteroides intermedium was also determined in the patients studied. In the 500 periodontitis patients, yeasts were detected in 84 (16.8%), enteric rods or pseudo‐monads in 51 (10.2%), and both yeasts and enterics or pseudomonads in 6 (1.2%). Candida albicans comprised 83.3% of the isolated yeasts. Enterobacteriaceae averaged 21–39% of the cultivable flora in culture‐positive cases, with Enterobacter cloacae, Enterobacter agglomerans, Proteus mirabilis, Klebsietta pneumonias, and Klebsiella oxytoca being the most frequent species. Pseudomonas aeruginosa was isolated from 10 patients, averaging 23.4% of the cultivable subgingival flora. All Candida isolates, and 86–95% of the enteric rods and pseudomonads, were resistant to 1 μg/ml of tetracycline, penicillin G, and erythromycin. In patients positive for yeasts, enteric rods or pseudomonads, A. actinomycetemcomitans was isolated from about one‐fifth, B. intermedius from about one‐third, and B. gingivalis from 5% of the individuals. The present findings suggest that yeasts or enteric rods or pseudomonads occur in the subgingival flora of about one‐third of “refractory” adult periodontitis patients. We caution against using antibiotics without prior microbiological screening in treating this patient group.

The periodontal probe has been and continues to be used as an important diagnostic instrument by the dental profession. The measurements recorded with the probe have generally been considered to represent a reasonably accurate estimate of sulcus or pocket depth. Recent reports on the histopathology of the periodontal lesion and the histological features of a healing lesion, together with histological studies on the relationship of the probe to periodontal tissues, have shed some new light on periodontal probing. It is now apparent that probing depth measured from the gingival margin seldom corresponds to sulcus or pocket depth. The discrepancy is least in the absence of inflammatory changes and increases with increasing degrees of inflammation. In the presence of periodontitis the probe tip passes through the inflamed tissues to stop at the level of the most coronal intact dento-gingival fibers, approximately 0.3-0.5 mm apical to the apical termination of the junctional epithelium. Decreased probing depth measurements following periodontal therapy may be due in part to decreased penetrability of the gingival tissues by the probe. Following treatment aimed at obtaining new attachment in periodontal defects, wider variations may occur between the location of the probe tip and the most coronal dento-gingival fibers than in the case of untreated sites. This is due in part to the formation of a so-called "long" junctional epithelium. In the absence of inflammation this epithelium may not be penetrable during ordinary probing, but could account for a rapid increase in probing depth measurements when inflammatory changes allow the probe to traverse the epithelium and/or the adjacent infiltrated connective tissue. In view of the difficulty inherent in relating periodontal probing measurements to actual sulcus or pocket depth, the interpretation of periodontal probing in the practice of periodontics may need reappraisal.

The effect of a single session of scaling and root planing on the subgingival periodontal flora of 14-adult human subjects was investigated by darkfield microscopy. At baseline, one randomly selected periodontally diseased site in each subject was assessed for GI and PlI scores, probing depth and the percentage distribution in subgingival debris of coccoid cells, spirochetes, motile cells and other microorganisms. Following a single full mouth scaling and root planing session, these criteria were reevaluated at other initially diseased sites, one per subject and time interval. The intervals tested were days 3, 7, 14, 21, 28, 35, 42, 49, 56, 70 and 90. The PlI and GI scores tended to decrease during the first 14 days, returning to baseline around days 21-28. After another transient decline around 35-42 days the values stabilized around baseline levels till the end of the experiment. Probing depth decreased below baseline during the first 7 days and with the exception of day 28, remained below baseline level till the end of the experiment. Coccoid cells increased from 25.1 % at baseline to 76.1 % on day 3. Return to the baseline level occurred by day 21. Spirochetes did not return to baseline imtil day 42. The percentage of motile cells decreased significantly from baseline on day 3 only (14.8 % to 3.8 %).The results indicated that a single session of scaling and root planing is capable of disturbing the proportions of certain bacterial forms in the subgingival periodontal flora, and that it may require approximately 42 days for the proportions to return to baseline levels. Probing depth was significantly decreased by the debridement throughout most of the 90-day experimental period. The proportion of coccoid cells was negatively correlated with both GI and PlI scores, while the percentage of spirochetes was positively correlated with GI and PlI scores as well as probing depth measurements.