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Notes: Abstract Histatins, histidine-rich proteins found within parotid and submandibular secretions, are a novel class of endogenous peptides with antimicrobial properties. This masked, randomized, placebo-controlled preclinical investigation examined the effect of 3 topical histatins on the development of plaque and gingivitis in beagle dogs. 16, female, 1-year-old beagles were brought to optimal gingival health by mechanical scaling and polishing followed by rigorous daily tooth brushing. At the conclusion of this pretreatment period, dogs were randomly divided into 4 groups for the application of test formulations, and were placed on a plaque-promoting diet, Test agents included 3 synthetic salivary histatins (histatin 5, P-113 and P-113D) which were incorporated in hydroxypropyl methylcellulose gel at a concentration of 0.125%, and a placebo, or negative control, which was the gel vehicle alone. Throughout the 10-week treatment period, test formulations (2.0 ml) were applied 2xdaily to all premolar teeth using a Monojet syringe. Plaque formation and gingival inflammation were assessed using the plaque (PI) and gingival (GI) indices on days 0, 7, 14, 21, 28, 42, 56 and 70. Furthermore, bleeding to probing was recorded as a percent of sites (%BOP) and according to the modified sulcus bleeding index (mSBI). Comparisons among groups and between group pairs (active versus placebo) were made with Kruskal-Wallis tests with the average of data over the interval, days 14–42, being the primary focus of the analysis. From baseline to day 7, all groups expressed similar indices. Thereafter, overall significant differences among the groups were noted at day 42 for PI, at days 21, 28, 42 and 70 for GI, and at days 14 and 28 for %BOP (p〈0.05). In particular, beagles treated with P-113 demonstrated significantly lower PI scores at day 42 (p〈0.05), significantly lower GI scores from days 21 through 42 (〈0.05), and significantly lower %BOP scores at days 14 and 28 (p〈0.05) compared to beagles treated with placebo. Beagles treated with P-113D exhibited significantly lower GI at day 42 compared to the placebo (p〈0.05). For the primary analysis conducted over the midtreatment interval (days 14–42), significant differences were detected for all parameters except mSBI (p〈0.05). Accordingly, significantly lower PI scores were found for P-113, lower GI scores for P-113 and P-113D, and lower %BOP for P-113 and P-113D compared to placebo (p〈0.05). These data indicate that in the beagle model, salivary histatins, P-113 and P-113D, topically applied, can significantly reduce clinical signs of plaque formation and gingival inflammation.

Notes: Abstract Clinical responses of facial grade II molar furcations to closed (C) versus open (O) debridement were evaluated. 25 teeth were treated at baseline (BL) with scaling/root planing (S/RP) and evaluated at 4 months. 12 of the teeth were then treated with open flap debridement and the remaining teeth were treated with further S/RP. Clinical parameters of plaque, gingival inflammation, bleeding on probing, gingival fluid flow, pocket depth and probing attachment level were taken at BL, 4, 7, 10, 13 and 16 months. Pairwise differences were determined between visits and a Z-test was applied to differences for C and O. For both treatment groups, the greatest changes in clinical parameters occurred from BL–4 months. Plaque and gingival inflammation showed a gradual reduction from BL throughout the study for both groups. A reduction in pocket depth from BL–16 months was noted in both groups (mid-furcal, C= 1.5 mm, O= 1.2 mm; root prominence, C= 1.02 mm, O = 0.84 mm)! There was a gain in probing attachment level in the midfurcal area for the C group (0.6 mm) while the O group lost (−0.46 mm). There were no statistically significant differences found for any clinical parameter between closed and open debridement. The presence of plaque and bleeding at a furcal site had not significant effect on treatment response.

Notes: Abstract This investigation was designed to determine the reproducibility of probing pocket depths in maxillary facial and mandibular facial and lingual grade II and III molar furcation sites. 80 untreated molar teeth with 102 furcation invasions due to periodontitis were probed with a pressure-sensitive periodontal probe by 3 examiners. 8 sites per furcation were measured by each examiner at a single examination. The sequence of examiner probing was rotated in order to evaluate the effect of sequential probing. Tracings were made from radiographs of the inter-root separations in order to classify the interradicular space and to determine the effect of root separation on reproducibility. Data was analyzed by regression analysis, Pearson correlations, intraclass correlations, and the Student-Newman-Keuls test. Analysis indicated a high reproducibility of the maxillary facial and mandibular facial and lingual furcation sites in this untreated adult sample. No effect was due to probing sequence. The mid-root prominences, the line angles, and the internal surface sites of the furcation roots were recordable and reproducible, while the horizontal measurements were not consistently recordable The reproducibility of the facial and lingual furcation sites that were probed decreased with an increase in probing pocket depth and an increased degree of root separation.

Notes: Abstract 19 adult periodontitis patients were treated with plaque control and a single episode of root debridement. Results of this treatment were monitored in non-molar sites, molar flat surface sites, and molar furcation sites by probing attachment level measurements every 3rd month for 24 months. After 24 months, sites with probing attachment loss were identified using linear regression analysis. Clinical scores for supragingival plaque, bleeding on probing, suppuration on probing, and probing depth, obtained from these sites during the 24-month study, were analyzed to determine if they could be used diagnostically as indicators of probing attachment loss. The results demonstrated that the diagnostic accuracy for these clinical indicators was generally low at all 3 anatomical site locations. A possible explanation for this limited diagnostic accuracy may be that some areas of probing attachment loss following basic periodontal therapy are caused by factors other than the progression of an inflammatory periodontal disease of microbial etiology.

Notes: Abstract The healing response of non-molar sites, molar flat surface sites, and molar furcation sites was investigated in 19 adult periodontitis patients following a periodontal therapy of plaque control and root debridement. A total of 2472 sites were monitored by recordings of dental plaque, bleeding on probing, probing depth, and probing attachment levels every 3rd month for 24 months. The results demonstrated that in sites with initial probing depth of 4.0 mm or greater, molar furcation sites responded less favorably to the therapy as compared to molar flat surface sites or non-molar sites. This was demonstrated by higher mean scores for bleeding on probing, less reduction in probing depth, and a mean loss of probing attachment of 0.5 mm over 24 months. Site analyses using linear regression showed a higher % of deeper sites with probing attachment loss for the molar furcations than either molar flat surface or non-molar sites. Among sites initially 7.0 mm or deeper, 21% of molar furcations were identified as showing probing attachment loss as compared to 7% of the molar flat surface sites and 11 % of the non-molar sites.

Notes: Abstract 11 adult patients with moderate to advanced periodontitis were treated with oral hygiene instruction and an initial, single episode of root debridement. Before therapy, 3 independent clinicians examined all patients and identified sites that in their opinion probably would not respond to the therapy and would continue to lose attachment. On 2 occasions, 3 and 12 months later, the clinicians reexamined and reevaluated all patients and all sites. The results of therapy were also monitored by probing attachment level measurements performed every 3rd month. All 11 patients completed 24 months of follow-up, and 6 subjects were available until 36 months. Sites with probing attachment loss after 12, 24 and 36 months were identified using linear regression analysis and compared to the clinicians' prediction of probing attachment loss. The results demonstrated a limited agreement between probing attachment loss determined by linear regression and the clinicians' predictions of probing attachment loss. It appears that the traditional clinical signs and factors used to forecast and identify periodontal disease activity are only moderately associated with probing attachment loss. This suggests that attachment loss may be caused by several factors, at least following initial therapy. The progression of an inflammatory disease of microbial etiology may be only 1 of such causes. Further studies are needed to clarify the nature and cause of probing attachment loss.

Notes: Abstract The purpose of this investigation was to histologically determine the position of the periodontal probe tip when probing the deepest in terra dicular pocket depth in grade II and III facial molar furcation sites. Facial furcation pockets (5.8 mm+ 1.3) were probed with a pressure-sensitive probe set at 50 g pressure. The probe tip was attached to the tooth with an acid etched composite resin. Surgical block biopsies were removed, fixed, decalcified and processed for histological sectioning. Buccolingual serial sections (6 μ) were cut from 9 biopsies and apicocoronal serial sections were cut from 3 biopsies. The sections were histometrically analyzed. The probe tip penetrated the inflamed furcation connective tissue an average depth of 2.1 mm (±0.6), The probe tip was located 0.4 mm (± 1.4) apical to the crest of the interradicular bone. The % of inflammatory cell infiltrate in the connective tissue (ICT) around the probe tip was 56% (± 15%). There was no correlation between the % of ICT and the depth of probe penetration. This investigation demonstrated that probing of untreated facial molar furcation sites does not measure the attachment level of the interradicular root surfaces, but rather records the depth of probe penetration into the inflamed furcation connective tissue.