Predictors of clinical outcomes after periodontal treatment of aggressive periodontitis : 12-month randomized trial

Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≥7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis

Predictors of clinical outcomes after periodontal treatment of aggressive periodontitis : 12-month randomized trial

Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≥7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis

S-Nitrosoglutathione Accelerates Recovery from 5-Fluorouracil-Induced Oral Mucositis

<div><p>Introduction</p><p>Mucositis induced by anti-neoplastic drugs is an important, dose-limiting and costly side-effect of cancer therapy.</p><p>Aim</p><p>To evaluate the effect of the topical application of S-nitrosoglutathione (GSNO), a nitric oxide donor, on 5-fluorouracil (5-FU)-induced oral mucositis in hamsters.</p><p>Materials and Methods</p><p>Oral mucositis was induced in male hamsters by two intraperitoneal administrations of 5-FU on the first and second days of the experiment (60 and 40 mg/kg, respectively) followed by mechanical trauma on the fourth day. Animals received saline, HPMC or HPMC/GSNO (0.1, 0.5 or 2.0 mM) 1 h prior to the 5-FU injection and twice a day for 10 or 14 days. Samples of cheek pouches were harvested for: histopathological analysis, TNF-α and IL-1β levels, immunohistochemical staining for iNOS, TNF-α, IL-1β, Ki67 and TGF-β RII and a TUNEL assay. The presence and levels of 39 bacterial taxa were analyzed using the Checkerboard DNA-DNA hybridization method. The profiles of NO released from the HPMC/GSNO formulations were characterized using chemiluminescence.</p><p>Results</p><p>The HPMC/GSNO formulations were found to provide sustained release of NO for more than 4 h at concentration-dependent rates of 14 to 80 nmol/mL/h. Treatment with HPMC/GSNO (0.5 mM) significantly reduced mucosal damage, inflammatory alterations and cell death associated with 5-FU-induced oral mucositis on day 14 but not on day 10. HPMC/GSNO administration also reversed the inhibitory effect of 5-FU on cell proliferation on day 14. In addition, we observed that the chemotherapy significantly increased the levels and/or prevalence of several bacterial species.</p><p>Conclusion</p><p>Topical HPMC/GSNO accelerates mucosal recovery, reduces inflammatory parameters, speeds up re-epithelization and decreases levels of periodontopathic species in mucosal ulcers.</p></div

Bacterial strains used to construct whole genomic DNA probes that were then used for testing hamster buccal epithelial cell samples.

<p>* ATCC (American Type Culture Collection, Rockville, MD);</p>†<p>The Forsyth Institute, Cambridge, MA.</p><p>Bacterial strains used to construct whole genomic DNA probes that were then used for testing hamster buccal epithelial cell samples.</p

Quantification of TNF-α- (A), IL-1β- (B), iNOS- (C) and TGF-β RII - (D) positive cells in cheek pouch tissues of hamsters subjected to 5-FU-induced oral mucositis, on day 14.

<p>Oral mucositis was induced in hamsters by intraperitoneal (i.p.) injection of 5-FU followed by mechanical trauma (MT) of the cheek pouch. Animals received topical applications of a gel containing 0.5 mM S-nitrosoglutathione (GSNO) 30 min prior to 5-FU and twice daily thereafter for 10 days or 14 days. Control groups comprised healthy animals (H) and animals subjected to 5-FU-induced oral mucositis that received local applications of saline (Saline). Cells positive for staining were counted (10 fields per slide, 400×) for statistical comparisons. Bars denote the means ± standard errors of positive cells from four slides per group (4 animals per group). *denotes significant differences (P<0.05) compared with the Healthy group; +denotes a significant difference (P<0.05) compared with the Saline group; #denotes a significant difference (P<0.05) compared with the HPMC group. Data were analyzed using the Kruskal Wallis and Mann Whitney tests.</p

Real-time NO release profiles of the HPMC/GSNO formulations.

<p>(A) Kinetic curves of NO release from the 0.5 mM and 2.0 mM HPMC/GSNO formulations, measured by chemiluminescence. (B) Integrated NO signals extracted from the curves of Fig. 1A, which indicate the total NO released from the formulations over the same time-scale. The straight lines denote linear regressions of the experimental data.</p

Cell death and proliferation in the cheek pouches of hamsters subjected to 5-FU-induced oral mucositis, on day 14.

<p>Oral mucositis was induced in hamsters by intraperitoneal (i.p.) injection of 5-FU followed by mechanical trauma (MT) of the cheek pouch. Animals received topical applications of a gel containing 0.5 mM S-nitrosoglutathione (GSNO) 30 min prior to 5-FU and twice daily thereafter for 10 days or 14 days. Control groups comprised healthy animals (H) and animals subjected to 5-FU-induced oral mucositis that received local applications of saline (saline). The TUNEL- and Ki67-positive cells were counted (10 fields per slide, 400×) for statistical comparisons. Bars denote the means ± standard errors of stained cells from at four slides per group (4 animals per group). *denotes a significant difference (P<0.05) compared with the Healthy group; **denotes a significant difference (P<0.05) compared with the MT group, +denotes a significant difference (P<0.05) compared with the Saline group; #denotes a significant difference (P<0.05) compared with the HPMC group. Data were analyzed using the Kruskal Wallis and Mann Whitney tests.</p