Aim: This randomized placebo‐controlled clinical trial evaluated the effect of Bifidobacterium animalis subsp. lactis (B. lactis) HN019‐containing probiotic lozenges as adjuvant to scaling and root planing (SRP) in patients with generalized chronic periodontitis.Materials and Methods: Forty‐one chronic periodontitis patients were recruited and monitored clinically, immunologically, and microbiologically at baseline (before SRP) and 30 and 90 days after SRP. All patients were randomly assigned to a Test (SRP + Probiotic, n = 20) or Control (SRP + Placebo, n = 21) group. The probiotic lozenges were used twice a day for 30 days. The data were statistically analysed.Results: The Test group presented a decrease in probing pocket depth and a clinical attachment gain significantly higher than those of the Control group at 90 days. The Test group also demonstrated significantly fewer periodontal pathogens of red and orange complexes, as well as lower proinflammatory cytokine levels when compared to the Control group. Only the Test group showed an increase in the number of B. lactis HN019 DNA copies on subgingival biofilm at 30 and 90 days.Conclusion: The use of B. lactis HN019 as an adjunct to SRP promotes additional clinical, microbiological, and immunological benefits in the treatment of chronic periodontitis (NCT03408548).

Background: Micro‐computed tomography (micro‐CT) offers significant potential for identifying mineralized structures. However, three‐dimensional (3‐D) micro‐CT of alveolar bone has not been adapted readily for quantification. Moreover, conventional methods are not highly sensitive for analyzing bone loss or bone gain following periodontal disease or reconstructive therapy. The objective of this investigation was to develop a micro‐CT methodology for quantifying tooth‐supporting alveolar bone in 3‐D following experimental preclinical situations of periodontitis or reconstructive therapy.Methods: Experimental in vivo bone loss or regeneration situations were developed to validate the micro‐CT imaging techniques. Twenty mature Sprague‐Dawley rats were divided into two groups: bone loss (Porphyromonas gingivalis lipopolysaccharide‐mediated bone resorption) and regenerative therapy. Micro‐CT and software digitized specimens were reconstructed three‐dimensionally for linear and volumetric parameter assessment of alveolar bone (linear bone height, bone volume, bone volume fraction, bone mineral content, and bone mineral density). Intra‐ and interexaminer reproducibility and reliability were compared for methodology validation.Results: The results demonstrated high examiner reproducibility for linear and volumetric parameters with high intraclass correlation coefficient (ICC) and coefficient of variation (CV). The ICC showed that the methodology was highly reliable and reproducible (ICC >0.99; 9‐% confidence interval, 0.937 to 1.000; CV <1.5%), suggesting that 3‐D measurements may provide better alveolar bone analysis than conventional 2‐D methods.Conclusions: The developed methods allow for highly accurate and reproducible static measurements of tooth‐supporting alveolar bone following preclinical situations of bone destruction or regeneration. Future investigations should focus on using in vivo micro‐CT imaging for real‐time assessments of alveolar bone changes.

Background: The literature suggests that an alteration in glucose metabolism occurs as a result of antibacterial periodontal therapy. The objective of this study was to monitor the effect of non‐surgical periodontal therapy on glycemic control in patients with type 2 diabetes mellitus (DM).Methods: Thirty type 2 DM subjects with periodontitis were randomly divided into two groups. Group 1 (G1), 15 subjects, received one‐stage full‐mouth scaling and root planing (FMSRP) plus amoxicillin/clavulanic acid 875 mg; group 2 (G2), 15 patients, received only FMSRP. At baseline and after 3 months, the glycated hemoglobin (HbA_1c) values, fasting glucose, and clinical parameters (with computerized probing and individualized acrylic stents) were recorded. Following therapy, the subjects were enrolled in a 2‐week interval maintenance program for 3 months.Results: After treatment, both groups showed clinical improvements. A probing depth (PD) reduction of 0.8 ± 0.6 mm (P <0.05) occurred in G1 and 0.9 ± 0.4 mm in G2 (P <0.05), but there were no significant changes in attachment level. Treatment reduced the HbA1c values after the 3‐month observation period in both groups; however, the reduction in HbA_1c values for the G2 group was statistically significant, but not for the G1 group. The changes in fasting glucose levels were not significant for either group.Conclusions: Periodontal therapy improved glycemic control in patients with type 2 DM in both groups; however, the reduction in HbA1c values reached statistical significance only in the group receiving scaling and root planing alone. J Periodontol 2003;74:1361‐1367.

Background: Prevention of alveolar bone destruction is a clinical challenge in periodontal disease treatment. The receptor activator of nuclear factor‐kappa B ligand (RANKL) inhibitor osteoprotegerin (OPG) inhibits osteoclastogenesis and suppresses bone resorption.Methods: To study the effects of RANKL inhibition on alveolar bone loss, an experimental ligature‐induced model of periodontitis was used. A total of 32 rats were administered human OPG‐Fc fusion protein (10 mg/kg) or vehicle by subcutaneous delivery twice weekly for 6 weeks. Negative or positive controls received no treatment or disease through vehicle delivery, respectively. Biopsies were harvested after 3 and 6 weeks, and mandibulae were evaluated by microcomputed tomography (μCT) and histology. Serum levels of human OPG‐Fc and tartrate‐resistant acid phosphatase‐‐b (TRAP‐5b) were measured throughout the study by enzyme‐linked immunosorbent assay (ELISA). Statistical analyses included analysis of variance (ANOVA) and Tukey tests.Results: Human OPG‐Fc was detected in the sera of OPG‐Fc–treated animals by 3 days and throughout the study. Serum TRAP‐‐b was sharply decreased by OPG‐Fc treatment soon after OPG‐Fc delivery and remained low for the observation period. Significant preservation of alveolar bone volume was observed among OPG‐Fc–treated animals compared to the controls at weeks 3 and 6 (P <0.05). Descriptive histology revealed that OPG‐Fc significantly suppressed osteoclast surface area at the alveolar crest.Conclusion: Systemic delivery of OPG‐Fc inhibits alveolar bone resorption in experimental periodontitis, suggesting that RANKL inhibition may represent an important therapeutic strategy for the prevention of progressive alveolar bone loss.

Background: The treatment of aggressive periodontitis has always presented a challenge for clinicians, but there are no established protocols and guidelines for the efficient control of the disease.Methods: Ten patients with a clinical diagnosis of aggressive periodontitis were treated in a split‐mouth design study to either photodynamic therapy (PDT) using a laser source with a wavelength of 690 nm associated with a phenothiazine photosensitizer or scaling and root planing (SRP) with hand instruments. Clinical assessment of plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing depth (PD), gingival recession (GR), and relative clinical attachment level (RCAL) were made at baseline and 3 months after treatment with an automated periodontal probe.Results: Initially, the PI was 1.0 ± 0.5 in both groups. At the 3‐month evaluation, the plaque scores were reduced and remained low throughout the study. A significant reduction of GI and BOP occurred in both groups after 3 months (P <0.05). The mean PD decreased in the PDT group from 4.92 ± 1.61 mm at baseline to 3.49 ± 0.98 mm after 3 months (P <0.05) and in SRP group from 4.92 ± 1.14 mm at baseline to 3.98 ± 1.76 mm after 3 months (P <0.05). The mean RCAL decreased in the PDT group from 9.93 ± 2.10 mm at baseline to 8.74 ± 2.12 mm after 3 months (P <0.05), and in the SRP group, from 10.53 ± 2.30 mm at baseline to 9.01 ± 3.05 mm after 3 months.Conclusion: PDT and SRP showed similar clinical results in the non‐surgical treatment of aggressive periodontitis.