Host defense peptides are immediate responders of the innate immunity that express antimicrobial, immunoregulatory, and wound-healing activities. Neutrophils are a major source for oral host defense peptides, and phagocytosis by neutrophils is a major mechanism for bacterial clearance in the gingival tissue. Dysfunction of or reduction in the numbers of neutrophils or deficiency in the LL-37 host defense peptide was each previously linked with proliferation of oral Aggregatibacter actinomycetemcomitans which resulted in an aggressive periodontal disease. Surprisingly, A. actinomycetemcomitans shows resistance to high concentrations of LL-37. In this study, we demonstrated that submicrocidal concentrations of LL-37 inhibit biofilm formation by A. actinomycetemcomitans and act as opsonins and agglutinins that greatly enhance its clearance by neutrophils and macrophages. Improved uptake of A. actinomycetemcomitans by neutrophils was mediated by their opsonization with LL-37. Enhanced phagocytosis and killing of A. actinomycetemcomitans by murine macrophage-like RAW 264.7 cells were dependent on their preagglutination by LL-37. Although A. actinomycetemcomitans is resistant to the bactericidal effect of LL-37, our results offer a rationale for the epidemiological association between LL-37 deficiency and the expansion of oral A. actinomycetemcomitans and indicate a possible therapeutic use of cationic peptides for host defense.

Results of this study suggest potential benefit in using photometric analysis to assess gingival changes after therapy.

Aims The study's aim was to assess the clinical outcome 6 and 12 months after a nonsurgical treatment of peri‐implantitis per se or in conjunction with a combination of local antiseptic and anti‐inflammatory treatment. Materials and methods Included were 69 patients with periodontitis, with 106 implants, diagnosed with peri‐implantitis. Peri‐implantitis was defined as radiographic bone loss ≥3 mm, probing depth (PD) ≥ 6 mm, with bleeding on probing. Group M peri‐implantitis was treated with ultrasonic debridement and soft tissue curettage. Group P had additional implant surface treatment with rotatory hand piece composed of chitosan bristle, soft tissue curettage combined with application of 0.95% hypochlorite and 1 mg minocycline HCl. Results After 6 months, both groups demonstrated significant reduction of mean plaque index, PD, and clinical attachment level (0.71 ± 0.57, 0.81 ± 0.55; 4.77 ± 0.73 mm, 4.42 ± 0.5 mm; 5.03 ± 0.86 mm, 5.13 ± 0.73 mm; respectively) and bleeding on probing. After 6 and 12 months, group P showed significantly better PD results compared to group M. The bleeding was significantly less in group P after 12 months (15.3% ± 6.2, 25.1% ± 8.2, respectively). Conclusions Adjunctive treatment with local antiseptic and anti‐inflammatories during mechanical phase was positively associated with inflammation reduction and connective tissue reattachment.

The results of this study demonstrating higher vitality and proliferation of MSCs seeded onto BB. Furthermore, following ridge preservation, higher percentage of new bone and lower residual scaffold were found in the BB compared with BO. This enhanced regenerative response might be the result of an enhancement of metabolic activity in cells attached to it. Further research will be needed to understand the precise mechanism.