Abstract
Aim of the study: The aim was to evaluate the effects of two LED devices, TL-01 and TL-03 in photodynamic therapy (PDT), on Enterococcus faecalis and on human gingival fibroblasts (HGFs). TL-01, characterized by a single emitter, irradiates one periodontal site at a time, whereas the multi-led device (TL-03) irradiates all vestibular sites of a single arch at a time. Methods: E. faecalis bacterial suspensions and HGFs were incubated for 45 min with Aladent gel (ALAD) containing 5-aminolevulinic acid and then exposed to LED devices (ALAD-PDT), having different distance and timing of irradiation (TL-01 N (0.5 mm, for 7 min), TL-03 N (0.5 mm, 15 min) and TL-03 F (30.0 mm, 15 min)). For bacterial suspension, the colony forming units and the live/dead staining were evaluated after 24 h, while the protoporphyrin IX (PpIX) content was monitored in all phases of the experimentation. For HGFs, the cell viability, proliferation, cell morphology, and adhesion were evaluated at 24 h. Results: Both TL-01 and TL-03 showed a significant reduction of bacterial load. The photoinactivation was inversely proportional to the PpIX accumulation. TL-01 and TL-03 promoted proliferation and adhesion of HGFs. Conclusions: Both tested devices for ALAD-PDT were equally effective in significantly reducing Enterococcus faecalis growth and in promoting HGFs proliferation and adhesion, in vitro.
Highlights
A significantly higher antibacterial effect was found in TL-01 N vs. TL-03 F (** p = 0.025)
No statistically significant difference was recorded among test groups TL-01 N, TL-03 N, and TL-03 F
Current treatments of periodontitis and peri-implantitis have the main objective of Current treatments of periodontitis and peri-implantitis have the main objective of bacterial and biofilm removal by means of chemical/physical disinfection and mechanical bacterial and biofilm removal byand means of chemical/physical andismechanical decontamination of periodontal peri-implant sites
Summary
Periodontitis and peri-implantitis are two chronic inflammatory pathologies that promote the irreversible break down of the bone and soft tissues that surround teeth and implants. Common etiology of both diseases is the bacterial dysbiosis that promotes tissue destruction, directly because of the presence of proteolytic bacteria and indirectly by triggering the host’s inflammatory response. In both diseases, the chances to treat the contaminated sites successfully are increased with an early diagnosis and intervention. All available treatments are based on mechanical, chemical, and physical methods that aim to disrupt the bacterial biofilm, promoting the root/implant decontamination [1,2]
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