title: Antimicrobial photodynamic therapy may promote periodontal healing through multiple mechanisms.
abstract: BACKGROUND
  Antimicrobial photodynamic therapy (aPDT) as an adjunctive treatment in addition to scaling and root planing for the treatment of periodontitis has been shown to be clinically useful. Its beneficial effect is reported to be due to its potent bactericidal activity. However, aPDT treatment has the potential to inactivate bacterial and host factors that contribute to disease. In this report, we demonstrate that aPDT treatment can simultaneously kill Porphyromonas gingivalis and inactivate its virulence-associated protease. It also inactivates host destructive cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1 beta.
  
  
  METHODS
  We developed a 96-well-based bacterial killing and protease inactivation assay that determined aPDT bactericidal and protease inactivation from the same sample. A cytokine inactivation assay that measured E-selectin expression in response to TNF-alpha and IL-1 beta was developed to measure the ability of aPDT to inactivate cytokine function.
  
  
  RESULTS
  A single aPDT treatment in vitro potently inactivated protease activity and resulted in a 4-log(10) reduction in the viability of P. gingivalis. Dose and time-of-exposure experiments revealed that protease inactivation occurred at lower concentrations of photosensitizer and less time of light exposure. Also, aPDT treatment potently and functionally inactivated IL-1 beta and TNF-alpha.
  
  
  CONCLUSIONS
  aPDT treatment may augment periodontal treatment by increasing bacterial killing, inactivating bacterial virulence factors, and inactivating host cytokines that impair periodontal restoration. Therefore, aPDT treatment may provide a more favorable healing environment.
authors.affiliation: Department of Periodontics, University of Washington, Seattle, WA 98195-7444, USA.
authors.forename: Pam
authors.initials: P
authors.lastname: Braham
authors.forename: Caroline
authors.initials: C
authors.lastname: Herron
authors.forename: Cale
authors.initials: C
authors.lastname: Street
authors.forename: Richard
authors.initials: R
authors.lastname: Darveau
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000890:Anti-Infective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002478:Cells, Cultured; D015169:Colony Count, Microbial; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000276:immunology; D005456:Fluorescent Dyes; D006801:Humans; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors; D054023:Lasers, Semiconductor / Q000627:therapeutic use; D008751:Methylene Blue / Q000008:administration & dosage / Q000494:pharmacology; D008911:Minocycline / Q000494:pharmacology; D010778:Photochemotherapy / Q000379:methods*; D017319:Photosensitizing Agents / Q000008:administration & dosage / Q000494:pharmacology*; D016966:Porphyromonas gingivalis / Q000187:drug effects* / Q000201:enzymology; D011480:Protease Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D037521:Virulence Factors / Q000037:antagonists & inhibitors
chemical_list: D000900:Anti-Bacterial Agents; D000890:Anti-Infective Agents; D019040:E-Selectin; D005456:Fluorescent Dyes; D053583:Interleukin-1beta; D017319:Photosensitizing Agents; D011480:Protease Inhibitors; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors; D008911:Minocycline; D008751:Methylene Blue