title: Laser-activated transforming growth factor-β1 induces human β-defensin 2: implications for laser therapies for periodontitis and peri-implantitis.
abstract: BACKGROUND
  There is increasing popularity of high-power lasers for surgical debridement and antimicrobial therapy in the management of peri-implantitis and periodontal therapy. Removal of the noxious foci would naturally promote tissue healing directly. However, there are also anecdotal reports of better healing around routine high-power laser procedures. The precise mechanisms mediating these effects remain to be fully elucidated. This work examines these low-dose laser bystander effects on oral human epithelial and fibroblasts, particularly focusing on the role of human β-defensin 2 (HBD-2 or DEFB4A), a potent factor capable of antimicrobial effects and promoting wound healing.
  
  
  METHODS
  Laser treatments were performed using a near-infrared laser (810 nm diode) at low doses. Normal human oral keratinocytes and fibroblast cells were used and HBD-2 mRNA and protein expression was assessed with real time polymerase chain reaction, western blotting and immunostaining. Role of transforming growth factor (TGF)-β1 signaling in this process was dissected using pathway-specific small molecule inhibitors.
  
  
  RESULTS
  We observed laser treatments robustly induced HBD-2 expression in an oral fibroblast cell line compared to a keratinocyte cell line. Low-dose laser treatments results in activation of the TGF-β1 pathway that mediated HBD-2 expression. The two arms of TGF-β1 signaling, Smad and non-Smad are involved in laser-mediated HBD-2 expression.
  
  
  CONCLUSIONS
  Laser-activated TGF-β1 signaling and induced expression of HBD-2, both of which are individually capable of promoting healing in tissues adjacent to high-power surgical laser applications. Moreover, the use of low-dose laser therapy itself can provide additional therapeutic benefits for effective clinical management of periodontal or peri-implant disease.
authors.affiliation: Cell Regulation and Control Unit, NIDCR, National Institutes of Health, Bethesda, MD, USA.
authors.forename: E
authors.initials: E
authors.lastname: Tang
authors.affiliation: Cell Regulation and Control Unit, NIDCR, National Institutes of Health, Bethesda, MD, USA.
authors.forename: I
authors.initials: I
authors.lastname: Khan
authors.affiliation: Restorative and Implant Dentistry, School of Dental Medicine, University at Buffalo, Buffalo, NY, USA.
authors.forename: S
authors.initials: S
authors.lastname: Andreana
authors.affiliation: Cell Regulation and Control Unit, NIDCR, National Institutes of Health, Bethesda, MD, USA.|Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, NY, USA.
authors.forename: P R
authors.initials: PR
authors.lastname: Arany
mesh_terms: D015153:Blotting, Western; D005347:Fibroblasts / Q000378:metabolism / Q000528:radiation effects; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism / Q000528:radiation effects; D028022:Low-Level Light Therapy / Q000379:methods; D057873:Peri-Implantitis / Q000532:radiotherapy*; D010518:Periodontitis / Q000532:radiotherapy*; D060888:Real-Time Polymerase Chain Reaction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*; D023083:beta-Defensins / Q000378:metabolism*
chemical_list: C106641:DEFB4A protein, human; D053773:Transforming Growth Factor beta1; D023083:beta-Defensins
keywords: defensins; lasers; low-level light/laser therapy; peri-implantitis; periodontitis; photobiomodulation therapy