title: Waveform modulation of negative-pressure wound therapy in the murine model.
abstract: BACKGROUND
  Negative-pressure wound therapy applied with a porous foam interface has been shown to accelerate granulation-tissue formation when a cyclic application mode of suction is applied, but the optimal waveform has not been determined. The authors hypothesized that changes in the suction waveform applied to wounds would modulate the biological response of granulation tissue formation.
  
  
  METHODS
  A vacuum-assisted closure device (Kinetic Concepts, Inc., San Antonio, Texas) was applied to full-thickness wounds in 48 male diabetic mice (C57BL/KsJ-Lepr db), which were treated with six different waveforms: square waveforms of 125 mmHg of suction for 2 minutes, alternating with 50 mmHg of suction for 2 minutes, 5 minutes, or 10 minutes; triangular waveform with a 7-minute period oscillating between 50 and 125 mmHg; and static suction at 125 mmHg or static suction at 0 mmHg (occlusive dressing). Wounds were quantitatively evaluated for granulation tissue thickness as well as the number of proliferating cells and the number of blood vessels of the newly formed granulation tissue.
  
  
  RESULTS
  At 7 days, the continuous and triangular waveforms induced the thickest granulation tissue, with high rates of cellular proliferation and blood vessel counts compared with square wave and occlusive dressing control wounds. Decreasing square waveform frequency significantly increased granulation tissue thickness, cellular proliferation, and blood vessel counts.
  
  
  CONCLUSIONS
  Waveform modulation has a significant effect on granulation tissue formation, angiogenesis, and cellular proliferation in excisional wounds in diabetic mice. The rapid change in pressure seen in our square wave model may be detrimental to granulation tissue formation.
authors: Boston, Mass.; and Geneva, Switzerland From the Division of Plastic Surgery, Brigham and Women's Hospital, Harvard Medical School, and the Division of Plastic Surgery, Hopitaux Universitaires de Geneve.
authors: Pouya
authors: P
authors: Dastouri
authors: Douglas L
authors: DL
authors: Helm
authors: Saja S
authors: SS
authors: Scherer
authors: Giorgio
authors: G
authors: Pietramaggiori
authors: George
authors: G
authors: Younan
authors: Dennis P
authors: DP
authors: Orgill
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D006097:Granulation Tissue / Q000473:pathology / Q000502:physiology; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D054843:Negative-Pressure Wound Therapy / Q000379:methods*; D018919:Neovascularization, Physiologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D012867:Skin / Q000098:blood supply / Q000293:injuries*; D013396:Suction / Q000379:methods; D014945:Wound Healing / Q000502:physiology*
chemical_list: D019394:Ki-67 Antigen; D019408:Platelet Endothelial Cell Adhesion Molecule-1