title: Short periodic applications of the vacuum-assisted closure device cause an extended tissue response in the diabetic mouse model.
abstract: BACKGROUND
  The vacuum-assisted closure device is a widely used mechanical modulator of wound healing; however, the optimal time kinetics of application have not been determined. The objective of the study was to optimize the kinetics of vacuum-assisted closure application.
  
  
  METHODS
  Full-thickness wounds in seven diabetic mice per study group were treated with either an occlusive dressing alone, the vacuum-assisted closure device for 6 or 12 hours, or the vacuum-assisted closure device periodically for 4 hours every other day or continuously for 7 days. Wound closure and tissue response were evaluated by macroscopic, histologic, and immunohistochemical analyses on day 7.
  
  
  RESULTS
  Wound closure was significantly faster after short initial vacuum-assisted closure (6-hour and 12-hour groups) when compared with continuous treatment. Increased granulation tissue formation was seen in the 12-hour group (2.4-fold increase) and in those treated periodically for 4 hours every other day (3.2-fold increase) compared with the dressing-alone controls. Significant stimulation of cell proliferation was seen after all vacuum-assisted closure patterns (3.6- to 5.3-fold increase), whereas angiogenesis was augmented only after the device was applied for either three times for 4 hours (4.3-fold) or continuously (4.7-fold) when compared with dressing-treated wounds. Treatment three times for 4 hours showed a superior angiogenic effect also when compared with short initial applications (6-hour and 12-hour groups).
  
  
  CONCLUSIONS
  Short vacuum-assisted closure treatment induced an extended biological response in the wound. A total of 12 hours of periodically applied vacuum-assisted closure reached a similar wound tissue response as continuously applied vacuum-assisted closure for 7 days. These findings suggest new clinical approaches for mechanical wound-healing devices.
authors.affiliation: Boston, Mass.; and Geneva, Switzerland From the Division of Plastic Surgery, Brigham and Women's Hospital, Harvard Medical School, and the Department of Surgery, University Hospital of Geneva.
authors.forename: Sandra Saja
authors.initials: SS
authors.lastname: Scherer
authors.forename: Giorgio
authors.initials: G
authors.lastname: Pietramaggiori
authors.forename: Jasmine C
authors.initials: JC
authors.lastname: Mathews
authors.forename: Dennis P
authors.initials: DP
authors.lastname: Orgill
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D049109:Cell Proliferation; D003921:Diabetes Mellitus, Experimental; D006097:Granulation Tissue / Q000378:metabolism; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D054843:Negative-Pressure Wound Therapy / Q000295:instrumentation; D018919:Neovascularization, Physiologic; D009779:Occlusive Dressings; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology
chemical_list: D015415:Biomarkers; D019394:Ki-67 Antigen; D019010:Vascular Cell Adhesion Molecule-1