Abstract
In the past year, three papers have been published exploring the role of the matricellular protein periostin in excisional skin repair. These papers all show a delay in wound closure and the kinetics of this delay are strikingly similar across the three reports. The similarities between these papers end, however, when each investigates the mechanism through which periostin influences skin repair. Three proposed mechanisms have been identified: (1) myofibroblast differentiation, (2) keratinocyte proliferation and (3) fibroblast proliferation and migration. The aim of this commentary is to compare and contrast the three studies performed to date in an attempt to decipher the role of periostin in the repair of full-thickness skin wounds.