Description
Presentation Blocks: 03-22-2018 - Thursday - 03:45 PM - 05:00 PM

Title: Characterizing the Effect of Periostin Deletion on Palatal Wound Healing

Authors:

Georgia Nikoloudaki (Presenter)
Western University

Paige Snider, Indiana University School of Medicine
Olga Simmons, Indiana University School of Medicine
Simon Conway, Indiana University School of Medicine
Douglas Hamilton, Western University

Abstract:

Objectives: In the palate wound contraction and scarring are the two main processes in wound healing responsible for the growth disturbances after cleft palate reconstruction surgery. Periostin is a matricellular protein which is highly expressed in fibrotic scars of human skin and plays a pivotal role in cutaneous wound repair, by modulating wound contraction and myofibroblasts differentiation. Objective: To assess the effect of periostin deletion on palatal wound healing.

Methods: 1.5mm full-thickness excisional wounds were created on the hard palate of periostin-knockout (KO) and wild-type (WT) mice. Wounds were photographed and their size was assessed using ImageJ software immediately after wounding from day3 to 15 post-wounding. Wounded tissues used for histological analysis (n=5), in situ hybridization (ISH) (n=5) and Reverse-Transcription-quantitative-Polymerase-Chain-Reaction (n=7) assessing several Extracellular Matrix (ECM) components, such as fibronectin, βigh3, αSMA/acta2, and the presence of fibroblasts and inflammatory cells.

Results: In WT mice, periostin was induced 6 days after wounding, peaking at day12. Genetic deletion of periostin significantly reduced wound closure rates compared to WT mice. This alteration corresponds with the onset in WT animals, as well as with the peak of βigh3 and acta2 expression. βigh3 is upregulated during palatal healing but its expression is reduced in KO wounds. Absence of periostin resulted in reduction in the mRNA levels of pivotal genes in wound repair, such as αSMA/acta2, fibronectin and βigh3, and impaired recruitment of fibroblasts and inflammatory cells, as visualized by immunofluorescent staining for fibroblast specific factor-1 and macrophages markers Arginase-1 and iNOS.

Conclusions: By elucidating the role of periostin in palatal wound healing the findings of our study further contribute to the better understanding of the underlying healing mechanisms and could provide new insights that can be used towards the development of novel approaches to accelerate and enhance the healing process after dental and maxillofacial surgical procedures.

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