Abstract
Wound healing is a multistep process that concludes with scar formation. A common clinical observation is that oral wounds exhibit privileged healing compared to extra-oral wounds. Current data demonstrates reduced inflammation and more rapid reepithelialization of oral wounds suggesting that reduced inflammation is vital to privileged repair. To examine the initiation of inflammation, the present study examines IL-1α, IL-β and TNFα production by oral versus cutaneous keratinocytes and compares mast cell infiltration in oral versus cutaneous wounds. Two 1 mm diameter excisional wounds were placed on the lateral tongue or dorsal skin of anesthetized BALB/c mice. At 3, 6, 12, and 24 hours after injury, wound tissue was harvested for analysis. Cytokine expression levels were measured by semiquantitative RT-PCR normalized to actin. At every time point, levels of IL-1α, IL-β and TNFα mRNA were less in oral than dermal wounds. When analyzed by ELISA, IL-1 protein levels peaked at 6 hours in both oral and cutaneous wounds, yet the levels were lower in oral wounds. Mast cell infiltration was measured by counting toluidine blue positive cells in fixed wound sections. The number of mast cells/mm2 was decreased overall in oral mucosal wounds. These findings suggest that a decreased early inflammatory response to injury may be responsible for the privileged repair of oral mucosa.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.