Abstract
The purpose of this paper is to compare and contrast the discrete biology differentiating fetal wound repair from its adult counterpart. Integumentary wound healing in mammalian fetuses is essentially different from wound healing in adult skin. Adult (postnatal) skin wound healing is a complex and well-orchestrated process spurred by attendant inflammation that leads to wound closure with scar formation. In contrast, fetal wound repair occurs with minimal inflammation, faster re-epithelialization, and without the accumulation of scar. Although research into scarless healing began decades ago, the critical molecular mechanisms driving the process of regenerative fetal healing remain uncertain. Understanding the molecular and cellular events during regenerative healing may provide clues that one day enable us to modulate adult wound healing and consequently reduce scarring.
Highlights
In adult mammalian organisms, injury to cutaneous tissue with disruption of normal skin architecture is repaired by means of an inflammatory and fibrotic response that leads to accumulation of scar [1]
Because early- to mid-gestational fetal wound healing occurs with evident restoration of normal skin architecture and no significant scar deposition, it has been termed “regenerative,” and has been taken as a model by which we may attempt to engineer the same process in adults
Other extracellular matrix (ECM) molecules differentially expressed in developing fetal skin and wounds include decorin, a proteoglycan implicated in regulation of TGF-β bioactivity, which has been shown to increase during the ontogenic transition from scarless fetal healing to adult wound healing, but which is decreased by wounding during the scarless healing period [60]
Summary
In adult (postnatal) mammalian organisms, injury to cutaneous tissue with disruption of normal skin architecture is repaired by means of an inflammatory and fibrotic response that leads to accumulation of scar [1]. Scar contractures following burn injury are well known to progress to microstomia, nasal stenosis, lip or eyelid ectropion if severe enough They can lead to restriction of neck movement and permanent mouth opening [2,3,4]. The scarless character of fetal wound repair persists until roughly the middle of the third trimester of intrauterine gestation, at which point a transition to the adult, scar-forming pattern of wound repair occurs [13,14,15]. Because early- to mid-gestational fetal wound healing occurs with evident restoration of normal skin architecture and no significant scar deposition, it has been termed “regenerative,” and has been taken as a model by which we may attempt to engineer the same process in adults. It becomes important to understand at the cellular and molecular level the distinctions between these two physiologies, in the hopes that an understanding of fetal biology may one day enable its recapitulation in the adult
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