Review of Small Intestine Submucosa Matrix Technology
Review of Small Intestine Submucosa Matrix Technology
Wound healing normally proceeds in a 4-phase process of hemostasis, inflammation, proliferation, and remodeling. The remodeling phase can begin as early as day 8 but can last for months. These 4 phases and their physiological functions must occur in the appropriate sequence, timing, and duration for wound healing to occur properly in the minimal amount of time. In contrast to acute wounds, chronic wounds typically do not follow this organized process, but enter a state of pathologic inflammation or proliferation.
The most obvious feature of chronic wounds is the failure to reepithelialize, which is due to a failure of keratinocyte migration rather than proliferation. Failure of migration may occur due to the lack of a functional ECM, when fibronectin and collagen molecules needed for the cells to attach to the surface and migrate are deficient. The composition of the ECM must be accurate and precise for the epithelial cells to detach from the wound edge and to migrate across the ECM scaffold. The abnormal ECM delays reepithelialization, which is detrimental, as the likelihood of successful healing decreases the longer a wound remains open.
Additionally, chronic wounds frequently harbor other factors that may impede ECM function, such as high concentrations of ECM-degrading proteases, a misregulated rate of matrix repair and degradation, increased numbers of senescent fibroblasts, or altered cytokine expression and distribution. As a result, new ECM cannot be reorganized or becomes unresponsive to critical signals in the healing response and, ultimately, proper healing of the wound cannot take place.
As the ECM is essential for proper wound healing, strategies that correct ECM dysfunction may be beneficial in wound management.
Coordination of Wound Healing Process With ECM Activity
Wound healing normally proceeds in a 4-phase process of hemostasis, inflammation, proliferation, and remodeling. The remodeling phase can begin as early as day 8 but can last for months. These 4 phases and their physiological functions must occur in the appropriate sequence, timing, and duration for wound healing to occur properly in the minimal amount of time. In contrast to acute wounds, chronic wounds typically do not follow this organized process, but enter a state of pathologic inflammation or proliferation.
The most obvious feature of chronic wounds is the failure to reepithelialize, which is due to a failure of keratinocyte migration rather than proliferation. Failure of migration may occur due to the lack of a functional ECM, when fibronectin and collagen molecules needed for the cells to attach to the surface and migrate are deficient. The composition of the ECM must be accurate and precise for the epithelial cells to detach from the wound edge and to migrate across the ECM scaffold. The abnormal ECM delays reepithelialization, which is detrimental, as the likelihood of successful healing decreases the longer a wound remains open.
Additionally, chronic wounds frequently harbor other factors that may impede ECM function, such as high concentrations of ECM-degrading proteases, a misregulated rate of matrix repair and degradation, increased numbers of senescent fibroblasts, or altered cytokine expression and distribution. As a result, new ECM cannot be reorganized or becomes unresponsive to critical signals in the healing response and, ultimately, proper healing of the wound cannot take place.
As the ECM is essential for proper wound healing, strategies that correct ECM dysfunction may be beneficial in wound management.
