Treatment Considerations for Keloids and Hypertropic Scars: A Systematic Review
Location
Philadelphia, PA
Start Date
11-5-2022 1:00 PM
End Date
11-5-2022 4:00 PM
Description
BACKGROUND: Scar formation is an important component of overall wound health. Defects in scar formation can lead to the accumulation of excess extracellular matrix within the tissue. The tissue repair mechanism utilizes a conglomerate of complex biological processes including cytokine activation, fibroblast and myofibroblast proliferation as well as the utilization of other cell molecules to achieve the ultimate aim of forming a healthy scar. Defects in this process lead to a phenomenon called pathological scarring. Pathological scarring can lead to chronic non-healing wounds most often seen in practice as keloids or other forms of hypertrophic scars. Investigation into the pathogenesis of pathological scars has shown evidence for an interplay between wound depth, skin tension and underlying systemic processes. There are currently two possible systemic mechanisms for the formation of hypertrophic scars and keloids: decreased presence of myofibroblasts and the effect of inflammation. On a relative scale, mechanisms underlying keloids have been described as inflammatory while the mechanism underlying hypertrophic scars have been described as mildly inflammatory. Among the numerous cytokines involved in cell homeostasis, persistent activation of IL-4 and IL-13 have been majorly implicated in the pathogenesis of hypertrophic scars. These cytokines are profibrotic and may trigger the action of TGFB to target connective tissue growth factor, α-SMA, collagens, matrix metalloproteinases, and tissue inhibitors of metalloproteinases, leading to deposition of excess collagen in the extracellular matrix.
METHODS: A literature review was performed from 2017 to 2022 using the databases: PubMed database of the National Center of Biotechnology Information, MEDLINE, Google Scholar, and Cochrane database. Articles were reviewed for treatment regimen, patient demographics, follow up, recurrence, and complications.
RESULTS: Over 15000 results were pooled from the original database searches. Articles were compared against inclusion and exclusion criteria narrow down accordingly.
CONCLUSIONS: The treatments for keloids and hypertrophic scarring have been stable and predictable over the past couple of years. There is room for more exploration and improvement and ultimately better patient outcomes in this condition.
Embargo Period
5-26-2022
Treatment Considerations for Keloids and Hypertropic Scars: A Systematic Review
Philadelphia, PA
BACKGROUND: Scar formation is an important component of overall wound health. Defects in scar formation can lead to the accumulation of excess extracellular matrix within the tissue. The tissue repair mechanism utilizes a conglomerate of complex biological processes including cytokine activation, fibroblast and myofibroblast proliferation as well as the utilization of other cell molecules to achieve the ultimate aim of forming a healthy scar. Defects in this process lead to a phenomenon called pathological scarring. Pathological scarring can lead to chronic non-healing wounds most often seen in practice as keloids or other forms of hypertrophic scars. Investigation into the pathogenesis of pathological scars has shown evidence for an interplay between wound depth, skin tension and underlying systemic processes. There are currently two possible systemic mechanisms for the formation of hypertrophic scars and keloids: decreased presence of myofibroblasts and the effect of inflammation. On a relative scale, mechanisms underlying keloids have been described as inflammatory while the mechanism underlying hypertrophic scars have been described as mildly inflammatory. Among the numerous cytokines involved in cell homeostasis, persistent activation of IL-4 and IL-13 have been majorly implicated in the pathogenesis of hypertrophic scars. These cytokines are profibrotic and may trigger the action of TGFB to target connective tissue growth factor, α-SMA, collagens, matrix metalloproteinases, and tissue inhibitors of metalloproteinases, leading to deposition of excess collagen in the extracellular matrix.
METHODS: A literature review was performed from 2017 to 2022 using the databases: PubMed database of the National Center of Biotechnology Information, MEDLINE, Google Scholar, and Cochrane database. Articles were reviewed for treatment regimen, patient demographics, follow up, recurrence, and complications.
RESULTS: Over 15000 results were pooled from the original database searches. Articles were compared against inclusion and exclusion criteria narrow down accordingly.
CONCLUSIONS: The treatments for keloids and hypertrophic scarring have been stable and predictable over the past couple of years. There is room for more exploration and improvement and ultimately better patient outcomes in this condition.