Cicatrización en piel fotoenvejecida: implicaciones en cirugía estética facial del paciente geriátrico.

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Bibliographic Details
Title:	Cicatrización en piel fotoenvejecida: implicaciones en cirugía estética facial del paciente geriátrico.
Alternate Title:	Wound healing in photoaged skin: implications for facial aesthetic surgery in geriatric patients.
Authors:	Sierra-Duque, Miguel A.¹ miguelsierra1998@gmail.com, Pichardo-Arzeno, Natalia A.², Gutierrez-Galvis, Ariel E.³
Source:	Revista de Cirugia. 2026, Vol. 78 Issue 4, p411-419. 9p.
Abstract (English):	Population aging has led to a six-fold increase in cosmetic procedures in geriatric patients. Photoaging, resulting from chronic ultraviolet radiation exposure, represents approximately 80% of facial aging and generates a qualitatively distinct biological substrate characterized by massive extracellular matrix degradation, fibroblast dysfunction, and chronic proinflammatory state (inflammaging) that compromises surgical wound healing. This narrative review synthesizes current concepts on the pathophysiology of wound healing in photoaged skin and its implications for facial aesthetic surgery in geriatric patients. Photoaging produces solar elastosis, dermoepidermal junction flattening, and type I collagen fragmentation, reducing tissue tensile strength to maximum 80% of uninjured skin. Molecular mechanisms involve ROS-mediated MAPK cascade activation, AP-1 and NF-κB stimulation inducing matrix metalloproteinases (MMP-1, MMP-3, MMP-9), and TGF-β pathway inhibition blocking type I procollagen synthesis. These alterations necessitate specific surgical modifications: SMAS approach in severe photoaging to transfer tensional load to deep planes, conservative undermining preserving subdermal vasculature, and adapted suture removal timing. Photoaged skin behaves as an organ blocked in perpetual damage phase with a microenvironment favoring protein degradation over synthesis. Surgical success depends on understanding these pathophysiological mechanisms and adapting technique to available biological substrate, prioritizing safety through individualized assessment based on physiological age. [ABSTRACT FROM AUTHOR]
Abstract (Spanish):	El envejecimiento poblacional ha incrementado seis veces los procedimientos cosméticos en pacientes geriátricos. El fotoenvejecimiento, resultado de exposición crónica a radiación ultravioleta, representa aproximadamente el 80% del envejecimiento facial y genera un sustrato biológico cualitativamente distinto caracterizado por degradación masiva de matriz extracelular, disfunción fibroblástica y estado proinflamatorio crónico (inflammaging) que compromete la cicatrización quirúrgica. Esta revisión narrativa sintetiza conceptos actuales sobre fisiopatología de cicatrización en piel fotoenvejecida y sus implicaciones en cirugía estética facial geriátrica. El fotoenvejecimiento produce elastosis solar, aplanamiento de la unión dermoepidérmica y fragmentación de colágeno tipo I, reduciendo la resistencia tensil tisular a máximo 80% de piel no lesionada. Los mecanismos moleculares involucran activación de cascada MAPK mediada por ROS, estimulación de AP-1 y NF-κB, induciendo metaloproteinasas de matriz (MMP-1, MMP-3, MMP-9), e inhibición de vía TGF-β bloqueando síntesis de procolágeno tipo I. Estas alteraciones condicionan modificaciones quirúrgicas específicas: abordaje sistema músculoaponeurótico superficial (SMAS) en fotodaño severo para transferir carga tensional a planos profundos, socavamiento conservador preservando vascularización subdérmica, y tiempos de retiro de suturas adaptados. La piel fotoenvejecida se comporta como órgano bloqueado en fase de daño perpetuo con microambiente que favorece degradación proteica sobre síntesis. El éxito quirúrgico depende de comprender estos mecanismos fisiopatológicos y adaptar la técnica al sustrato biológico disponible, priorizando seguridad mediante evaluación individualizada basada en edad fisiológica. [ABSTRACT FROM AUTHOR]
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Database:	MedicLatina

Description
Abstract:	Population aging has led to a six-fold increase in cosmetic procedures in geriatric patients. Photoaging, resulting from chronic ultraviolet radiation exposure, represents approximately 80% of facial aging and generates a qualitatively distinct biological substrate characterized by massive extracellular matrix degradation, fibroblast dysfunction, and chronic proinflammatory state (inflammaging) that compromises surgical wound healing. This narrative review synthesizes current concepts on the pathophysiology of wound healing in photoaged skin and its implications for facial aesthetic surgery in geriatric patients. Photoaging produces solar elastosis, dermoepidermal junction flattening, and type I collagen fragmentation, reducing tissue tensile strength to maximum 80% of uninjured skin. Molecular mechanisms involve ROS-mediated MAPK cascade activation, AP-1 and NF-κB stimulation inducing matrix metalloproteinases (MMP-1, MMP-3, MMP-9), and TGF-β pathway inhibition blocking type I procollagen synthesis. These alterations necessitate specific surgical modifications: SMAS approach in severe photoaging to transfer tensional load to deep planes, conservative undermining preserving subdermal vasculature, and adapted suture removal timing. Photoaged skin behaves as an organ blocked in perpetual damage phase with a microenvironment favoring protein degradation over synthesis. Surgical success depends on understanding these pathophysiological mechanisms and adapting technique to available biological substrate, prioritizing safety through individualized assessment based on physiological age. [ABSTRACT FROM AUTHOR]
ISSN:	24524557
DOI:	10.35687/s2452-454920260043053