Hypertrophic scar therapy : pressure-induced remodelling and its determinants
Hypertrophic scars are cosmetically unattractive products of abnormal wound healing and, if they occur over flexor aspects of joints, considerable functional impairment often results. Pressure, as a therapy for hypertrophic- scarring has considerable attraction since it is effective and nonsurgical. Previous reports of this therapy have not quantified magnitudes or durations of pressure required to induce remodelling. Correlation of these parameters is necessary to define guidelines to optimise pressure therapy. Measurement of pressure applied to hypertrophic scars by garments with elastic properties was achieved using a monitoring system based on a thin (0.2mm) flat (1cm²) capacitive transducer. Pressures of 15 - 40mnmHg produced, in general, accelerated scar remodelling with superior cosmesis resulting from higher pressures. Clinical studies suggested that 6-9 months pressure is sufficient to induce permanent remodelling, although studies of rates of collagen biosynthesis in p ressure-treated and untreated scars indicated 9- 12 months pressure was necessary. Two types of pressure applying garments, Tubigrip and Lycra, were studied and compared. Tubigrip garments demonstrated superior elastic properties for maintaining pressure with-time. Investigations of two hypotheses for pressure-induced remodelling were performed. A first hypothesis that pressure induces ischaemia in scars, implying remodelling by autolysis, was investigated with vital microscopy using a hamster cheek pouch model. Pressure magnitudes which induced scar remodelling did not disturb the microcirculation sufficiently to cause permanent damage, therefore this hypothesis was thought unlikely to be correct. A second hypothesis that pressure-induced vascular changes produce scar resorption via a collagen-based mechanism was investigated using a radioactive isotope assay of the rate of collagen biosynthesis. The time for which the rate of collagen biosynthesis approached normal scar levels was reduced by half in pressure-treated compared to untreated scars. A two-phase scar remodelling theory was introduced comprising a pressure-magnitude dependent phase followed by a time-dependent phase. The second hypothesis was thought to be partially correct and the complexity of the pressure-induced remodelling mechanism is discussed.