The panniculus carnosus layer exhibits poor regeneration and deformed geometry following pressure injury: Implications for biomechanical protection

Abstract

Background Human pressure injuries (PI) exhibit delayed healing and are classified as chronic wounds, and muscle damage increases the chronicity and severity of PIs. Pressure or load redistribution is typically the gold standard for preventing PIs in bedridden patients or those with limited mobility. The panniculus carnosus (PC) is a thin muscle in the cutaneous layer. Although evidence of the PC layer in multiple anatomical locations such as the heel has been reported, with high inter-individual variability, the PC is traditionally considered to be vestigial in humans. In this work, we investigate the role of the PC layer in biomechanics and load distribution, and ask how the PC regenerates after a pressure-induced injury. Methods To examine the biomechanical function of the PC, a finite element analysis was performed on a three-dimensional model of the human heel, comparing the change in soft tissue deformation during supine weight-bearing, with and without the PC. To assess PC regeneration, a mouse with inducible confetti-colored fluorescent satellite cells (muscle stem cells) was developed by crossing the Brainbow2.1 mouse with a conditional Pax7CreER mouse. The resulting mouse, upon tamoxifen induction, provides fluorescent colors for lineage tracing of muscle regeneration in vivo. Muscle PIs were created in these mice by applying a pair of 12mm magnets to the dorsal skinfold and PC muscle, in two intervals of 12 hours. Results In computational simulations of heel tissue, we find extensive overall displacement of soft tissues around the bony prominence during weight bearing, which was greatly decreased in the presence of the PC layer. Additionally, the presence of PC decreased the volume of tissue experiencing high strain and stress. When the PCs of mice were injured by pressure, tissue histology and fluorescent tracing of endogenous stem cells showed that the PC failed to regenerate across the distances necessary for this two-dimensional sheet-like structure. Even at 90 days following injury, a hole remained in the PC, while the other tissue layers regenerated successfully. Furthermore, multiple split and deformed myofibers were observed in the newly regenerated muscle at the wound edge. Conclusions Our work shows that the PC layer is sufficient to redistribute load around the posterior of the heel bone, reducing the volume of displaced tissue and the volume of soft tissue experiencing high strain and stress. Moreover, upon pressure injury, the PC layer is highly susceptible to poor regeneration and abnormalities in the geometry of the resulting fibers. Split or deformed fibers are weaker and more susceptible to repeated injury and this could be an underlying pathology of recurrent human PIs. We conclude that the PC might play an important protective function in pressure redistribution and that the PC regenerates poorly after PI. This absence or deformation of PC could be a potential risk factor for PI recurrence.