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Published on: May 31, 2018
Influence of pressure on mandibular angiosomes: What implications for decellularization?
Corentin Serra1, Romain Monchaux2, Benjamin Salmon3
1Laboratory of Mechanics and Interfaces, ENSTA, Institut Polytechnique de Paris, 91120, Palaiseau, France; Faculté de Santé, Université Paris Cité, 75005, Paris, France; Maxillofacial and Plastic Surgery, Necker Children Hospital, APHP, 75015, Paris, France.
Abstract:
The vascularization of bone still holds several unknowns, crucial to future developments in reconstructive surgery: both for bone transplantation and decellularized allograft. This study introduces a novel method to analyze pressure-dependent vascular territories in the human mandible, with direct implications for the optimization of decellularization by perfusion protocols. Traditional anatomical approaches have struggled to delineate perfusion territories due to the complexity of multiple arterial inputs and the dynamic nature of blood flow. Our methodology integrates pressure-controlled perfusion with 3D imaging to map vascular distribution within the mandibular bone under varying perfusion pressures. We conducted controlled perfusions on human cadaveric mandibles, progressively increasing pressure while monitoring the expansion of perfused territories using contrast-enhanced cone beam computed tomography. A custom segmentation pipeline allowed for the reconstruction of pressure maps detailing the minimal pressure required to perfuse different regions of the mandible. Our results demonstrate a low-pressure anastomosis of the maxillary artery to the facial artery through the mental artery, suggesting the equivalence of intraosseous territories, followed by a radial perfusion pattern from the inferior alveolar artery, with increasing resistance at the cortical bone. Perfusion saturation was achieved at approximately 100-125 hPa, in accordance with physiological arterial pressures. Furthermore, cortical bone exhibited higher perfusion thresholds than cancellous bone, emphasizing differential vascular resistance across bone structures. These findings suggest that pressure-driven perfusion analysis can provide crucial insights into bone vascularization. By optimizing pressure parameters, it may be possible to achieve more effective decellularization by perfusion in massive bone allografts, improving graft integration and long-term viability. This study also underscores the need for pressure-controlled anatomical studies, as perfusion territories vary significantly with applied pressure, challenging traditional static angiosoma models. Future research should explore the applicability of these findings in living tissues and refine decellularization techniques based on controlled perfusion dynamics.
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