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      Diffusion and Perfusion: The Keys to Fat Grafting

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          Abstract

          Background:

          Fat grafting is now widely used in plastic surgery. Long-term graft retention can be unpredictable. Fat grafts must obtain oxygen via diffusion until neovascularization occurs, so oxygen delivery may be the overarching variable in graft retention.

          Methods:

          We studied the peer-reviewed literature to determine which aspects of a fat graft and the microenvironment surrounding a fat graft affect oxygen delivery and created 3 models relating distinct variables to oxygen delivery and graft retention.

          Results:

          Our models confirm that thin microribbons of fat maximize oxygen transport when injected into a large, compliant, well-vascularized recipient site. The “Microribbon Model” predicts that, in a typical human, fat injections larger than 0.16 cm in radius will have a region of central necrosis. Our “Fluid Accommodation Model” predicts that once grafted tissues approach a critical interstitial fluid pressure of 9 mm Hg, any additional fluid will drastically increase interstitial fluid pressure and reduce capillary perfusion and oxygen delivery. Our “External Volume Expansion Effect Model” predicts the effect of vascular changes induced by preoperative external volume expansion that allow for greater volumes of fat to be successfully grafted.

          Conclusions:

          These models confirm that initial fat grafting survival is limited by oxygen diffusion. Preoperative expansion increases oxygen diffusion capacity allowing for additional graft retention. These models provide a scientific framework for testing the current fat grafting theories.

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          Most cited references71

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          Tensegrity: the architectural basis of cellular mechanotransduction.

          D. Ingber (1997)
          Physical forces of gravity, hemodynamic stresses, and movement play a critical role in tissue development. Yet, little is known about how cells convert these mechanical signals into a chemical response. This review attempts to place the potential molecular mediators of mechanotransduction (e.g. stretch-sensitive ion channels, signaling molecules, cytoskeleton, integrins) within the context of the structural complexity of living cells. The model presented relies on recent experimental findings, which suggests that cells use tensegrity architecture for their organization. Tensegrity predicts that cells are hard-wired to respond immediately to mechanical stresses transmitted over cell surface receptors that physically couple the cytoskeleton to extracellular matrix (e.g. integrins) or to other cells (cadherins, selectins, CAMs). Many signal transducing molecules that are activated by cell binding to growth factors and extracellular matrix associate with cytoskeletal scaffolds within focal adhesion complexes. Mechanical signals, therefore, may be integrated with other environmental signals and transduced into a biochemical response through force-dependent changes in scaffold geometry or molecular mechanics. Tensegrity also provides a mechanism to focus mechanical energy on molecular transducers and to orchestrate and tune the cellular response.
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            Lymphatic vascular defects promoted by Prox1 haploinsufficiency cause adult-onset obesity.

            Multiple organs cooperate to regulate appetite, metabolism, and glucose and fatty acid homeostasis. Here, we identified and characterized lymphatic vasculature dysfunction as a cause of adult-onset obesity. We found that functional inactivation of a single allele of the homeobox gene Prox1 led to adult-onset obesity due to abnormal lymph leakage from mispatterned and ruptured lymphatic vessels. Prox1 heterozygous mice are a new model for adult-onset obesity and lymphatic vascular disease.
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              Vacuum-assisted closure: microdeformations of wounds and cell proliferation.

              The mechanism of action of the Vacuum Assisted Closure Therapy (VAC; KCI, San Antonio, Texas), a recent novel innovation in the care of wounds, remains unknown. In vitro studies have revealed that cells allowed to stretch tend to divide and proliferate in the presence of soluble mitogens, whereas retracted cells remain quiescent. The authors hypothesize that application of micromechanical forces to wounds in vivo can promote wound healing through this cell shape-dependent, mechanical control mechanism. The authors created a computer model (finite element) of a wound and simulated VAC application. Finite element modeling is commonly used to engineer complex systems by breaking them down into simple discrete elements. In this model, the authors altered the pressure, pore diameter, and pore volume fraction to study the effects of vacuum-induced material deformations. The authors compared the morphology of deformation of this wound model with histologic sections of wounds treated with the VAC. The finite element model showed that most elements stretched by VAC application experienced deformations of 5 to 20 percent strain, which are similar to in vitro strain levels shown to promote cellular proliferation. Importantly, the deformation predicted by the model also was similar in morphology to the surface undulations observed in histologic cross-sections of the wounds. The authors hypothesize that this tissue deformation stretches individual cells, thereby promoting proliferation in the wound microenvironment. The application of micromechanical forces may be a useful method with which to stimulate wound healing through promotion of cell division, angiogenesis, and local elaboration of growth factors. Finite element modeling of the VAC device is consistent with this mechanism of action.
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                Author and article information

                Journal
                Plast Reconstr Surg Glob Open
                Plast Reconstr Surg Glob Open
                GOX
                Plastic and Reconstructive Surgery Global Open
                Wolters Kluwer Health
                2169-7574
                September 2014
                07 October 2014
                : 2
                : 9
                : e220
                Affiliations
                From the [* ]Division of Plastic Surgery, Brigham and Women’s Hospital, Boston, Mass.; []University of Michigan Medical School, Ann Arbor, Mich.; []Gulliver Preparatory School, Pinecrest, Fla.; [§ ]College of Engineering, Boston University, Boston, Mass.; []Institute of Plastic Reconstructive and Aesthetic Surgery, University of Padova, Padova, Italy; and []Harvard Medical School, Boston, Mass.
                Author notes
                Dennis P. Orgill, MD, PhD, Division of Plastic Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, E-mail: dorgill@ 123456partners.org
                Article
                00002
                10.1097/GOX.0000000000000183
                4229279
                25426403
                f788c1a7-1e25-4298-8524-8bd9fddd2a78
                Copyright © 2014 The Authors. Published by Lippincott Williams & Wilkins on behalf of The American Society of Plastic Surgeons. PRS Global Open is a publication of the American Society of Plastic Surgeons.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.

                History
                : 8 April 2014
                : 22 July 2014
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