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Plastic and Reconstructive Surgery - Global Open:
doi: 10.1097/GOX.0000000000000015
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Are We Killing Our Fat Cells before Grafting Them?

Sieber, David A. MD; Van Beek, Allen L. MD

Open Access
United States
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Division of Plastic and Reconstructive Surgery, University of Minnesota, Minneapolis, Minn.

Correspondence to Dr. Sieber, Division of Plastic and Reconstructive Surgery, University of Minnesota, 420 Delaware Street SE, MMC 122, Minneapolis, MN, siebe076@umn.edu

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.

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Sir:

Since its inception by Neuber in 1893, there have been numerous modifications in fat grafting techniques, all attempting to maximize posttransplant adipocyte survival. Despite ongoing research, there remains wide variations in viability after autologous fat grafting, with reported loss ranging from 40% to 60%.1 Research studying various methods of harvesting, force and time of centrifugation, effects of local anesthetic, cannula size, hand versus machine aspiration, and location of donor sites are discussed.2,3 However, the question remains: why are so many adipocytes being resorbed after transfer?

There is suggestion in the literature that high negative pressures may contribute to cellular rupture before injection.4 Our study was able to identify that high negative pressures are generated through hand aspiration with minimal amounts of distraction. The maximum negative pressure generated exceeds 600 mm Hg, which is likely enough negative pressure to cause cellular rupture and also creates excess pressure with distractions greater than 3 mL.

To date, there has been a lack of convincing research to define a range of negative pressures that cause direct cellular rupture of living adipocytes. A single study suggests that cells begin to rupture at negative pressures over 20 mm Hg, but the scientific literature has never addressed this issue directly.4 Coleman5 recommends displacing the plunger by 1–2 mL in a 10-mL syringe. This distraction amount generates negative pressures in the range of 50–115 mm Hg (Fig. 1). The pressure at which cell rupture occurs has yet to be determined; however, some studies do suggest higher cell viability with low pressure harvesting of aggregates of cells. The current literature evaluates cells under negative 760mm Hg and negative 380mm Hg of pressure but is lacking in comparing high negative pressures of 760 mm Hg with low negative pressures of <150 mm Hg.

Fig. 1
Fig. 1
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Persistent issues in the literature are the lack of a standardized protocol for lipoaspiration and a need for a quantitative method of evaluating adipocyte viability. Without standard methods, available studies have multiple variables that potentially confound the data and provide conflicting results. This may be the reason that so many of the currently published studies have not been able to show significance between experimental and control groups.

Many authors have attempted to determine cell viability by preserving cells in fixative. This merely suspends the cell in time, providing a snapshot of healthy cellular architecture, but it does not provide an accurate picture of eventual cell death due to programmed apoptosis or induced cell death. Newer assays measuring cytoplasmic enzymes such as 3-phosphate dehydrogenase do a better of job of determining viable cells from those that are programmed to die, but it still does not provide a quantitative evaluation of living cells ability to survive.

Clinical fat grafting is an evolving process where the end result is variable, and the factors creating that variability have yet to be adequately studied. It seems likely that high negative pressure and other technical factors during aspiration and grafting contribute to premature cellular death. However, more stringent standardized protocols and quantitative measurements of cell viability need to be developed before that question can be answered.

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DISCLOSURE

The authors have no financial interest to declare in relation to the content of this article. The Article Processing Charge was paid for by the authors.

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REFERENCES

1. Rubin A, Hoefflin SM. Fat purification: survival of the fittest. Plast Reconstr Surg. 2002;109:1463–1464

2. Illouz YG, Sterodimas A. Autologous fat transplantation to the breast: a personal technique with 25 years of experience. Aesthetic Plast Surg. 2009;33:706–715

3. Rohrich RJ, Sorokin ES, Brown SA. In search of improved fat transfer viability: a quantitative analysis of the role of centrifugation and harvest site. Plast Reconstr Surg. 2004;113:391–395 discussion 396–397.

4. Prado A, Castillo P, Gaete F. Does vacuum pressure extraction of fat affect the infranatant cellularity of liposuction specimens? Plast Reconstr Surg. 2005;116:1832–1833

5. Coleman S Structural Fat Grafting. 2004 Quality Medical Pub

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