Search

Background: Anatomical studies have identified separate superficial and deep facial fat compartments, leading some to theorize that volume loss from the deep midface causes overlying superficial fat pseudoptosis. Unfortunately, a paucity of evidence exists regarding whether facial fat volume is truly lost with age and, if so, whether it is lost equally or differentially from the superficial and deep compartments. The aim of this study was to quantify volume changes occurring with age within the superficial, deep, and buccal fat compartments of the midface., Methods: A retrospective longitudinal study was performed evaluating individuals aged 30 to 65 years who underwent facial computed tomography followed by facial computed tomography greater than or equal to 10 years later. Superficial midface, deep midface, and buccal fat volumes were quantified using Horos radiology software., Results: Nineteen subjects met inclusion criteria. Mean total fat volume decreased significantly from 46.47 cc to 40.81 cc (p < 0.01). The mean superficial and deep fat volumes both decreased significantly from 26.10 cc to 23.15 cc (p < 0.01) and from 11.01 cc to 8.98 cc (p < 0.01), respectively. No significant difference was observed in buccal fat volume over time (9.36 cc to 8.68 cc; p = 0.04). Patients lost an average of 11.3 percent of their initial superficial fat volume and 18.4 percent of their initial deep fat volume., Conclusions: Significant volume loss was observed from both superficial and deep facial fat compartments over a mean 11.3 years. Patients lost a greater percentage of deep facial fat volume, providing support for the theory of pseudoptosis caused by deep midface fat loss., (Copyright © 2020 by the American Society of Plastic Surgeons.)

Background: Neck fat distribution plays an important role in aging, yet how fat distribution changes with age is largely unknown. This study used volumetric computed tomography in live patients to characterize neck fat volume and distribution in young and elderly women., Methods: A retrospective analysis was conducted of head and neck computed tomographic angiographs of 20 young (aged 20 to 35 years) and 20 old (aged 65 to 89 years) women. Fat volume in the supraplatysmal and subplatysmal planes was quantified. Distribution of fat volume was assessed by dividing each supraplatysmal and subplatysmal compartment into upper, middle, and lower thirds., Results: Total supraplatysmal fat volume was greater than subplatysmal in all patients. Young patients had more total supraplatysmal fat than old patients (p < 0.0001). No difference was found between age groups in subplatysmal fat (p > 0.05). No difference was found between upper/middle/lower third supraplatysmal fat volumes in young patients. When comparing supraplatysmal thirds within the elderly population, the middle third fat volume (28.58 ± 20.01 cm3) was greater than both upper (18.93 ± 10.35 cm3) and lower thirds (15.46 ± 11.57 cm3) (p < 0.01)., Conclusions: This study suggests that total supraplatysmal fat volume decreases with age. Older patients had more fat volume in the upper and middle thirds compared with the lower third of the supraplatysmal fat compartment, whereas young patients had more evenly distributed fat. These results suggest that fat deposition and redistribution in the neck occur with age and may be a contributing factor to the obtuse cervicomandibular angle of the elderly., (Copyright © 2020 by the American Society of Plastic Surgeons.)

Summary: Facial aging is a multifactorial process governed by both intrinsic and extrinsic factors that impart a change to each component of the facial anatomy. Our understanding of the science of aging has evolved over the years. A recent and valuable addition to our understanding is the knowledge of both the superficial and deep facial fat compartments. The deep compartments provide structural support to the midface and the superficial fat compartments. Understanding the anatomy and the spectrum of their changes helps to tailor management options for facial rejuvenation. The authors present a review on facial aging as it relates to these fat compartments and provide a management algorithm based on the longitudinal changes seen during aging., (Copyright © 2020 by the American Society of Plastic Surgeons.)

Background: The clinical unpredictability of autologous fat grafting originates partially from the unique characteristics of adipose tissue. Evidence of adipose remodeling toward browning (developing of brown-like adipocytes in white adipose tissue) in response to trauma has been emerging. With regard to fat grafting surgery by which adipose tissue depots are directly and ubiquitously traumatized, whether it affects adipose phenotype change toward browning has not been previously reported., Methods: Human subcutaneous adipose tissues were harvested from the abdominal region of female patients by means of liposuction and were then injected into the dorsal flanks of athymic nude mice. After 12 weeks, fat grafts were harvested and subjected to histologic analysis., Results: Hematoxylin and eosin staining showed the appearance of small multilocular adipocytes in the peripheral region of the grafts. These adipocytes exhibited higher staining for uncoupling protein 1 (a fat browning-specific marker), mitochondrial protein, and CD31 compared with the central ones, indicating the presence of brown-like adipocytes (i.e., beige adipocytes) in this area. Furthermore, immunofluorescence staining demonstrated that these beige adipocytes might be derived from de novo adipogenesis from progenitors of graft origin., Conclusion: Results of this study suggest that browning of subcutaneous white adipose tissue participates in adaptive tissue remodeling following grafting and contributes to adipose tissue repair.

Background: Fat grafting remains unpredictable in the clinical setting, and variables that influence adipocyte survival, such as age, body mass index, and specific donor sites, are still not well understood., Methods: Twenty-four female subjects were enrolled in this research after institutional review board approval and signed consent to participate was obtained. Subjects were separated into groups according to (1) age (younger, ≤45 years; and older, ≥46 years) and (2) body mass index (normal weight, body mass index<25; and overweight, body mass index≥25). All fat samples were obtained through dry liposuction of three donor sites: lower abdomen, inner thigh, and flank. They were processed identically for dissociation of adipose tissue and isolation of adipocytes. Adipocyte viability was measured using the Nexcelom Cellometer Auto T4., Results: In younger patients, adipocyte viability was greater in the lower abdomen than in the flank; in older patients, this difference was not seen. When lower abdominal fat from younger was compared with that from older patients, the viability was higher in younger patients. However, adipocytes from the flank depot had higher viability in the older group compared with the younger group. Inner thigh fat viability was not significantly different across the two age groups. The authors also found no significant differences in fat viability for any given donor site between the normal weight and overweight body mass index groups., Conclusions: The optimal choice site for fat harvest should take patient age into consideration. In younger patients, both lower abdomen and inner thigh appear to be good options., Clinical Question/level of Evidence: Therapeutic, II.

Background: This pilot study examined the efficacy of 5-bromo-2-deoxyuridine-labeled autologous adipose-derived stem cells seeded onto collagen scaffolds to augment and/or regenerate the fat-enriched hypodermal tissue in an acute porcine wound model., Methods: Porcine autologous adipose-derived stem cells were isolated and cultured. At passage 2, the cells were labeled with 5-bromo-2-deoxyuridine, seeded onto a three-dimensional collagen scaffold, and cultured for 10 days. Scaffolds were implanted subcutaneously in adult pigs with two adipose-derived stem cell scaffolds and two control scaffolds. Animals were euthanized at 2, 4, 8, and 12 weeks; all scaffold conditions were explanted for histology and immunohistochemistry analyses., Results: For all time points, adipose-derived stem cell scaffolds had increased connective tissue matrix within the subcutaneous tissue compared with scaffold alone and untreated porcine skin (p < 0.01). The neosynthesized connective tissue was vascularized and composed of small cells within an abundant extracellular matrix organized in layers. 5-Bromo-2-deoxyuridine cells were detectable only up to 4 weeks and mature adipocytes were absent. Levels of collagen types I, III, and VI differed among the experimental groups, with increased extracellular matrix associated with the presence of adipose-derived stem cells., Conclusions: The authors' data clearly show the efficacy of adipose-derived stem cells for soft-tissue repair and skin aging because it induces a significant increase of the dermis thickness. Moreover, the authors' results demonstrate the interest of their acute wound model and allowed them to show the skin thickness variation over time of the experiment, which is one of the challenges with which clinicians struggle in fat grafting.

Background: Although fat deposition is a defining clinical characteristic of lymphedema, the cellular mechanisms that regulate this response remain unknown. The goals of this two-part study were to determine the effect of lymphatic fluid stasis on adipogenesis and inflammation (part I) and how these changes regulate the temporal and spatial expression of fat differentiation genes (part II)., Methods: Adult female mice underwent tail lymphatic ablation and were euthanized 6 weeks after surgery (n = 20). Fat deposition, fibrosis, and inflammation were then analyzed in the regions of the tail exposed to lymphatic fluid stasis as compared with normal lymphatic flow., Results: Lymphatic fluid stasis in the tail resulted in significant subcutaneous fat deposition, with a 2-fold increase in fat thickness (p < 0.01). In addition, lymphatic stasis was associated with subcutaneous fat fibrosis and collagen deposition. Adipogenesis in response to lymphatic fluid stasis was associated with a marked mononuclear cell inflammatory response (5-fold increase in CD45 cells; p < 0.001). In addition, the authors noted a significant increase in the number of monocytes/macrophages as identified by F4/80 immunohistochemistry (p < 0.001)., Conclusions: The mouse-tail model has pathologic findings that are similar to clinical lymphedema, including fat deposition, fibrosis, and inflammation. Adipogenesis in response to lymphatic fluid stasis closely resembles this process in obesity. This model therefore provides an excellent means with which to study the molecular mechanisms that regulate the pathophysiology of lymphedema.

Background: Although fat deposition is a defining clinical characteristic of lymphedema, the cellular mechanisms that regulate this response remain unknown. The goal of this study was to determine how lymphatic fluid stasis regulates adipogenic gene activation and fat deposition., Methods: Adult female mice underwent tail lymphatic ablation and were euthanied at 1, 3, or 6 weeks postoperatively (n = 8 per group). Samples were analyzed by immunohistochemistry and Western blot analysis. An alternative group of mice underwent axillary dissections or sham incisions, and limb tissues were harvested 3 weeks postoperatively (n = 8 per group)., Results: Lymphatic fluid stasis resulted in significant subcutaneous fat deposition and fibrosis in lymphedematous tail regions (p < 0.001). Western blot analysis demonstrated that proteins regulating adipose differentiation including CCAAT/enhancer-binding protein-α and adiponectin were markedly up-regulated in response to lymphatic fluid stasis in the tail and axillary models. Expression of these markers increased in edematous tissues according to the gradient of lymphatic stasis distal to the wound. Immunohistochemical analysis further demonstrated that adiponectin and peroxisome proliferator-activated receptor-γ, another critical adipogenic transcription factor, followed similar expression gradients. Finally, adiponectin and peroxisome proliferator-activated receptor-γ expression localized to a variety of cell types in newly formed subcutaneous fat., Conclusions: The mouse-tail model of lymphedema demonstrates pathologic findings similar to clinical lymphedema, including fat deposition and fibrosis. The authors show that lymphatic fluid stasis potently up-regulates the expression of fat differentiation markers both spatially and temporally. These studies elucidate mechanisms regulating abnormal fat deposition in lymphedema pathogenesis and therefore provide a basis for developing targeted treatments.

Background: Gynoid lipodystrophy (cellulite) affects most women, and many seek plastic surgery consultation to improve appearance. Various products are offered, but the literature on the cause and treatment is limited. Understanding the biological and biophysical factors that affect severity may facilitate the development of effective therapies. There has been a dramatic increase in the number of people who have lost significant weight as a result of bariatric surgery or medically supervised weight programs. The effect of weight loss on cellulite severity has not been systematically studied and remains a common patient concern. The authors hypothesized that cellulite severity would decrease with weight loss and subsequent decrease in subcutaneous fat in most subjects., Methods: The authors examined the cellulite changes in female subjects who were enrolled in medically supervised weight loss programs using quantitative surface roughness by three-dimensional laser surface scanning, tissue composition by dual energy x-ray absorptiometry, dermal-subcutaneous structure with three-dimensional ultrasound, and tissue elasticity with biomechanical measurements., Results: The majority of subjects had an improvement in cellulite with weight loss, but the condition worsened for others. Improvement was associated with significant reductions in weight and percentage of thigh fat, significantly higher starting body mass index, and significantly greater initial severity. Cellulite worsened with a significantly smaller starting body mass index, smaller reductions in weight accompanied by no change in percentage of thigh fat, and significant increases in tissue compliance., Conclusions: Cellulite is a complex condition, and treatments such as weight loss have variable effects on the improvement or worsening of this condition. Additional studies are required to understand how the factors that influence and modulate cellulite severity, particularly those at the level of the subcutaneous tissue septa, can be manipulated to improve this condition.