Parry-Romberg Reconstruction

Slack, Ginger; Tabit, Christina J.; Allam, Karam A.; Kawamoto, Henry K.; Bradley, James P.

doi:10.1097/sap.0b013e31827aeb0d

Cited by 48 publications

(21 citation statements)

References 20 publications

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“…If surgical therapy is indeed delayed until disease burns out, proper mandibular development and parallelism of facial planes can be guided with orthodontic rehabilitation and orthodontic appliances [ 142 , 143 ]. For mild to moderate atrophy, fat grafting, as well as lipoinjection and other soft tissue fillers, can be employed [ 142 , 144 , 149 , 153 , 154 ]. For more severe atrophy, a combined approach of skeletal and soft tissue augmentation is often recommended.…”

Section: Treatmentmentioning

confidence: 99%

Progressive hemifacial atrophy: a review

Tolkachjov

Patel

Tollefson

2015

Orphanet J Rare Dis

115

187

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BackgroundProgressive Hemifacial Atrophy (PHA) is an acquired, typically unilateral, facial distortion with unknown etiology. The true incidence of this disorder has not been reported, but it is often regarded as a subtype of localized scleroderma. Historically, a debate existed whether PHA is a form of linear scleroderma, called morphea en coup de sabre (ECDS), or whether these conditions are inherently different processes or appear on a spectrum (; Adv Exp Med Biol 455:101–4, 1999; J Eur Acad Dermatol Venereol 19:403–4, 2005). Currently, it is generally accepted that both diseases exist on a spectrum of localized scleroderma and often coexist.The pathogenesis of PHA has not been delineated, but trauma, autoimmunity, infection, and autonomic dysregulation have all been suggested. The majority of patients have initial manifestations in the first two decades of life; however, late presentations in 6th and 7th decades are also described [J Am Acad Dermatol 56:257–63, 2007; J Postgrad Med 51:135–6, 2005; Neurology 61:674–6, 2003]. The typical course of PHA is slow progression over 2-20 years and eventually reaching quiescence.Systemic associations of PHA are protean, but neurological manifestations of seizures and headaches are common [J Am Acad Dermatol 56:257–63, 2007; Neurology 48:1013–8, 1997; Semin Arthritis Rheum 43:335–47, 2013]. As in many rare diseases, standard guidelines for imaging, treatment, and follow-up are not defined.MethodsThis review is based on a literature search using PubMed including original articles, reviews, cases and clinical guidelines. The search terms were “idiopathic hemifacial atrophy”, “Parry-Romberg syndrome”, “Romberg’s syndrome”, “progressive hemifacial atrophy”, “progressive facial hemiatrophy”, “juvenile localized scleroderma”, “linear scleroderma”, and “morphea en coup de sabre”. The goal of this review is to summarize clinical findings, theories of pathogenesis, diagnosis, clinical course, and proposed treatments of progressive hemifacial atrophy using a detailed review of literature.Inclusion- and exclusion criteriaReview articles were used to identify primary papers of interest while retrospective cohort studies, case series, case reports, and treatment analyses in the English language literature or available translations of international literature were included.

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Section: Treatmentmentioning

confidence: 99%

Progressive hemifacial atrophy: a review

Tolkachjov

Patel

Tollefson

2015

Orphanet J Rare Dis

115

187

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“…However, poorer engraftment was noted in progressive hemifacial atrophy patients, suggesting that these more difficult cases may require the use of serial injections to achieve the desired volume. 72,73 …”

Section: Recipient-site Variablesmentioning

confidence: 99%

The Current State of Fat Grafting

Strong

Cederna

Rubin

et al. 2015

Plastic and Reconstructive Surgery

340

129

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Background Interest in and acceptance of autologous fat grafting for use in contour abnormalities, breast reconstruction, and cosmetic procedures have increased. However, there are many procedural variations that alter the effectiveness of the procedure and may account for the unpredictable resorption rates observed. Methods The authors highlighted studies investigating the effects of harvesting procedures, processing techniques, and reinjection methods on the survival of fat grafts. This review focused on the impact different techniques have on outcomes observed in the following: in vitro analyses, in vivo animal experiments, and human studies. Results This systemic review revealed the current state of the literature. There was no significant difference in the outcomes of grafted fat obtained from different donor sites, different donor-site preparations, harvest technique, fat harvesting cannula size, or centrifugation speed, when tumescent solution was used. Gauze rolling was found to enhance the volume of grafted fat, and no significant difference in retention was observed following centrifugation, filtration, or sedimentation in animal experiments. In contrast, clinical studies in patients found more favorable outcomes with fat processed by centrifugation compared with sedimentation. In addition, higher retention was observed with slower reinjection speed and when introduced into less mobile areas. Conclusions There has been a substantial increase in research interest to identify methodologies for optimizing fat graft survival. Despite some differences in harvest and implantation technique in the laboratory, these findings have not translated into a universal protocol for fat grafting. Therefore, additional human studies are necessary to aid in the development of a universal protocol for clinical practice.

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“…Fat grafting is a promising regenerative cell-directed therapy that has shown good results in several applications such as breast augmentation and reconstruction, treatment of contour deformities and scars, and wound healing (Klinger et al, 2008;Slack et al, 2014;Condé-Green et al, 2015;Katzel and Bucky, 2017;Ruan et al, 2019). However, fat graft fibrosis is a major grafting-related complication (Mineda et al, 2014;Cai et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Necroptosis in Macrophage Foam Cells Promotes Fat Graft Fibrosis in Mice

Chen

Deng

Feng

et al. 2021

Front. Cell Dev. Biol.

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Background: Fibrosis is a major grafting-related complication that leads to fat tissue dysfunction. Macrophage-induced inflammation is related to the development of fat tissue fibrosis. Necroptosis is a recently discovered pathway of programmed cell necrosis that results in severe inflammation and subsequent tissue fibrosis. Thus, in this study, we investigated the role of macrophage necroptosis in fat graft fibrosis and the underlying mechanisms.Methods: Fibrosis and necroptosis were investigated in mouse fat tissue before and after grafting. An in vitro “crown-like” structure (CLS) cell culture model was developed by co-culturing RAW 264.7 macrophages with apoptotic adipocytes to reproduce in vivo CLS macrophage-adipocyte interactions. Lipid uptake and necroptosis in CLS macrophages were analyzed using Oil-Red-O staining, western blotting, and immunofluorescence. RAW264.7 macrophages were cultured alone or with apoptotic adipocytes and treated with a necroptosis inhibitor (Nec-1 or GSK872) to explore the paracrine effect of necroptotic CLS macrophages on collagen synthesis in fibroblasts in vitro. Mice were treated with Nec-1 to analyze the effect of blocking necroptosis on fat graft fibrosis.Results: Fibrosis was increased after grafting in fat grafts of mice. Macrophages clustered around apoptotic adipocytes or large oil droplets to form a typical CLS in fibrotic depots. This was accompanied by formation and necroptosis of macrophage foam cells (MFCs) in CLSs. RAW 264.7 macrophages co-cultured with apoptotic adipocytes induced CLS formation in vitro, and lipid accumulation in CLS macrophages resulted in the formation and necroptosis of MFCs. Necroptosis of MFCs altered the expression of collagen I and VI in fibroblasts via a paracrine mechanism involving inflammatory cytokines/chemokines, which was reversed by GSK872 or Nec-1 treatment. Furthermore, treatment with Nec-1 ameliorated fat graft fibrosis in mice.Conclusion: Apoptotic adipocytes induced necroptosis of MFCs, and necroptosis of these cells activated collagen synthesis in fibroblasts via a paracrine mechanism. Inhibition of necroptosis in macrophages is a potential approach to prevent fibrosis in fat grafts.

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Parry-Romberg Reconstruction

Abstract: Despite poorer fat graft take within the disease region of Romberg patients, fat grafting resulted in long-term improvement in hypoplasia and skin hyperpigmentation.

Cited by 48 publications

References 20 publications

Progressive hemifacial atrophy: a review

Progressive hemifacial atrophy: a review

The Current State of Fat Grafting

Necroptosis in Macrophage Foam Cells Promotes Fat Graft Fibrosis in Mice

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