Tissue Expansion Research Articles

Reconstructing Failure: Assessing Surgical and Patient Reported Outcomes Following Loss of Initial Breast Reconstruction.

Breast reconstruction failure, defined as the removal of a prosthetic device or flap without immediate replacement, can be traumatic for patients. We aim to describe the progression of patients who experience tissue expander (TE), implant, or autologous breast reconstructive failure and assess the patient reported outcomes (PROs) among patients who undergo additional reconstruction. Patients undergoing TE, implant, or autologous breast reconstruction between 2017 and 2022 were included, and patients with reconstructive failures were identified. Outcomes of interests included (1) receipt of additional reconstruction and (2) BREAST-Q scores 1-year after reconstructive failure. We also performed a propensity-matched analysis between patients who undergo secondary reconstruction and patients who had an uncomplicated reconstruction. 4,258 TE, 4,420 implant, and 1,545 autologous breast reconstruction patients were included. Of patients who experienced reconstructive failures, 49.5% of TE, 4.8% of implant, and 53.8% of autologous patients underwent secondary reconstruction. Age, psychiatric diagnosis, chemotherapy, radiation, and mastectomy type were associated with increased likelihood of secondary reconstruction. Between patients with and without additional reconstruction, higher Psychosocial Well-being trended towards the former cohort (61 [Interquartile Range: 56, 80] vs 50 [46, 65], p=0.085). Propensity-matched analysis demonstrated comparable PROs at 1-year after definite reconstruction. Less than half of reconstructive failure patients undergo an additional reconstruction. Patients with secondary reconstruction may have improved Psychosocial Well-being than those who do not and comparable PROs to those who had uncomplicated initial reconstruction. Surgeons should counsel patients with reconstructive failures that although traumatizing, secondary reconstruction may be beneficial.

Tissue expansion mitigates radiation-induced skin fibrosis in a porcine model

Tissue expansion (TE) is the primary method for breast reconstruction after mastectomy. In many cases, mastectomy patients undergo radiation treatment (XR). Radiation is known to induce skin fibrosis and is one of the main causes for complications during post-mastectomy breast reconstruction. TE, on the other hand, induces a pro-regenerative response that culminates in growth of new skin. However, the combined effect of XR and TE on skin mechanics is unknown. Here we used the porcine model of TE to study the effect of radiation on skin fibrosis through biaxial testing, histological analysis, and kinematic analysis of skin deformation over time. We found that XR leads to stiffening of skin compared to control based on a shift in the transition stretch (transition between a low stiffness and an exponential stress-strain region characteristic of collagenous tissue) and an increase in the high modulus (modulus computed with stress-stretch data past the transition point). The change in transition stretch can be explained by thicker, more aligned collagen fiber bundles measured in histology images. Skin subjected to both XR+TE showed similar microstructure to controls as well as similar biaxial response, suggesting that physiological remodeling of collagen induced by TE partially counteracts pro-fibrotic XR effects. Skin growth was indirectly assessed with a kinematic approach that quantified increase in permanent area changes without reduction in thickness, suggesting production of new tissue driven by TE even in the presence of radiation treatment. Future work will focus on the detailed biological mechanisms by which TE counteracts radiation induced fibrosis. Statement of significanceBreast cancer is the most prevalent in women and its treatment often results in total breast removal (mastectomy), followed by reconstruction using tissue expanders. Radiation, which is used in about a third of breast reconstruction cases, can lead to significant complications. The timing of radiation treatment remains controversial. Radiation is known to cause immediate skin damage and long-term fibrosis. Tissue expansion leads to a pro-regenerative response involving collagen remodeling. Here we show that tissue expansion immediately prior to radiation can reduce the level of radiation-induced fibrosis. Thus, we anticipate that this new evidence will open up new avenues of investigation into how the collagen remodeling and pro-regenerative effects of tissue expansion can be leverage to prevent radiation-induced fibrosis.

A Lifeboat for Failed Nasal Reconstructions: The Supraclavicular-Submental Sandwich Flap.

Many failures in total or subtotal nasal reconstruction result from an underestimation of the amount of skin required for an adequate result, especially for sufficient lining. Such planning errors usually lead to poor results, with exposure of structural grafts, infection, scar retraction, airway obstruction, and finally loss of projection and shape of the reconstructed nose. Reconstruction options for cases in which previous attempts have failed are always limited, as well as in cases of trauma or burns affecting the soft tissues of the forehead and face. In such complex situations, one may employ free flaps or tissue expansion, but such resources may not be always available. We describe a technique indicated for salvage surgeries in patients whose previous nasal reconstructions have failed, allowing a generous amount of tissue transfer for the nasal region. The technique combines the use of supraclavicular and submental flaps, with simple execution, not requiring microsurgical skills or devices such as tissue expanders. Done in three stages, the described technique provides enough skin for a total nasal reconstruction. The final result is obtained after subsequent refinements, and the total number of procedures is equivalent to when more sophisticated techniques are employed, such as tissue expansion or microsurgery.

Comparing Cortiva Silhouette to AlloDerm for Use in Prepectoral Two-stage Prosthetic Breast Reconstruction.

The use of acellular dermal matrices (ADMs) in implant-based breast reconstruction has become increasingly routine during the past 20 years. ADMs improve soft-tissue support, facilitate greater tissue expander (TE) fill volumes, and reduce rates of capsular contracture. As the ADM market continues to grow, outcomes studies are necessary to assess the risks and benefits of each product. In this study, we compare the performance of Cortiva Silhouette, the thinnest ADM widely available, to AlloDerm, commonly considered the industry standard. We performed a retrospective review of 178 consecutive two-stage prosthetic breast reconstructions performed by the senior author. In every case, either Cortiva or AlloDerm was used to provide soft-tissue support during TE placement. Subjects were divided into Cortiva and AlloDerm cohorts and compared across patient characteristics and reconstructive outcomes variables. During the study period, AlloDerm was used in 116 reconstructions; Cortiva was used in 62. After propensity score matching (62 AlloDerm, 62 Cortiva), Cortiva was associated with greater intraoperative and final TE fill volumes, as well as larger silicone implants. Cortiva was also associated with fewer complications overall, and fewer instances of mastectomy skin necrosis, delayed wound healing, and seroma. Cortiva Silhouette is noninferior to AlloDerm in terms of safety and providing soft-tissue support in prepectoral two-stage implant-based breast reconstruction. In this study, Cortiva supported greater TE fill volumes and larger silicone implants relative to AlloDerm and was associated with fewer complications.

Use of Fascia Lata as Matrix for Subpectoral Breast Reconstruction.

Matrices are used with increased frequency to assist with tissue expander or implant-based breast reconstruction. These devices usually have a high cost, especially when they are human-derived. We present the use of fascia lata for implant and expander-based subpectoral reconstruction. According to our review of the literature, this is the first report of the use of a patient's own fascia lata instead of a matrix.

Implant-based Breast Reconstruction Salvage with Negative Pressure Wound Therapy with Instillation: An Evaluation of Outcomes.

Implant infection is problematic in breast reconstruction. Traditionally, infected tissue expanders (TE)/implants are removed for several months before replacement, resulting in breast reconstruction delay. Salvage involving device removal, negative pressure wound therapy with instillation and dwell (NPWTi-d) placement, and early staged TE/implant replacement within a few days has been described. The purpose of this study was to compare outcomes of the NPWTi-d salvage pathway with traditional implant removal. A retrospective review was performed on patients who underwent implant-based reconstruction and developed TE/implant infection/exposure requiring removal. Patients were divided into two groups. Group 1 had TE/implant removal, NPWTi-d placement, and TE/implant replacement 1-4 days later. Group 2 (control) underwent standard TE/implant removal and no NPWTi-d. Reinfection after TE/implant salvage, TE/implant-free days, and time to final reconstruction were assessed. The study included 47 patients (76 TE/implants) in group 1 (13 patients, 16 TE/implants) and group 2 (34 patients, 60 TE/implants). The success rate (no surgical-site infection within 90 days) of implant salvage was 81.3% in group 1. No group 1 patients abandoned completing reconstruction after TE/implant loss versus 38.2% (13 of 34) in group 2 (P = 0.0094). Mean implant-free days was 2.5 ± 1.2 in group 1 versus 134.6 ± 78.5 in group 2 (P = 0.0001). The interval to final implant-based reconstruction was 69.0 ± 69.7 days in group 1 versus 225.6 ± 93.6 days in group 2 (P = 0.0001). A breast implant salvage pathway with infected device removal, NPWTi-d placement, and early TE/implant replacement was successful in 81.3%. Patients experienced 132 less implant-free days and faster time to final reconstruction.

A natural small molecule pinocembrin resists high-fat diet-induced obesity through GPR120-ERK1/2 pathway

Obesity is a widely concerned health problem. Mobilizing white adipose tissue and reducing fat synthesis are considered as effective strategies in the treatment of obesity. Here, using Connectivity Map (CMap) approach, we identified the pinocembrin (PB), a natural flavonoid primarily found in propolis, as a potential anti-obesity drug. Therefore, high-fat-diet (HFD) mice were randomly divided into two groups and fed a HFD or HFD with PB in this study. In vivo experiments showed that supplementation of PB reduced the body weight gain and ameliorated insulin resistance in HFD-induced mice. More importantly, PB did not cause side effect through detecting the levels of alanine transaminase (ALT), aspartate aminotransferase (AST), creatinine (CRE) and blood urea nitrogen (BUN) in serum of mice. Additionally, PB reduced expansion of white adipose tissue with upregulation of genes related lipolysis and downregulation of genes related lipogenesis. Furthermore, in vitro experiments revealed that PB treatment dose-dependently inhibited lipid droplet formation with upregulation of genes related lipolysis and downregulation of genes related lipogenesis. Molecular docking analysis combined with cellular thermal shift assay (CETSA) suggested that PB has a high affinity to the G protein-coupled receptor 120 (GPR120). Meanwhile, we confirmed that PB efficiently inhibited adipogenic differentiation of preadipocytes by directly binding to GPR120 and subsequently activating the downstream phosphorylation extracellular regulated kinase 1/2 (ERK1/2). Collectively, PB exerted anti-obesity effect through GPR120-ERK1/2 signaling pathway, providing a novel and promising natural drug for the treatment of obesity.

Direct-to-implant and tissue expander-based immediate breast reconstruction in Chinese women: A comparison of surgical complications and patient-reported outcomes

BackgroundDirect-to-implant (DTI) breast reconstruction restores the patient's body image immediately after the mastectomy but may increase postoperative complications compared to tissue expander (TE)-based breast reconstruction. There are very few studies that compared the surgical complications and patient-reported outcomes of DTI and TE breast reconstructions in Asian women. MethodThe study compares postoperative complications and patient-reported outcomes (PROs) between DTI and TE breast reconstruction in Chinese women and explores the risk factors of postoperative complications and influencing factors of PROs. Retrospective chart review of patients undergoing immediate breast reconstruction between 2008 and 2022 was conducted and BREAST-Q questionnaires of the breast reconstruction module were distributed to eligible patients. Multivariate regression models were used to explore risk factors for postoperative complications and factors that influence BREAST-Q scores. ResultsDTI was associated with lower rates of major complication and implant loss but has no significant influence on patients’ satisfaction or quality of life. Age and axillary lymph node dissection are important complication risk factors for both DTI and TE. The application of ADM significantly increased the risk of seroma or hematoma. In the DTI group, capsular contracture significantly reduced patients’ satisfaction with breast scores. ConclusionDTI dual-plane breast reconstruction does not increase complication rates in appropriately selected Chinese patients. In DTI patients, the management of capsular contracture is crucial for improving patient satisfaction.

Potential of the Thoracoepigastric Vein as a Drainage Vein in Breast Reconstruction With a Free Flap: An Anatomical Study Using Computed Tomography.

The recipient vessel choice is very important when performing free-flap breast reconstructions. Usually, the concomitant vein of the recipient artery is anastomosed, and mismatches in the diameter are occasionally observed. We consider the thoracoepigastric vein (TEV) as a potential useful recipient vein. The use of the TEV is not a novel technique. It has been used by surgeons for free-flap anastomoses in the axillary region, but usually as an anastomotic site for the second vein. However, anatomical findings such as TEV diameter, its deficiency rate, and influence on mastectomy are not clear. In this study, computed tomography (CT) was performed to evaluate the use of the TEV as a recipient vein for breast reconstruction. The medical records of patients who underwent breast reconstruction with free-flap transfer were retrospectively evaluated. In most cases, CT was performed using a tissue expander inserted after mastectomy. The TEV was considered suitable if its diameter on the mastectomy side was >1 mm and the vertical distance from the most distal slice level where the TEV could be seen at the third costal cartilage height of the parasternal region was <50 mm. Sixty-six sides of 33 patients were evaluated. The mean age of the patients was 49.3 ± 5.1 years. The TEV was used in five flaps. TEV diameters were not significantly different between the left and right sides (1.85 ± 0.53 vs. 1.82 ± 0.6, respectively, p = 0.836). On the mastectomy side, eight (25%) TEVs were injured, but only three (8.6%) were considered unavailable. On the healthy side, 96.4% TEVs were available. TEVs may be a good choice as vein anastomosis targets for breast reconstruction with a free flap because of their relatively large vessel diameter. UMIN-CTR: R000061573.

A Century of Prolactin: Emerging Perspectives as a Metabolic Regulator.

Prolactin, a hormone that has been studied for almost a century, has evolved from a reproductive regulator to a key player in metabolic health. Initially identified for its lactogenic role, the impact of prolactin on glucose and lipid metabolism became evident in the 1970s, leading to a paradigm shift in our understanding. Deviations in prolactin levels, including hyperprolactinaemia and hypoprolactinaemia, have been associated with adverse effects on glucose and lipid metabolism. Mechanistically, prolactin regulates metabolic homoeostasis by maintaining islet abundance, regulating the hypothalamic energy regulatory centre, balancing adipose tissue expansion, and regulating hepatic metabolism. Given the widespread use of pharmaceutical agents that affect prolactin levels, it is important to examine prolactin-related metabolic effects. Recently, a profound exploration of the intricate metabolic role of prolactin has been conducted, encompassing its rhythm-dependent regulatory influence on metabolism and its correlation with cognitive impairment associated with metabolic diseases. In this review, we highlight the role of prolactin as a metabolic regulator, summarise its metabolic effects, and discuss topics related to the association between prolactin and metabolic comorbidities.

Current status of prepectoral breast reconstruction in Argentina.

Breast cancer is among the most common cancers diagnosed in women, affecting one in eight women per year. Immediate implant-based breast reconstruction has emerged as the predominant approach for postmastectomy reconstruction, with a growing preference for the direct-to-implant (DTI) method over the traditional tissue expander technique. While conventionally, implants were typically positioned beneath the pectoralis major muscle, recent advancements have paved the way for implant placement above the muscle, in the prepectoral plane. Nipple-sparing mastectomy (NSM) and skin-sparing mastectomy (SSM) techniques can be combined with prepectoral breast reconstruction. The presence of sufficient fatty tissue coverage is considered one of the foremost independent factors influencing the success of immediate breast reconstruction and flap viability. DTI is a safe approach for prepectoral implant-based reconstruction with a number of advantages. However, careful patient selection and judicious assessment of flap perfusion help identify an appropriate subset of patients for prepectoral DTI reconstruction. Proposed breast tissue coverage classification (BTCC) and rigorous perfusion assessment techniques will aid to minimize postoperative complications and reconstruction failure. Based on the obtained range of coverage values (distance between the Cooper's ligaments and the skin) of preoperative digital mammogram evaluation, a three-type BTCC is as follows: Type 1: <1 cm (poor coverage), Type 2: between 1 and 2 cm (medium coverage), Type 3: >2 cm (good coverage). Prepectoral DTI reconstruction provides good results with complication rates similar to those of subpectoral techniques, eliminating breast animation. A meticulous surgical technique is essential to preserve the vascular network that guarantees the survival of the skin flap and nipple-areola complex (NAC). In the good coverage group (Type 3), an immediate DTI reconstruction could be safely performed. Aesthetic complications as rippling can occur if prepectoral implants are placed in Type 1 patients. Preoperative planning for prepectoral placement should not depend on breast volume, but on breast tissue coverage. Flap evaluation based on preoperative imaging measurements may be helpful when planning a conservative mastectomy. Patient selection, preoperative and intraoperative mastectomy flap evaluation, and modifications in implant technology play a critical role in this new and rapidly growing method for implant-based breast reconstruction.

Loss of tyrosine 211 phosphorylation of proliferating cell nuclear antigen (PCNA) enhances postnatal mammary gland development.

The intricately orchestrated progression of mammary tissue development involves the precise coordination of gland differentiation and cellular proliferation. Nevertheless, the understanding of the role and regulatory mechanisms governing the DNA replication machinery in mammary gland development remains limited. Given the essential role of DNA replication in the viability of living cells, any genetic disturbance to its replicative function, in any form, will impede organ development. This circumstance poses a technical challenge in elucidating the potential function of cell proliferation in mammary morphogenesis. PCNA is crucial in DNA replication, playing a pivotal role in the development of complete eukaryotic organisms. The phosphorylation of PCNA at tyrosine 211 (Y211) has been demonstrated to play a significant role in supporting replication forks and, consequently, cell proliferation. Therefore, the utilization of a knock-in mouse model, wherein the Y211 residue of PCNA is replaced with phenylalanine (211F), presents an opportunity to evaluate the impact of reduced cell proliferation potential on mammary gland development. Interestingly, the lack of Y211 phosphorylation did not significantly impact the rates of proliferation or cell death in the mammary gland. In contrast, the absence of Y211PCNA led to an increased, rather than reduced, growth of the mammary gland. This was evident in assessments of gland length and the number of terminal end buds (TEBs) in both postnatal and virgin mammary glands. Notably, this observation correlated with an elevation in tissue stemness within the 211F glands compared to the WT glands. Additionally, it was consistent with the greater body weight gains observed in 211F pups compared to WT pups during the weaning period. Our findings unveil an unexpected aspect that may carry significance for mammary development. This newfound is associated with the regulation of a central component within the DNA replication machinery, providing insights into the intricate interplay governing mammary tissue expansion.

Role for BLT1 in regulating inflammation within adipose tissue immune cells of aged mice

BackgroundAging is a complex biological process characterized by obesity and immunosenescence throughout the organism. Immunosenescence involves a decline in immune function and the increase in chronic-low grade inflammation, called inflammaging. Adipose tissue expansion, particularly that of visceral adipose tissue (VAT), is associated with an increase in pro-inflammatory macrophages that play an important role in modulating immune responses and producing inflammatory cytokines. The leukotriene B4 receptor 1 (BLT1) is a regulator of obesity-induced inflammation. Its ligand, LTB4, acts as a chemoattractant for immune cells and induces inflammation. Studies have shown that BLT1 is crucial for cytokine production during lipopolysaccharide (LPS) endotoxemia challenge in younger organisms. However, the expression patterns and function of BLT1 in older organisms remains unknown.ResultsIn this study, we investigated BLT1 expression in immune cell subsets within the VAT of aged male and female mice. Moreover, we examined how antagonizing BLT1 signaling could alter the inflammatory response to LPS in aged mice. Our results demonstrate that aged mice exhibit increased adiposity and inflammation, characterized by elevated frequencies of B and T cells, along with pro-inflammatory macrophages in VAT. BLT1 expression is the highest in VAT macrophages. LPS and LTB4 treatment result in increased BLT1 in young and aged bone marrow-derived macrophages (BMDMs). However, LTB4 treatment resulted in amplified Il6 from aged, but not young BMDMs. Treatment of aged mice with the BLT1 antagonist, U75302, followed by LPS-induced endotoxemia resulted in an increase in anti-inflammatory macrophages, reduced phosphorylated NFκB and reduced Il6.ConclusionsThis study provides valuable insights into the age- and sex- specific changes in BLT1 expression on immune cell subsets within VAT. This study offers support for the potential of BLT1 in modulating inflammation in aging.

Mesenchymal stem cells from adipose tissue prone to lose their stemness associated markers in obesity related stress conditions

Obesity is a health problem characterized by large expansion of adipose tissue. During this expansion, genotoxic stressors can be accumulated and negatively affect the mesenchymal stem cells (MSCs) of adipose tissue. Due to the oxidative stress generated by these genotoxic stressors, senescence phenotype might be observed in adipose tissue MSCs. Senescent MSCs lose their proliferations and differentiation properties and secrete senescence-associated molecules to their niche thus triggering senescence for the rest of the tissue. Accumulation of senescent cells in adipose tissue results in decreased tissue regeneration and functional impairment not only in the close vicinity but also in the other tissues. Here we hypothesized that declined tissue regeneration might be associated with loss of stemness markers in MSCs population. We analyzed the expression of several stemness-associated genes of in vitro cultured MSCs originated from adipose tissue of high-fat diet and normal diet mice models. Since the heterogenous MSCs population covers a small percentage of the pluripotent stem cells, which have roles in proliferation and tissue regeneration, we measured the percentage of these cells via TRA-1-60 pluripotent state antigen. Additionally, by conducting a shotgun proteomic approach using LC-MS/MS, whole cell proteome of the adipose tissue MSCs of high-fat diet and normal diet mice were analyzed and identified proteins were evaluated via gene ontology and PPI network analysis. MSCs of obese mice showed senescent phenotype and altered cell cycle distribution due to a hostile environment with oxidative stress in adipose tissue where they reside. Additionally, the number of pluripotent markers expressing cells declined in the MSC population of the high-fat diet mice. Gene expression analysis evidenced the loss of stemness with a decrease in the expression of stemness-associated genes. Of the proteomic comparison of the normal and the high-fat diet group, MSCs revealed that stemness-associated molecules were decreased while inflammation and senescence-associated phenotypes emerged in obese mice MSCs. Our results showed us that the MSCs of adipose tissue may lose their stemness properties due to obesity-associated stress conditions.

New concepts in the roles of AMPK in adipocyte stem cell biology.

Obesity is a major risk factor for many life-threatening diseases. Adipose tissue dysfunction is emerging as a driving factor in the transition from excess adiposity to comorbidities such as metabolic-associated fatty liver disease, cardiovascular disease, Type 2 diabetes and cancer. However, the transition from healthy adipose expansion to the development of these conditions is poorly understood. Adipose stem cells, residing in the vasculature and stromal regions of subcutaneous and visceral depots, are responsible for the expansion and maintenance of organ function, and are now recognised as key mediators of pathological transformation. Impaired tissue expansion drives inflammation, dysregulation of endocrine function and the deposition of lipids in the liver, muscle and around vital organs, where it is toxic. Contrary to previous hypotheses, it is the promotion of healthy adipose tissue expansion and function, not inhibition of adipogenesis, that presents the most attractive therapeutic strategy in the treatment of metabolic disease. AMP-activated protein kinase, a master regulator of energy homeostasis, has been regarded as one such target, due to its central role in adipose tissue lipid metabolism, and its apparent inhibition of adipogenesis. However, recent studies utilising AMP-activated protein kinase (AMPK)-specific compounds highlight a more subtle, time-dependent role for AMPK in the process of adipogenesis, and in a previously unexplored repression of leptin, independent of adipocyte maturity. In this article, I discuss historic evidence for AMPK-mediated adipogenesis inhibition and the multi-faceted roles for AMPK in adipose tissue.

Additional treatments after curettage of congenital melanocytic nevi in the craniofacial region: A report from a single center in Japan

BackgroundCongenital melanocytic nevus (CMN) is a benign skin lesion present from birth, which may present with a risk of malignant transformation if extensive. Curettage, a treatment method involving the removal of the superficial layer of the nevus, is often used in the early stages of life. However, recurrence of the nevus and postoperative scarring may present as problems. Additional treatments, such as resection and/or laser treatment, are regularly required after curettage, particularly in the craniofacial region. However, no systematic treatment strategy has been reported. This study investigated additional treatments used after curettage to treat CMN in the craniofacial region and compared the frequency of treatments with respect to specific sites. MethodsCMN cases involving curettage as an initial treatment were retrospectively reviewed at Kyoto University Hospital between May 2019 and April 2022. ResultsThis study comprised 23 cases. Curettage was performed at a mean of 3.8 (1–10) months of age. No additional treatments were provided for 80% of head CMN. Additional treatments were performed in all cases, including the forehead and cheek. Laser treatment was performed in 86% of eyelid CMN and 75% of nasal CMN. Tissue expansion and flap closure were used in 33% of forehead CMN and 33% of cheek CMN. ConclusionsAdditional treatments used for CMN in the craniofacial region varied in accordance with the lesion site.

A 10/14 French silicone urinary catheter with inflatable balloon used as novel expansion device in lid reconstruction surgery.

To describe the surgical technique using a 10/14 French silicone urinary catheter as a novel tissue expander for repair of defects after removal of eyelid tumors. This device recruits additional tissue by tissue expansion for repair of large eyelid defects. A prospective noncomparative, interventional case study was conducted over a period of 3 years in which 30 patients were enrolled. All the 30 patients were selected for upper or lower lid Tenzel rotational flap after removal of large malignant tumor, using the tissue expander. A 10/14-French silicone urinary catheter was placed in the periocular region and expanded by graded inflation with normal saline to a total volume of 10 or 14 ml, respectively, over a period of 3 days. On the fourth day before the planned surgery, the catheter balloon was deflated and a modified Tenzel rotational flap was performed to close the defect. Postoperative blink reflex was preserved. There were no cases of wound dehiscence. There was a significant reduction of incision length in upper and lower lid reconstruction with modified Tenzel flap reconstruction. This approach allows for temporary tissue expansion, permitting the closure of large eyelid defects, typically not possible with a conventional Tenzel flap. This also provides excellent functional outcomes without closing patients' eyelids (which limits vision for weeks to months) as is typical of other reconstructive modalities (e.g. Cutler Beard procedure). The device is cost-effective and readily available. The authors believe it is an excellent alternative in the developing world where access to more expensive options is limited.

Super‐Resolution Imaging in Collagen‐Abundant Thick Tissues

Expansion microscopy (ExM) has gained increasing popularity for 3D ultrastructural imaging of cultured cells and tissue slices at nanoscale resolution using conventional microscopes via physical expansion of biological tissues. However, its application to collagen‐abundant thick tissues is still challenging. Herein, a new method, collagen ExM (ColExM), optimized for expanding tissues containing more than 70% collagen, is demonstrated. ColExM succeeds in 4.5‐fold linear expansion with minimal structural distortion of corneal and skin tissues. It is compatible with immunostaining, allowing super‐resolution visualization of 3D neural structures innervating hair follicles, corneas, and pancreatic tumors with high stromal collagen content. The method succeeds in identifying individual mitochondria and previously unrecognized dendritic spinelike structures of corneal nerves. It also enables fine mapping of structural rearrangement of tight junctions and actin cytoskeletons. Therefore, ColExM can facilitate the exploration of 3D nanoscale structures in collagen‐rich tissues.

Data quality assessment of the Dutch Breast Implant Registry by automated data verification using medical billing data

The Dutch Breast Implant Registry (DBIR) provides real-time population-based data to monitor and improve the quality and safety of breast implants and to trace patients in the event of an (inter)national recall. To serve these main goals, the capture rate and percentage of implants that are actually registered should be known and data should be complete. This study aimed to describe an automated verification process for capture rates and data completeness using medical billing data as the external source. DBIR-data on reconstructive permanent breast implants and tissue expanders (TEs) from 2019 were compared to medical billing data. At the hospital level, the capture rate of DBIR and accuracy of the selected data points were assessed. In total, 2389 implants (1420 patients) were included from 12 participating hospitals (11% of all healthcare institutions registering in DBIR). DBIR had capture rates of 99% to 114% for inserted permanent implants and TEs and 49% for explanted permanent implants and TEs. Among the 9015 data points analyzed in DBIR, 8861 (98%) matched the medical billing data. Mastopexy had the highest matching percentage (100%) and capsulectomy the lowest (86%). This study showed varying capture rates in DBIR depending on the intervention group, indicating that registration of DBIR-data and medical billing codes could be further optimized. Data accuracy was high as only 2% of data points did not correspond to medical billing data. For future data verification, other external data sources could be explored, including sources that enable verification of cosmetic implants.

A conserved regulation of cell expansion underlies notochord mechanics, spine morphogenesis, and endochondral bone lengthening.

Cell size is a key contributor to tissue morphogenesis 1 . As a notable example, growth plate hypertrophic chondrocytes use cellular biogenesis and disproportionate fluid uptake to expand 10-20 times in size to drive lengthening of endochondral bone 2,3 . Similarly, notochordal cells expand to one of the largest cell types in the developing embryo to drive axial extension 4-6 . In zebrafish, the notochord vacuolated cells undergo vacuole fusion to form a single large, fluid-filled vacuole that fills the cytoplasmic space and contributes to vacuolated cell expansion 7 . When this process goes awry, the notochord lacks sufficient hydrostatic pressure to support vertebral bone deposition resulting in adult spines with misshapen vertebral bones and scoliosis 8 . However, it remains unclear whether endochondral bone and the notochord share common genetic and cellular mechanisms for regulating cell and tissue expansion. Here, we demonstrate that the 5'-inositol phosphatase gene, inppl1a , regulates notochord expansion, spine morphogenesis, and endochondral bone lengthening in zebrafish. Furthermore, we show that inppl1a regulates notochord expansion independent of vacuole fusion, thereby genetically decoupling these processes. We demonstrate that inppl1a -dependent notochord expansion is essential to establish normal mechanical properties of the notochord to facilitate the development of a straight spine. Finally, we find that inppl1a is also important for endochondral bone lengthening in fish, as has been shown in the human INPPL1 -related endochondral bone disorder, Opsismodysplasia 9 . Overall, this work reveals a conserved mechanism of cell size regulation that influences disparate tissues critical for skeletal development and short-stature disorders.