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BACKGROUND: Pilonidal sinus can be treated with excision and flap reconstruction, but treatment is often complicated by wound dehiscence, infection, and recurrence. Understanding the mechanical forces on the sacrococcygeal area during posture change could help guide optimal flap choice. METHODS: Sixteen volunteers underwent measurements of skin-stretching, pressure, and shear stress on the sacrum when sitting relative to standing. Skin-stretching was measured by drawing a 4 × 4 cm square on the sacrum and measuring the vertical, horizontal, and diagonal axes. Pressure and shear stress was measured at six sacral points with a device. The data analysis highlighted the potential of the superior gluteal artery perforator (SGAP) flap for dissipating mechanical forces. Ten pilonidal sinus cases treated with SGAP flaps were retrospectively reviewed for 6-month outcomes. RESULTS: Sitting is associated with high stretching tension in the horizontal direction [estimated marginal mean (95% confidence intervals) = 17.3% (15.4%-22.6%)]. The lower sacrum experienced the highest pressure [106.6 (96.6-116.5) mm Hg] and shear stress [11.6 (9.7-13.5) N] during sitting. The transposed SGAP flap was deemed to be optimal for releasing the horizontal tension and providing sufficient subcutaneous tissue for ameliorating pressure/shear stress during sitting. It also has high blood flow and can therefore be used with large lesions. Moreover, its donor site is above the high-pressure/stress lower sacrum. Retrospective analysis showed that no patients experienced complications. CONCLUSIONS: Sitting is associated with high mechanical forces on the sacrococcygeal skin. The transposed SGAP flap may ameliorate these forces and thereby reduce the risk of complications of pilonidal sinus reconstruction for large defects.

DOI： 10.1097/GOX.0000000000005923

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Language：English   Publishing type：Research paper (scientific journal)  

UNLABELLED: Keloids are red' invasive scars that are driven by chronic inflammation in the reticular dermis. The role of blood vessels in keloid behavior remains poorly understood. In the present study with 32 keloid patients, we examined the hemodynamics of keloid tissue, the anatomy of the blood vessels feeding and draining the keloids, and the vascular histology of keloids. METHODS: Ten patients with large anterior chest keloids underwent near-infrared spectroscopy, which measured regional saturation of oxygen and total hemoglobin index in the keloid and surrounding skin. Another 10 patients with large chest keloids and three healthy volunteers underwent multidetector-low computed tomography. The extirpated chest keloids of 12 patients were subjected to histology with optical, CD31 immunohistochemical, and electron microscopy. RESULTS: All keloids had a low regional saturation of oxygen and a high total hemoglobin index, which is indicative of blood congestion. Multidetector-low computed tomography revealed dilation of the arteries and veins that were respectively feeding and draining the keloid leading edge. Hematoxylin-eosin staining and CD31 immunohistochemisty revealed considerable neovascularization in the keloid leading edge but not in the center. Electron microscopy showed that the lumens of many vessels in the keloid center appeared to be occluded or narrowed. CONCLUSIONS: Keloids seem to be congested because of increased neovascularization and arterial inflow at the leading edge and blocked outflow due to vascular destruction in the center. The surrounding veins seem to expand in response to this congested state. Methods that improve the blood circulation in keloids may be effective therapies.

DOI： 10.1097/GOX.0000000000004374

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Language：English   Publishing type：Research paper (scientific journal)  

Wound healing is a complex biological process, and imbalances of various substances in the wound environment may prolong healing and lead to excessive scarring. Keloid is abnormal proliferation of scar tissue beyond the original wound margins with excessive deposition of extracellular matrix (ECM) and chronic inflammation. Despite numerous previous research efforts, the pathogenesis of keloid remains unknown. Vascular endothelial cells (VECs) are a major type of inductive cell in inflammation and fibrosis. Despite several studies on vascular morphology in keloid formation, there has been no functional analysis of the role of VECs. In the present study, we isolated living VECs from keloid tissues and investigated gene expression patterns using microarray analysis. We obtained 5 keloid tissue samples and 6 normal skin samples from patients without keloid. Immediately after excision, tissue samples were gently minced and living cells were isolated. Magnetic-activated cell sorting of VECs was performed by negative selection of fibroblasts and CD45+ cells and by positive selection of CD31+cells. After RNA extraction, gene expression analysis was performed to compare VECs isolated from keloid tissue (KVECs) with VECs from normal skin (NVECs). After cell isolation, the percentage of CD31+ cells as measured by flow cytometry ranged from 81.8%-98.6%. Principal component analysis was used to identify distinct molecular phenotypes in KVECs versus NVECs and these were divided into two subgroups. In total, 15 genes were upregulated, and 3 genes were downregulated in KVECs compared with NVECs using the t-test (< 0.05). Quantitative RT-PCR and immunohistochemistry showed 16-fold and 11-fold overexpression of SERPINA3 and LAMC2, respectively. SERPINA3 encodes the serine protease inhibitor, α1-antichymotripsin. Laminin γ2-Chain (LAMC2) is a subunit of laminin-5 that induces retraction of vascular endothelial cells and enhances vascular permeability. This is the first report of VEC isolation and gene expression analysis in keloid tissue. Our data suggest that SERPINA3 and LAMC2 upregulation in KVECs may contribute to the development of fibrosis and prolonged inflammation in keloid. Further functional investigation of these genes will help clarify the mechanisms of abnormal scar tissue proliferation.

DOI： 10.3389/fcell.2020.00658

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Language：Japanese   Publisher：克誠堂出版(株)  

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2016&ichushi_jid=J00398&link_issn=&doc_id=20160714240006&doc_link_id=%2Fad3ksgke%2F2016%2F005907%2F008%2F0738-0748%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fad3ksgke%2F2016%2F005907%2F008%2F0738-0748%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1097/PRS.0b013e31824a9f76

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Language：Japanese   Publisher：日本医科大学医学会  

J-GLOBAL

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Language：Japanese   Publisher：日本医科大学医学会  

J-GLOBAL

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