Angiogenesis induction and regression in human surgical wounds
Angiogenesis in human wound healing is not well characterized, with only sparse information available regarding the maturation and fate of vessels formed as a consequence of human tissue repair. Therefore, this study aimed to establish the temporal profile of angiogenesis in human dermal wounds. Pun...
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Veröffentlicht in: | Wound repair and regeneration 2002-07, Vol.10 (4), p.245-251 |
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description | Angiogenesis in human wound healing is not well characterized, with only sparse information available regarding the maturation and fate of vessels formed as a consequence of human tissue repair. Therefore, this study aimed to establish the temporal profile of angiogenesis in human dermal wounds. Punch biopsies were obtained under local anesthesia from 45 patients following breast surgery. Scars were predominantly between 2 and 52 weeks after surgery but in five patients were > 52 weeks. Control samples were taken from breast skin peroperatively (n=24). Quantification of vascular density was performed using the Chalkley grid, following antibody staining for platelet endothelial cell adhesion molecule. Vascular patterns, wound cellularity and morphology were also determined. Cumulative microvessel density was increased in all samples when compared to controls (p 52 weeks. Control tissue showed an ordered morphological arrangement of dermal structures, collagen, and elastic fibers. However, wounding resulted in marked structural distortion for up to 15 weeks. In conclusion, this study shows for the first time the prolonged persistence of both microvessels and cellularity (fibroblastic cells), in addition to structural distortion in human dermal wounds, which is in contrast to previous in vitro and in vivo studies. (WOUND REP REG 2002;10:245–251) |
doi_str_mv | 10.1046/j.1524-475X.2002.10408.x |
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Cumulative microvessel density was increased in all samples when compared to controls (p < 0.05). This was greatest 2 to 24 weeks following surgery 17 (15–21) median (range), decreased thereafter, but remained elevated compared to controls even in the mature scars > 52 weeks. Control tissue showed an ordered morphological arrangement of dermal structures, collagen, and elastic fibers. However, wounding resulted in marked structural distortion for up to 15 weeks. In conclusion, this study shows for the first time the prolonged persistence of both microvessels and cellularity (fibroblastic cells), in addition to structural distortion in human dermal wounds, which is in contrast to previous in vitro and in vivo studies. 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E.</creatorcontrib><creatorcontrib>Cross, Simon S.</creatorcontrib><creatorcontrib>Reed, Malcolm W. R.</creatorcontrib><title>Angiogenesis induction and regression in human surgical wounds</title><title>Wound repair and regeneration</title><addtitle>Wound Repair Regen</addtitle><description>Angiogenesis in human wound healing is not well characterized, with only sparse information available regarding the maturation and fate of vessels formed as a consequence of human tissue repair. Therefore, this study aimed to establish the temporal profile of angiogenesis in human dermal wounds. Punch biopsies were obtained under local anesthesia from 45 patients following breast surgery. Scars were predominantly between 2 and 52 weeks after surgery but in five patients were > 52 weeks. Control samples were taken from breast skin peroperatively (n=24). Quantification of vascular density was performed using the Chalkley grid, following antibody staining for platelet endothelial cell adhesion molecule. Vascular patterns, wound cellularity and morphology were also determined. Cumulative microvessel density was increased in all samples when compared to controls (p < 0.05). This was greatest 2 to 24 weeks following surgery 17 (15–21) median (range), decreased thereafter, but remained elevated compared to controls even in the mature scars > 52 weeks. Control tissue showed an ordered morphological arrangement of dermal structures, collagen, and elastic fibers. However, wounding resulted in marked structural distortion for up to 15 weeks. In conclusion, this study shows for the first time the prolonged persistence of both microvessels and cellularity (fibroblastic cells), in addition to structural distortion in human dermal wounds, which is in contrast to previous in vitro and in vivo studies. (WOUND REP REG 2002;10:245–251)</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biopsy, Needle - adverse effects</subject><subject>Cicatrix - etiology</subject><subject>Cicatrix - pathology</subject><subject>Cicatrix - physiopathology</subject><subject>Dermis - blood supply</subject><subject>Dermis - injuries</subject><subject>Dermis - physiopathology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Middle Aged</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Remission Induction</subject><subject>Time Factors</subject><subject>Wound Healing - physiology</subject><subject>Wounds, Penetrating - etiology</subject><subject>Wounds, Penetrating - pathology</subject><subject>Wounds, Penetrating - physiopathology</subject><issn>1067-1927</issn><issn>1524-475X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkF1PwjAUhhujEUX_gtmVd8N-rGt3Q0KIognBhGjgrum6Foujw5YF-PduQPDWq572vOdpzgNAhGAPwSR9WvYQxUmcMDrvYQhx-wp5b3cBbs6Ny6aGKYtRhlkH3IawhBBSmvFr0EEYZQhCdgP6A7ew1UI7HWyIrCtqtbGVi6QrIq8XXofQXq2LvuqVdFGo_cIqWUbbqnZFuANXRpZB35_OLvh8ef4Yvsbj99HbcDCOVUIIj3GSy9yYVDLKWcKhQUYpxDgjhuZIGZaRlPIsxTrNckaYlHmR5AxTZVCOCSJd8Hjkrn31U-uwESsblC5L6XRVB8EwRDxhvAnyY1D5KgSvjVh7u5J-LxAUrTuxFK0i0SoSrTtxcCd2zejD6Y86X-nib_Akqwn0j4GtLfX-32Axm04PZQOIjwAbNnp3Bkj_LdJmaypmk5Gg8wnPGBkLSn4BbbqMyA</recordid><startdate>200207</startdate><enddate>200207</enddate><creator>Brown, Nicola J.</creator><creator>Smyth, Edward A. E.</creator><creator>Cross, Simon S.</creator><creator>Reed, Malcolm W. R.</creator><general>Blackwell Science Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200207</creationdate><title>Angiogenesis induction and regression in human surgical wounds</title><author>Brown, Nicola J. ; Smyth, Edward A. E. ; Cross, Simon S. ; Reed, Malcolm W. R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4338-24babff6a7587480f1fcc17873f5b1cf793658962e69b737aabd4b725cf1b2313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biopsy, Needle - adverse effects</topic><topic>Cicatrix - etiology</topic><topic>Cicatrix - pathology</topic><topic>Cicatrix - physiopathology</topic><topic>Dermis - blood supply</topic><topic>Dermis - injuries</topic><topic>Dermis - physiopathology</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Middle Aged</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Remission Induction</topic><topic>Time Factors</topic><topic>Wound Healing - physiology</topic><topic>Wounds, Penetrating - etiology</topic><topic>Wounds, Penetrating - pathology</topic><topic>Wounds, Penetrating - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, Nicola J.</creatorcontrib><creatorcontrib>Smyth, Edward A. E.</creatorcontrib><creatorcontrib>Cross, Simon S.</creatorcontrib><creatorcontrib>Reed, Malcolm W. R.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Wound repair and regeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Nicola J.</au><au>Smyth, Edward A. E.</au><au>Cross, Simon S.</au><au>Reed, Malcolm W. R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiogenesis induction and regression in human surgical wounds</atitle><jtitle>Wound repair and regeneration</jtitle><addtitle>Wound Repair Regen</addtitle><date>2002-07</date><risdate>2002</risdate><volume>10</volume><issue>4</issue><spage>245</spage><epage>251</epage><pages>245-251</pages><issn>1067-1927</issn><eissn>1524-475X</eissn><abstract>Angiogenesis in human wound healing is not well characterized, with only sparse information available regarding the maturation and fate of vessels formed as a consequence of human tissue repair. Therefore, this study aimed to establish the temporal profile of angiogenesis in human dermal wounds. Punch biopsies were obtained under local anesthesia from 45 patients following breast surgery. Scars were predominantly between 2 and 52 weeks after surgery but in five patients were > 52 weeks. Control samples were taken from breast skin peroperatively (n=24). Quantification of vascular density was performed using the Chalkley grid, following antibody staining for platelet endothelial cell adhesion molecule. Vascular patterns, wound cellularity and morphology were also determined. Cumulative microvessel density was increased in all samples when compared to controls (p < 0.05). This was greatest 2 to 24 weeks following surgery 17 (15–21) median (range), decreased thereafter, but remained elevated compared to controls even in the mature scars > 52 weeks. Control tissue showed an ordered morphological arrangement of dermal structures, collagen, and elastic fibers. However, wounding resulted in marked structural distortion for up to 15 weeks. In conclusion, this study shows for the first time the prolonged persistence of both microvessels and cellularity (fibroblastic cells), in addition to structural distortion in human dermal wounds, which is in contrast to previous in vitro and in vivo studies. (WOUND REP REG 2002;10:245–251)</abstract><cop>Malden, USA</cop><pub>Blackwell Science Inc</pub><pmid>12191007</pmid><doi>10.1046/j.1524-475X.2002.10408.x</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Aged Aged, 80 and over Biopsy, Needle - adverse effects Cicatrix - etiology Cicatrix - pathology Cicatrix - physiopathology Dermis - blood supply Dermis - injuries Dermis - physiopathology Female Follow-Up Studies Humans Middle Aged Neovascularization, Physiologic - physiology Remission Induction Time Factors Wound Healing - physiology Wounds, Penetrating - etiology Wounds, Penetrating - pathology Wounds, Penetrating - physiopathology |
title | Angiogenesis induction and regression in human surgical wounds |
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