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Michael T. Longaker - One of the best experts on this subject based on the ideXlab platform.
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Scarless Fetal Skin wound healing update
Birth defects research. Part C Embryo today : reviews, 2012Co-Authors: A.s. Zimmermann, Michael T. Longaker, Allison Nauta, H. Peter LorenzAbstract:Scar formation, a physiologic process in adult wound healing, can have devastating effects for patients; a multitude of pathologic outcomes, affecting all organ systems, stems from an amplification of this process. In contrast to adult wound repair, the early-gestation Fetal Skin wound heals without scar formation, a phenomenon that appears to be intrinsic to Fetal Skin. An intensive research effort has focused on unraveling the mechanisms that underlie scarless Fetal wound healing in an attempt to improve the quality of healing in both children and adults. Unique properties of Fetal cells, extracellular matrix, cytokine profile, and gene expression contribute to this scarless repair. Despite the great increase in knowledge gained over the past decades, the precise mechanisms regulating scarless Fetal healing remain unknown. Herein, we describe the current proposed mechanisms underlying Fetal scarless wound healing in an effort to recapitulate the Fetal phenotype in the postnatal environment. Birth Defects Research (Part C) 96:237–247, 2012. © 2012 Wiley Periodicals, Inc.
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Chapter 6 Fetal Skin Wound Healing
Advances in clinical chemistry, 2009Co-Authors: Edward P. Buchanan, Michael T. Longaker, H. Peter LorenzAbstract:1. Abstract The developing fetus has the ability to heal wounds by regenerating normal epidermis and dermis with restoration of the extracellular matrix (ECM) architecture, strength, and function. In contrast, adult wounds heal with fibrosis and scar. Scar tissue remains weaker than normal Skin with an altered ECM composition. Despite extensive investigation, the mechanism of Fetal wound healing remains largely unknown. We do know that early in gestation, Fetal Skin is developing at a rapid pace and the ECM is a loose network facilitating cellular migration. Wounding in this unique environment triggers a complex cascade of tightly controlled events culminating in a scarless wound phenotype of fine reticular collagen and abundant hyaluronic acid. Comparison between postnatal and Fetal wound healing has revealed differences in inflammatory response, cellular mediators, cytokines, growth factors, and ECM modulators. Investigation into cell signaling pathways and transcription factors has demonstrated differences in secondary messenger phosphorylation patterns and homeobox gene expression. Further research may reveal novel genes essential to scarless repair that can be manipulated in the adult wound and thus ameliorate scar.
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Fetal Skin wound healing.
Advances in clinical chemistry, 2009Co-Authors: Edward P. Buchanan, Michael T. Longaker, H. Peter LorenzAbstract:The developing fetus has the ability to heal wounds by regenerating normal epidermis and dermis with restoration of the extracellular matrix (ECM) architecture, strength, and function. In contrast, adult wounds heal with fibrosis and scar. Scar tissue remains weaker than normal Skin with an altered ECM composition. Despite extensive investigation, the mechanism of Fetal wound healing remains largely unknown. We do know that early in gestation, Fetal Skin is developing at a rapid pace and the ECM is a loose network facilitating cellular migration. Wounding in this unique environment triggers a complex cascade of tightly controlled events culminating in a scarless wound phenotype of fine reticular collagen and abundant hyaluronic acid. Comparison between postnatal and Fetal wound healing has revealed differences in inflammatory response, cellular mediators, cytokines, growth factors, and ECM modulators. Investigation into cell signaling pathways and transcription factors has demonstrated differences in secondary messenger phosphorylation patterns and homeobox gene expression. Further research may reveal novel genes essential to scarless repair that can be manipulated in the adult wound and thus ameliorate scar.
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The Fetal Fibroblast: The Effector Cell of Scarless Fetal Skin Repair
Plastic and reconstructive surgery, 1995Co-Authors: H P Lorenz, Michael T. Longaker, Richard Y. Lin, David J. WhitbyAbstract:Human Fetal Skin heals without scar formation when it is transplanted to a subcutaneous location on an adult athymic mouse and subsequently wounded. In contrast, human Fetal Skin of identical gestational age heals with scar formation when transplanted to a cutaneous location on the athymic mouse recipient. To determine if mouse (adult) or human (Fetal) fibroblasts are healing the graft wounds, we performed indirect immunohistochemistry for mouse and human collagen types I and III. Full-thickness Skin grafts (n = 51) from human fetuses at 18 weeks' (n = 4) or 24 weeks' (n = 2) gestational age were placed onto athymic mice in two locations: cutaneously onto a fascial bed and subcutaneously in a pocket under the murine panniculus carnosus. Linear incisions were made in each graft 7 days after transplantation. Grafts were harvested at 7, 14, and 21 days after wounding and stained with hematoxylin and eosin or Mallory's trichrome. Immunohistochemistry for either human collagen type I or type III or for mouse collagen type I was performed. The subcutaneous grafts healed with human collagen types I and III in a scarless pattern. The wound collagen pattern was reticular and unrecognizable from the surrounding dermis. Hair follicles and sebaceous gland patterns were unchanged in the wounded dermis. Conversely, the cutaneous grafts healed with mouse collagen in a scar pattern with disorganized collagen fibers and no appendages. Mouse collagen scar was present along the base of the cutaneous grafts and as a thin capsule around the subcutaneous grafts. We conclude that (1) subcutaneous grafts heal with human Fetal collagen and no scar formation, and (2) cutaneous grafts heal with mouse collagen in a scar pattern. Fetal fibroblasts can heal Fetal Skin wounds without scar despite being perfused by adult serum and inflammatory cells in an adult environment. These data suggest that the Fetal fibroblast is the major effector cell for scarless Fetal Skin repair.
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The Fetal fibroblast : the effector cell of scarless Fetal Skin repair. Discussion
Plastic and Reconstructive Surgery, 1995Co-Authors: Hermann P. Lorenz, Michael T. Longaker, Richard Y. Lin, David J. Whitby, P. MartinAbstract:Human Fetal Skin heals without scar formation when it is transplanted to a subcutaneous location on an adult athymic mouse and subsequently wounded. In contrast, human Fetal Skin of identical gestational age heals with scar formation when transplanted to a cutaneous location on the athymic mouse recipient. To determine if mouse (adult) or human (Fetal) fibroblasts are healing the graft wounds, we performed indirect immunohistochemistry for mouse and human collagen types I and III. Full-thickness Skin grafts (n = 51) from human fetuses at 18 weeks' (n = 4) or 24 weeks' (n = 2) gestational age were placed onto athymic mice in two locations : cutaneously onto a fascial bed and subcutaneously in a pocket under the murine panniculus carnosus. Linear incisions were made in each graft 7 days after transplantation. Grafts were harvested at 7, 14, and 21 days after wounding and stained with hematoxylin and eosin or Mallory's trichrome. Immunohistochemistry for either human collagen type I or type III or for mouse collagen type I was performed. The subcutaneous grafts healed with human collagen types I and III in a scarless pattern. The wound collagen pattern was reticular and unrecognizable from the surrounding dermis. Hair follicles and sebaceous gland patterns were unchanged in the wounded dermis. Conversely, the cutaneous grafts healed with mouse collagen in a scar pattern with disorganized collagen fibers and no appendages. Mouse collagen scar was present along the base of the cutaneous grafts and as a thin capsule around the subcutaneous grafts. We conclude that (1) subcutaneous grafts heal with human Fetal collagen and no scar formation, and (2) cutaneous grafts heal with mouse collagen in a scar pattern. Fetal fibroblasts can heal Fetal Skin wounds without scar despite being perfused by adult serum and inflammatory cells in an adult environment. These data suggest that the Fetal fibroblast is the major effector cell for scarless Fetal Skin repair.
Karen A Holbrook - One of the best experts on this subject based on the ideXlab platform.
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ultrasound guided Fetal Skin sampling for prenatal diagnosis of genodermatoses
Obstetrics & Gynecology, 1994Co-Authors: Donald S Emerson, Joe Leigh Simpson, Sherman Elias, Lee P Shulman, Karen A HolbrookAbstract:Objective: To evaluate the safety and diagnostic efficacy of ultrasound-guided Fetal Skin sampling for the prenatal diagnosis of genodermatoses. Methods: Seventeen pregnancies seen over 6.5 yearn were analyzed retrospectively. Fifteen were at risk for junctional epidermolysis bullosa and two for recessive dystrophic epidermolysis bullosa. Under ultrasound guidance, a biopsy forceps was inserted through a 14-gauge catheter and directed toward the fetus (thorax, back, or buttocks) to obtain Skin samples. The procedures were performed at a mean of 18.3 weeks'gestation (range 16.5-19.5). Results: Fetal Skin sampling was successful in all cases; the mean number of biopsies taken was 3.6 (range two to five)
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Ultrasound-guided Fetal Skin sampling for prenatal diagnosis of genodermatoses.
Obstetrics and gynecology, 1994Co-Authors: Sherman Elias, Donald S Emerson, Joe Leigh Simpson, Lee P Shulman, Karen A HolbrookAbstract:OBJECTIVE To evaluate the safety and diagnostic efficacy of ultrasound-guided Fetal Skin sampling for the prenatal diagnosis of genodermatoses. METHODS Seventeen pregnancies seen over 6.5 years were analyzed retrospectively. Fifteen were at risk for junctional epidermolysis bullosa and two for recessive dystrophic epidermolysis bullosa. Under ultrasound guidance, a biopsy forceps was inserted through a 14-gauge catheter and directed toward the fetus (thorax, back, or buttocks) to obtain Skin samples. The procedures were performed at a mean of 18.3 weeks' gestation (range 16.5-19.5). RESULTS Fetal Skin sampling was successful in all cases; the mean number of biopsies taken was 3.6 (range two to five). Five of the 17 fetuses were determined to be affected, each with junctional epidermolysis bullosa; these pregnancies were terminated electively and the prenatal diagnoses confirmed. The remaining 12 pregnancies resulted in the delivery of healthy infants at or after 37 weeks' gestation. There were no pregnancy-related complications, specifically preterm rupture of the membranes or preterm labor. Three of the 12 infants had minor Skin blemishes believed to be due to the Skin sampling. CONCLUSION Ultrasound-guided Fetal Skin sampling is the procedure of choice when Fetal Skin is required for prenatal diagnosis of genodermatoses.
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Prenatal diagnosis of genetic Skin disease using Fetal Skin biopsy samples
Archives of dermatology, 1993Co-Authors: Karen A Holbrook, Lynne T. Smith, Sherman EliasAbstract:Background: Understanding normal Skin development and identifying markers of genetic Skin disease expressed in postnatal Skin have permitted the prenatal diagnosis of many severe genodermatoses: bullous diseases, keratinization diseases, pigment cell disorders, and disorders of the epidermal appendages (ectodermal dysplasias). Samples of 16 to 22 weeks' gestation Fetal Skin obtained by ultrasound-guided biopsy are evaluated using morphologic, immunohistochemical, and biochemical methods. Observations: The 12-year experience in evaluating samples from fetuses at risk of these disorders has allowed us to establish conditions that must be met before the samples are taken and the criteria for recognizing the disorder, to recommend the site(s) for sampling, and to be mindful of pitfalls that may be encountered in interpreting the tissue structure. Conclusions: Fetal Skin biopsy is an important diagnostic tool that has permitted families in which members carry the abnormal gene for one of these severe Skin diseases to undertake a pregnancy knowing that the condition of the fetus can be determined. Nonetheless, the ultimate goal is phase out this procedure when linkage of more of these disorders to specific genes is understood, specific mutations are characterized, and probes are available for molecular diagnoses using tissue obtained at earlier Fetal ages. Until this is possible, Fetal Skin biopsy remains an important tool that can be used with reasonably high levels of safety and confidence. ( Arch Dermatol. 1993;129:1437-1454)
H. Peter Lorenz - One of the best experts on this subject based on the ideXlab platform.
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Scarless Fetal Skin wound healing update
Birth defects research. Part C Embryo today : reviews, 2012Co-Authors: A.s. Zimmermann, Michael T. Longaker, Allison Nauta, H. Peter LorenzAbstract:Scar formation, a physiologic process in adult wound healing, can have devastating effects for patients; a multitude of pathologic outcomes, affecting all organ systems, stems from an amplification of this process. In contrast to adult wound repair, the early-gestation Fetal Skin wound heals without scar formation, a phenomenon that appears to be intrinsic to Fetal Skin. An intensive research effort has focused on unraveling the mechanisms that underlie scarless Fetal wound healing in an attempt to improve the quality of healing in both children and adults. Unique properties of Fetal cells, extracellular matrix, cytokine profile, and gene expression contribute to this scarless repair. Despite the great increase in knowledge gained over the past decades, the precise mechanisms regulating scarless Fetal healing remain unknown. Herein, we describe the current proposed mechanisms underlying Fetal scarless wound healing in an effort to recapitulate the Fetal phenotype in the postnatal environment. Birth Defects Research (Part C) 96:237–247, 2012. © 2012 Wiley Periodicals, Inc.
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Chapter 6 Fetal Skin Wound Healing
Advances in clinical chemistry, 2009Co-Authors: Edward P. Buchanan, Michael T. Longaker, H. Peter LorenzAbstract:1. Abstract The developing fetus has the ability to heal wounds by regenerating normal epidermis and dermis with restoration of the extracellular matrix (ECM) architecture, strength, and function. In contrast, adult wounds heal with fibrosis and scar. Scar tissue remains weaker than normal Skin with an altered ECM composition. Despite extensive investigation, the mechanism of Fetal wound healing remains largely unknown. We do know that early in gestation, Fetal Skin is developing at a rapid pace and the ECM is a loose network facilitating cellular migration. Wounding in this unique environment triggers a complex cascade of tightly controlled events culminating in a scarless wound phenotype of fine reticular collagen and abundant hyaluronic acid. Comparison between postnatal and Fetal wound healing has revealed differences in inflammatory response, cellular mediators, cytokines, growth factors, and ECM modulators. Investigation into cell signaling pathways and transcription factors has demonstrated differences in secondary messenger phosphorylation patterns and homeobox gene expression. Further research may reveal novel genes essential to scarless repair that can be manipulated in the adult wound and thus ameliorate scar.
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Fetal Skin wound healing.
Advances in clinical chemistry, 2009Co-Authors: Edward P. Buchanan, Michael T. Longaker, H. Peter LorenzAbstract:The developing fetus has the ability to heal wounds by regenerating normal epidermis and dermis with restoration of the extracellular matrix (ECM) architecture, strength, and function. In contrast, adult wounds heal with fibrosis and scar. Scar tissue remains weaker than normal Skin with an altered ECM composition. Despite extensive investigation, the mechanism of Fetal wound healing remains largely unknown. We do know that early in gestation, Fetal Skin is developing at a rapid pace and the ECM is a loose network facilitating cellular migration. Wounding in this unique environment triggers a complex cascade of tightly controlled events culminating in a scarless wound phenotype of fine reticular collagen and abundant hyaluronic acid. Comparison between postnatal and Fetal wound healing has revealed differences in inflammatory response, cellular mediators, cytokines, growth factors, and ECM modulators. Investigation into cell signaling pathways and transcription factors has demonstrated differences in secondary messenger phosphorylation patterns and homeobox gene expression. Further research may reveal novel genes essential to scarless repair that can be manipulated in the adult wound and thus ameliorate scar.
H P Lorenz - One of the best experts on this subject based on the ideXlab platform.
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exogenous transforming growth factor beta amplifies its own expression and induces scar formation in a model of human Fetal Skin repair
Annals of Surgery, 1995Co-Authors: Kerry M Sullivan, Peter A Argenta, Martin Meuli, H P Lorenz, N S AdzickAbstract:OBJECTIVE: Fetal Skin wounds heal without scarring. To determine the role of TGF-beta 1 in Fetal wound healing, mRNA expression of TGF-beta 1 was analyzed in human Fetal and adult Skin wounds. METHODS: Human Fetal Skin transplanted to a subcutaneous location on an adult athymic mouse that was subsequently wounded heals without scar, whereas human adult Skin heals with scar formation in that location. In situ hybridization for TGF-beta 1 mRNA expression and species-specific immunohistochemistry for fibroblasts, macrophages, and neutrophils were performed in human adult wounds, Fetal wounds, and Fetal wounds treated with a TGF-beta 1 slow release disk. RESULTS: Transforming growth factor-beta 1 mRNA expression was induced by wounding adult Skin. No TGF-beta 1 mRNA upregulation was detected in human Fetal Skin after wounding. However, when exogenous TGF-beta 1 was added to human Fetal Skin, induction of TGF-beta 1 mRNA expression in human Fetal fibroblasts occurred, an adult-like inflammatory response was detected, and the Skin healed with scar formation. CONCLUSIONS: Transforming growth factor-beta 1 is an important modulator in scar formation. Anti-TGF-beta 1 strategies may promote scarless healing in adult wounds.
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The Fetal Fibroblast: The Effector Cell of Scarless Fetal Skin Repair
Plastic and reconstructive surgery, 1995Co-Authors: H P Lorenz, Michael T. Longaker, Richard Y. Lin, David J. WhitbyAbstract:Human Fetal Skin heals without scar formation when it is transplanted to a subcutaneous location on an adult athymic mouse and subsequently wounded. In contrast, human Fetal Skin of identical gestational age heals with scar formation when transplanted to a cutaneous location on the athymic mouse recipient. To determine if mouse (adult) or human (Fetal) fibroblasts are healing the graft wounds, we performed indirect immunohistochemistry for mouse and human collagen types I and III. Full-thickness Skin grafts (n = 51) from human fetuses at 18 weeks' (n = 4) or 24 weeks' (n = 2) gestational age were placed onto athymic mice in two locations: cutaneously onto a fascial bed and subcutaneously in a pocket under the murine panniculus carnosus. Linear incisions were made in each graft 7 days after transplantation. Grafts were harvested at 7, 14, and 21 days after wounding and stained with hematoxylin and eosin or Mallory's trichrome. Immunohistochemistry for either human collagen type I or type III or for mouse collagen type I was performed. The subcutaneous grafts healed with human collagen types I and III in a scarless pattern. The wound collagen pattern was reticular and unrecognizable from the surrounding dermis. Hair follicles and sebaceous gland patterns were unchanged in the wounded dermis. Conversely, the cutaneous grafts healed with mouse collagen in a scar pattern with disorganized collagen fibers and no appendages. Mouse collagen scar was present along the base of the cutaneous grafts and as a thin capsule around the subcutaneous grafts. We conclude that (1) subcutaneous grafts heal with human Fetal collagen and no scar formation, and (2) cutaneous grafts heal with mouse collagen in a scar pattern. Fetal fibroblasts can heal Fetal Skin wounds without scar despite being perfused by adult serum and inflammatory cells in an adult environment. These data suggest that the Fetal fibroblast is the major effector cell for scarless Fetal Skin repair.
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Scarless wound repair: a human Fetal Skin model
Development (Cambridge England), 1992Co-Authors: H P Lorenz, Michael T. Longaker, L.a. Perkocha, Russell W. Jennings, M R HarrisonAbstract:Animal studies demonstrate that the fetus heals cutaneous wounds by reformation of normal tissue architecture without scar formation. We have developed a new model to study human Fetal Skin wound healing. Grafts of human Fetal Skin placed onto athymic mice retain the morphologic features of normal development, although they differentiate at an accelerated rate when placed cutaneously compared to subcutaneously. Full-thickness Skin grafts from human fetuses at 15 (n = 12), 17 (n = 11), 18 (n = 25), 19 (n = 20) and 22 (n = 13) weeks gestational age were placed onto athymic (nu/nu) mice in 2 locations: (1) cutaneously onto a fascial bed and thereby exposed to air or (2) subcutaneously in a pocket under the murine panniculus carnosus. Linear incisions were made in each graft 7 days after transplantation. Grafts were harvested at 7, 14 and 21 days postwounding and analyzed histologically for scar formation. By hematoxylin & eosin and Mallory's trichrome stains, complete epidermal and dermal graft wound healing without scar formation was demonstrated in the subcutaneous grafts at each gestational age studied. In contrast, scar was seen at all time points in the cutaneous grafts in both the incisional wound and at the interface of the Fetal human Skin graft and adult mouse Skin, regardless of Fetal Skin gestational age.(ABSTRACT TRUNCATED AT 250 WORDS)
Sherman Elias - One of the best experts on this subject based on the ideXlab platform.
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ultrasound guided Fetal Skin sampling for prenatal diagnosis of genodermatoses
Obstetrics & Gynecology, 1994Co-Authors: Donald S Emerson, Joe Leigh Simpson, Sherman Elias, Lee P Shulman, Karen A HolbrookAbstract:Objective: To evaluate the safety and diagnostic efficacy of ultrasound-guided Fetal Skin sampling for the prenatal diagnosis of genodermatoses. Methods: Seventeen pregnancies seen over 6.5 yearn were analyzed retrospectively. Fifteen were at risk for junctional epidermolysis bullosa and two for recessive dystrophic epidermolysis bullosa. Under ultrasound guidance, a biopsy forceps was inserted through a 14-gauge catheter and directed toward the fetus (thorax, back, or buttocks) to obtain Skin samples. The procedures were performed at a mean of 18.3 weeks'gestation (range 16.5-19.5). Results: Fetal Skin sampling was successful in all cases; the mean number of biopsies taken was 3.6 (range two to five)
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Ultrasound-guided Fetal Skin sampling for prenatal diagnosis of genodermatoses.
Obstetrics and gynecology, 1994Co-Authors: Sherman Elias, Donald S Emerson, Joe Leigh Simpson, Lee P Shulman, Karen A HolbrookAbstract:OBJECTIVE To evaluate the safety and diagnostic efficacy of ultrasound-guided Fetal Skin sampling for the prenatal diagnosis of genodermatoses. METHODS Seventeen pregnancies seen over 6.5 years were analyzed retrospectively. Fifteen were at risk for junctional epidermolysis bullosa and two for recessive dystrophic epidermolysis bullosa. Under ultrasound guidance, a biopsy forceps was inserted through a 14-gauge catheter and directed toward the fetus (thorax, back, or buttocks) to obtain Skin samples. The procedures were performed at a mean of 18.3 weeks' gestation (range 16.5-19.5). RESULTS Fetal Skin sampling was successful in all cases; the mean number of biopsies taken was 3.6 (range two to five). Five of the 17 fetuses were determined to be affected, each with junctional epidermolysis bullosa; these pregnancies were terminated electively and the prenatal diagnoses confirmed. The remaining 12 pregnancies resulted in the delivery of healthy infants at or after 37 weeks' gestation. There were no pregnancy-related complications, specifically preterm rupture of the membranes or preterm labor. Three of the 12 infants had minor Skin blemishes believed to be due to the Skin sampling. CONCLUSION Ultrasound-guided Fetal Skin sampling is the procedure of choice when Fetal Skin is required for prenatal diagnosis of genodermatoses.
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Prenatal diagnosis of genetic Skin disease using Fetal Skin biopsy samples
Archives of dermatology, 1993Co-Authors: Karen A Holbrook, Lynne T. Smith, Sherman EliasAbstract:Background: Understanding normal Skin development and identifying markers of genetic Skin disease expressed in postnatal Skin have permitted the prenatal diagnosis of many severe genodermatoses: bullous diseases, keratinization diseases, pigment cell disorders, and disorders of the epidermal appendages (ectodermal dysplasias). Samples of 16 to 22 weeks' gestation Fetal Skin obtained by ultrasound-guided biopsy are evaluated using morphologic, immunohistochemical, and biochemical methods. Observations: The 12-year experience in evaluating samples from fetuses at risk of these disorders has allowed us to establish conditions that must be met before the samples are taken and the criteria for recognizing the disorder, to recommend the site(s) for sampling, and to be mindful of pitfalls that may be encountered in interpreting the tissue structure. Conclusions: Fetal Skin biopsy is an important diagnostic tool that has permitted families in which members carry the abnormal gene for one of these severe Skin diseases to undertake a pregnancy knowing that the condition of the fetus can be determined. Nonetheless, the ultimate goal is phase out this procedure when linkage of more of these disorders to specific genes is understood, specific mutations are characterized, and probes are available for molecular diagnoses using tissue obtained at earlier Fetal ages. Until this is possible, Fetal Skin biopsy remains an important tool that can be used with reasonably high levels of safety and confidence. ( Arch Dermatol. 1993;129:1437-1454)