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Nicole M. Le Douarin - One of the best experts on this subject based on the ideXlab platform.
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BIOLOGICAL SCIENCES / DEVELOPMENTAL BIOLOGY THE CEPHALIC NEURAL CREST EXERTS A CRITICAL EFFECT ON FORE- AND MIDBRAIN DEVELOPMENT
2015Co-Authors: Sophie E. Creuzet, Nicole M. Le Douarin, Salavador Martinez, Contributed Nicole, Le M. DouarinAbstract:1 Encephalisation is the most important characteristic in the evolutionary transition leading from protochordates to vertebrates. This event has coincided with the emergence of a transient and pluripotent structure, the neural crest (NC) which is absent in protochordates. In vertebrates, NC provides the rostral cephalic vesicles with skeletal protection and functional vascularization. The surgical extirpation of the cephalic NC, which is responsible for building up the cranio-Facial Skeleton, results in the absence of Facial Skeleton together with severe defects of pre-otic brain development leading to exencephaly. Here, we have analysed the role of the NC in fore- and midbrain development. We show that i) NC cells (NCC) control Fgf8 expression in the anterior neural ridge (ANR) which is considered as the prosencephalic organizer, ii) the cephalic NCC are necessary for the closure of the neural tube, and iii) NCC contribute to the proper patterning of genes that are expressed in the prosencephalic and mesencephalic alar plate. Along with the development of the roof plate, NCC also concur to the patterning of the pallial and subpallial structures: we show that the NC-dependen
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neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse `mesenchymal9 derivatives. Experiments in avian embryos have revealed that the differentiation of the NC `neural9 precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of `mesenchymal9 NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
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neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse 'mesenchymal' derivatives. Experiments in avian embryos have revealed that the differentiation of the NC 'neural' precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of 'mesenchymal' NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
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Reciprocal relationships between Fgf8 and neural crest cells in Facial and forebrain development.
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Sophie Creuzet, B. Schuler, Gérard Couly, Nicole M. Le DouarinAbstract:Fgf8 exerts a strong effect on the mesenchymal cells of neural crest (NC) origin that are fated to form the Facial Skeleton. Surgical extirpation of Facial skeletogenic NC domain (including mid-diencephalon down through rhombomere 2), which does not express Hox genes, results in the failure of Facial Skeleton development and inhibition of the closure of the forebrain neural tube, while Fgf8 expression in the telencephalon and in the branchial arch (BA) ectoderm is abolished. We demonstrate here that (i) exogenous FGF8 is able to rescue Facial Skeleton development by promoting the proliferation of NC cells from a single rhombomere, r3, which in normal development contributes only marginally to mesenchyme of BA1, and (ii) expression of Fgf8 in forebrain and in BA ectoderm is subjected to signal(s) arising from NC cells, thus showing that the development of cephalic NC-derived structures depends on FGF8 signaling, which is itself triggered by the NC cells.
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negative effect of hox gene expression on the development of the neural crest derived Facial Skeleton
Development, 2002Co-Authors: Sophie Creuzet, Gérard Couly, Christine Vincent, Nicole M. Le DouarinAbstract:Diencephalic, mesencephalic and metencephalic neural crest cells are skeletogenic and derive from neural folds that do not express Hox genes. In order to examine the influence of Hox gene expression on skull morphogenesis, expression of Hoxa2, Hoxa3 and Hoxb4 in conjunction with that of the green fluorescent protein has been selectively targeted to the Hox-negative neural folds of the avian embryo prior to the onset of crest cell emigration. Hoxa2 expression precludes the development of the entire Facial Skeleton. Transgenic Hoxa2 embryos such as those from which the Hox-negative domain of the cephalic neural crest has been removed have no upper or lower jaws and no frontonasal structures. Embryos subjected to the forced expression of Hoxa3 and Hoxb4 show severe defects in the Facial Skeleton but not a complete absence of Facial cartilage. Hoxa3 prevents the formation of the Skeleton derived from the first branchial arch, but allows the development (albeit reduced) of the nasal septum. Hoxb4, by contrast, hampers the formation of the nasal bud-derived Skeleton, while allowing that of a proximal (but not distal) segment of the lower jaw. The combined effect of Hoxa3 and Hoxb4 prevents the formation of Facial skeletal structures, comparable with Hoxa2. None of these genes impairs the formation of neural derivatives of the crest. These results suggest that over the course of evolution, the absence of Hox gene expression in the anterior part of the chordate embryo was crucial in the vertebrate phylum for the development of a face, jaws and brain case, and, hence, also for that of the forebrain.
Peter T Dziegielewski - One of the best experts on this subject based on the ideXlab platform.
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follicular thyroid carcinoma metastasis to the Facial Skeleton a systematic review
BMC Cancer, 2017Co-Authors: Varun V Varadarajan, Elizabeth Pace, Vatsal Patel, Raja Sawhney, Robert J Amdur, Peter T DziegielewskiAbstract:Follicular thyroid carcinoma (FTC) metastasis to the Facial Skeleton is exceedingly rare. A case of FTC metastasizing to the mandible is presented and a systematic review of the literature describing thyroid metastasis to the Facial Skeleton is performed. A 73-year-old female presented with metastatic FTC to the mandible and underwent total thyroidectomy, segmental mandibulectomy, bone impacted fibular free flap reconstruction, and adjuvant radioactive iodine treatment. The PubMed database was searched for literature describing thyroid cancer with Facial Skeleton metastasis using the key words “thyroid,” “cancer,” “carcinoma,” “metastasis,” and “malignancy” with “oral cavity,” “maxilla,” “mandible,” “sinus,” “paranasal,” and “orbit.” Reports that only involved the soft tissues were excluded. Systematic review revealed 59 cases of well-differentiated thyroid cancer with Facial Skeleton metastasis: 35 mandibular metastases (21 = FTC), 6 maxilla metastases (2 = FTC), 9 orbital metastases (4 = FTC), and 11 paranasal sinus metastases (7 = FTC). Treatment included surgery, RAI, external beam radiotherapy (XRT), or a combination of these modalities. The one, two, and five-year survival rates were 100%, 79%, and 16%, respectively. Facial Skeleton metastasis of FTC is a rare clinical challenge. Optimal treatment appears to include total thyroidectomy and resection of involved structures with or without adjuvant treatment.
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Follicular thyroid carcinoma metastasis to the Facial Skeleton: a systematic review
BMC Cancer, 2017Co-Authors: Varun V Varadarajan, Vatsal Patel, Raja Sawhney, Robert J Amdur, Elizabeth K. Pace, Peter T DziegielewskiAbstract:Background Follicular thyroid carcinoma (FTC) metastasis to the Facial Skeleton is exceedingly rare. A case of FTC metastasizing to the mandible is presented and a systematic review of the literature describing thyroid metastasis to the Facial Skeleton is performed. Case presentation A 73-year-old female presented with metastatic FTC to the mandible and underwent total thyroidectomy, segmental mandibulectomy, bone impacted fibular free flap reconstruction, and adjuvant radioactive iodine treatment. The PubMed database was searched for literature describing thyroid cancer with Facial Skeleton metastasis using the key words “thyroid,” “cancer,” “carcinoma,” “metastasis,” and “malignancy” with “oral cavity,” “maxilla,” “mandible,” “sinus,” “paranasal,” and “orbit.” Reports that only involved the soft tissues were excluded. Systematic review revealed 59 cases of well-differentiated thyroid cancer with Facial Skeleton metastasis: 35 mandibular metastases (21 = FTC), 6 maxilla metastases (2 = FTC), 9 orbital metastases (4 = FTC), and 11 paranasal sinus metastases (7 = FTC). Treatment included surgery, RAI, external beam radiotherapy (XRT), or a combination of these modalities. The one, two, and five-year survival rates were 100%, 79%, and 16%, respectively. Conclusion Facial Skeleton metastasis of FTC is a rare clinical challenge. Optimal treatment appears to include total thyroidectomy and resection of involved structures with or without adjuvant treatment.
Sophie Creuzet - One of the best experts on this subject based on the ideXlab platform.
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neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse `mesenchymal9 derivatives. Experiments in avian embryos have revealed that the differentiation of the NC `neural9 precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of `mesenchymal9 NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
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neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse 'mesenchymal' derivatives. Experiments in avian embryos have revealed that the differentiation of the NC 'neural' precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of 'mesenchymal' NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
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Reciprocal relationships between Fgf8 and neural crest cells in Facial and forebrain development.
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Sophie Creuzet, B. Schuler, Gérard Couly, Nicole M. Le DouarinAbstract:Fgf8 exerts a strong effect on the mesenchymal cells of neural crest (NC) origin that are fated to form the Facial Skeleton. Surgical extirpation of Facial skeletogenic NC domain (including mid-diencephalon down through rhombomere 2), which does not express Hox genes, results in the failure of Facial Skeleton development and inhibition of the closure of the forebrain neural tube, while Fgf8 expression in the telencephalon and in the branchial arch (BA) ectoderm is abolished. We demonstrate here that (i) exogenous FGF8 is able to rescue Facial Skeleton development by promoting the proliferation of NC cells from a single rhombomere, r3, which in normal development contributes only marginally to mesenchyme of BA1, and (ii) expression of Fgf8 in forebrain and in BA ectoderm is subjected to signal(s) arising from NC cells, thus showing that the development of cephalic NC-derived structures depends on FGF8 signaling, which is itself triggered by the NC cells.
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negative effect of hox gene expression on the development of the neural crest derived Facial Skeleton
Development, 2002Co-Authors: Sophie Creuzet, Gérard Couly, Christine Vincent, Nicole M. Le DouarinAbstract:Diencephalic, mesencephalic and metencephalic neural crest cells are skeletogenic and derive from neural folds that do not express Hox genes. In order to examine the influence of Hox gene expression on skull morphogenesis, expression of Hoxa2, Hoxa3 and Hoxb4 in conjunction with that of the green fluorescent protein has been selectively targeted to the Hox-negative neural folds of the avian embryo prior to the onset of crest cell emigration. Hoxa2 expression precludes the development of the entire Facial Skeleton. Transgenic Hoxa2 embryos such as those from which the Hox-negative domain of the cephalic neural crest has been removed have no upper or lower jaws and no frontonasal structures. Embryos subjected to the forced expression of Hoxa3 and Hoxb4 show severe defects in the Facial Skeleton but not a complete absence of Facial cartilage. Hoxa3 prevents the formation of the Skeleton derived from the first branchial arch, but allows the development (albeit reduced) of the nasal septum. Hoxb4, by contrast, hampers the formation of the nasal bud-derived Skeleton, while allowing that of a proximal (but not distal) segment of the lower jaw. The combined effect of Hoxa3 and Hoxb4 prevents the formation of Facial skeletal structures, comparable with Hoxa2. None of these genes impairs the formation of neural derivatives of the crest. These results suggest that over the course of evolution, the absence of Hox gene expression in the anterior part of the chordate embryo was crucial in the vertebrate phylum for the development of a face, jaws and brain case, and, hence, also for that of the forebrain.
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interactions between hox negative cephalic neural crest cells and the foregut endoderm in patterning the Facial Skeleton in the vertebrate head
Development, 2002Co-Authors: Gérard Couly, Sophie Creuzet, Christine Vincent, S Bennaceur, Nicole M. Le DouarinAbstract:The vertebrate face contains bones that differentiate from mesenchymal cells of neural crest origin, which colonize the median nasofrontal bud and the first branchial arches. The patterning of individual Facial bones and their relative positions occurs through mechanisms that remained elusive. During the early stages of head morphogenesis, an endodermal cul-de-sac, destined to become Sessel's pouch, underlies the nasofrontal bud. Reiterative outpocketings of the foregut then form the branchial pouches. We have tested the capacity of endoderm of the avian neurula to specify the Facial Skeleton by performing ablations or grafts of defined endodermal regions. Neural crest cells that do not express Hox genes respond to patterning cues produced regionally in the anterior endoderm to yield distinct skeletal components of the upper face and jaws. However, Hox-expressing neural crest cells do not respond to these cues. Bone orientation is likewise dependent on the position of the endoderm relative to the embryonic axes. Our findings thus indicate that the endoderm instructs neural crest cells as to the size, shape and position of all the Facial skeletal elements, whether they are cartilage or membrane bones.
Gérard Couly - One of the best experts on this subject based on the ideXlab platform.
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neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse `mesenchymal9 derivatives. Experiments in avian embryos have revealed that the differentiation of the NC `neural9 precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of `mesenchymal9 NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
-
neural crest cell plasticity and its limits
Development, 2004Co-Authors: Nicole M. Le Douarin, Sophie Creuzet, Gérard Couly, Elisabeth DupinAbstract:The neural crest (NC) yields pluripotent cells endowed with migratory properties. They give rise to neurons, glia, melanocytes and endocrine cells, and to diverse 'mesenchymal' derivatives. Experiments in avian embryos have revealed that the differentiation of the NC 'neural' precursors is strongly influenced by environmental cues. The reversibility of differentiated cells (such as melanocytes or glia) to a pluripotent precursor state can even be induced in vitro by a cytokine, endothelin 3. The fate of 'mesenchymal' NC precursors is strongly restricted by Hox gene expression. In this context, however, Facial Skeleton morphogenesis is under the control of a multistep crosstalk between the epithelia (endoderm and ectoderm) and NC cells.
-
Reciprocal relationships between Fgf8 and neural crest cells in Facial and forebrain development.
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Sophie Creuzet, B. Schuler, Gérard Couly, Nicole M. Le DouarinAbstract:Fgf8 exerts a strong effect on the mesenchymal cells of neural crest (NC) origin that are fated to form the Facial Skeleton. Surgical extirpation of Facial skeletogenic NC domain (including mid-diencephalon down through rhombomere 2), which does not express Hox genes, results in the failure of Facial Skeleton development and inhibition of the closure of the forebrain neural tube, while Fgf8 expression in the telencephalon and in the branchial arch (BA) ectoderm is abolished. We demonstrate here that (i) exogenous FGF8 is able to rescue Facial Skeleton development by promoting the proliferation of NC cells from a single rhombomere, r3, which in normal development contributes only marginally to mesenchyme of BA1, and (ii) expression of Fgf8 in forebrain and in BA ectoderm is subjected to signal(s) arising from NC cells, thus showing that the development of cephalic NC-derived structures depends on FGF8 signaling, which is itself triggered by the NC cells.
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negative effect of hox gene expression on the development of the neural crest derived Facial Skeleton
Development, 2002Co-Authors: Sophie Creuzet, Gérard Couly, Christine Vincent, Nicole M. Le DouarinAbstract:Diencephalic, mesencephalic and metencephalic neural crest cells are skeletogenic and derive from neural folds that do not express Hox genes. In order to examine the influence of Hox gene expression on skull morphogenesis, expression of Hoxa2, Hoxa3 and Hoxb4 in conjunction with that of the green fluorescent protein has been selectively targeted to the Hox-negative neural folds of the avian embryo prior to the onset of crest cell emigration. Hoxa2 expression precludes the development of the entire Facial Skeleton. Transgenic Hoxa2 embryos such as those from which the Hox-negative domain of the cephalic neural crest has been removed have no upper or lower jaws and no frontonasal structures. Embryos subjected to the forced expression of Hoxa3 and Hoxb4 show severe defects in the Facial Skeleton but not a complete absence of Facial cartilage. Hoxa3 prevents the formation of the Skeleton derived from the first branchial arch, but allows the development (albeit reduced) of the nasal septum. Hoxb4, by contrast, hampers the formation of the nasal bud-derived Skeleton, while allowing that of a proximal (but not distal) segment of the lower jaw. The combined effect of Hoxa3 and Hoxb4 prevents the formation of Facial skeletal structures, comparable with Hoxa2. None of these genes impairs the formation of neural derivatives of the crest. These results suggest that over the course of evolution, the absence of Hox gene expression in the anterior part of the chordate embryo was crucial in the vertebrate phylum for the development of a face, jaws and brain case, and, hence, also for that of the forebrain.
-
interactions between hox negative cephalic neural crest cells and the foregut endoderm in patterning the Facial Skeleton in the vertebrate head
Development, 2002Co-Authors: Gérard Couly, Sophie Creuzet, Christine Vincent, S Bennaceur, Nicole M. Le DouarinAbstract:The vertebrate face contains bones that differentiate from mesenchymal cells of neural crest origin, which colonize the median nasofrontal bud and the first branchial arches. The patterning of individual Facial bones and their relative positions occurs through mechanisms that remained elusive. During the early stages of head morphogenesis, an endodermal cul-de-sac, destined to become Sessel's pouch, underlies the nasofrontal bud. Reiterative outpocketings of the foregut then form the branchial pouches. We have tested the capacity of endoderm of the avian neurula to specify the Facial Skeleton by performing ablations or grafts of defined endodermal regions. Neural crest cells that do not express Hox genes respond to patterning cues produced regionally in the anterior endoderm to yield distinct skeletal components of the upper face and jaws. However, Hox-expressing neural crest cells do not respond to these cues. Bone orientation is likewise dependent on the position of the endoderm relative to the embryonic axes. Our findings thus indicate that the endoderm instructs neural crest cells as to the size, shape and position of all the Facial skeletal elements, whether they are cartilage or membrane bones.
Robert J Amdur - One of the best experts on this subject based on the ideXlab platform.
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follicular thyroid carcinoma metastasis to the Facial Skeleton a systematic review
BMC Cancer, 2017Co-Authors: Varun V Varadarajan, Elizabeth Pace, Vatsal Patel, Raja Sawhney, Robert J Amdur, Peter T DziegielewskiAbstract:Follicular thyroid carcinoma (FTC) metastasis to the Facial Skeleton is exceedingly rare. A case of FTC metastasizing to the mandible is presented and a systematic review of the literature describing thyroid metastasis to the Facial Skeleton is performed. A 73-year-old female presented with metastatic FTC to the mandible and underwent total thyroidectomy, segmental mandibulectomy, bone impacted fibular free flap reconstruction, and adjuvant radioactive iodine treatment. The PubMed database was searched for literature describing thyroid cancer with Facial Skeleton metastasis using the key words “thyroid,” “cancer,” “carcinoma,” “metastasis,” and “malignancy” with “oral cavity,” “maxilla,” “mandible,” “sinus,” “paranasal,” and “orbit.” Reports that only involved the soft tissues were excluded. Systematic review revealed 59 cases of well-differentiated thyroid cancer with Facial Skeleton metastasis: 35 mandibular metastases (21 = FTC), 6 maxilla metastases (2 = FTC), 9 orbital metastases (4 = FTC), and 11 paranasal sinus metastases (7 = FTC). Treatment included surgery, RAI, external beam radiotherapy (XRT), or a combination of these modalities. The one, two, and five-year survival rates were 100%, 79%, and 16%, respectively. Facial Skeleton metastasis of FTC is a rare clinical challenge. Optimal treatment appears to include total thyroidectomy and resection of involved structures with or without adjuvant treatment.
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Follicular thyroid carcinoma metastasis to the Facial Skeleton: a systematic review
BMC Cancer, 2017Co-Authors: Varun V Varadarajan, Vatsal Patel, Raja Sawhney, Robert J Amdur, Elizabeth K. Pace, Peter T DziegielewskiAbstract:Background Follicular thyroid carcinoma (FTC) metastasis to the Facial Skeleton is exceedingly rare. A case of FTC metastasizing to the mandible is presented and a systematic review of the literature describing thyroid metastasis to the Facial Skeleton is performed. Case presentation A 73-year-old female presented with metastatic FTC to the mandible and underwent total thyroidectomy, segmental mandibulectomy, bone impacted fibular free flap reconstruction, and adjuvant radioactive iodine treatment. The PubMed database was searched for literature describing thyroid cancer with Facial Skeleton metastasis using the key words “thyroid,” “cancer,” “carcinoma,” “metastasis,” and “malignancy” with “oral cavity,” “maxilla,” “mandible,” “sinus,” “paranasal,” and “orbit.” Reports that only involved the soft tissues were excluded. Systematic review revealed 59 cases of well-differentiated thyroid cancer with Facial Skeleton metastasis: 35 mandibular metastases (21 = FTC), 6 maxilla metastases (2 = FTC), 9 orbital metastases (4 = FTC), and 11 paranasal sinus metastases (7 = FTC). Treatment included surgery, RAI, external beam radiotherapy (XRT), or a combination of these modalities. The one, two, and five-year survival rates were 100%, 79%, and 16%, respectively. Conclusion Facial Skeleton metastasis of FTC is a rare clinical challenge. Optimal treatment appears to include total thyroidectomy and resection of involved structures with or without adjuvant treatment.
