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Increased Microvessel and Arteriole Density in the Contracted Side of the Relapsed Clubfoot
T. Novotny, A. Eckhardt, J. Knitlova, M. Doubkova, M. Ostadal, J. Uhlik, J. Musilkova
Language English Country United States
Document type Journal Article
Grant support
NV17-31564A
MZ0
CEP Register
- MeSH
- Arterioles * MeSH
- beta Catenin metabolism MeSH
- Humans MeSH
- Neovascularization, Pathologic * MeSH
- Clubfoot etiology metabolism therapy MeSH
- Child, Preschool MeSH
- Prospective Studies MeSH
- Vascular Endothelial Growth Factor Receptor-2 metabolism MeSH
- Recurrence MeSH
- Casts, Surgical MeSH
- Vascular Endothelial Growth Factor A metabolism MeSH
- Treatment Outcome MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
BACKGROUND: Clubfoot deformity (pes equinovarus) is one of the most common birth defects, and its etiology is still unknown. Initial clubfoot treatment is based on the Ponseti method throughout most of the world. Despite the effectiveness of this therapy, clubfoot may relapse. Recent studies confirm the theory of active fibrotic remodeling processes in the extracellular matrix of the affected tissue. The aim of this study was to clarify whether relapses in clubfoot therapy are associated with altered angiogenesis and to suggest possible regulatory pathways of this pathologic process. METHODS: We compared microvessel density, arteriole density, and concentration of angioproliferative-related proteins found between tissues in the contracted, that is, the medial side (M-side), and noncontracted, that is, the lateral side (L-side) of the relapsed clubfeet. Tissue samples from 10 patients were analyzed. Histopathologic analysis consisted of immunohistochemistry and image analysis. Real-time polymerase chain reaction was used to study mRNA expression. RESULTS: An increase in microvessel and arteriole density was noted in contracted, relapsed clubfoot tissue. This was accompanied by a significant increase in the levels of the vascular endothelial growth factor, vascular endothelial growth factor receptor 2, β catenin and active β catenin. Vascular endothelial growth factor, vascular endothelial growth factor receptor 2, and CD31 overexpression was also seen with mRNA analysis. CONCLUSIONS: Increased microvessel and arteriole density in the contracted side of the relapsed clubfoot was noted. These processes are mediated by specific proangiogenic proteins that are overexpressed in the contracted tissue. These findings contribute to the etiology and the development of relapses in the treatment of clubfoot. LEVEL OF EVIDENCE: Level II-analytical and prospective.
2nd Faculty of Medicine Charles University
Department of Orthopaedics Masaryk Hospital
Department of Orthopaedics University Hospital Bulovka Charles University Prague Czech Republic
Faculty of Health Studies Jan Evangelista Purkyne University Usti nad Labem
References provided by Crossref.org
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- $a BACKGROUND: Clubfoot deformity (pes equinovarus) is one of the most common birth defects, and its etiology is still unknown. Initial clubfoot treatment is based on the Ponseti method throughout most of the world. Despite the effectiveness of this therapy, clubfoot may relapse. Recent studies confirm the theory of active fibrotic remodeling processes in the extracellular matrix of the affected tissue. The aim of this study was to clarify whether relapses in clubfoot therapy are associated with altered angiogenesis and to suggest possible regulatory pathways of this pathologic process. METHODS: We compared microvessel density, arteriole density, and concentration of angioproliferative-related proteins found between tissues in the contracted, that is, the medial side (M-side), and noncontracted, that is, the lateral side (L-side) of the relapsed clubfeet. Tissue samples from 10 patients were analyzed. Histopathologic analysis consisted of immunohistochemistry and image analysis. Real-time polymerase chain reaction was used to study mRNA expression. RESULTS: An increase in microvessel and arteriole density was noted in contracted, relapsed clubfoot tissue. This was accompanied by a significant increase in the levels of the vascular endothelial growth factor, vascular endothelial growth factor receptor 2, β catenin and active β catenin. Vascular endothelial growth factor, vascular endothelial growth factor receptor 2, and CD31 overexpression was also seen with mRNA analysis. CONCLUSIONS: Increased microvessel and arteriole density in the contracted side of the relapsed clubfoot was noted. These processes are mediated by specific proangiogenic proteins that are overexpressed in the contracted tissue. These findings contribute to the etiology and the development of relapses in the treatment of clubfoot. LEVEL OF EVIDENCE: Level II-analytical and prospective.
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