César Pacheco-Tena1, Ruy Pérez-Tamayo1, Carlos Pineda1, Susana A González-Chávez1, Celia Quiñonez-Flores1, Antonio Ugalde Vitelly1, Robert D Inman1, Jane E Aubin1, Janitzia Vázquez-Mellado1, Rubén Burgos-Vargas2. 1. From the Facultad de Medicina, Universidad Autónoma de Chihuahua, Chihuahua; Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México; Instituto Nacional de Rehabilitación; Servicio de Cirugía Plástica y Reconstructiva, and Servicio de Reumatología, Hospital General de México, México D.F., México; Arthritis Centre for Excellence, Toronto Western Hospital, and Department of Molecular Genetics University of Toronto, Toronto, Ontario, Canada.C. Pacheco-Tena, MD; S.A. González-Chávez, MSc; C. Quiñonez-Flores, MSc, Facultad de Medicina, Universidad Autónoma de Chihuahua; R. Pérez-Tamayo, MD, Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México; C. Pineda, MD, Dirección de Investigación, Instituto Nacional de Rehabilitación; A. Ugalde Vitelly, MD, Servicio de Cirugía Plástica y Reconstructiva, Hospital General de México; J. Vázquez-Mellado, PhD; R. Burgos-Vargas, MD, Servicio de Reumatología, Hospital General de México, Facultad de Medicina, Universidad Nacional Autónoma de México; R.D. Inman, MD, Arthritis Centre for Excellence, Toronto Western Hospital; J.E. Aubin, PhD, Department of Molecular Genetics, University of Toronto. 2. From the Facultad de Medicina, Universidad Autónoma de Chihuahua, Chihuahua; Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México; Instituto Nacional de Rehabilitación; Servicio de Cirugía Plástica y Reconstructiva, and Servicio de Reumatología, Hospital General de México, México D.F., México; Arthritis Centre for Excellence, Toronto Western Hospital, and Department of Molecular Genetics University of Toronto, Toronto, Ontario, Canada.C. Pacheco-Tena, MD; S.A. González-Chávez, MSc; C. Quiñonez-Flores, MSc, Facultad de Medicina, Universidad Autónoma de Chihuahua; R. Pérez-Tamayo, MD, Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México; C. Pineda, MD, Dirección de Investigación, Instituto Nacional de Rehabilitación; A. Ugalde Vitelly, MD, Servicio de Cirugía Plástica y Reconstructiva, Hospital General de México; J. Vázquez-Mellado, PhD; R. Burgos-Vargas, MD, Servicio de Reumatología, Hospital General de México, Facultad de Medicina, Universidad Nacional Autónoma de México; R.D. Inman, MD, Arthritis Centre for Excellence, Toronto Western Hospital; J.E. Aubin, PhD, Department of Molecular Genetics, University of Toronto. r.burgos.vargas@gmail.com.
Abstract
OBJECTIVE: Patients with juvenile-onset spondyloarthritis (SpA) may develop ankylosis of the midfoot resembling the spinal changes seen in patients with ankylosing spondylitis (AS). The study of the histopathology of the feet of patients with tarsitis could help us understand the pathogenesis of bone formation in affected structures in the SpA. The objective of our study was to describe the histopathologic characteristics of the midfoot in patients with tarsitis associated with SpA. METHODS: We obtained synovial sheaths, entheses, and bone samples from 20 patients with SpA with midfoot pain/tenderness and swelling. Tissue samples underwent H&E staining; immunohistochemistry for CD3, CD4, CD8, CD68, and CD20 cell identification; and immunofluorescence for bone lineage proteins, including osteocalcin, osteopontin, parathyroid hormone-related protein, bone sialoprotein, and alkaline phosphatase. RESULTS: Slight edema and hyalinization were found in some tendon sheaths, and few inflammatory cells were detected in the entheses. In bones, we found some changes suggesting osteoproliferation, including endochondral and intramembranous ossification, but no inflammatory cells. In entheses showing bone proliferation, we detected osteocalcin and osteopontin in cells with a fibroblast-mesenchymal phenotype, suggesting the induction of entheseal cells toward an osteoblast phenotype. CONCLUSION: Osteoproliferation and abnormal expression of bone lineage proteins, but no inflammatory infiltration, characterize midfoot involvement in patients with SpA. In this sense, tarsitis (or ankylosing tarsitis) resembles the involvement of the spine in patients with AS. Ossification may be in part explained by the differentiation of mesenchymal entheseal cells toward the osteoblastic lineage.
OBJECTIVE:Patients with juvenile-onset spondyloarthritis (SpA) may develop ankylosis of the midfoot resembling the spinal changes seen in patients with ankylosing spondylitis (AS). The study of the histopathology of the feet of patients with tarsitis could help us understand the pathogenesis of bone formation in affected structures in the SpA. The objective of our study was to describe the histopathologic characteristics of the midfoot in patients with tarsitis associated with SpA. METHODS: We obtained synovial sheaths, entheses, and bone samples from 20 patients with SpA with midfoot pain/tenderness and swelling. Tissue samples underwent H&E staining; immunohistochemistry for CD3, CD4, CD8, CD68, and CD20 cell identification; and immunofluorescence for bone lineage proteins, including osteocalcin, osteopontin, parathyroid hormone-related protein, bone sialoprotein, and alkaline phosphatase. RESULTS: Slight edema and hyalinization were found in some tendon sheaths, and few inflammatory cells were detected in the entheses. In bones, we found some changes suggesting osteoproliferation, including endochondral and intramembranous ossification, but no inflammatory cells. In entheses showing bone proliferation, we detected osteocalcin and osteopontin in cells with a fibroblast-mesenchymal phenotype, suggesting the induction of entheseal cells toward an osteoblast phenotype. CONCLUSION: Osteoproliferation and abnormal expression of bone lineage proteins, but no inflammatory infiltration, characterize midfoot involvement in patients with SpA. In this sense, tarsitis (or ankylosing tarsitis) resembles the involvement of the spine in patients with AS. Ossification may be in part explained by the differentiation of mesenchymal entheseal cells toward the osteoblastic lineage.
Authors: José Pablo Romero-López; María Lilia Domínguez-López; Rubén Burgos-Vargas; Ethel García-Latorre Journal: Rheumatol Int Date: 2018-05-31 Impact factor: 2.631
Authors: Clementina López-Medina; Anna Molto; Joachim Sieper; Tuncay Duruöz; Uta Kiltz; Bassel Elzorkany; Najia Hajjaj-Hassouni; Ruben Burgos-Vargas; José Maldonado-Cocco; Nelly Ziade; Meghna Gavali; Victoria Navarro-Compan; Shue-Fen Luo; Sara Monti; Kim Tae-Jong; Mitsumasa Kishimoto; F M Pimentel-Santos; Jieruo Gu; Ruxandra Schiotis; Floris A van Gaalen; Pál Geher; Marina Magrey; Sebastián E Ibáñez Vodnizza; Wilson Bautista-Molano; Walter Maksymowych; Pedro M Machado; Robert Landewé; Desirée van der Heijde; Maxime Dougados Journal: RMD Open Date: 2021-01