Scientific Reports (Oct 2022)

Histoarchitecture of the fibrillary matrix of human fetal posterior tibial tendons

  • Rodrigo Sousa Macedo,
  • Walcy Rosolia Teodoro,
  • Vera Luiza Capellozzi,
  • Dov Lagus Rosemberg,
  • Rafael Barban Sposeto,
  • Cesar de Cesar Netto,
  • Jonathan T. Deland,
  • Nicola Maffulli,
  • Scott J. Ellis,
  • Alexandre Leme Godoy-Santos

DOI
https://doi.org/10.1038/s41598-022-19695-3
Journal volume & issue
Vol. 12, no. 1
pp. 1 – 8

Abstract

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Abstract Adult tendons are highly differentiated. In mature individuals, tendon healing after an injury occurs through fibrotic tissue formation. Understanding the intrinsic reparative properties of fetal tendons would help to understand the maturation tissue process and tendon tissue repair. The present study evaluated the evolution of histoarchitecture, cellularity and the distribution of collagens I, III and V in the posterior tibial tendon in human fetuses at different gestational ages. Morphological profiles were assessed in nine fresh spontaneously aborted fetuses (Group I: five fetuses aged between 22 and 28 weeks of gestation; Group II: four fetuses aged between 32 and 38 weeks of gestation), characterized by a combination of histology, fluorescence and immunohistochemistry. In Group I, the posterior tibial tendon showed statistically significant greater cellularity and presence of collagen III and V than in Group II tendon, which showed a predominance of collagenous I and a better organization of the extracellular matrix compared with Group I tendons. In addition, a statistically significant higher rate of CD90, a marker of mesenchymal cells, was found in Group I tendons. In fetuses with gestational age between 22 and 28 weeks, the posterior tibialis tendons showed a thin and disorganized fibrillar structure, with an increase in collagen III and V fibers and mesenchymal cells. In the posterior tibialis tendons of fetuses with gestational age between 32 and 38 weeks, the fibrillar structure was thicker with a statistically significant increase in type I collagen and decreased cellularity.