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Achilles Tendon Ablation Induces Scleraxis Expression and Neotendon Formation in the Plantaris Tendon
Author(s) -
Flood Michael D,
Phan Anthony C,
Gumucio Jonathan P,
Mendias Christopher L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1142.52
Subject(s) - tendon , achilles tendon , fibril , chemistry , collagen fibril , anatomy , matrix (chemical analysis) , muscle hypertrophy , ablation , hyperplasia , microbiology and biotechnology , pathology , biology , medicine , endocrinology , biochemistry , chromatography
Tendons are organized into functional cable‐like units of matrix and cells called fibrils, and surrounded by a basement membrane layer of tissue known as the epitenon. In response to mechanical stimuli tendons grow by increasing their cross‐sectional area, however it is not known whether tendons grow by adding additional fibrils (hyperplasia) or by increasing the size of existing fibrils (hypertrophy). To gain a greater understanding of the cellular mechanisms of adult tendon growth, we used a synergist ablation model whereby a tenectomy of the Achilles tendon was performed to induce growth of the synergist plantaris tendon. We hypothesized that following synergist ablation, cells in the epitenon would migrate toward the interior of the tendon and increase the size of existing tendon fibrils. Two weeks following surgery, tendons were prepared for histology and gene expression analysis. Following Achilles tenectomy, there was an outward expansion of the epitenon surrounded by eccentric layers of immature matrix containing scleraxis‐positive fibroblasts, while no change in the size or cell density of the original tendon tissue was observed. This growth was coupled with an upregulation of scleraxis and collagen I expression. Our results suggest that following mechanical loading, tendon growth occurs through the addition of new fibrils to existing tendon, rather than hypertrophy of existing fibrils.