gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017)

24.10. - 27.10.2017, Berlin

Uncovering the role of tenomodulin gene in tendon healing

Meeting Abstract

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  • presenting/speaker Manuel Delgado Caceres - Laboratory for Experimental Trauma Surgery , Department of Trauma Surgery , Universitiy Regensburg Medical Centre, Regensburg, Germany
  • Dasheng Lin - Experimental Surgery and Regenerative Medicine, Department of Surgery, Ludwig-Maximilians-University, Munich, Germany
  • Denitsa Docheva - Laboratory for Experimental Trauma Surgery , Department of Trauma Surgery , Universitiy Regensburg Medical Centre, Regensburg, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017). Berlin, 24.-27.10.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocGR20-440

doi: 10.3205/17dkou551, urn:nbn:de:0183-17dkou5516

Veröffentlicht: 23. Oktober 2017

© 2017 Delgado Caceres et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Objectives: Recently we have reviewed the so far known roles of Tenomodulin (Tnmd) is a gene factor important for tendon maturation and residing tendon stem/progenitor cell functions (Dex et al. 2016).. The putative signaling of Tnmd participates is just starting to be better understood. However, its exact role during tendon healing process still remains puzzling. Therefore, the aims of this study were to carry out a pilot analyses on the effect of Tnmd in early tendon healing by applying an Achilles tendon rupture model in Tnmd-deficient mice.

Methods: Adult Tnmd-KO (n = 8) and wild-type (WT) (n = 8) mice underwent unilateral surgery of Achilles tendon based on Palmes et al. 2002 and were compared at day 8 postoperatively by: 1) H&E staining for overall assessment; 2) immunohistochemical BrdU analysis for cell proliferation; 3) Safranin O staining for endochondral formation and 4) Perilipin staining for fat accumulation.

Results and Conclusion: Our pilot surgical study showed a very different scar organization in Tnmd-KO with a clearly reduced cell density. BrdU analysis confirmed a lower number of proliferating cells in Tnmd-KO scar area. Endochondral formation was not observed in the scar tissues in either of the genotypes at day 8. However, a very interesting tendency was detected in Tnmd-KO animals by Perilipin staining, namely the scars of this group contained significatly more adipose-rich areas. In literature several papers have linked Tnmd gene to fat formation and function in patient genetic studies (reviewed in Dex et al. 2016) and experimental mouse models (Jiang et al. 2016 and Senol-Cosar et al. 2016).

Taken together, we can report for the first time that loss of Tnmd leads to an inferior repair process with increased risk of fat accumulation.