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Extended report
Endogenous regeneration after collagenase-induced knee joint damage in the adult newt Notophthalmus viridescens
  1. Matthias Geyer1,
  2. Thilo Borchardt2,
  3. Carina Schreiyäck1,
  4. Astrid Wietelmann2,
  5. Florian Müller-Schrobsdorff1,
  6. Clemens Müller3,
  7. Ulf Müller-Ladner1,
  8. Robert Dinser1
  1. 1Department of Rheumatology and Clinical Immunology, Justus-Liebig-University of Gießen, Kerckhoff-Klinik, Bad Nauheim, Germany
  2. 2Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany
  3. 3Department of Radiology, Kerckhoff-Klinik, Bad Nauheim, Germany
  1. Correspondence to Dr Matthias Geyer, Department of Rheumatology and Clinical Immunology, Justus-Liebig-University of Gießen, Internal Medicine and Rheumatology, Kerckhoff-Klinik, Benekestr. 2-8, D-61231 Bad Nauheim; m.geyer{at}


Objectives To determine whether adult newts (Notophthalmus viridescens) are able to repair experimentally-induced joint damage in order to generate a model system for the study of endogenous joint regeneration.

Methods Joint instability and articular cartilage lesions of the knee joint of adult newts (N viridescens) were induced by intra-articular injection of collagenase. The changes over time were analysed clinically, by MRI, histologically and by reverse transcription PCR to detect selected relevant markers.

Results After rapid onset of disease with joint luxation, loss of proteoglycans and cartilage volume, the signs ameliorated continuously by regeneration of the affected joint compartments. The majority of joints were morphologically intact and functionally operative after 10 weeks. Upregulation of chondrogenic key genes, homogenous expression levels of factors implicated in cartilage homeostasis and limb regeneration as well as the distribution of the blastemal marker 22/18 in both treated and untreated knees suggest that joint regeneration in adult newts only partially invokes pathways of embryological organogenesis.

Conclusions Newts are able to regenerate articular cartilage injuries and to restore tissue integrity and function after induction of damage using a procedure known to induce experimental osteoarthritis in murine models. Further analysis of the underlying molecular mechanisms may contribute to the development of novel treatment approaches in joint failure.

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  • Funding This work was funded by the Robert-and-Willy-Pitzer-Stiftung and by an unconditional grant dedicated from Dr Sigrid Schuler.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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