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Structure of the human tibialis posterior tendon

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Archives of Orthopaedic and Trauma Surgery Aims and scope Submit manuscript

Abstract

Background

The most common site of rupture of the posterior tibial tendon is the retromalleolar region where the tendon changes its direction of pull. The aim of this study was to characterize the tissue of the gliding zone of the tibialis posterior tendon to gain further knowledge about possible structural causes for spontaneous tendon rupture.

Methods

Light microscopy, transmission electron microscopy and immunohistochemical methods were used to describe the structure of the human tibialis posterior tendon.

Results

In the region where the tendon wraps around the medial malleolus, the structure of the tissue changes from the typical structure of a traction tendon. The superficial zone which was directed towards the pulley tissue had the structure of fibrocartilage with a specific three-dimensional collagen fibril texture. Transmission electron microscopy showed chondrocytes with a felt-like pericellular matrix that increased in size towards the gliding surface. The extracellular matrix of the fibrocartilage was rich in acid glycosaminoglycans and stained intensively with alcian blue at pH 1. Immunohistochemical staining of cartilage-specific extracellular matrix components such as type II collagen, chondroitin-4-sulphate, chondroitin-6-sulphate, keratan sulphate and aggrecan was positive.

Conclusion

The location of the fibrocartilage corresponds to the region where the tibialis posterior tendon wraps around the medial malleolus, which serves as a pulley. According to the theory of 'causal histogenesis', the stimulus for the development of fibrocartilage within dense connective tissue is intermittent compressive and shear stress. The fibrocartilaginous region is the region where most spontaneous ruptures of the tibialis posterior tendon occur. Due to its structure, the fibrocartilaginous region may be more vulnerable to repetitive tensile microtrauma; degeneration may occur due to the poor repair response of the avascular fibrocartilaginous tissue.

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Acknowledgements

We want to thank Mrs. R Worm, Mrs. K. Stengel, Mrs. S. Seiters, Mrs. H. Siebke and Mrs. H. Waluk, members of the Department of Anatomy of the Christian Albrechts University Kiel, for their expert technical assistance. The work was supported by a grant from the 'Forschungsschwerpunkt Muskel und Skelettsystem' of CAU Kiel. The monoclonal aggrecan antibody developed by B. Caterson was obtained from the Developmental Studies Hybridoma Bank developed under the auspices of the NICHD and maintained by the University of Iowa, Department of Biological Sciences, Iowa City, IA 52242, USA.

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Authors and Affiliations

  1. Department of Orthopaedic Surgery, Christian Albrechts University Kiel, Michaelisstrasse 40, 24098, Kiel, Germany

    Wolf Petersen & Thore Zantop

  2. Department of Anatomy, Christian Albrechts University Kiel, Olshausenstr. 40, 24098, Kiel, Germany

    Gerrit Hohmann, Thomas Pufe, Friedrich Paulsen & Bernhard Tillmann

  3. Department of Legal Medicine, University Hospital Eppendorf, Hamburg, Germany

    Michael Tsokos

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  1. Wolf Petersen
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  2. Gerrit Hohmann
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  4. Michael Tsokos
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  5. Thore Zantop
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  6. Friedrich Paulsen
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  7. Bernhard Tillmann
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Correspondence to Wolf Petersen.

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Petersen, W., Hohmann, G., Pufe, T. et al. Structure of the human tibialis posterior tendon. Arch Orthop Trauma Surg 124, 237–242 (2004). https://doi.org/10.1007/s00402-003-0500-5

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  • DOI: https://doi.org/10.1007/s00402-003-0500-5

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