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Review
. 2011;99(1):211-25.
doi: 10.1093/bmb/ldr025. Epub 2011 Jul 4.

Musculoskeletal diseases--tendon

Tomoya Sakabe  1 , Takao Sakai
Affiliations
Review

Musculoskeletal diseases--tendon

Tomoya Sakabe et al. Br Med Bull. 2011.

Abstract

Introduction: Tendons establish specific connections between muscles and the skeleton by transferring contraction forces from skeletal muscle to bone thereby allowing body movement. Tendon physiology and pathology are heavily dependent on mechanical stimuli. Tendon injuries clinically represent a serious and still unresolved problem since damaged tendon tissues heal very slowly and no surgical treatment can restore a damaged tendon to its normal structural integrity and mechanical strength. Understanding how mechanical stimuli regulate tendon tissue homeostasis and regeneration will improve the treatment of adult tendon injuries that still pose a great challenge in today's medicine.

Source of data: This review summarizes the current status of tendon treatment and discusses new directions from the point of view of cell-based therapy and regenerative medicine approach. We searched the available literature using PubMed for relevant original articles and reviews.

Growing points: Identification of tendon cell markers has enabled us to study precisely tendon healing and homeostasis. Clinically, tissue engineering for tendon injuries is an emerging technology comprising elements from the fields of cellular source, scaffold materials, growth factors/cytokines and gene delivering systems.

Areas timely for developing research: The clinical settings to establish appropriate microenvironment for injured tendons with the combination of these novel cellular- and molecular-based scaffolds will be critical for the treatment.

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Figures

Fig. 1
Fig. 1
Tensile loading plays a crucial role in tenocytes. (a) Achilles tendons in adult Scleraxis-GFP transgenic mice. Left panel: under fluorescence stereomicroscope; right panel: under microscope with GFP/ultraviolet (UV) filters to show scleraxis-GFP (green) and nucleus [4′6-diamidino-2-phenylinodole (DAPI) blue]. AT, Achilles tendon. Bar = 100 µm. (b) Analysis of cell death at 2 h after complete transection of adult Achilles tendon in Scleraxis-GFP transgenic mice. Arrows indicate the transection edge of tendons. Note that the expression of scleraxis-GFP (green) is diminished and cells positive by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay (TUNEL assay: a marker for cell death, red) are evident in the transected Achilles tendon. Bar = 100 µm.
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