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Review
. 2002;4(4):252-60.
doi: 10.1186/ar416. Epub 2002 Feb 13.

The vasculature and its role in the damaged and healing tendon

Affiliations
Review

The vasculature and its role in the damaged and healing tendon

Steven A Fenwick et al. Arthritis Res. 2002.

Abstract

Tendon pathology has many manifestations, from spontaneous rupture to chronic tendinitis or tendinosis; the etiology and pathology of each are very different, and poorly understood. Tendon is a comparatively poorly vascularised tissue that relies heavily upon synovial fluid diffusion to provide nutrition. During tendon injury, as with damage to any tissue, there is a requirement for cell infiltration from the blood system to provide the necessary reparative factors for tissue healing. We describe in this review the response of the vasculature to tendon damage in a number of forms, and how and when the revascularisation or neovascularisation process occurs. We also include a section on the revascularisation of tendon during its use as a tendon graft in both ligament reconstruction and tendon-tendon grafting.

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Figures

Figure 1
Figure 1
The structure and vascular supply of tendon. (a) The hierarchical structure of a typical tendon, composed of bundles of collagen fibrils bound together into fibres by the endotenon and surrounded by the epitenon. Adapted from Connective Tissue Research [94]. (b) Diagram showing the vincula supply to the sheathed digital flexor tendons (grey line with arrowheads). Published with permission from Journal of Bone and Joint Surgery [32]. (c) The supplying artery forms branches (mesotenon) into the tendon, passing through the sheath at a number of sites. Published with permission from Grant's Atlas of Anatomy [95]. (d) Blood vessels are arranged longitudinally in the epitenon, with frequent cross-anastomoses, and pass through the endotenon surrounding the fibre bundles (fascicles). Published with permission from Journal of Bone and Joint Surgery [32].
Figure 2
Figure 2
Schematic diagram illustrating two basic consequences of tendon damage. We postulate that the abundant neovascularisation in chronic tendinopathy is responsible for the clinical symptoms (pain, swelling). In the absence of a vascular response, the degenerative process is asymptomatic, and may lead directly to tendon rupture. Subclinical degeneration may also lead to the clinical condition of tendinopathy. Painful tendinopathy, however, does not necessarily lead to tendon rupture. The black box signifies our lack of understanding of the processes that distinguish these two potentially different pathways.

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