Tendons are often thought of as mere attachments; cords or connectors of the force generating engines of muscle to the bony effectors of motion.  New research into the structure-function relationships of tendons and connective tissue is changing this old archetype, and now the enigmatic methods of cellular signaling in tendon mechanical force transduction is being elucidated. The purpose of this article is to present a general overview of tendon structure and function, starting with a discussion of biochemical and cellular tendon composition. For a full review of tendon biology, biochemistry, and biomechanics, a list of papers is provided at the end of this discourse.

Like many connective tissues exposed to mechanical stress, tendons are primarily composed of an extensive extracellular matrix (ECM).  This tendinous matrix is mostly Type I collagen (representing 70-86 percent dry fat-free weight respectively) forming microfibrils.  This collagen is a triple helix held together by hydrogen and covalent bonds augmented by extensive post-translational modification.  This is known as tropocollagen.  These tropocollagen macromolecules are arranged in a "quarternary stagger" pattern, allowing the alignment of oppositely charged collagenous amino-acid side chains to interact, greatly increasing microfibril stability under tension.  Other collagens such as II, III, V, VII, IX, and XII are also present in varying degrees depending on specific local factors of tendinous morphology (aponeurotic versus cylindrical morphology).  The second and notably important component of proteoglycans are critical for imparting the unique viscoelasticity of tendons due to their hydrophilicity and ability to prevent collagenous microfibrillar deformation during tension.  Of particular note is the macromolecular morphology of this tendinous extracellular matrix.  Collagen microfibrils aggregate to form fibrils, which are then grouped into fibers.  Fibers are in turn grouped into fiber bundles, and fiber bundles into the visible fascicles that are seen during dissection.  The nomenclature of this organization varies between authors, but it does illustrate the heterogeneity of extracellular matrix organization and its interdepndence between differing levels of organization.  The overall organization of a prototypical tendon is helical, somewhat akin to manmade ropes.  The fibrils are also known to possess a quality loosely called "crimp," or a zig-zag pattern of arrangement of fibrils and higher structural levels that imparts flexibility.  This crimp pattern is ill defined, but is known to converge at sites of tendinous attachment, leading some anatomists to hypothesize that they add to force transduction for small diameter muscle attachments.

The component cells of tendons are a specialized lineage of fibroblasts known as tenocytes.  These cells are arranged in longitudinal rows, with intimal attachment to the extensive ECM described previously.  These tenocytes develop a system of intercellular attachments that facilitate communication between adjacent cells, usually through gap junctions.  This process is analogous to the mature osteocytes of mature compact bone that communicate through canaliculi.  Tenocytes are not a static tissue, but rather actively participate in ECM modification and maintenance, a process poorly understood but known to occur in response to mechanical stress.  This perhaps represents a tendinous psuedohypertrophy, in which the tenocyte diameter increases to upregulate ECM production.  The application of this fact to the understanding of tendon healing modalities is obvious.  Glucocorticoids, for instance, suppress tenocyte ECM synthesis whilst nitric oxide (EDGF) upregulates production of ECM.

Tendons are often thought of as a uniquely avascular tissue, with very little in the way of neurovascular connectivity.  This view, espoused by early anatomists, is now known to be mostly false, although the vascularity of tendons (and ligaments) still is incredibly diminished compared to their neighboring tissues such as bone or muscle.  New research indicates that small tendinous vessels course between fascicles and larger vessels course through surrounding peritendinous fat and paratenon.  These inter-tendinous vessels originate at the myotendinous juncture, and exhibit mutiple anastomoses between each other.  There is also vascular continuity at tendon insertions in bone, commonly called entheses.  Certain regions of tendon, however, can be very avascular, particularly in the regions near bony pulleys, such as the medial malleolus.  These regions are thought to be the structurally weakest part of their respective tendons.

Basic tendon biology is an evolving discipline, with particular interest in the transcriptional regulation of fibroblastic precursors to mature tenocytes and the role of native local and systemic hormonal influences in tendon repair and healing.  A solid understanding of basic tendon biology, however, is necessary for the budding orthopedic surgeon.   Please check the list of additional references for further study.


Benjamin M, Kaiser E, and Milz S. (2008) Structure-Function Relationships in Tendons: A Review.  J. Anat. 212, pp211-228.

Kjaer M. (2004) Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading.  Physiol Rev 84, pp649-698.