From what I read on wikipedia they are made of collagen. Collagen is just a protein. Right? How is this collagen structured (I imagine like fibers). Aren't there cells in this fibers as well?

From this picture:
Tendon H&E

Is the pink stuff the collagen? and the purple stuff the tenocytes?

If someone can expand on this with a picture preferably, it would be great.


As you correctly say, tendons are made up of collagen fibers. Collagen is one of the most important proteins (or, to be more specific, family of proteins, as there are many types of collagen) forming connective tissue in the body.

Collagen molecules have a particular structure that allows them to form long fibers, composed by three different strands that form a triple helix. This is a schema of a collagen helix (each ball represents one aminoacid):

Collagen helix
(source: Wikipedia)

These helices can then be bound together to form a collagen fiber, through the action of an enzyme called lysyl oxidase which binds two lysine residues from two different helices together (lysine is one of the aminoacids that makes up collagen).

Here is a scanning electron microscope of a collagen fiber:

Collagen fiber, SEM
(source: Science photo library)

Collagen is secreted out of the cells that produce it so, although there may be cells around the collagen molecules, it is important to understand that it is part of what is called the extracellular matrix, the extracellular structure that supports the cells in our body.

As for the photo you linked, it is an hematoxylin and eosin (H&E) stain of a tendon. Hematoxylin colours cell nuclei in dark blue, so the dark spots are definitely cells. The pink "waves" are indeed collagen fibers, the cells are probably the tenocytes, the specialized fibroblasts of the tendon, which produce the collagen.

  • $\begingroup$ Do these tenocytes move around the collagen fibers? Sort of like spiders in a web? $\endgroup$ – user952 Jun 17 '12 at 15:28
  • $\begingroup$ @user952: I don't really know. I would say no, but I may be wrong. $\endgroup$ – nico Jun 17 '12 at 15:44

{4} for has a similar image as yours but with some labels:

enter image description here

with the caption:

Figure 1.2: Tendon microstructure of healthy tendons: nuclei of tenocytes are darker in color and vascularization does not disrupt collagen arrays. arrays http://www.onlineveterinaryanatomy.net/content/tendon-histology-labelled (mirror)

Some illustrations showing the tendon structure:

enter image description here

(image source) (mirror)

enter image description here

(image source) (mirror)

Another illustration from {3}:

enter image description here

Regarding the cellular content of tendons, quote from {1}

The cellular content of tendons accounts for 20% of the overall tissue volume (Nordin et al., 2001). The main cell type present within tendons, which is responsible for the production and regulation of ECM, is the tenocyte (Maffulli et al., 2002). These are bipolar cells with elongated nuclei and spindle-shaped morphologies; they are regularly anchored in columns amongst the collagen bundles (Bernard-Beaubois et al., 1997). Other cells (though present in smaller numbers) include chondrocytes present at OTJ insertion sites, synovial cells composing the tendon sheath and vascular cells such as capillary endothelial and arteriole smooth muscle cells (Sharma and Maffulli, 2005).

Some more details from {2}:

The matrix is far more conspicuous than the cells. However, it is now widely recognised that the cellular elements hold the key to understanding development, repair and the ability of tendons and ligaments to respond to changing mechanical load. Tenocytes are mechanosensitive cells that are hardwired in a way that allows them to deploy a tensegrity architectural system to detect changes in mechanical load via deformation of their cell membrane and cytoskeleton (Wang, 2006). Strain in the extracellular matrix (ECM) tenses cytoskeletal fibres via integrin receptors in the cell membrane, and this in turn is relayed to the cell nucleus so that gene expression can be altered. An important principle of the tensegrity system is fibre continuity between the ECM and the cells. As Myers et al. (2007) point out, the implication is that the existence of a continuous network of fibres (i.e. collagen fibres in the ECM; cytoskeletal fibres in the cells) means that stress on one part of one cell can be dissipated throughout the entire tissue. Consequently, individual cells are protected from damage and a small mechanical stimulus can potentially affect many cells (Ingber, 1997; Myers et al., 2007). It is also worth noting that an under-stimulation of tenocytes that results from an altered cell–ECM interaction consequent upon tendinopathy could down-regulate cell activity (Arnoczky et al., 2007). Thus, the tendon becomes weakened and more vulnerable to damage from mechanical overload.

Although tenocytes and ligament fibroblasts are unremarkable cells in routine histological preparations and seemingly isolated within the ECM (Figs 14.2 and 14.3), they have a much more elaborate form when viewed by confocal microscopy (McNeilly et al., 1996). Each cell has numerous finger-like and sheet-like processes, extending around groups of collagen fibres and creating a 3D network of intercellular contacts throughout the tissue that fits well with the tensegrity model discussed above. The tenocytes are typically arranged in longitudinal rows, where the long axis is parallel to the tendon itself (Fig. 14.3). This reduces the risk of cell damage accompanying tendon or ligament loading. Adjacent cells communicate with each other via gap junctions – structures that allow ions and small molecules to be rapidly exchanged between individual cells. Two types of gap junctions are present in tendons – those expressing the protein connexin (cxn) 32 and those expressing cxn 43 (McNeilly et al., 1996; Ralphs et al., 1998). It is notable that the distribution of these two connexins is distinctive and implies they have independent functions. Connexin 32 is only present between cells within a longitudinal row, whereas cxn 43 also links cells in adjacent rows. Consequently, gap junctions containing cxn 32 are oriented along the line of tensile loading of a tendon, but cxn 43 junctions link cells in all directions. Waggett et al. (2006) have since shown that collagen synthesis is inhibited in avian tendon cells subject to cyclic mechanical loading in vitro, via cxn 43 and stimulated via cxn 32. Thus, it seems likely that the interplay between these junctions in response to load changes in tendons and ligament is critical in allowing them to adapt their ECM to changing mechanical load (Waggett et al., 2006). The integrity of the cell junctions in a compliant tendon seems to be ensured by the presence of longitudinally oriented, actin stress fibres within the tenocytes, which are associated with adherens junctions that link cells within the same longitudinal row (Ralphs et al., 2002).



Your Answer

By clicking “Post Your Answer”, you agree to our terms of service, privacy policy and cookie policy

Not the answer you're looking for? Browse other questions tagged or ask your own question.