Tendon Physiology

 

The immature form of a tenocyte is referred to as tenoblast and both are arranged in rows between the collagen fibres (Tan and Chan 2008). Together these cells comprise of 90-95% of the cellular composition of tendons. The remaining 5-10% of the cellular distribution is made up of chondrocytes (at the osteotendinous junctions), synovial cells (tendon sheath) and vascular cells which are smooth muscle cells of arterioles and endothelial cells of capillaries (Sharma and Maffuli 2005). Tenoblasts are spindle shaped and are highly metabolically active, as is reflected in the large presence of cytoplasmic organelles (Sharma and Maffulli 2005). As the tenoblast begins to mature it transforms into the elongated form of a tenocyte with a lower nucleus to cytoplasm ratio and a lower resultant metabolic activity. Tenocytes are involved in the synthesis of collagen and all components of the ECM. To provide the energy required to complete the above roles, tenocytes are involved in energy generation through the krebs cycle, anaerobic glycolsis and the pentose phosphate shunt (Sharma and Maffuli 2005).

 

As outlined previously collagen fibrils unite to form fascicles ranging from primary to tertiary bundles. More specifically collagen fibrils are the smallest tendon component which can be tested mechanically and are visible under microscopy (Sharma and Maffuli 2005). However collagen fibrils can be dissected further into their smallest constituent, tropocollagen. A triple-helix peptide chain, tropocollagen is water soluble. Only when a number of tropocollagen join and crosslink do they become insoluble fibrils (Sharma and Maffuli 2005).

 

Surrounding and enveloping the collagen and tenocytes, within the extracellular matrix, is the ground substance. Aside from providing structural support to the collagen, a number of molecules within the ground substance hold important roles within the tendon structure. Proteoglycans (PG) for example are highly hydrophilic, thereby enabling rapid diffusion of water-soluble molecules and the migration of cells (Sharma and Maffuli 2005). A specific PG called decorin helps improve connection, tensile strength and viscoelasticity between the collagen fibrils (Lawerence 2014). Other molecules such as adhesive glycoproteins play a role in tendon repair and healing (Sharma and Maffuli 2005). Tenascin-C is a molecule found in abundance within the tendon. This molecule may play a role in collagen fibre orientation and alignment as the expression of this molecule is regulated by mechanical strain (Sharma and Maffuli 2005).

 

Tendons which are exposed to mechanical stress are often enveloped in a tendon sheath. Examples of this are the tendons of the hand and feet, where effective lubrication is required (Sharma and Maffuli 2005). Tendon sheaths are two layered with the deepest layer being known as the synovial sheath. This sheath functions to provide synovial fluid to improve lubrication of tendon and limit friction. The outer layer of the tendon sheath is called the fibrotic sheath helps as a fulcrum to improve tendon function. (Sharma and Maffuli 2005). The TA and PT, as mentioned earlier, lack this tendon sheath and instead have a dual layer paratenon.

 

Complex architecture is necessary at the myotendinous junction to ensure efficient transmission of force from the muscle, through the tendon, and to the bone. At this junction collagen fibrils of the tendon insert into grooves or recesses formed by the processes of long tubular myocytes. Proteins crucial to the integrity of this location include laminin, integrin, Vinculin, fibronectin and talin; they ensure that actin filaments which extend beyond the z-line interlock with collagen fibrils. This anchors the collagen and muscle fibres in place, enabling tension created by the contractile proteins of muscle fibres to be passed to the collagen fibrils (Sharma and Maffuli 2005). Even with this complex architecture in place, the myotendinous junction remains the weakest point of the muscle-tendon unit (Sharma and Maffulli 2005).

 

As the tendon joins with muscle, the tendon must also join with bone which occurs at the osteotendinous junction. The area can be subdivided into four zones: dense tendon zone, fibrocartilage, mineralized fibrocartilage and bone (Sharma and Maffulli 2005). These zones increase in stiffness from their preceding zone, with the transition from tenocytes to fibrochondorcytes and finally osteocytes. The unique structure of the osteotendinous junction limits collagen fibre bending, shearing and failure (Sharma and Maffuli 2005). 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Fig 1.7: Schematic drawing to basic tendon structure (Docheva et al 2014).

 

 

Key References

• Sharma, P. and Maffuli, M. (2005) ‘Tendon Injury and Tendinopathy: Healing and Repair’, The journal of Joint and Bone Surgery, 87: 187-202.

• Maffulli, N., Longo, U., Maffulli, G., Khanna, G., Denaro, V. (2011) ‘Achilles Tendon Ruptures in Elite Athlete’, Foot & Ankle International, 32(1): 9-15.