Tissue Mechanics Of Tendon Tissue Biology Essay


Tendons are tissues that are responsible for locomotion and joint stability; they are made of tough fibrous connective tissues consisting mostly of closely packed parallel arrays of collagen fibers. Unlike ligaments or fascia, tendons connect muscles to bones, while the ligament connects between two bones and fascia connects one muscle to the other.

Tendons permit locomotion by relying mechanical forces generated by the muscles to bones, therefore tendons are able to sustain extremely large forces acting on them. The goal of this review is to provide an overall perspective on the mechanics of the tendon tissue.

First, I will touch on the structure of tendons and its composition, followed by its mechanical properties. Finally, I will cover forces experienced by tendons in vivo, and finally look at its response to mechanical loading during the healing process.

Tendon contains several different protein molecules; they include mostly collagen proteins, and traces of other proteins such as elastin and proteoglycans. Proteoglycans vary in amounts at different sites of the tendon. Higher proteoglycans expression is found in regions of higher compression, as proteoglycan proteins are hydrophilic and attract water molecules, which resist compression. While lesser proteoglycans proteins are found in tensile bearing regions of the tendon. Elastin on the other hand is responsible in the recovery of the tendon structure after stretching.

Lady using a tablet
Lady using a tablet


Essay Writers

Lady Using Tablet

Get your grade
or your money back

using our Essay Writing Service!

Essay Writing Service

Collagen protein is the building block of tendon; there are various type of collagen proteins found in a health tendon. Type I collagen proteins account for about 98% of the collagen population, while the remaining 2% consist of a mixture of type II, VI, IX, X and XI collagen proteins. Collagen proteins especially type I, exhibit great tensile strength properties.

The fibril structure is the basic tendon structural unit made up of parallel-aligned collagen proteins, and has a diameter ranging from 10 nm to 500 nm. These variations of sizes depend on the type of animal, age and location of tendon. In younger animals, fibrils are uniformly smaller than older animals, which have a mixture of small and large fibrils.

Fibril bundles bounded by endotenons, forms the next unit of tendon structure, collagen fibers. Endotenons consist of blood vessls, lymphatics and nerves in a layer of connective tissue. Next, these collagen fibers bundles form the subfascicle, which then forms the secondary fiber bundles forming the fascicle. Fascicle is enclosed in epitenon, which are connective tissues sheath carrying blood, nerve and lymphatic supply. Fascicle then bundles to form tertiary fiber bundles forming the tendon tissue.

A connective tissue layer known as paratenon, which consist of synovial sheath, encloses the tendon tissue. Collectively, these inter-layering of connective tissues reduce friction between the tissues. The unique parallel and "wave-like" formation of the tendon structure provides the tensile strength required to endure large amounts of tensile stress. Figure 1 below shows the different levels of tendon structure as described above.

Fig. 1. Diagram showing the hierarchical structure of tendon tissue. (Silver et al, 2003)

Tendons link muscle and bones together, the junction in which the tendons meet with bones and vice versa is known as the enthesis. There are two different types of enthesis junction; they are fibro-cartilaginous and fibrous enthesis. The fibrous enthesis connects the muscles to the bones in adults or attaches to the periosteum during adolescence.

Comparatively, the fibro-cartilaginous enthesis containing a section of hyaline fibro-cartilage distributes mechanical loadings. Both enthesis junctions have the ability to bear most of the tensile, shear and compressive forces. These forces changes the physiological properties of the junction by inducing an increase expression of proteoglycans, which are proteins found in the extracellular matrix.

Mechanical Properties of Tendon

Tendons experience high mechanical forces during locomotion or vigorous exercises. It is necessary to obtain the stress versus strain graph from experiments, to understand how it reacts to different mechanical loadings. Figure 2 below shows the relationship between stress-strain of the tendon fibers. The initial portion of the curve labeled "toe region" represents the straightening of the "wave-like" tendon fibers.

As the fibers straightened out it transits into the elastic region of the curve, where young's modulus can be determined as stress increases linearly with strain. Beyond this region, the tendon fibers begin to rupture and the tendon tissue experience plastic deformation. At about 10% strain, the tendon tissue reaches its ultimate stress and true fracture stress.

Lady using a tablet
Lady using a tablet


Writing Services

Lady Using Tablet

Always on Time

Marked to Standard

Order Now

Fig. 2. Stress vs Strain plot of tendon fibers.

Figure 3 captures the "wave like" arrangement of the tendon fascicle under a confocal laser-scanning microscope. The left image depicts a strained fascicle, and it has a lesser "wave like" arrangement compared to the right, which shows an unstrained fascicle.



Fig. 3. Microscopy scans of strained (left) and Unstrain (right)tendon fasicles displaying "wave like" arrangement clearly.

The data in table 1 represents the experimental findings of the human patellar tendon, which compares two distinct age groups. The result suggest that mechanical properties of tendons deteriorate with age, and this result correlates with our daily observations that adults experience more straining of the tendons compared to youths.




Ultimate Tensile Strength

53.6 MPa

64.7 MPa

Table 1. Tensile properties of human patellar tendon. (Johnson et al. 1994)

Young's Modulus

660 MPa

504 MPa

Effects of Exercise on Tendons

Exercising has a profound effect on the host body; the coordination of movement invokes the muscles, tendons and bones. To achieve greater strength, muscles undergo hypertrophy, a process in which muscle fibers thicken to increase output forces. As such, tendons experience increase mechanical loading as it transfers forces generated by the muscles to the bones. This increase in stress induces remodeling of the tendon tissues by influencing its chemical composition, and mechanical properties. Understanding the effects of exercising on tendons will clarify the cause of injuries associated with health tendons and long-term exercise, while shedding light on better treatment methodologies for suffering individuals.

Biochemical Changes

Collagen proteins associated with the tensile strength of tendons, increased dramatically by up to 46% after 8 weeks of endurance training. (Curwin, 1988) The experiment also shows that there was about 50% decrease in pyridinoline cross-linking between the tendon fibers, suggesting that the maturation of tendons slowed down. Interestingly, insulin-like growth factor I (IGF-I) responsible in collagen synthesis and cell proliferation had an increased expression. Also noted in the experiments, were quick turnover rate for the type I collagens. (Langberg, 2001) Collectively, the experiment showed a higher tendon synthesis compared to degradation, suggest that exercising increases the synthesis of new tendon tissues that replaces older worn out tendons. (Magnusson, 2003)

Tensile Strength & Stiffness (Mechanical Properties)

Studies have shown that engaging in long-term training increase both tensile strength and stiffness in tendons. This observation was noted when an increase in tensile strength of up to 5% and stiffness of up to 10% in the achilles tendons of rabbits after undergoing 40 weeks of exercise. (Kubo, 2000). Also increase in tendon bundles as well as cross-sectional area of tendons have be found comparing mice that underwent one week of exercise compared to the controls. (Michna, 1989)

Injuries Associated With Worn Out Tendons

Injuries due to worn out tendons are known as tendinopathy, this injury is common among athletes and people that exercise routinely. The major cause for this injury is due to constant stress exerting on the tendon overtime. This type of stress can be classified under fatigue where the loading is well below the maximum stress level however exerted over an extended amount of time, leading to inflammation of the tendon. This inflammation is due to the release of prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4), in response to constant repeated mechanical loading. Both PGE2 and LTB4 are naturally occurring molecules, which are involved in the inflammation process. LTB4 produced by leukocytes in response to inflammatory mediators induce neutrophil activation and infiltration across the endothelium. Besides tendon injuries, another common tendon related injury is at the tendon-bone junction (enthesis), also known as enthesopathy. The characteristics of enthesopathy include, loosening of collagen bundles, lipid accumulation and micro calcification. (Jarvinen, 1997)

In addition, damaged due to trauma to the paratenon, would lead to paratenonitis. Paratenon or the tissue consisting of synovial sheath, encloses the tendon bundle, when damaged could lead to edema, swelling and infiltration of white blood cells within the tendon fibers. (Jarvinen, 1997)

Treatments available for injuries to the tendon include, non-medicinal treatments such as physical therapy, stretching or controlled motion via immobilization. Painkillers such as non-steroidal anti-inflammatory drugs (NSAIDs) are used frequently to suppress and provide symptomatic relief of the accompanying pain. In order to treat tendon injuries effectively, the mechanism behind tendinopathy recovery must be elucidated.

Lady using a tablet
Lady using a tablet

This Essay is

a Student's Work

Lady Using Tablet

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.

Examples of our work

Tendon Recovery


~1 Day

~ 2 Month

~ 1 Month

The recovery process of tendon healing consist of three slightly overlapping main phases, they include the inflammatory, repairing and remodeling phases. Figure 4 below illustrates the three phases as well as the duration of each phase.

Fig 4. Illustration of the tendon recovery phases

During the 1st 24 hours after tendon injuries has occurred, neutrophils, monocytes, macrophages, erythrocytes, platelets, and inflammatory cells migrate to the site of inflammation. These immune cells work to clear the injury site of toxic materials via phagocytosis. Concurrently, these immune cells release signaling molecules and growth factors that initiate collagen repair and synthesis by recruiting fibroblasts cells.

Next, cellular repairing phase begins which last for about one month. Fibroblasts cells that were recruited in the inflammation phase, increase collagen synthesis and other extracellular matrix (ECM) components. These ECM components include protreoglycans, which attracts water molecules aiding repair.

After the repair phase, remodeling phase begins which last for about two months. During this phase, newly repaired tissues modify itself into fibrous tissue, which subsequently changes into scar-like tendon tissue. Subsequently, the covalent bonding between the collagen molecules increase which increases the tendon's tensile strength and stiffness. As the phase nears completion, the cells responsible for remodeling decline in numbers.

Growth Factors

In addition to cell mediated repair, growth factors used by these cells play an important role in tendon healing. To date, five important grow factors involved in tendon repair have been elucidated. Namely, insulin-like growth factor I (IGF-I), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and transforming growth factor beta (TGF-β).

The expression levels for all of the mentioned growth factor increased dramatically after tendon injury. Expression of the IGF-I is highest at the early stage of inflammation, it promotes fibroblasts proliferation and migration. Which in turns increase collagen and proteoglycan synthesis. (Abrahamsson, 1996) Shortly after tendon injury, PDGF expression increases which stimulates production of other growth factors.

VEGF increases blood supply to the site of injury through a process known as angiogenesis. It also increases proliferation of endothelial cells. bFGF aids repair of tendons by coordinating cell migration and proliferation. TGF-β exist in three different types of isoforms namely, TGF-β1, TGF-β2, TGF-β3. TGF-β1 aids the process of increasing ECM at the site of injury; an overexpression of TGF-β1 is detrimental as it forms tissue fibrosis, which is not ideal. Next TGF-β2, has similar functions to the TGF-β1 isoform, however it improves tissue scarring during the remodeling process. Collectively, the TGF-β family of growth factors plays an important part in the recovery and remodeling of damaged tendon tissues.

Effects of Mechanical Stress on Tendon Healing

It had been noted that though exercising and stretching of injured tendons should be avoided, controlled movement of an injured tendon however enhances the recovery of the damaged tissue. Studies have shown that early mobilization of the flexor tendons of canine, improve the rate of recovery as well as increased its tensile strength. (Gelberman, 1986)

Taken together, experiments as well as clinical treatments of injured tendons have shown that early mobilization of recovering tendons increases recovery rate as well as tensile strength while reducing immobility of the tendon. Mechanical loadings for the treatment of tendinopathy have shown reduced chronic pains, suggesting that the loadings improved tendon recovery. (Amiel, 1982)

Fibroblast Role in Tendon Healing

The healing of tendon tissue results in the formation of scar tissue. The formation of scar tissue occurs when fibroblast cells contract at the site of injury. The forces generated by these contractions are essential in the closure of wound openings. However, excessive contractive forces exerted by the fibroblast to the surround ECM results in the formation of scar tissues. However, the reduction of contractive forces by inhibiting fibroblast contraction has shown to impair wound recovery. (Coleman, 1998) Therefore, optimal level of contraction is required to expedite wound healing while reducing scar tissue formation.

Figure 5 below shows the three main phases of tendon recovery as well as the tensile strength of an injured tissue. Compared to a healthy uninjured tendon, a fully recovered injured tendon can never fully recover its original tensile strength. This observation is due to the remodeling of the damaged tendon tissues, in which scar tissues formed; do not have the same tensile properties as native tendon tissues. This difference in tensile strength is due to the difference in the biochemical and biomechanical properties.

Fig 5. tendon strength at different recovery phases

Response of Cells in Tendon to Mechanical Load

Effects of Mechanical Loading on Fibroblast

Until now, we have discussed the effects mechanical loadings on tendon tissue. Mechanical loading causes the tendon fibers to change in biochemical, mechanical properties as well as composition. Being a biological tissue, cells such as fibroblasts exist among the tendon fibers

Effects of Mechanical loading on Gene Expression

The ability for tendons to adapt under mechanical loading as describe in the first half of this review, is a testimony to the ability of the cells to induce alterations to tendons. These cells, which are known as tenocytes, are specialized elongated fibroblasts that exist between the collagen fibers. Upon sensing changes in mechanical loadings, the tenocytes react by altering its gene expression causing a change in protein synthesis leading to the desired phenotypic change of the tendon tissue. This process is known as mechanotransduction, and it involves a series of complex reaction cascade. The reaction cascade involves a wide array of biomolecules they include, the ECM, integrins, cytoskeleton, G proteins, MAPKs and stretch-activated ion channels.

The primary role of ECM is to support its surrounding tissue structure as well as a medium for nutrients and waste products to travel in. They provide cell support, proliferation, cell adhesion, differentiation by acting as a substrate for proper cell adhesion. Studies have shown that ECM promotes growth factors such as TGF-β, bFGF and PFGF under mechanical stress. These growth factors as mentioned in the previous section have an important role in promoting collagen synthesis and repair. Besides this, ECM contains vast amount of fibrous proteins and glycosaminoglycans, fibrous proteins such as proteoglycans mitigate forces by dissipating mechanical stresses. The resultant forces that exist after dampening gets transmitted to the cytoskeleton of the tenocytes.

The cytoskeleton of the tenocytes like majority of cells, is made up of microfilaments, microtubules and intermediate filaments. In accordance with the tensegrity theory, the forces acted by the cell equalize forces acting on the cell by the ECM.

These specialized tendon fibroblast, react by inducing a change in its gene expression which will eventually alter the properties of the tendon tissue.