Biomechanics of Tendon and Ligament Tissue

Massage therapists focus a great deal of attention on muscles when addressing client’s pain and injury complaints. However, other soft tissues may also play a prominent role in various pain complaints. Tendon and ligament injuries comprise a significant number of musculoskeletal disorders. Understanding structure and function of tendons and ligaments and how they are injured helps us construct the most appropriate treatment plans when dealing with them. Let’s take a look at some key issues of tendon and ligament structure that influence how they work and how they are injured.

 

Structure and Function

Both tendons and ligaments are composed of dense regular connective tissue. However, there are significant differences that are important. These two tissues are most commonly distinguished by their main function: tendons connect muscle to bone, while ligaments connect bone to bone.

The functional difference of connecting muscle to bone vs. bone to bone is important but can also lead to misunderstanding. For example, the patellar tendon begins at the distal end of the quadriceps muscles and continues to its attachment site on the tibial tuberosity. The patella is a sesamoid bone that is actually embedded within this tendon. Yet, numerous anatomical texts designate the portion of this structure between the distal patella and the tibial tuberosity as the patellar ligament because it is connecting bone (patella) with bone (tibia) (Image 1).

Image 1
Infrapatellar tendon is often listed as the patellar ligament because of its connection between the patella and tibia
Image is from 3D4Medical’s Complete Anatomy application

It is more important to focus on the structure and function of these tissues rather than simply their anatomical attachment points. The entire connective tissue extending from the distal quadriceps to the tibial tuberosity clearly functions as a tendon and not a ligament despite the fact that the patella is embedded within the tissue itself. In addition, the fibrous composition of the structure is clearly tendinous and not ligamentous.

The biomechanical function of tendon is to transmit the contraction force of a muscle to the bone while minimizing the loss of tensile force. Tendons have their collagen fibers oriented in almost an exclusively parallel direction. That gives the tendon the greatest amount of tensile strength to resist forces directed along the orientation of these fibers (Image 2).1

Image 2
Collagen fibers in the tendon are much more parallel aligned. In ligament they are looser and also run in multiple directions.

This parallel fiber orientation allows the tendon to be very stiff so it can transmit the muscle’s contraction force more like a wire and less like a rubber band. The capability of tendons to withstand very strong tensile forces is indicated by how infrequently you hear of tendon tearing compared to muscle tearing in strain injuries.

The forces a tendon is subjected to are primarily in one direction. However, there are a few locations where tendons may also have tensile loading that is not directly in line with their primary muscle’s angle of pull. Tendons of the finger flexors and extensors in the hand are a good example. There are lateral connections between the individual tendons that allow finger tendons to work as a network.2 These fibrous networks seem to be important in maintaining appropriate space between the flexor and extensor tendons and channeling forces between them in order to coordinate movement of the fingers and toes. Attempting to move a finger or toe independently of the others illustrates how this connecting network functions.

Some tendons are also surrounded by a synovial sheath. Tendons surrounded by a synovial sheath are generally located in the distal extremities where the tendons take sharp angular turns and are held to close to the joint by a binding retinaculum (Image 3). The primary function of the sheath is to reduce friction between the tendon and the retinaculum during movement.

Image 3
Tendon sheaths and their binding retinacula
Image is from 3D4Medical’s Complete Anatomy application

Tendons are primarily for transmitting forces. Ligaments, on the other hand are mainly for establishing skeletal stability. The primary function of the ligament is to connect bones to each other and to guide appropriate movement at each joint. Guiding movement at the joint helps maintain the most optimal joint contact surface and prevent excessive wear between bones, as there are substantial friction forces from movement and weight bearing.

Ligaments are generally smaller and shorter than most tendons. They usually only span one joint and it is important for their attachment points to be relatively close together to guide movement and give the joint the greatest degree of stability.

Ligaments, similar to tendons, have their collagen fiber orientation primarily in a parallel direction from one end of the ligament to the other. However, there are also numerous fibers running in multiple directions within the ligament (Image 2). Fibers running in multiple directions indicate that ligament can withstand forces that are in multiple directions even though they are mainly designed to resist force in one particular direction.

Ligaments also have a higher concentration of elastin then tendons which also allows them to be more pliable than tendon. The ligament needs to have a certain degree of pliability to absorb joint loads with a little bit of give in multiple conditions. Unlike tendons, ligaments don’t need synovial sheaths because they don’t span multiple joints with sharp turns and they aren’t sliding back and forth like tendons.

 

Common Pathologies

Tendon and ligament injuries are both relatively common soft-tissue disorders. However, their injuries differ in how they occur and what happens to the tissue in these injuries. Tendons are most commonly injured by repetitive loads over time while ligaments are mostly injured from sudden high force loads. Let’s take a look at both of these injury processes.

The most common tendon disorder that people are familiar with is tendinitis. As its name implies, tendinitis would be an inflammatory condition of the tendon. However, in recent years research has indicated that there may be very little, if any, inflammation associated with these common overuse tendon disorders. If not inflammation, than what is occurring?

Instead of inflammation there may be a degree of structural breakdown of the collagen matrix within the tendon in these overuse disorders. For that reason, the terms tendinosis or tendinopathy (which simply indicate pathology of the tendon) are now frequently preferred because they don’t emphasize an inflammatory component. It is definitely possible to have true tendinitis where inflammation is a factor, but it is actually not common.

Whether we have collagen degeneration or a true inflammatory process in the tendon makes significant difference in choosing treatment strategies. For example, if there is a true inflammatory tendon pathology, the administration of anti-inflammatory medications such as corticosteroid injections would make sense. However, steroid injections into tendons also impair collagen synthesis and adversely affect overall tendon strength in the long-term. For that reason, treating a collagen degeneration tendinosis complaint with steroid injections could actually make the condition worse instead of better.

One question that frequently comes up with tendon pathologies is what causes pain for these overuse tendon disorders if it isn’t an inflammatory condition with tendon fiber tearing. The answer is simply that we aren’t sure yet. There are several theories but there is not a definitive model yet for what is the pain producing mechanism in tendon disorders. One promising theory is that there are numerous nociceptors in tendons that are sensitive to chemical irritation. The chronic overload on tendons causes a series of biochemical and metabolic challenges in the stressed tendons which may activate nociceptors and cause tendon pain.3

Mechanical overload is clearly the most frequent cause for tendon pathology. However, tendinosis can also occur in the absence of significant mechanical overload. Research has shown a strong connection between tendinosis and the fluoroquinolone family of antibiotics. These antibiotics are generally taken for things completely unrelated to tendon or musculoskeletal disorders but they can have an adverse impact on the structural integrity of tendons. Consequently, if a client is complaining of tendon pathology, it would be a good idea to find out in the initial history if the client has been taking any fluoroquinolone antibiotics. If so, mechanically oriented treatment strategies such as increasing load on the tendon may not be the best choice.

Another relatively common tendon pathology is tenosynovitis. Unlike the common overuse condition frequently called tendinitis, tenosynovitis is an inflammatory condition. Tendons that are contained within a synovial sheath are subjected to significant friction between the tendon and its sheath. As a result of chronic overuse, inflammation and fibrous adhesions can develop between the tendon and surrounding sheath. These fibrous adhesions make it more difficult for the tendon to move smoothly inside the sheath and can produce pain. Because tendon sheaths are only in certain places, tenosynovitis will only occur in those tendons that are housed in a synovial sheath (mostly in the distal extremities).

Ligament injuries are a bit simpler than the tendon pathologies described above. Ligament injuries occur most frequently when there is a very high force load that overwhelms the ligaments capability to withstand the force. This is called a sprain and differentiated from a strain, which is an injury to the muscle-tendon unit. Ligament sprains are graded in three different categories of grade 1 (mild), grade 2 (moderate) and grade 3 (severe- including complete rupture). There are various different clinical signs and symptoms associated with each degree of ligament sprain to determine how severe the injury is.

Because of the multiple fiber directions and higher elastin content, ligaments can withstand some degree of sudden stretch load. If the force load extends beyond what the ligament can withstand, the ligament may be permanently elongated. Permanent elongation occurs in second and third degree sprains, although third degree sprains may also include a complete rupture of the ligament.

When a ligament becomes permanently elongated, also referred to as plastic deformation, there is an increasing degree of mobility at the joint because the ligament is not restricting movement the way it should. The increasing degree of movement at the joint is called hypermobility and can be one factor in an earlier development of osteoarthritis at that joint. Ligamentous laxity and hypermobility can also be a factor in other disorders. For example, laxity in the capsular ligaments of the shoulder has been implicated as one cause for subacromial impingement due to excessive movement of the humeral head.

 

Treatment Strategies

Identifying when a ligament or tendon has been injured is helpful in designing an appropriate treatment strategy. Gentle protected movement is a mainstay in the treatment strategy for both tendon and ligament injuries. For ligament sprains treatment formerly emphasized maintaining the joint in an immobilized position so the ligament would not be stressed and could appropriately heal. However, recent research has indicated that movement within normal limits is far more effective and beneficial in producing an ideal healing environment for the ligament, so now movement that does not overstress the ligament is strongly encouraged.

Treatment for chronic overuse tendon pathologies can be a little counterintuitive. It would seem like the most effective means of healing the collagen degeneration within the tendon would be to completely rest it and allow the tissue to rebuild. Some degree of rest from offending activity is certainly helpful. However, we have now learned that stressing the tendon with certain types of load, especially eccentric muscle load, helps the tendon adapt to the stresses and can lead to quicker recovery. So, despite the fact that injury was caused by excessive use, exercising the tendon is actually a crucial part of the healing process as well.

One of the questions for massage therapists is the role that massage can play in addressing tendon and ligament injuries. Deep friction massage has been used frequently to address chronic overuse tendon disorders. Formerly, it was thought that the primary benefit to this treatment was reducing unhealthy scarring within the torn tendon fibers. Now that we realize most of these tendon disorders involve collagen degeneration and not fiber tearing, that treatment approach does not make sense. Still, we know that deep friction massage does often produce clinically beneficial results for overuse tendon disorders. Although there is still research to be done in this area, one possible explanation is that pressure and movement applied to the tendon may stimulate fibroblast activity and can encourage tissue healing within the damaged collagen matrix of the tendon.

Similarly, friction massage is still used to treat tenosynovitis. The primary theory around massage for tenosynovitis is that friction massage can help reduce dysfunctional adhesion and binding between the tendon and surrounding synovial sheath. This has never been confirmed through research, so right now we recognize this treatment strategy as beneficial, but still need further investigation.

Another very important facet of treating any tendon pathology is working on the muscles associated with the injured tendons. In addition to decreasing aggravating activities, tensile loads can be reduced on the tendon by decreasing tightness in the tendon’s muscle. A wide variety of massage techniques can be quite effective in achieving that goal.

Treating ligament sprains follows a similar track. It is unclear if massage can do anything significant to encourage the healing process of a sprained ligament. It may help to some degree with encouraging tissue regeneration as with tendons. In addition, a joint that is not properly mobilized during the healing process may develop fibrous adhesion between the healing ligament fibers and adjacent tissues. Frequent friction of the healing ligament, including self-massage multiple times during the day, may help reduce the likelihood that adhesions adversely bind the healing ligament and prevent full range of motion in the future.

It is important to remember that ligaments do not contain contractile tissue. As a result, they do not contract. It is not unusual to find massage treatment techniques where the practitioner advocates “releasing” the ligament. We must remember that because ligaments don’t contract, they also don’t release. In fact, releasing a ligament is probably one of main things you don’t want to do because it’s primarily designed to be stiff and hold joint contact surfaces in proper orientation with each other.

It is important for us to understand how different soft tissues function, what happens to them when injured, and how our massage treatments interface with those tissues disorders. As we continue to learn more about tendon and ligament physiology, may also develop more appropriate treatment strategies that will help our clients get back to activities even sooner.

 

Notes

  1. Rumian AP, Wallace AL, Birch HL. Tendons and ligaments are anatomically distinct but overlap in molecular and morphological features—a comparative study in an ovine model. J Orthop Res. 2007;25(4):458-464. doi:10.1002/jor.20218.
  2. Müller SA, Todorov A, Heisterbach PE, Martin I, Majewski M. Tendon healing: an overview of physiology, biology, and pathology of tendon healing and systematic review of state of the art in tendon bioengineering. Knee Surgery, Sport Traumatol Arthrosc. 2015;23(7):2097-2105. doi:10.1007/s00167-013-2680-z.
  3. Danielson P. Reviving the “biochemical” hypothesis for tendinopathy: New findings suggest the involvement of locally produced signal substances. Br J Sports Med. 2009;43(4):265-268. doi:10.1136/bjsm.2008.054593.

 

 

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