By Ground Up Strength

Many strength trainees, bodybuilders, and exercisers are told that there should be a certain ratio between the strength of their hamstring and quadriceps muscles. Called the H/Q ratio and reported to be anywhere from .50 to .75 with a normative value of .60, the strength ratio of this important agonist/antagonist pairing is considered essential to the stability of the knee joint and to prevent ACL and other injuries. It is also sometimes thought to be predictive of those at risk for hamstring strain.

Some strength and conditioning experts actually test the maximal strength of the quadriceps and hamstring muscles of their clients, using leg extensions and leg curls, respectively, believing that they should observe a certain ratio in maximum weight of each movement and that this relationship will tell them whether their clients are at risk for a knee injury. To calculate the hamstring-quadriceps strength ratio, the maximal knee extensor moment and the maximal knee flexor moment is tested at identical velocities (isokinetic), and the flexion result is divided by the extension result.

It is quite true that the functional relationships between an agonist muscle, like the quadriceps, and its antagonist muscle, the hamstrings are very important, the idea that testing the strength of each muscle for an ideal ratio is an accurate screen for injury potential is rather crude and simplistic.

In reality there is not one ratio for concentric hamstring and quadriceps torque ratios but a range of ratios depending on joint angle and speed of movement. These have been well studied, producing averages anywhere from 0.5 to 0.75. The mechanical advantage of a muscle tends to change with the joint angle which changes the angle of pull of the muscle. As the mechanical advantage of one muscle increases the mechanical advantage of the other muscle may decrease. Also, the speed of the movement changes the angle at which peak torque occurs. Therefore, although important considerations for screening, these agonist/antagonist muscle relationships certainly are not static entities.

Another problem is that conventional testing, as described above, involves testing the maximal strength of the quadriceps and hamstrings using the same concentric action. This may make no sense because these muscles do not function in terms of concentric-concentric actions but concentric-eccentric actions.

Another observation is that quadriceps weakness is a feature of ACL deficiency. When people with anterior knee pain are tested, weakened quadriceps with normal hamstring strength is often found. In other words, weak quadriceps are typical in those with ACL dysfunction but this does not mean that weak quadriceps are a cause of ACL problems.

See DEVELOPMENTS IN THE USE OF THE HAMSTRING/QUADRICEPS RATIO FOR THE ASSESSMENT OF MUSCLE BALANCE for an indepth review of this subject, including conventional viewpoints and new developments concerning joint angle and muscle action.

References

Coombs, Rosalind, and Gerard Garbutt. "DEVELOPMENTS IN THE USE OF THE HAMSTRING/ QUADRICEPS RATIO FOR THE ASSESSMENT OF MUSCLE BALANCE." Journal of Sports Science and Medicine 1 (2002): 56-62. <http://ww.jssm.org/vol1/n3/1/n3-1pdf.pdf>

Dvir, Zeevi. Isokinetics: Muscle Testing, Interpretation, and Clinical Applications. Edinburgh: Churchill Livingstone, 2004. Print.

Brown, Lee E. Isokinetics in Human Performance. Champaign, IL: Human Kinetics, 2000. Print.

Bennell, K., H. Wajswelner, P. Lew, A. Schall-Riaucour, S. Leslie, D. Plant, and J. Cirone. "Isokinetic Strength Testing Does Not Predict Hamstring Injury in Australian Rules Footballers." British Journal of Sports Medicine 32.4 (1998): 309-14.

by EricT

Inversion: Turning the sole of the foot inward or medially, toward the midline of the body. This occurs, for example, when you are standing on the outer edge of your foot. When an ankle sprain occurs as a result of forcible movement in this direction, it is called an inversion sprain or lateral ankle sprain. The lateral ligaments of the ankle are injured in inversion sprains usually occuring from the front to back (anteriorly to posteriorly) as plantar flexion accompanies the movement. The anterior talofibular ligament (ATF) is typically injured first followed by the calcaneofibular and posterior talofibular ligaments, depending on the severity of the injury. The peroneal muscles, which are located on lateral lower leg and produce eversion of the foot, may also be damaged.

by EricT

Eversion: Turning the foot so that the sole faces outwards, or laterally, such as when you are standing on the iner edge of your foot. The sole of the foot is moved away from the body's midline. Movement of the intertarsal joints such as the talocalcaneal and subtalar joint is responsible for this action. When an ankle sprain occurs as a result of this forcible eversion movement it is called an eversion sprain or medial ankle sprain, which affect the deltoid ligament of the ankle (much less common than inversion sprains).

by EricT

Quick forum thread discussion on whether the male athletic supporter serves any real purpose.

Topics Covered

• What was the original purpose of the athletic support?
• Can an athletic supporter protect you from an inguinal hernia
• Do you need a firm undergarment to protect you from a hernia?
• The athletic supporter and the 'cup' to protect the genitalia

See also the hernia category.

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by EricT

Strain (2): A measure of deformation which describes the changes in the dimensions of a body as a result of load application. In mathematics strain is designated by the Greek letter Epsilon: ?. Although many laypeople think of stress and strain as the same thing they are not.

by EricT

By Eric Troy

Turf toe, which is actually a sprain of the first metatarsophalangeal joint (MTP), is one of the most common athletic foot injuries. You may not realize how important your big toe is until you sprain it. This seemingly little sprain is a big problem and it can take you out of the game for three or more weeks. If you expect it to heel quickly you have to be able to protect the toe from the constant aggravation of walking.

Turf toe got its name from the injury's association with artificial turf. The term has become a generic term for any injury to the MTP of the big toe, but the most common cause of this condition is a hyperextension or hyperflexion sprain injury to the joint. It is quite common in football players, especially linebackers and offensive linemen.

Mechanisms of Injury

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More of these injuries are reported to occur on artificial turf because of its stickiness. When an athlete plants his foot and flexes his ankle to push off, the shoe sticks to the turf, which may be old and inflexible, causing the big toe to hyperextend as the body's weight is transferred to it. Alternatively, when an athlete comes to a quick stop the toe may be jammed into the front of the shoe, causing hyperflexion of the MTP. Over-flexible lightweight shoes may be a culprit as they allow the toe this excess motion. Obviously, barefoot athletes may be even more likely to sustain this injury.

Despite how this common injury got its name, however, it can occur on any playing surface. Other predisposing factors are a stiff MTP joint, too little or too much ankle mobility, excess weight, and prior injury. The many variables contributing to these injuries are still inconclusive.

Symptoms and Initial Treatment

The main symptom of an MTP joint sprain is pain at the base of the big toe at the first joint. When the toe is bent upwards the pain can become quite severe. There may be swelling and discoloration in the area of the joint as well, depending upon the severity of the injury. Initial treatment is standard first aid for sprain injuries using rest, ice, compression, and elevation (RICE). Also in the early phase of injury, NSAIDS may be used to reduce pain and inflammation. Although running should not be attempted until the pain goes away, walking may also aggravate the injured tissues because of the extension of the toe during the push-off phase of gait. To protect the toe from the stress of walking and to reduce associated pain, the first thing to do is wear a pair of stiff soled shoes. This in itself may not be enough, however, as it is difficult to keep the big toe motionless even in the best of circumstances. Therefore a special tape bracing procedure is used.

Big Toe Bracing: Taping Procedure for Turf Toe

This explanation assumes that you do not have access to a professional athletic trainer to tape your toe for you. Although you can perform this procedure yourself, it is much easier to have a friend help out.

The supplies needed to tape a big toe are a roll of 1.5 inch athletic tape and spray adherent. The adherent is used to make sure the tape sticks well to the skin as even adhesive tape tends to slip over time, reducing its effectiveness and causing chafing.

Follow these steps:

1. Prepare the Skin. Skin should always be thoroughly washed and dried before taping. Male athletes may have a bit of hair on the top of their big toe. If desired, carefully shave the toe free of hair to facilitate pain free removal of the tape later.

2. Spray adherent on the bottom of the big toe and the rest of the bottom of the foot where the tape will be applied. Although it is not absolutely necessary to use a spray adherent if the skin is clean and dry, the feet are so subject to moisture that adherent is advised in this case.

3. Place an anchor strip around the middle of the big toe. This strip is simply there to anchor the other pieces of tape to.

4. Tear off three pieces of tape that are measured to fit from the anchor strip to the heel and combine these pieces into one thick piece of tape. This strip will be the piece that actually holds the toe in position, so it must be extra strong.

5. Secure one end of the thick strip to the anchor strip on the toe and then pull the tape down toward the heel so that the toe is in line with the foot. Maintaining this tension, attach the tape along the bottom of the foot all the way to mid-heel. Be sure that the toe is not bent down (flexed) or bent up (extended). The toe must be held straight and in line with the foot to reduce tension on the injured joint tissues.

6. Tear eight or more pieces of tape long enough to cover the bottom of the foot crosswise. These strips must be able to reach up the lateral surfaces of each side of the foot but they should not reach all the way around the foot. Use these strips to cover the thick strip you placed on the bottom of the foot, to hold it in place. Starting just under the ball of the foot overlap each piece of tape by half the width of the tape until the entire arch of the foot is covered down to the end of the thick strip.

7. Tear a piece of tape in half lengthwise and place this piece around the big toe to help secure the tensioning strip. Walk to make sure the big toe is stabilized.

Tips for Using the Athletic Tape

Tearing athletic tape can be a bit tricky at first but once you know the method it is easy to do, with practice. Using the forefingers and thumbs, pinch the very edge of the tape, placing the fingers of each hand as close to each other as possible. Pinch hard and quickly tear. You may be tempted to use scissors but the blades will stick to the adhesive on the tape, making it difficult to cut and causing the tape to fold over on itself.

Once you know the taping procedure, it is best to tear all of your strips in advance and place them on the edge of your work surface by securing one end of the tape, allowing most of the tape’s length to hang down to be easily retrieved when needed. Place the strips in the order you plan to use them.

Alternatives to Taping for Turf Toe

Chronic turf toe may require daily taping for weeks or months, which may quickly become an unwelcome chore. Fortunately, there are several products on the market called turf toe straps, typically made from mole-skin, which perform the same function as taping the toe. These affordable straps can be easily slipped onto the foot and are much more comfortable than tape.

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References

Starkey, Chad, and Glen Johnson. Athletic Training and Sports Medicine. Sudbury, MA: Jones and Bartlett, 2006. 65-67. Print.

France, Robert C. Introduction to Sports Medicine and Athletic Training. New York: Thomson and Delmar Learning, 2004. 236. Print.

Perrin, David H. Athletic Taping and Bracing. Champaign, IL: Human Kinetics, 2005. Print.

Baxter, Donald E., David A. Porter, and Lew Schon. Baxter's the Foot and Ankle in Sport. Philadelphia, PA: Mosby Elsevier, 2008. Print.

by EricT

By Eric Troy, Ground Up Strength

If you ask a doctor what shin splints are you probably will not get a straight answer. That is because there are no straight answers to give. Shin splints is the generic name we use for any leg pain that is below the knee and above the ankle. The term is nondescriptive and does not refer to any one type of pain or pathophysiology. It is often called a "wastebasket" diagnosis.

Shin splints therefore should not be considered an adequate diagnosis of chronic lower leg pain as this will offer no guidance to treatment and avoidance. Basically, if your doctor tells you that you have shin splints they are basically telling you that you have shin pain, which you probably already knew!

However, there is a typical pain syndrome, called Medial Tibial Stress Syndrome, that can be considered somewhat synonymous with shin splints. This syndrome causes pain that typically occurs in the lateral front of the lower leg or more to the inside of the lower leg, called the "posteromedial" region. It is most common following repetitive running and jumping activities such as running, volleyball, soccer. There are many articles that will run through all the complexities of shin pain and try to tell you the truth about shin splints by dumping data about all the many causes..but most of them are rare compared to MTSS.

Medial tibial stress syndrome (MTSS), also called Medial Tibial Periostalgia or Medial Periostalgia, usually follows an abrupt increase in activity or training. The culprit, simply put, is doing too much too soon. Those who play seasonal sports but fail to train at a proper level off-season may suffer from them. Also, if you are used to only playing tennis for recreation and suddenly switch to long distance running, don't be surprised by the abrupt appearance of shin splints. Therefore, this condition could be considered to be the bane of those who consider themselves in shape but forget that fitness is specific and all activities must be approached with a proper buildup in training level.

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Running on hard surfaces and running on the toes of your feet are also associated factors. Besides running, any high impact activities, such as gymnastics and ballet dancing, are associated with this condition. If you are getting ready to go into military basic training, expect the possibility of shin splint pain due to marching in combat boots and hard shoes, often on hard surfaces, with no shock absorption capabilities.

At first the pain may tend to decrease rapidly with rest but as it grows worse it becomes more persistent and severe. The pain may eventually occur even when the leg is not bearing weight.

Be aware that the onset of this syndrome may mimic that of stress fractures. However, stress fractures are associated with point tenderness over a specific area. With MTSS, the tenderness will occur over a much broader zone. It is also important that medial tibial stress syndrome not be confused with acute compartment syndrome, which is a much more serious condition. All three of these, MTSS, stress fracture, and compartment syndrome, may be diagnosed under the blanket term "shin splints." All three have been variously described as causes of shin splint in various articles and literature but this is improper since shin splints are usually thought of as a benign condition. The American Medical Association has limited the definition of shin splints to musculotendinous inflammation, excluding stress fractures and acute and chronic compartment syndromes. This is proper since it is very foolish to lump a benign inflammatory condition like MTSS with conditions such as stress fractures, compartment syndromes, or other serious conditions. Ischemic disorders, popiteal artery entrapment or even fascial hernia are possible, any of which could be considered medical emergencies.

Even though MTSS may be the most common benign cause of shin splint symptoms, other causes of shin pain are still possible besides the above mentioned serious conditions. As well, the term has been applied to inflammation of the tendons of the anterior and posterior tibialis muscles and inflammation of the interosseous membrane between the fibula and tibia.

What is Medial Tibial Stress Syndrome (MTSS) Exactly?

The pathogensis of MTSS is unknown although there are several common theories. Medial tibial stress syndrome is thought to be a periostitis. A periostitis is an inflammation of the periosteum. In MTSS, the inflammation occurs along the posteromedial border of the tibia, commonly in the distal third of the bone.

Previously it was thought that MTSS was due to myostitis, fascitis, or periostitis of the posterior tibialis muscle but now the soleus muscle, which covers the medial third of the heel core as it inserts into the calcaneus, is thought to be the culprit.

It may be caused by excessive stress on the medial tibial fascia by the deep posterior compartment muscles like the tibialis, soleus, and flexor digitorum longus. During overpronation, an eccentric contraction of the soleus occurs to control pronation, causing periostitis of the soleus insertion along the posterior medial tibial border. According to Detmer 6, there is an actual separation of the periosteum from the tibial cortex due to rupture of the sharpey's fibers (the fibers that actually attach the muscle to the periosteum). For this reason some texts prefer the term medial periostalgia, medial tibial periostalgia, soleus periostalgia, or chronic periostalgia, etc. since the term periostalgia denotes a painful condition of the periosteum but not necessarily an inflammatory one.

Specific Factors

The specific etiology of shin splints is yet to be pinned down. There are several biomechanical factors and external factors that may contribute to the syndrome.

• Over-pronation
• variations in foot structure and functions:
  • • rearfoot valgus - extremely extremely rare but associated with severe tibial valgum (knock-knees) and excessive subtalar pronation. 5
    • forefoot varus - inverted position of the forefoot relative to the rearfoot at the level of the midtarsal joint 5
• weakness of lower leg musculature
• leg lenghth discrepancy
• tibial torsion - inward twisting of shin bones
• tibial varum (bow-leggedness, bandiness, bandy-leg, or tibia vara)
• excessive femoral anteversion
• increased Q angle
• tightness of gasrocneumeus and soleus muscles and limited ankle dorsiflexion
• worn or ill-fitting shoes and shoes with no shock absorption

Symptoms and Presentation

The presentation of shin splints of MTSS origin can vary from person to person. Typically, however, the pain develops during later stages of training or exercise and gets better after rest. As the condition progresses the pain may develop earlier in the training session, may be more intense, and may linger after exercise. With severe and chronic cases, the pain may go away with rest only to come back later even if the leg is not bearing weight. As stated above, the presentation may be somewhat similar to stress fracture, at first, but the pain and tenderness from stress fracture is usually very focal, and does not respond to rest and other treatment as quickly as MTSS. There may also be:

• tenderness over a broad zone of the tibia, usually the middle third
• mild swelling

Treatment

Shin splints will generally respond to conservative treatment, modification of activity, and attention to proper footwear.

• Initially, only do activities or exercise than can be done without pain. For instance, if you have shin splints from running, switch to bike riding. If a simple reduction in volume (mileage) or intensity will allow you to exercise without pain, this is fine. Sometimes, it may be best to take a couple of weeks off from training, especially with more severe cases.

• For acute shin splints (MTSS) use RICE can be used although as stated above, the "Rest" portion may be relative rest. Ice can be useful for the acute pain symptoms, generally after exercise. Wrapping for support can help in severe cases. See Shin-Splint Taping Instructions below.

• NSAID's (Nonsteroidal Anti-Inflammatories) can be used to control pain, initially. Avoid long-term use.

• Stretch the gastrocnemius and soleus, the achiles tendon, in general the "anterior compartment" of the lower leg, to establish greater ankle dorsiflexion range of motion.

• Self-massage of the calf muscles and soleus are recommended. Use a tennis ball or self massage tool like the Tiger Tail Stick Massager to work these muscles

• Engage in regular comprehensive mobility training with an emphasis on lower extremity mobility, including hip mobility as well as ankle mobility

• Strengthening the muscles at the front of the lower leg can be useful. Toe taps progressed to toe curls with very light weight and moderate volume can be used

• Consult a podiatrist for foot issues like flat feet, etc.

What About Trigger Points? Do They Cause Shin Splints?

Shin Splints of MTSS origin are not associated with the referred pain from trigger points, although Davies misleadingly implies that they are by saying that trigger points in the shin muscles "result" in shin splints although this pain is "not the same as referred pain from trigger points," a statement that makes no sense sense since an operating definition of a trigger point is a localized band of taut tissue that refers pain to other areas, rather than "chronic overload tension."¹

Note that trigger points in the shin muscles themselves, the tibialis anterior, extensor digitorum longus, and extensor hallucis longus do not send pain to the medial mid shin area, as with MTSS shin splints, but to the top of the foot and toes. Trigger points in the soleus muscle sends pain to the calf area, the achilles tendon and heel area, and the medial ankle.

According to Travell and Simons "the strong relation of periostalgic shin splints [shin splints from MTSS] to the kind and amount of exercise, and the localization of pain and tenderness to the insertion of the overstressed muscle distinguishes this condition clinically from myofascial TrP syndromes."² Why Davies chose to associate shin splints with trigger points is unknown. Nevertheless, general self myofascial release of the shin muscles is recommended and could certainly be helpful. 7

Shin Splint Taping Instructions

A compressive wrap around the lower leg can provide some gentle support and relief of pain for shin splints. The taping procedure is simple, and will use 1.5 or 2 inch elastic or non-elastic athletic tape.

• If needed shave the skin, then wash and dry the area.

• And under-wrap can be used first, before taping, if desired. A spray adhesive can be applied to the skin prior to taping, to help the tape stick better.

• Prepare separate strips of tape long enough to wrap about the lower leg.

• Starting just above the achiles tendon and apply separate strips, overlapping each strip by half the width of the strip, to about 6 to 8 inches above the ankle

• Do not wrap the leg too tightly, only gentle support is needed!

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GUS Member Comments

by EricT

The three common terms used to refer to tendon injuries or overuse injuries are extremely confusing. Much of the time, the difference between these entities is not apparent at all and they seem to be used interchangeably. Since there also exists disagreement among practitioners as to what internal changes actually constitute what condition, the layperson is left even more befuddled. Both tendonitis and tendonosis are much more common terms than tendonopathy.

The most common of the three terms is tendonitis. The suffix "-itis" means inflammation. So the term tendonitis means inflammation of the tendon and of the tendon-muscle attachments. This term is used to refer to most tendon injuries even though such injuries may feature degenerative changes with little evidence of inflammatory cells. In fact, little evidence of an inflammatory process has been found in experimental models of tendonitis using chronically overloaded animal limb muscles.

An alternative model is tendonosis. The suffix "-osis" refers to a diseased or abnormal state. Therefore, the term tendonosis would refer to a tendon being abnormal or diseased. This condition is described as degenerative changes brought on by acute trauma or several strains to the tissue that exceed the ability of the tissue to heal, thus resulting in repetitive injury and the deposition of scar tissue.

The difference between tendonosis and tendonitis is that tendonosis features tendon damage at the cellular level which does not show inflammation and is degenerative in nature. Many conditions referred to as tendonitis may more accurately be called tendonosis.

It may well be that there is no difference between overuse injuries commonly called tendonitis versus those called tendonosis. When the tissues of "tendonitis" are looked at under a microscope there seems to be no neutrophil reaction, which would indicate an acute inflammatory response, but rather the tissue changes seem to be consistent with chronic degenerative changes, lending credence to the tendonosis theory.

Since corticosteroid injections sometimes help conditions without apparent inflammation, even more questions emerge as to the role of cytokines in these conditions and the merit of the two classifications.

The suffix "-pathy" comes from the Greek word pathos meaning suffering or disease. Tendonopathy, therefore, is a catchall term meaning "disease of the tendon" and does not try to differentiate the role of inflammation versus other changes. It may be that tendonopathy is a better term in general for these conditions. In fact, some recent studies have considered whether "tendonitis" is but a myth due to the aforementioned absence of inflammatory cells in histological examination.

Some experts have therefore decided that "tendonosis" is a better term whereas by others "tendonopathy" is considered to be a better choice. Clearly, acute traumatic injuries are different than chronic overuse injuries that are the result of accumulated micro-trauma, and this guides the treatment of such injuries.

However, for the layperson, there is no need to be confused by these terms. It probably does not matter whether you call your condition tendonitis or tendonosis, as long as your health professional is not confused!

Other terms used to describe overuse injuries include myositis, myotendonitis, and tenosynovitis.

Note to the reader: Even more confusion may be generated by some frequently used alternative spellings. Tendonosis is sometimes spelled as tendinosis and tendonopathy as tendinopathy. Since there is no such thing as a tendin this article avoids using these misspellings, except in the title, as tendinopathy is such a widespread usage I used it to help people find this article in searches.

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References

1. Stone, John H. A Clinician's Pearls and Myths in Rheumatology. New York: Springer, 2009. Print.

2. Hammer, Warren I. Functional Soft-tissue Examination and Treatment by Manual Methods. Sudbury, MA: Jones and Bartlett Pub., 2007. Print.

3. Mellion, Morris B., Margot Putukian, and Christopher C. Madden. Sports Medicine Secrets. Philadelphia: Hanley & Belfus, 2003. Print.

by EricT

By Nathan Wei

The first non-steroidal anti-inflammatory drug (NSAID), aspirin, is still used to treat aches and pains. It is unique in that it has many other useful properties above and beyond its effectiveness for arthritis and related problems.

The second NSAID was a drug called phenylbutazone (Butazolidin), which was eventually removed from the market by the FDA because of a myriad of side effects, among them being aplastic anemia, and stomach ulcers. "Bute" was also a favorite at the racetracks because its pain-relieving properties allowed horses to race "through the pain."

Following the introduction of phenylbutazone, there was a proliferation of NSAIDS for the treatment of both osteoarthritis and rheumatoid arthritis. They are still used today and are effective for relieving pain and inflammation.

However, they also have potential side effects including the elevation of cardiovascular risk leading to stroke and heart attack, hypertension, kidney malfunction, and gastrointestinal ulceration. Nonetheless, they are helpful in alleviating arthritis symptoms.

Less clear is their role for other conditions involving aches and pains and musculoskeletal injury. For example, short term use of NSAIDS for relief of pain due to fractures can be beneficial.

The downside is longer term use (more than one week) has been shown in multiple animal studies to slow fracture healing. This deleterious effect on fracture healing has not been seen with the use of acetaminophen.

Studies in humans have had mixed conclusions. One study by Giannoudis and colleagues in the Journal of Bone and Joint Surgery found NSAID use to be associated with poor fracture healing. On the other hand, a review of studies carried out by Dodwell and associates in Calcified Tissue International did not find this to be true.

Nonetheless, it is advisable to limit the use of NSAIDS to one or two weeks maximum when treating a patient with fractures. NSAIDS are useful during the first few days after a fracture since they help reduce pain and other symptoms related to inflammation. One situation commonly seen in a rheumatology practice is a patient who is on NSAID therapy and develops a fracture due to osteoporosis.

Tendonitis is another condition for which NSAIDS are prescribed. Again, the current consensus is that short term use for pain relief can be beneficial but longer term use is not helpful.

The same holds true for ligament and muscle injuries. The key role of NSAIDS in these situations is to reduce symptoms enough so patients can return to a normal level of activity.

This topic also brings up the issue of whether methotrexate and biologic therapy dosing need to be adjusted when patients have a fracture. The answer is not known.

[For a more detailed discussion of the use of NSAIDS with musculoskeletal injury, readers are referred to an excellent article (Patel DS, Adrian BA. Do NSAIDS Impair Healing in Musculoskeletal Injuries? J Musculoskel Med. June 2011, pp207-212)]

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis Treatment Center http://www.arthritistreatmentcenter.com. For more info: Arthritis Treatment

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by EricT

By Sai-Chuen Fu¹, Christer Rolf², Yau-Chuk Cheuk³, Pauline PY Lui⁴, and Kai-Ming Chan⁵

Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology Journal, 2010

Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments.

Introduction

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In the past decades, our concepts on chronic tendon pain have evolved from "tendinitis" which focused on clinical inflammatory signs, into "tendinosis" which stressed the pathologic features of the free tendon as observed by histology and biochemistry, and then "tendinopathy" which declared nothing further about its nature, just introducing a new label for chronic tendon and insertion problems in general [1] . Woo and Renstrom [2] concludes that the pathogenesis, etiology and mechanisms in most of the myriads of conditions related to tendinopathy are unknown. However, with clear definitions outlining and discriminating the various diagnoses of "tendinopathy", it is still possible to propose a unified model for the pathogenesis based on available experimental evidences, which we propose as our theory to be proved or rejected by future investigation.

In general, tendinopathy is characterized by longstanding localized activity-related pain and the patients in general respond poorly to most "conservative treatments". However, a wide spectrum of tendon pathologies is put under the umbrella entity of tendinopathy based on some common features [3] (Table 1), leading to an impression that there is no single general pathogenesis or aetiology involved which can explain all conditions. If so, we firmly believe that these pathologies should be classified as different entities. As the current research evidences are confusing, it is very important to identify if there are common denominators and diversifiers for various manifestations of what we loosely call "tendinopathy" to help us understand the pathogeneses of these conditions.

In this article, we review previous investigations according to the nature of the studies, for example, clinical observations, characterization of clinical samples, evaluation of treatments to patients with tendinopathy, animal models of tendinopathy and cell culture studies related to the effects of risk factors. Certainly we do not answer all questions with the integration of various research evidences, but we take the bold step to propose an integrative theory for the pathogenesis of tendinopathy based on the underlying messages in these studies.

Clinical observations of tendinopathy

To understand the pathogenesis of what today is labeled as "tendinopathy" we have to make some clear distinctions. Firstly we must consider the varying clinical presentations. Most tendon problems are presented to the clinician either as a rupture or localized pain, often including stiffness and swelling. Symptomatic tendinopathy refers to chronic localized pain with "degenerative" changes in tendons as observed by imaging or histology; while asymptomatic tendinopathy is identified from ruptures or partial rupture cases shown to be associated with non symptomatic pre-existing degenerative changes. Pathologies primarily manifested as passive loss of range of motion (i.e. trigger finger, frozen shoulder, etc) are not considered as tendinopathy in this discussion. Dating back to 1938, Codman reported degeneration in complete ruptures of rotator cuff [4] . Kannus and Josza reported in 1991 from a large number of histological samples that an absolute majority of patients with complete Achilles tendon ruptures had pathologic alterations which he described as "mucoid degeneration" [5] . This "mucoid degeneration" is almost equivalent to the histological alterations characterized for tendinosis [6] . It is very likely that these pathological changes in tendons imposed mechanical weakness and higher susceptibility to ruptures. Similar histopathological characteristics were also described in clinical samples of symptomatic tendinopathy [7,8] . It suggests that the "typical" histopathological changes characterized by tendon degeneration may not necessarily be directly linked to increased nociception giving the patients warning signals; while in painful cases, the mechanically weaker tendons may be protected from ruptures due to decreased impact levels since painful activities will be avoided.

Secondly, we must consider the etiology and epidemiology. Unfortunately, well defined epidemiological studies on "tendinopathy" are virtually nonexistent. Age-related changes in tendons were reported [9] , but tendinopathy is not an age-related degeneration because similar pathological changes are observed in young people [10] . Higher number of cases in males presented in clinical studies [11,12] may not reflect higher susceptibility of male gender to tendinopathy; on the contrary, it is reported that female gender was more susceptible to repetitive trauma in rotator cuff [13] and female cyclists suffer a higher risk for "overuse injury" in general than their male counterparts [14] . There were significant gender differences in tendon microcirculation [15] and the neuropeptide responsiveness in rabbit tendon explants was influenced by gender and pregnancy [16] . Diabetes [17] and metabolic alterations such as dislipidemia [18] has been proposed as risk factor for developing tendinopathy. These findings suggest that the hormonal background may affect the development of tendinopathy. Fluoroquinolone [19] and corticosteroids [20] were found to be associated with Achilles tendon ruptures; suggesting pharmacological influence on the development of tendon pathology. Overuse, repetitive strain or mechanical overload to tendons are considered as primary trigger of symptomatic tendinopathy in various regions [21] , as implied by the names such as "jumper's knee", "runner's heel", "swimmer's shoulder" and "tennis elbow". The prevalence of supraspinatous tendinopathy could be as high 69 % in elite swimmers [22] . However, there are frequent tendinopathy cases (pain or rupture) in the non-athlete population [23,20] . Thus overuse injury should not be equated to tendinopathy, but it may be one of the major triggers of the pathological development in some individuals. Furthermore, overuse as a risk factor for tendinopathy is not simply a quantitative increase in activities, but may also be attributed to improper gait or training errors [24,25] .

Thirdly, the anatomical sites of tendinopathic changes add further complexity. Since overuse or cumulative trauma may also affect other peritendinous tissues, tendinopathy was sometimes presented with pathological changes in tenosynovium, bursa and nerves. Our discussion on the pathogenesis of tendinopathy should be focused on changes primarily initiated and observed in tendons; otherwise the pathogenesis pathways will be very heterogeneous. It follows that infectious tenosynovitis, bursitis, adhesive capsulitis or tendon and nerve entrapment in case of carpel tunnel syndrome will not be included in our model, but "paratenonitis" [26] and "insertional tendinopathies" [27] will be discussed since they are parts of a tendon. The pathological changes in different forms of tendinopathy are localized in different regions of the affected tendons, for example, the proximal deep posterior portion of the patellar tendon is affected in patellar tendinopathy, while mid-substance or insertion pathological changes can be observed in Achilles tendinopathy. The medial musculotendinous junction or lateral Humerus insertion was affected in Rotator cuff tendinopathy, while in lateral epicondylitis the fascial collagen structure on the extensor carpi radialis brevis tendon was pathological. Based on the involvement of pathological changes in the paratenon, different sub-classes can be further identified in Achilles tendinopathy [28] . Owing to these variations in the sites of pathological changes, it suggests the common denominator of the pathogenesis of tendinopathy may probably involve a process that can affect all parts of tendons [29] , including musculotendinous junction, mid-substance, insertion and paratenons. The "communication" between these structures around the tendons is poorly investigated.
Medical imaging of tendinopathy

Tendinopathy exhibited characteristic pathological changes which are visible under ultrasound or magnetic resonance imaging (MRI). Tendon thickening or swelling is revealed, localized hypoechogenic signals were detected by ultrasound [30] and an increased T1 and T2 contrast signal was shown by MRI [31,32] . It suggests an increased water content which is probably related to increased accumulation of water-retaining proteoglycans. Doppler ultrasound imaging showed increased vascularity and blood flow in the pathological regions but the oxygen tension was not significantly different [33] . These findings suggested an inflammatory component [34] with localized changes in the tendinous matrix and hypervascularity may be associated with the pathogenesis of tendinopathy.
Characterization of clinical samples of tendinopathy

Direct investigation of tendinopathy started with histological examination of the pathological tissues. Classical characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer "tendinitis" [35,6] . Further characterizations are basically extrapolation of these findings, for examples, measurement of proliferation and apoptosis to explain the changes in cellularity [36,37] , detection of extracellular matrix components [38-41] , collagen crosslink [42] and degradative enzymes [43,44] to explain the matrix disturbances, and detection of the expression of various cytokines to account for the deregulation of cellular activities [45,46] . Calcified tendinitis exhibited abnormal tendon calcification which is more common in rotator cuffs [47] . Recently, the findings of increased innervations [48] and nociceptive substances [49,50] suggest that the chronic pain of tendinopathy may directly be resulted from the pathological changes. The findings of increased apoptosis [51,52] and acquisition of chondrogenic phenotypes [53] in the injured tendons suggested a disturbance in cell differentiation. Increased proteoglycans with over-sulphation [40] and expression of different versican variant [54] may be related to abnormal chondrogenesis in the affected tendons. In contrast to early observations of a lack of inflammatory cells [11] , increased mast cell number was reported in human patellar tendinopathy [55] . Researchers are well aware of the limitation of the clinical samples, which may represent only the end-stage of the pathological processes with unknown duration and onset. Nevertheless, these observations have provided some direct clues to work out the pathogenesis of tendinopathy, and these histopathological characteristics are often used as endpoints in animal models of tendinopathy [56-58] . It should be noted that some of these pathological characteristics are sustained healing responses that failed to repair the initial injury, such as increased cell proliferation and elevated cytokines, which is also implicated in the normal healing process, as shown in the active remodeling sites in healthy tendons [59] . The histopathological features of tendinopathy we observed in animal models must be chronic and cannot be resolved spontaneously as compared to the normal course of tendon healing.

Genetic predisposition of tendinopathy

The possible genetic predisposition for Achilles tendinopathy has been investigated. It was found that variants within COL5A1 [60] , tenascin C [61] and matrix metalloproteinase 3 (MMP3) gene [62] was associated with increased risk of Achilles tendon injuries in general. Since these genes are related to homeostasis of extracellular matrix in tendons, it is suggested that the genetic variants modify the susceptibility of tendons to matrix disturbance observed in tendinopathy.

Evaluation of interventions to tendinopathy

The observed pathological changes of tendinopathy intuitively provided a lot of insights for the treatments. However, all current treatment methods may not significantly affect the natural history of the disease [63] . Surgical excision was reported to be used on animals over many years, in particular on horses [64] . Surgical excision of pathological tissues [65,66] and percutaneous multiple longitudinal incisions [67,68] were reported to be effective to relieve the symptoms similar to open excision of macroscopic pathologic tendon structures [23] . But ultrasonographic anomalies may still be evident in the healing tissues after surgical excision of pathological tissues; despite the painful symptoms were relieved [69] . Thus the current understanding of the relationship of structural changes and functional impairments is still inadequate to assure the degenerative features as specific "markers" for tendinopathy. Biophysical intervention such as extracorporeal shockwave therapy exhibited significant improvement especially for calcified tendinopathy [70,71] . It suggests that the pathological tissues might be responsive to mechanical stimulation. The observed effects of eccentric exercise for tendinopathy [72,73] also implied that a proper modulation of mechanical environment may exert positive effects on the diseased tendons, such as an increase in peritendinous collagen synthesis [74] . Other biophysical interventions included ultrasound therapy [75-77] , pulsed magnetic field therapy [78,79] , low level laser therapy [80-82] , radiofrequency [83] and acupuncture [84] . These studies claimed that modulation of inflammatory or neuronal components in the pathological tissues may exert beneficial effects. There are also reports on the use of nitric oxide [85] , sclerosing agents [86,87] , MMP inhibitors [88] , bone marrow plasma injection [89] , autologous blood injection [90,91] or platelet-rich plasma [92-94] for tendinopathy. Stem cell therapy was tried in horse models [95] . These studies may suggest the involvement of disturbances in cytokines, neovascularization, innervations or cell differentiation in the pathogenesis of tendinopathy.

Animal models of tendinopathy

The lack of a representative animal model is a major obstacle for tendinopathy research. Recent reviews discussed current animal models used for tendinopathy research [96-98] , including cytokine-induced tendon injuries [58,99,100] , collagenase-induced injury [56,101-105] and overuse induced injury [57,106-110] . Generally, histopathological characteristics derived from clinical samples are the main criteria for evaluation of tendinopathic changes. Ultrasonographic features were occasionally used in horse models [111] , and some studies reported pain-associated behavioral changes associated with the tendon injuries [112,113] . These animal models were established according to different hypotheses of pathogenesis, and aimed at reproducing the clinical signs of tendinopathy as far as possible. The use of cytokines to induce pathological changes implied the key roles of one or several cytokines in the development of the disease; while collagenase injection mimicked the pathological processes from the point when progressive matrix degradation was dominating. These chemically-induced tendinopathy models may reveal different starting points of the pathological process but the causes of increased cytokines or collagenases must be linked with clinically relevant etiological factors. Moreover, the acute induction of degenerative changes in these models cannot reflect the chronic development of the disease. On the other hand, animal models of overuse tendon injuries gained wide acceptance for the demonstration of the relationship between the mechanical overload and the development of histopathological changes [57,109,110] and increase in pro-inflammatory mediators [51,114,115] . Although overuse is sufficient to generate degenerative changes over a longer period of time, this form of injuries can be healed when the overuse training was ceased [116] ; while in clinical cases of tendinopathy the symptoms were not improved by rest. Obviously, overuse tendon injury does not equate to tendinopathy. The failed healing response to the injuries caused by mechanical overload of tendons should also be considered in the establishment of animal model of tendinopathy. With respect to the variability in clinical manifestation of tendinopathy, most animal models may only mimic parts of the pathogenesis pathways, or they may only represent one of the possible pathways from the generation of injuries to development of tendinopathy features (Table 1). In summary, it appears that degenerative tendon injuries can be resulted from repetitive strain injuries that exceed the normal thresholds (overuse); while abnormal levels of cytokines and collagenases could be the effectors to mediate this kind of degenerative injuries.

Cell culture studies of effects of risk factors on tendinopathy

Cell culture studies of tendinopathy included the characterization of abnormal activities in the cells isolated from pathological tissues of tendinopathy [36,44,45,53] , and the studies in normal cultured tendon cells in response to potential risk factors such as mechanical strain [117-123] and xenobiotics [124-129] . In cell cultures of tendinopathy tissues, the abnormal cellular activities were persistent during sub-cultures, indicating relatively stable cell phenotypes that are significantly different from tendon fibroblasts derived from healthy tendons [36,45] . On the other hand, numerous studies showed that repetitive mechanical stimulation can affect production of pro-inflammatory mediators [117,118,120-123,130] , metalloproteinases [123,131] and matrix syntheses [119] in cultured tendon fibroblasts; while non-tenogenic differentiation of tendon derived stem cells can also be triggered by mechanical stretching [132] . Corticosteroids also induced fibrocartilage phenotype in tendon cells [129] , affected matrix synthesis [127] , cell viability [126,128] and apoptosis [133] . Fluoroquinolones may also activate metalloproteinases in tendon cells and hence collagenolytic injuries [125] . These observations implied that activation of collagenolysis and erroneous differentiation may weaken the mechanical properties of tendons [134] . Interestingly, non-steroidal anti-inflammatory drugs (NSAIDs) also modulate tendon cell proliferation [124,135] , the expression of extracellular matrix components [124] and degradative enzymes [136] . As NSAID is commonly used for sports-related injuries and symptoms, it is possible that anti-inflammatory treatment used for overuse injury may contribute to the development of tendinopathy [137] which is normally diagnosed after NSAID treatment was failed.

Previous theories of pathogenesis of tendinopathy

Several theories of pathogenesis of tendinopathy have been proposed to explain the development of the histopathological features observed in the clinical samples of tendinopathy. Burry suggested that tendon lesions were not resolved properly and resulted in degenerative changes already in 1978 [138] . However, further elaboration of the idea of "improper resolution of tendon lesion" was not possible due to a lack of experimental evidences at that time. Leadbetter and Khan et al. have suggested that "tendinosis" are degenerative changes resulting from increased demand on tendons with inadequate repair and progressive cell death [139,140] . This model explained the generation of overuse injury, and the reasons for inadequate repair are attributed to adaptive response to tissue overload as elaborated by Kibler and Sorosky et al [141,142] . However, "inadequate repair" as quantitative decrease in healing cells cannot explain the findings of focal hypercellularity, active proliferation and metaplasia in tendinopathy samples. The "apoptosis theory" [143-145] proposed by Murrell also neglect the fact of increased cellularity; but this hypothesis linked up oxidative stress, acquisition of cartilage phenotype and activation of metalloproteinase with the development of degenerative injuries by high dose of cyclic strain. Unfavorable mechanical stimulation as repetitive tensile strain [120] , stress-shielding [146] , contractile tension overloads [147] or compression [148] was proposed as noxious triggers on tendon cells to induce tendon inflammation or degenerative changes. These theories pointed out that the interactions between tendon cells and their mechanical environment were deterministic for the pathogenesis. On the other hand, Pufe et al. suggested that hypoxia and increased vascular in-growth into tendons may be the causes of tendon weakening and ruptures [149] , while Riley provided a neurogenic hypothesis to explain the adaptive responses to mechanical overload by nerve and mast cells unit [150] and Fredberg et al. suggested neurogenic inflammation may be involved in the pathogenesis pathway [151] . These theories were formulated according to the findings of hypervascularity and increased innervations. In summary, the common motifs in these pathogenesis theories include unfavorable mechanical loading, adaptive cellular responses (including tendon, blood vessels and nerves) and the generation of histopathological features. In our opinion, it is possible to unify these ideas as "failed healing", which may be the integral part of various pathological processes that divert various tendon injuries into its different manifestations of tendinopathy. (Table 1)

A unified theory of pathogenesis of tendinopathy

Based on the information of various lines of investigation of tendinopathy, we can summarize some major points which must be considered in the formulation of the pathogenesis model of tendinopathy:

1. The interactions of tendon injuries and unfavorable mechanical environment would be the starting point of the pathological process. Instead of coining the phrase "adaptive responses of tendon cells", we think that the "adaptive healing responses to tendon injuries" would be a more comprehensive descriptor, which also includes vascular, neural and peri-tendinous reactions at different stages of healing.

2. The normal healing processes are diverted to an abnormal pathway, probably due to unfavorable mechanical environment, disturbances of local inflammatory responses, oxidative stress or pharmacological influences. Therefore, the healing capacity is not only inadequate but also incorrect and deviated from an ideal healing outcome.

3. The primary results of pathology are the progressive collagenolytic injuries co-existing with a failed healing response, thus both degenerative changes and active healing are observed in the pathological tissues.

4. These pathological tissues may aggravate the nociceptive responses by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis; otherwise the insidious mechanical deterioration without pain may render increased risk of ruptures.

Based on these points, we propose that the pathogenesis of tendinopathy can be perceived as a 3-stages process: injury, failed healing and clinical presentation. The first stage does not involve pathological changes and normal healing response could occur. The second stage is relatively insidious and discriminated from the third stage when clinical presentations are evident, such as ruptures or chronic pain, often resistant to conservative treatments.

Our theory of the pathogenesis of tendinopathy is summarized in Figure 1.

Figure 1. Failed healing theory for the pathogenesis of tendinopathy.

Stage 1. Injury

In the first stage, initiation of tendinopathy may involve generation of collagenolytic injuries. Overuse can evoke the release of pro-inflammatory mediators [115] , which would result in stimulation of metalloproteinases and hence collagenolytic injuries [152,153] . Recent findings showed that the expression of MMP and tissue inhibitor of metalloproteinase (TIMP) in tendon cells were sensitive to mechanical overload or stress-deprivation [131,154] . MMP inhibitor suppressed development of mechanical weakness induced by stress-deprivation [155] . Chemicals such as fluoroquinolone can induce tendon cell death [156] , oxidative damages [157] and collagenolysis [125] . A previous traumatic injury that has not been healed may also be susceptible to failed healing [158] . With the case reports of infectious tenosynovitis [159] , the involvement of pathogens to generate tendon injuries and inflammation could not be ruled out. Tendon pain and mechanical weakness is not significant at this stage and it is possible for the tendon injury to heal spontaneously.

Stage 2. Failed healing

In the failed healing stage, healing responses were activated but failed to repair the collagenolytic injuries. The exact causes for failed healing are still obscured. It is speculated that unfavorable mechanical environment, genetic pre-disposition, hormonal background and pharmacological exposures may affect the healing process. Since tendon healing includes many sequential processes such as inflammation, neovascularization, neural modulations [160] , recruitment of healing cells, proliferation, apoptosis [161] , matrix synthesis, tenogenic differentiation and matrix remodeling; disturbances occurred at different stages of healing may lead to different combinations of histopathological changes as what we observed in the clinical samples of tendinopathy (Table 1). Inflammatory responses are presumably elicited as the initial stage of tissue repair, but it may not be properly resolved under hostile mechanical environment or pharmacological intervention such as NSAIDs, resulting in elevated pro-inflammatory cytokines and a lack of ordinary inflammatory infiltration in the diseased tissues. Depending on the anatomical variations of the affected tendons, peritendinous reactions may be resulted as restrictive fibrosis, increased innervations and vascular in-growth from para-tenon structures may also take part in healing process [162] . The sustained activation of tendon progenitor cells with unfavorable micro-milieu for tendogenic differentiation may prone to erroneous differentiation into fibrochondrogenic [163] or calcifying phenotypes [104] , which are normally confined to the regions of bone-tendon junctions. Tendon pain becomes significant and conservative treatments such as NSAIDs are prescribed to the patients, which may further modify the pathways of the failed healing.

Stage 3. Clinical presentation

In the third stage, symptomatic tendinopathy is diagnosed as longstanding, activity-related pain with characteristic medical images; while spontaneous ruptures are resulted from mechanical weakness under normal activities in cases of asymptomatic tendinopathy. The consequences of failed healing to collagenolytic injuries involve significant changes in extracellular matrix, which are then visible under ultrasound or MRI. In symptomatic cases, inflammatory pain may be involved and controlled during the injury and failed healing stages, but the pain mechanism may gradually shift to non-phlogistic ones such as agitation to peritendinous nerves by nociceptive substances or swelling, rendering the resistance to common anti-inflammatory treatments. Though mechanical weakness may be involved in asymptomatic cases [164] , lower activities due to pain may reduce risk of ruptures. In asymptomatic cases, the matrix disturbance resulted from failed healing may not activate nociceptive response. The insidious deterioration in mechanical properties of the affected tendons may lead to ruptures. Owing to different combinations of etiological factors, temporal and spatial variations on the failed healing, the clinical manifestations of tendinopathy may exhibit high variability.

Explicability of the theory

With this theory for the pathogenesis of tendinopathy, we can explain the process of the generation of the pathological features of tendinopathy we observed in the clinical samples. The theory is in accordance with most of the evidences derived from tendinopathy studies. For example, overuse is a major etiological factor but there are tendinopathy patients without obvious history of repetitive injuries. It is possible that non-overuse tendon injuries may also be exposed to risk factors for failed healing and entered to the third stage of tendinopathy. Overuse induces collagenolytic tendon injuries and it also imposes repetitive mechanical strain which may be unfavorable for normal healing. Stress-deprivation also induces MMP expression and whether over- or under-stimulation is still an active debate [165] . It is possible that tenocyte is responsive to both over- and under-stimulation, both tensile and compressive loading. Because the cellular responses of healing tendon cells change in different stages of tendon healing [166] , we speculate that the cell responsiveness to mechanical loading may not be constant during tendon healing and failed healing may be resulted from a mismatch of healing stages and the mechanical environment. Our theory can also explain why animal models of collagenase-induced injuries can reproduce the histopathological characteristics and functional impairment similar to tendinopathy; despite the generation of collagenolytic injuries in these models are completely different from the insidious onset of tendinopathy. By proposing a process of failed healing to translate tendon injuries into tendinopathy, other extrinsic and intrinsic factors would probably enter the play at this stage, such as genetic predisposition, age [167] , xenobiotics (NSAIDs and corticosteroids) and mechanical loading on the tendons. For example, differential tensile forces acting on patellar tendon [168] may impose varying loading on tendon cells in different regions, it may explain why posterior proximal patellar tendon is pathological in patellar tendinopathy. Peritendinous structures may be disturbed to different extents in the healing response to tendon injuries, which may lead to different manifestations of "paratenonitis" or tendon adhesion. Investigations of how these factors affect tendon healing could help to further elucidate the mechanism of failed healing. The recent discovery of tendon-derived stem cells and characterization of pathological tissues of tendinopathy have provided evidences to support the ideas of erroneous cell differentiation that contribute to failed tendon healing. According to this theory of pathogenesis, we shall have a theoretical framework to develop a more representative animal model of tendinopathy for further study and verification. New ideas for treatments of tendinopathy may be inspired based on this theory, for example, a treatment which could override on the failed healing tissues and restart the healing process.

Missing links and limitations

As compared to previous theories of pathogenesis for tendinopathy which described a viscous cycle of inadequate repair and increased susceptibility of further injuries, this new theory attempts to describe the "vicious cycle" as an interaction between the vulnerability of the healing process to noxious mechanical and biochemical environments. Thus we can investigate the missing links as predicted in the theory, for example, the impact of mechanical stimulation on the cell differentiation of healing tendons cells, and the disturbances in cytokines triggered by re-injury on healing tendons. However, there are still some limitations in the current pathogenesis theory. Firstly, tendinopathies in different tendons exhibited specific patterns of affected regions and different forms of matrix disturbance, which may be presumably accounted by variations in local mechanical environment and vascular supplies; but it is difficult to explain for these variations at the present stage. Secondly, the interplay among innervations, increased nociception and tendon healing is unknown. It is still a black box for the mechanism of increased nociception by failed tendon healing. The factors which govern the development of chronic pain in tendinopathic tendons remain obscure. Finally, the interactions between healing tendons and the peritendinous tissues are seldom investigated and it is difficult to evaluate the potential involvement of peritendinous tissues in the development of tendinopathy.

Abbreviations

MMP3: Matrix metalloproteinase 3; MRI: Magnetic resonance imaging; NSAID: Non-steroidal anti-inflammatory drug; TIMP: Tissue inhibitor of metalloproteinase

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

SCF, RC and KMC planned and drafted the manuscript. YCC managed the references and assisted in drafting. PPYL approved the final version. All authors read and approved the final manuscript.

Acknowledgements

No funding has been received for this review.

© 2010 Fu et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Citation

FU, Sai-Chuen, Christopher Rolf, Yau-Chuk Cheuk, Pauline PY Lui, and Kai-Ming Chan. "Full Text | Deciphering the Pathogenesis of Tendinopathy: a Three-stage Process." Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology 2 (2010). SMARTT. BioMed Central. Web. 11 June 2011. <http://www.smarttjournal.com/content/2/1/30>.

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Arya S, Kulig K: Tendinopathy alters mechanical and material properties of the Achilles tendon. J Appl Physiol 2010, 108(3):670-675.

Arnoczky SP, Lavagnino M, Egerbacher M: The mechanobiological aetiopathogenesis of tendinopathy: is it the over-stimulation or the under-stimulation of tendon cells? Int J Exp Pathol 2007, 88(4):217-226.

Fu SC, Cheuk YC, Chan KM, Hung LK, Wong MW: Is cultured tendon fibroblast a good model to study tendon healing? J Orthop Res 2008, 26(3):374-383.

Dudhia J, Scott CM, Draper ER, Heinegård D, Pitsillides AA, Smith RK: Aging enhances a mechanically-induced reduction in tendon strength by an active process involving matrix metalloproteinase activity. Aging Cell 2007, 6(4):547-556.

Dillon EM, Erasmus PJ, Müller JH, Scheffer C, de Villiers RV: Differential forces within the proximal patellar tendon as an explanation for the characteristic lesion of patellar tendinopathy: an in vivo descriptive experimental study. Am J Sports Med 2008, 36(11):2119-2127.

by EricT

By Dr. Thomas Buividas

Diabetic Joint Disease is a destructive arthritis facilitated by neurological (nerve) disease. It is also known as Charcot Joint Disease. It is named for Jean-Marie Charcot a French neurologist who observed a severe pattern of joint destruction in patients with advanced syphilis. This advanced (tertiary) syphilis commonly causes absence of normal sensation; especially in the lower extremities (foot and ankle). Charcot noted this in 1868. For the last seventy years this has also been observed in patients with diabetic peripheral neuropathy (nerve disease). This neuropathy also causes a loss of normal sensation. Feet can become totally insensate (without feeling). It’s common for these feet to have normal arterial circulation. The last predisposing factor to Diabetic Joint Disease is trauma. Trauma can be acute as an injury like a fracture or sprain; or it can be subtle like a repetitive stress injury. A person whose foot musculoskeletal structure is even slightly dysfunctional is at a much greater risk for this destructive arthritis.

Who develops Diabetic Joint Disease?

The vast majority of patients who develop this arthropathy have diabetes mellitus. Specifically these patients have diabetic peripheral neuropathy. The incidence in the diabetic population is about 8.5 per 1000 patients. There are approximately sixteen million diagnosed and undiagnosed diabetics in the United States population; and another approximately forty million people with impaired glucose tolerance making them predisposed to diabetes mellitus.

Why do they develop Diabetic Joint Disease?

Simply put trauma with out pain. In the sensate foot even minor trauma causes pain. In the insensate foot the pain is not perceived. Pain is important for telling us something is wrong. Without the pain the diabetic person doesn’t feel strain, sprains, arthritis, fractures, and minor and major injuries. Without the pain telling the person there is a problem the person aggravates the condition which can lead to joint and bone destruction. Multiple fractures and total joint destruction are not uncommon. Diabetic Joint Disease can become so bad the foot or ankle becomes totally destroyed necessitating special shoes, foot orthosis, bracing, surgical care and even possible amputation.

Are there other conditions that lead to Charcot Joint Disease?

Any disease or disorder that leads to an insensate foot can cause Charcot Joint Disease.
Spine trauma can be a cause. Infectious disease such as syphilis and leprosy can be causes. Neurological disorders such as Charcot-Marie-Tooth disease; and vitamin deficiency can also be causes. These represent a miniscule incidence of Charcot Joint Disease. But the worse trend of all and the highest risk are probably in people who are both diabetic and alcoholic.

What are common symptoms of Diabetic Joint Disease?

Unexplained swelling of the foot and ankle usually unilateral (one side) usually without pain is a common presentation. Redness and heat maybe present. Common differential diagnosis includes gout, infection of soft tissues or bone and tendonitis.

How is Diabetic Joint Disease diagnosed?

Clinical examination with basic history are physical should lead a clinician to be highly suspicious of the disorder. An insensate diabetic patient who present with a unilateral warm, swollen, reddish foot with no history of significant should preliminarily treated as having Diabetic Joint Disease until proven otherwise. More advanced cases can have crepitating or grating noises between bone and joints when place through a range of motion.

Radiographs in early stages can often be inconclusive. In later stages they can be quite self evident with severe bone destruction, dislocations and fractures. Bone scans are helpful in making a diagnosis. Other testing such as MRI or CT scans can be helpful in diagnosing bone abscess and for surgical staging.

How is it treated?

Initial treatment consists of immobilization with a cast or cam-walker. Total non-weight bearing is mandatory. Use of crutches, walkers and knee walkers is a necessity also. Use of a wheelchair is not uncommon. After the condition becomes quiescent foot orthosis, special insoles, extra-depth shoes, custom shoes, braces and ankle foot orthosis may be needed to control the condition and stabilize deformity. Surgical care is sometimes needed.

About the Author

Dr. Thomas Buividas
Archer Foot and Ankle Clinic,
4554 S. Archer Avenue,
Chicago, IL 60632.
773-847-6784.
http://www.ArcherFootAndAnkle.com

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by EricT

By Asheesh Bedi, MD

In an adult population, ruptures of the Achilles tendon can be a common injury of the foot and ankle. While they can be seen in almost all level of competitive athletes, they have been historically linked with the “weekend warrior” athlete who may be somewhat de-conditioned but exerts themselves in brief periods of time in sporting activities. Recognition and treatment of an Achilles tendon injury is very important, as neglected or unrecognized ruptures can cause many future problems with both daily activities and sports competition.

What is the anatomy and function of the Achilles tendon?

The Achilles tendon connects the muscles of the calf and to the heelbone. The tendon is large and must be able to withstand and transmit the large forces generated by these powerful muscles to move the foot. These forces can be many times our own body weight. The tendon is particular active with pushing down (plantar flexion) of the foot, and is therefore critical to perform in all sports, especially those in which jumping is critical. Correspondingly, sports such as basketball, track and field, and volleyball place high stresses on the Achilles tendon with jumping and landing, and are likely the highest risk for tendon injury. However, ruptures have been reported with virtually every sport.

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What is an Achilles tendon rupture?

An achilles tendon rupture is a disruption in the integrity of the tendon somewhere between the muscle bellies and the heel bone (calcaneus). Most commonly, tears occur at the muscle-tendon junction 2 to 4 centimeters above the insertion into bone, but they can occur as avulsions directly from the calcaneus.

Tears can result from trauma or transection injuries which extend through the skin and underlying tendon. More commonly however, athletes suffer these injuries during sporting activities. Up to one-third of the athletes who suffer a rupture complained of some injury or symptoms in the tendon in the preceding weeks, suggesting that a preceding event may place the Achillies tendon at-risk for rupture. Chronic inflammation or irritation of the tendon for repetitive activities (“Achilles tendinitis”) can also weaken the tendon and render it vulnerable to rupture as well.

What places me at higher risk for an Achilles tendon rupture as an athlete?

Virtually anyone can suffer a rupture of the Achilles tendon, but certain pre-existing factors can place an athlete at greater risk and should be considered. These include:

• De-conditioning with weakness of the calf muscles, a common problem in “weekend” athletes who have not been training.
• Injections of steroid in or around the Achilles tendon – these can weaken the tendon and increase the risk of rupture with provocative activities, and should generally be avoided.
• Pre-existing Achilles tendinitis (inflammation of the tendon) with secondary degeneration and weakening of the tendon over time.
• Certain antibiotics (fluoroquinolones – Ciprofloxacin, Levofloxacin, Ofloxacin, etc) can place tendon at higher risk of injury
• Gout
• Hyper-parathyroidism
• Diabetes

How does an Achilles tendon rupture occur in athletes?

Most of the time, athletes will suffer an Achilles tendon rupture when a significant force is placed on the leg with the knee extended and foot pulled up (dorsi-flexed). This usually happens when awkwardly landing from a jump, and stresses the tendon when it is maximally stretched. This is a common occurrence and the basketball court.

Although Achilles tendon ruptures have been classically associated with the “weekend” athlete that is over the age of 30, they are certainly not restricted to them. Professional, well-conditioned athletes have suffered from them as well. These include NFL players Vinny Testaverde and Takeo Spikes, tennis champion Boris Becker, and many all-star NBA players, including Dominique Wilkins, Elton Brand, and Christian Laettner.

What are the symptoms of an Achilles tendon rupture in athletes?

The symptoms of an Achilles tendon rupture are generally not subtle. The athlete will usually complain about a “popping” that could be heard and felt when jumping or landing on the court or field. Up to one-third of the time, the athlete will have complained of some pain or symptoms in the Achilles in the prior weeks – it is thought that this inciting event may render it vulnerable to injury. The athlete will immediately complain of weakness with pushing off on the foot (plantar-flexion), reflected in difficulty walking and an inability to jump with the involved leg. Often there is a palpable defect at the location of rupture just above the heel bone, with loss of integrity of the “taut band” just deep to the skin. Examination of the opposite, normal side will help to detect these differences.

What are my treatment options for an Achilles rupture as an athlete?

Treatment options for an Achilles tendon rupture are quite simple: operative or nonoperative. Some prompt treatment is important, however, as an Achilles tendon rupture will seldom heal on their own. With rupture, the muscle belly and tendon retract proximally into the calf and leave a large “gap” defect that cannot heal. Furthermore, waiting for a long time before seeking medical attention (“chronic” rupture) or failing to recognize the injury can compromise treatment options – the tendon becomes stiff and scarred and sometimes cannot be repaired primarily (“end-to-end”).

Nonsurgical options offer the advantage of avoiding the complications of surgery. Typically, the foot is kept in a down position (plantar-flexed) to approximate the ruptured tendon ends as close as possible, and immobilized in a cast or rigid boot until healing occurs. The major limitation of nonoperative treatment, however, remains the risk of incomplete or no healing, and is a significant concern when there is significant tendon retraction. Correspondingly, the risk of recurrent rupture is higher with nonoperative treatment. This option is generally NOT pursued by athletes, given their desire to return to sporting and at-risk activities, and to therefore have the strongest repair possible.

Achilles tendon surgery offers the benefits of an immediate and secure “end-to-end” repair of the ruptured tendon. This allows for a predictable course of recovery and decreased risk of repeat rupture. The main risk of Achilles tendon surgery, however, relates to the surgical wound and healing. The Achilles tendon is directly beneath the skin, and the skin flaps for a repair can have a tenuous blood supply that can place healing of the both the skin and tendon at-risk. For this reason, meticulous handling of the skin and surrounding tendon sheath (“paratenon”) with a surgical repair is of critical importance.

What does Achilles tendon surgery involve?

Surgical repair is typically the treatment of choice for athletes. Surgical repair usually allows for:

• A more predictable postoperative course of healing
• Secure “end-to-end” repair of the tendon
• Earlier return to sports
• Lower risk of recurrent tendon rupture
• Earlier and more predictable return of muscle power

Ruptured Achilles Tendon Surgery

Open surgery is typically performed by making an incision just medial to the tendon. A medial incision avoids risk to the sural nerve and protects it from the risk of abrasion immediately on the back side of the Achilles tendon. The skin flaps are handled very gently to avoid trauma and injury to its blood supply. The enveloping sheath of the Achilles tendon (paratenon) is identified below and incised longitudinally over the tendon defect. The paratenon is also carefully handled and preserved so that it can be closed after tendon repair – this sheath nourishes the healing tendon and provides a protective layer between the tendon and overlying skin. A collection of blood (hematoma) from the trauma is typically encountered and irrigated away to visualize the ends of the ruptured tendon. The proximal end can sometimes “re-coil” deep into the calf and may need to retrieved into the wound. Any scar and adhesions of the ruptured tendon ends should be broken to allow full mobilization and “end-to-end” approximation of the tendon under minimal tension. Grasping sutures are then placed into both tendon ends and tied together to approximate the tendon to re-create its native, resting length. While various techniques and suture configuration have been described, the ultimate common goal is to resist gap formation and confer sufficient strength to the repair until interval healing of tendon occurs.

Repairs of chronic or neglected ruptures is more difficult. In certain cases, the tendon stumps can be so retracted, stiff, and scarred that they cannot be brought “end-to-end” for a primary repair. In these circumstances, augmentation with other tissue or tendon transfer from another muscle may be required and is usually associated with a less optimal result.

What is involved in postoperative rehabilitation?

A plaster splint is typically used to protect the wound for the first one to two postoperative weeks. After satisfactory wound healing is confirmed, the athlete is transitioned to a short leg cast or protective boot and protected weightbearing with crutches is allowed for the next 6 to 8 weeks. No active plantar flexion and passive stretching of the Achilles tendon repair is encouraged during this time. Roll-A-bouts can be useful during this period to improve mobility and completely protect the healing tendon from weight bearing. At approximately 6 weeks, gentle active plantar flexion and tendon stretching is initiated. Isotonic dorsiflexion and full weightbearing in the protective boot are gradually allowed as well. By 3 months, muscle strengthening and propioceptive training are initiated. These exercises can include:

• Isotonic plantar and dorsi-flexion exercises
• Isokinetics
• Balance Board and Perturbation Training
• Stairmaster or Versiclimber

Be sure to take a look at this Balance Exercise Video as well.

A Strong Lower Body with Balance Exercises.

How long will it take for me to get back to my sport?

Return to sport is highly variable, and depends upon the type and severity of injury, associated comorbidities, strength and rehabilitation, as well as treatment pursued. In general, healthy athletes who choose nonoperative treatment cannot expect a full return to sports for one year. On the other hand, an uncomplicated surgical repair in a healthy athlete often permits return to sport at 6 to 9 months.

Can I prevent an Achilles tendon rupture?

Unfortunately, it is hard to anticipate and therefore “prevent” an Achilles tendon rupture. However, there has been some evidence to support that de-conditioning, loss of propioception, and weakness of the calf musculature may increase the vulnerability to injury during exertion in sports. For this reason, staying well-conditioned and balanced with a steady training program is the most effective way to minimize the risk of an Achilles rupture. Nonetheless, even an athlete in “tip-top” condition can suffer an unfortunate, high-load injury! Daily exercises to consider include:

It is also advisable to avoid fluoroquinolone antibiotics which can predispose to risk of tendon injury with provocative activities.

For more information on “sports injuries” visit SportsMD Media Inc. SportsMD is the most trusted resource for sports health and fitness information for people engaged in sports everywhere. We have assembled the sports industry’s leading Doctors and health experts – each sharing valuable, practical advice to keep you playing injury-free.

References:

Inglis A, Scott W, Sculco T, Patterson A. Ruptures of the tendoachilles. An objective assessment of surgical and non-surgical treatment. J Bone Joint Surg Am 1976 Oct; 58(7): 990-3.

Nistor L. Conservative treatment of fresh subcutaneous rupture of the Achilles tendon. Acta Orthop Scand. 1976 Aug;47(4):459-62.

Nistor L. Surgical and non-surgical treatment of Achilles Tendon rupture. A prospective randomized study. J Bone Joint Surg Am. 1981 Mar;63(3):394-9.

About the Author:

Dr. Asheesh Bedi is an Assistant Professor of Sports Medicine and Shoulder Surgery at the University of Michigan and MedSport Program. He is a team physician for the University of Michigan Athletic Department and specializes in both arthroscopic and open surgery for athletic injuries of the shoulder, elbow, hip, and knee. Dr. Bedi completed his undergraduate training at Northwestern University where he graduated Summa Cum Laude. He graduated from the University of Michigan Medical School with AOA recognition, and remained in Ann Arbor to pursue residency training in Orthopaedic Surgery at the University of Michigan. After completing his training, Dr. Bedi completed a two-year fellowship in sports medicine and shoulder surgery at the Hospital for Special Surgery and Weill Cornell Medical College in New York. He has also pursued additional dedicated training with Dr. Bryan Kelly in arthroscopic hip surgery for young athletes. While in New York, he was an assistant team physician for the New Jersey Nets professional basketball and New York Mets professional baseball organizations with Dr. Riley Williams, Struan Coleman, and David Altchek. He was also an orthopaedic consultant for the U.S. Open Tennis Tournament in 2007 and 2008 with Dr. David Dines and an assistant team physician for Iona College Athletic Programs.

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by EricT

By Ground Up Strength

Plica syndrome is an post-traumatic or post-inflammatory thickening, chronic inflammation (synovitis), and/or fibrosis of the synovial plicae of the knee. This means that the plica (PLI-kah) have been irritated by overuse or injury to the knee. Most commonly affecting the medial plica, the symptoms mimic those of other other knee problems such as a torn meniscus, causing patella pain, snapping, clicking, and tenderness of the joint. There may be a sense of instability in the knee and a knee-locking sensation. 1,2

First described in 1918, the plica is a remnant band of synovial tissue that is left over from fetal development. Normally, as the fetus grows, it is thought that the knee is split into three separate compartments: the medial and lateral synovial compartments and the suprapatellar bursa. These compartments are separated by snynovial septa (a synovial membrane). At somewhere between two to three months of fetal development these plica resorb to form one large cavity called the synovial cavity. Sometimes they are not resorbed completely and their folds partially remain, becoming plica. This theory may not adequately explain all the plica remnants of the knee and and the many variations that are found but it is at least a partial explanation of their formation.

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There are several possible plicae that are found in the knee: the suprapatellar plica, the mediopetellar (medial) plica, the infrapatellar plica, and the lateral patellar plica (rare). When they were first seen during arthroscopy and excised they were thought to be abnormal but they are now known to be normal leftovers of the embryonic development. Although all the plica of the knee do not occur at the same rate and in everyone they do occur in many people. Their incidence, however, is controversial. Just the presence of plicae does not indicate a problem. Normally the plica are asymptomatic and problems are rare. They are simply viewed as vestigial tissues which have no real function but do not necessarily cause problems. 4,3

What Causes Plica Syndrome?

Plica syndrome is caused by chronic inflammation from trauma to the knee or other pathological knee conditions. Normally the plica synovial membranes are thin and elastic. When these membranes become inflamed over time they can lose their elasticity and become thickened and fibrotic. This causes the plica to interfere with the normal dynamic function of the knee, manifesting in symptoms that are similar to many other knee problems. Symptomatic plica, are, as stated, rare. The medial (mediopatellar) plica is the most widely reported to be symptomatic. Symptomatic suprapatella and lateral plicae have also been reported, but much more rarely.4

Medial Plica Syndrome

The most problematic of the plicae is the medial plicae, which arises from the medial retinaculum and inserts on the intrapatellar fat pad. It is located just to the inside of the patella, about the width of a finger away. Sources vary as to their incidence with estimates anywhere from 18% to 70% of the population but problems are rarely seen, ranging from 35 to 11% of all cases. The medial plica is in such a position to be at risk of impinging between the medial facet of the patella and the trochlea of the humerus. The plica can then become inflamed and enlarged leading to more problems. Or the impingement can stretch nerve endings to cause pain. The plica can also become inflamed from direct trauma to the knee or other inflammatory processes.3,4

Plica Syndrome Symptoms

Symptoms of plica syndrome include knee pain and swelling, a clicking sensation, and locking and weakness of the knee. Medial joint pain above the patella is often reported. Pain during knee flexion, from around 30 degrees to 60 degrees of flexion is also sometimes reported and there may be pain during extension. There may be a palpable tender and painful band or cord along the inside edge of the patella.3,2

Diagnosis of Plica Syndrome

Diagnosis of plica syndrome can be very challenging. Many other conditions that cause similar symptoms must be ruled out and then plica syndrome becomes a diagnosis of exclusion. Although the plica can be seen in MRI the mere presense of the plica does not mean it is causing a problem. The goal of imaging is to show fibrosis in the plica or hyperintense areas and to exclude other pathologic changes. Imaging is not always helpful in diagnosing the syndrome. The best way to diagnose plica syndrome is through arthroscopic surgery which "fixes the problem" by removing the offending plica and confirms the diagnoses at the same time. However, surgery is not the first line of treatment and conservative treatment is usually tried first.

Treatment

The treatment for plica syndrome is usually conservative. Ice, activity modification, and NSAIDs such as ibuprofen are used to reduce inflammation of the plica and its thickening. Compression wrapping of the knee may also be ordered. Cortisone injection into the plica folds are sometimes used as well an these may help about half of those treated.

If conservative treatment fails to relieve symptoms within 3 months, the doctor may recommend arthroscopic or open surgery to remove the plicae. Arthoscopic surgery should be sought, if possible as this is a much simpler and less invasive surgery. But if symptoms can be managed conservative treatment should be continued.

by EricT

By Jonathan Blood-Smyth

Flat footedness is divided into acquired flat foot which is a condition which develops after we have attained maturity and congenital flat foot which is a common condition and often not of pathological significance. Adult flat foot has many potential causes which include dislocation and fractures, foot abnormalities, arthritic changes and neurological conditions. The commonest cause however of this foot problem is a dysfunction of one of the foot tendons, the posterior tibial muscle tendon. The methods by which the tibialis posterior tendon malfunctions are varied and ascribed to degeneration, inflammation or trauma.

Studies of this condition have revealed that it is more common in groups who are obese, diabetic, hypertensive, on steroid medication or had previous trauma or operations to the mid part of the foot. Patients with arthritic conditions, often called spondyloarthropathies, have typically a family history of psoriasis or inflammatory conditions and have a higher incidence of this condition. Older people without specific medical problems are also seen, pointing to a mechanical cause secondary to age related degenerative changes. This tendon problem is moderately commonly seen in patients with rheumatoid arthritis.

Underneath the medial malleolus of the ankle and for a short distance forwards exists a region of limited blood supply which impacts on the tendon running through this area, contributing to an explanation of why degenerative change might occur more readily here. The tibialis posterior tendon contributes to the stability of the medial foot arch which has both passive and active supports. The static, passive supports for the arch include the spring ligament (calcaneonavicular ligament), the long and short plantar ligaments and the plantar fascia. The spring ligament is a support for the talus or ankle bone and stops it migrating inwards or downwards.

The medial foot arch is most powerfully supported in an active manner by the tibialis posterior muscle via its tendon. Its contraction lifts the inside of the medial longitudinal arch of the foot and inwardly turns the foot. If the tendon is ruptured or damaged and this supporting influence is lost then the outward turning foot muscles can work without being opposed. This permits the foot to suffer three main consequences: the hindfoot areas turns outwards; the medial foot arch loses its height and the front part of the foot can also turn outwards.

Flat Foot

The forefoot and the hindfoot combine to be a rigid and stable platform in gait and the tendon changes lead to a reduction or loss of this with a less efficient gait pattern. Because the tibialis posterior muscle's strong influence on the foot is diminished or removed by the tendon problems this allows the major calf muscles to act more at the ankle rather than further forward. Pressure on the talus or ankle bone leads it to move down and inwards which puts the spring ligament on a stretch and allows a collapse of the inside arch as the joints assume new positions.

When developing symptoms from acquired flat foot patients will complain of swelling and pain on the inside of the ankle and foot when they are standing on the foot. The arch may gradually reduce and the patient realise they are walking on the inner part of the foot instead of normally. There is a loss of strength as the patient pushes off in walking and they may limp, the changes in gait often reflected in abnormal patterns of wear underneath the shoes. Physiotherapy assessment of the foot initially involves comparing both feet in standing to see if the arch is different on either foot.

If the foot is seen from behind the heel it is typical to be able to see the two outer toes, and seeing more means the forefoot is turned outwards. The physiotherapist will measure the angle made by the lower leg in relation to that of the heel, an angle which is increased as the heel bone turns outwards, a position known as valgus. On going up on tiptoe a normal foot performs a slight inward deviation of the heel as the large calf muscles power up.

Jonathan Blood Smyth is the Superintendent of Physiotherapy at an NHS hospital in the South-West of the UK. He writes articles about back pain, neck pain, and injury management. If you are looking for physiotherapists in Sheffield visit his website.

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by EricT

By Jeff P. Anliker, LMT

Injuries can occur anywhere and at anytime, but the most prevalent place of occurrence is in the workplace. The reason for such a high rate of injury is that people spend 8-18 hours a day, 5-7 days a week performing unidirectional (one-way) movement patterns, causing an imbalance in the musculoskeletal system that results in the overuse and under use of certain muscle groups. If left unchecked, these injuries can be come chronic, resulting in pain and dysfunction that can last for years.

Usually, when one muscle group is overused, the opposing muscle group, acting as a stabilizer, becomes underused. When this imbalance establishes itself in the musculoskeletal system, the body does not function as designed. Instead of muscles working together to perform a specified function, they work against each other, causing the body to exert more energy to perform the same task that previously was perceived by the body as "simple".

When muscles become too short and tight, they lose their strength as they are in a chronic semi-contracted state and cannot contract (shorten) efficiently due to being pre-fatigued and the fact that they are already in a state where they are too short for proper function. If a muscle is already in a shortened, semi-contracted state, it cannot contract, or shorten very far. And the farther a muscle can contract (shorten) and move, the greater the strength and endurance the muscle will have. Chronically tight, restrictive muscles just don't function very well and they impinge structures around and beneath them such as nerves and blood vessels, causing disorders like Carpal Tunnel Syndrome, Cubital Tunnel Syndrome and many other associated Repetitive Strain injuries. Short muscles also pull bones out of alignment, which causes a joint imbalance, often resulting in severe pain and dysfunction.

The same goes for underused muscles. Underdeveloped muscles are weak due to lack of direct stimulation. Weak muscles are usually too long, unless they are in a state of spasm, which occurs as a protective response in order to keep from being overstretched. Weak underdeveloped muscles cannot act as efficient stabilizers when the opposing muscle(s) are called into action, which again causes a joint imbalance to develop, as weak muscles cannot stabilize bones in their proper position / alignment. Weather a muscle is short and tight or long and weak, the strength and length imbalance of the affected muscle(s) must be corrected for the body to function optimally without pain, dysfunction and reduced mobility of the involved muscles / joints.

Muscle imbalances are the cause of most biomechanical disorders in the body. From Carpal Tunnel Syndrome to Thoracic Outlet Syndrome, an existing muscle imbalance is at the root cause of the disorder in 90% of the cases. Too many modalities focus on the "band-aid principal", allowing the muscle imbalance go on for years with a little bit of relief here and there. Now is the time to focus on the actual "cause(s)" of these disorders and eliminate them altogether. With the appropriate exercise and stretch routine, most musculoskeletal disorders can be eliminated quickly and effectively.

Correcting muscle imbalances is achieved through a process consisting of a number of stretches and exercises. Soft-tissue treatment and hot/cold therapy may be utilized to help expedite the rate of recovery if it is so desired. Usually the nature of performing both stretches and exercises within the same program can be quite effective at eliminating the existing condition without the addition of the soft tissue treatment and hydrotherapy. Word of caution; there is a treatment sequence to addressing muscle imbalances if the best results are to be achieved. If random stretches and exercises are performed, an individual may cause themselves more harm than good.

A general rule when addressing a chronic muscle imbalance is to execute the following program:

1. Heat Therapy: Use heating-pad 5 Min. to warm the affected joint and surrounding muscles, preparing them for upcoming stretches and exercises. (Be sure that all sides of the joint and surrounding muscles are warmed-up.)

2. Soft-Tissue Treatment: Soft tissue treatment utilizing Effleurage and Trigger Point Therapy to reduce muscle spasm and relax the tight, restrictive overused muscles can be very effective in correcting muscle imbalances. Utilizing Transverse Friction Massage (TFM) on specifically weak, injured muscles and/or tendons to break down adhesions on the soft tissues can also be very effective in reducing overall pain and dysfunction.) Performing basic massage to the tight muscles is the easiest way to address the issue without getting too complex.)

3. Stretching Routine: Once the muscles are warmed up, stretching the tight, restrictive muscle group is key to increasing their length and reducing their impingement of surrounding tissues as well as reducing their effect on the misalignment of the joint. (Stretching the weak, underdeveloped muscles is not recommended as they are already too long and do not need to be lengthened further.)

4. Exercise Routine: Once the tight restrictive muscles have been lengthened from the stretches, it is time to exercise the opposing muscle group, the one that is weak and underdeveloped, in order to shorten and strengthen the muscles in order to reduce the tensile stresses imposed on them from the opposing tight muscle group. Exercising and strengthening the weak underdeveloped muscles not only forces the opposing muscle group to relax and lengthen further, but it also helps to maintain the length created in those muscles from the previous stretches. (Do not perform stretches after the exercises as this misaligns the joints and causes muscle rebounding. Always perform stretches first when addressing chronic muscle imbalances and then immediately follow with exercises.)

5. Contrast Bath: Utilizing a contrast bath at the end of the complete routine can be helpful in reducing muscle spasm, remove toxins from the muscles and increase circulation and overall nutrient flow to the injury, helping to aid an increase the speed of recovery. Basic procedure is 3-minutes heat to 1-minute of cold. Repeat 3-times, finishing with cold.¹

This general treatment program for chronic repetitive strain injuries resulting from muscle imbalances is very effective and often eliminates all of the symptoms previously associated with the injury, quickly and effectively. Always consult a physician before beginning any type of exercise or treatment program.

Remember, Your Health is in Your Hands!

Jeff P. Anliker is a Therapist, Author and Inventor of Flextend, Flextend-AC, Flextend-TFT and other therapeutic products that are utilized by Corporations, Consumers and Medical Facilities around the world. repetitive-strain.com.

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by EricT

By: Jeff P. Anliker, LMT

Carpal Tunnel Syndrome (CTS) is the most widely recognized form of Repetitive Strain Injury (RSI), but Trigger Finger is catching up fast, becoming all too common among society and affecting the youth and elderly in ever-increasing numbers. If the rising numbers keep on track, Trigger Finger may be recognized along with Carpal Tunnel Syndrome as having achieved epidemic proportions.

Trigger Finger On The Rise

Prior to the 1990's, Trigger Finger seemed to affect a small number of the elderly that had experienced some form of direct trauma or excessive strain to one or possibly several fingers. Trigger Finger was more prevalent in those that were already suffering with Osteoarthritis in the affected hand, making many healthcare professionals to believe that Trigger Finger was a byproduct of Osteoarthritis. But within the past 5-years, the age of those suffering from Trigger Finger became much “younger” while the overall number of individuals with the disorder increased. The belief of a direct correlation between those suffering with Osteoarthritis and Trigger Finger seems to be reducing in popularity as many of those suffering with Trigger Finger do not have Osteoarthritis, but instead, are involved in high-risk tasks that are already associated as the causative factor in many types of Repetitive Strain Injuries.

Injuries resulting from repeated motion (repetitive / cumulative trauma disorders — CTD's) are growing. According to recent annual statistics from the U.S. Survey of Occupational Injuries and Illnesses, over 302,000 CTD's account for nearly two-thirds all of workplace-related illnesses.

Ergonomic disorders are the fastest growing category of work-related illness. According to the most recent statistics from the U.S. Bureau of Labor Statistics, they account for 56 percent of illnesses reported to the Occupational Safety and Health Administration.

Trigger Finger – Recognized as a Repetitive Strain Injury

Now that Trigger Finger is rearing its head in the workplace with increased intensity, it has been added to the growing list of debilitating Repetitive strain Injuries. Trigger Finger now joins the ranks of Tendonitis, Carpal Tunnel Syndrome, Epicondylitis, Cubital Tunnel Syndrome, DeQuervain's and the many other debilitating workplace disorders affecting the upper extremity. So, what is Trigger Finger, how is it recognized and what are its symptoms?

Trigger Finger Explained

Trigger Finger is a form of overuse injury affecting any of the fingers (1-5) with symptoms ranging from a painless annoyance with occasional snapping/jerking of the finger(s), to severe dysfunction and pain with continuous locking of the finger(s) in a flexed downward / forward position into the palm of the hand.

The occurrence of this injury usually results from overuse of the flexor muscles/tendons and the formation of an adhesion or fibrotic nodule on the tendon. If left untreated, the adhesion/nodule becomes larger, therefore creating a conflicting ratio between the size of the tendon and the size of the entrance of the tendon sheath. In most cases, if the adhesion/nodule is not treated, it can continue to increase in size (Depending on activity/use of the affected finger) to the point where it still has the ability to pass into and through the tendon sheath when flexing the finger, but becomes stuck and cannot move back through the tendon sheath when trying to extend/straighten the finger, thus causing the finger to lock in the flexed forward / downward position.

The Trigger Finger Solution

Because Trigger Finger consists of an adhesion, nodule, and scar tissue buildup on the tendon due to excess strain, overuse, or direct trauma to that specific location on the tendon, it should be treated with stretching and strengthening exercises in order to break down the adhesion on the affected tendon. By breaking down the adhesion on the affected tendon, it reduces in size and slides through the pulley system in a normal manner, no longer “catching” and locking into the downward flexed position. (There is also a “thinning” of the tendon, which helps reduce the overall size of the tendon and nodule, therefore allowing it to pass through the tendon sheath with greater ease.) Creating strength in the opposing finger extensor tendons is very important as it allows the finger to return to an extended position in a more appropriate manner. This is where muscle balancing comes into play. By creating equality of tendon length and strength on both sides of the finger joint, individuals can help prevent the onset of Trigger Finger and/or keep it from re-occurring in the future.

Conservative therapy utilizing stretches and exercises has been highly effective, providing long-term and permanent relief. For those wanting to avoid surgery and for those where surgery was not effective in eliminating the condition, stretch and exercise therapy is the solution to both preventing and rehabilitating the devastating symptoms associated with Trigger finger.

Jeff P. Anliker is a Therapist and Inventor of Flextend and other therapeutic products that are utilized by Corporations, Consumers and Medical Facilities around the world for prevention, rehabilitation and performance enhancement. http://repetitive-strain.com.

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by EricT

By Asheesh Bedi, MD

Medial collateral ligament injuries to the knee are not uncommon. Many well-recognized professional athletes, including Hines Ward, Knowshan Moreno, and Troy Polamalu, have suffered from medial collateral ligament tears after injury on the football field. These can occur alone or in combination with other ligament or cartilage injuries of the knee in athletes.

What is the Medial Collateral Ligament?

The medial collateral ligament (MCL), together with the cruciates and lateral collateral ligament, is critical to the stability of the knee joint. The MCL is a fibrous band of tissue made up of collagen fibers that runs along the inner aspect of the knee from the end of the thigh bone (femur) to the top of the shin bone (tibia). In this location, the MCL provides “side-to-side” stability to the knee and prevents widening of the inner aspect of the joint with forces applied to the outside of aspect of the knee (valgus force). When significant forces are applied to the outside aspect of the knee, as can occur during a tackle in football or awkward slide into base with baseball, the ligament can be stretched (“sprained”) or torn.

The MCL is made up of a superficial and a deep layer. The superficial MCL runs from the distal femur to the tibia 4 or 5 centimeters below the knee joint line, and is found just below the sheath of the sartorius muscle tendon. The deeper MCL layer lies just outside of the knee capsule and inserts directly into the tibial plateau and medial meniscus. The superficial layers is much more mechanically important in resisting forces to the outside aspect of the knee (“valgus” force).

How is the MCL Injured in Athletes?

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Because the MCL resists widening of the inside of the knee joint, the MCL is usually injured indirectly by traumatic forces in the outside of the knee. These are certainly common in contact sports from tackles or “clipping injuries” in football and soccer. However, MCL injuries can also occur from noncontact mechanisms such as awkward landing or pivoting events in basketball or slides into base with baseball. MCL sprains or tears can occur in isolation or in combination with injury to the meniscus, cartilage, or cruciate ligaments.

What are the Signs of a Medial Collateral Ligament (MCL) Injury in Athletes?

The most common symptom following a MCL injury is pain directly over the medial aspect of the knee. The MCL can be tender to palpation over its attachment to the thighbone (femur) proximally, at its mid-substance, or distally over the shin bone (tibia) depending on the location of injury. The pain may also be reproduced by stressing the knee with a force applied to the outside aspect of the knee (“valgus force”), attempting to widen the inner aspect of the joint and stress the MCL. While a valgus force is applied, the inner aspect of the joint line can be palpated – widening that is 5 to 10mm greater than the normal, uninjured knee is significant for MCL injury. Swelling over the torn ligament may appear, and bruising or general swelling of the joint is not uncommon. In more severe injuries, patients may complain that the knee is unstable and feel as though their knee may 'give out' or buckle.

Based on physical examination, MCL injuries are graded in severity on a scale of I to III.

• Grade I injuries are incomplete tears of the MCL. The ligament is still intact but stretched, and the symptoms are mild. Patients usually complain of pain with palpation of the MCL.
• Grade II MCL tears are partial or incomplete tears of the MCL. There is significant pain with valgus stress of the knee and palpation along the medial aspect on the knee over the ligament. Athletes with these tears often complain of knee pain or instability when attempting to cut or pivot.
• Grade III tears are complete tears of the MCL. These athletes have significant pain along the medial aspect of the knee. Even deep bending of the knee is uncomfortable. These tears often occur in combination with other injuries in the knee, and complaints of “giving out” or instability with walking, running, or pivoting is common. A knee brace or a knee immobilizer is usually needed for comfort.

How are MCL Injuries in Athletes Treated?

Treatment of an isolated MCL injury in an athlete rarely requires surgical intervention. Usually rest and anti-inflammatory medications followed by rehabilitation will allow patients to resume their previous level of activity. All MCL injuries, however, are not created equal. Therefore, the time for an athlete to return-to-play is highly variable and dependent on the severity of the injury.

Grade I injuries usually resolve without complication. They are typically managed with rest, ice, and nonsteroidal anti-inflammatory medications until the knee is pain-free to examination or routine activities. Most athletes with a grade I MCL tear will be able to return to their sport within 1-2 weeks following their injury.

When a grade II MCL sprain occurs, a hinged knee brace is commonly used to protect the knee from valgus forces. Nonoperative treatment also ensues with icing, nonsteroidal medications, and controlled rehabilitation. Athletes with a grade II injury can return to activity once they are not having pain to palpation or stressing of the MCL with a valgus force. Athletes can often return to sports within 3-4 weeks after their injury, but may remain in a protective hinged brace with contact sports.

When a grade III injury occurs, the pain usually significant in the acute post-injury period. Athletes usually require a hinged brace locked in extension and crutches to protect against weightbearing for 1 to 2 weeks. As the pain resolves, the brace can be unlocked to allow range-of-motion as tolerated. Gradual weightbearing can be initiated as well. Once the athlete can comfortably flex the knee to 100 degrees, elliptical and stationary bicycle riding can begin. Light running can begin once the athlete has regained their quadriceps strength compared to the opposite side, and sporting activity can follow as long as the athlete remains pain-free. Complete rehabilitation from a grade III MCL tear can range from 6 weeks to 4 months.

For more helpful information on “sports injuries” and issues, please visit SportsMD Media Inc. SportsMD is the most trusted resource for sports health and fitness information for people engaged in sports everywhere. We have assembled the sports industry’s leading Doctors and health experts – each sharing valuable, practical advice to keep you playing injury-free.

References

Indelicato, PA. "Isolated Medial Collateral Ligament Injuries in the Knee" J. Am. Acad. Ortho. Surg., Jan 1995; 3: 9 - 14.

Grood E et al. Ligamentous and capsular restraints preventing straight medial and lateral laxity in intact human cadaver knees. J Bone Joint Surg 1981; 63A:1257-1269.

Dr. Asheesh Bedi is an Assistant Professor of Sports Medicine and Shoulder Surgery at the University of Michigan and MedSport Program. He is a team physician for the University of Michigan Athletic Department and specializes in both arthroscopic and open surgery for athletic injuries of the shoulder, elbow, hip, and knee. Dr. Bedi completed his undergraduate training at Northwestern University where he graduated Summa Cum Laude. He graduated from the University of Michigan Medical School with AOA recognition, and remained in Ann Arbor to pursue residency training in Orthopaedic Surgery at the University of Michigan. After completing his training, Dr. Bedi completed a two-year fellowship in sports medicine and shoulder surgery at the Hospital for Special Surgery and Weill Cornell Medical College in New York. He has also pursued additional dedicated training with Dr. Bryan Kelly in arthroscopic hip surgery for young athletes. While in New York, he was an assistant team physician for the New Jersey Nets professional basketball and New York Mets professional baseball organizations with Dr. Riley Williams, Struan Coleman, and David Altchek. He was also an orthopaedic consultant for the U.S. Open Tennis Tournament in 2007 and 2008 with Dr. David Dines and an assistant team physician for Iona College Athletic Programs.

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by EricT

By Asheesh Bedi, M.D.

What is the patellar tendon? What is patellar tendonitis?

Patellar tendonitis is defined by inflammation in the patellar tendon, and most commonly occurs at its origin just below the kneecap. The most common cause is overuse or repetitive injury, and it has been reported to occur in athletes of virtually every sport. However, jumping activities place particularly high strains on the tendon and the condition is therefore more common in basketball players, tennis players, volleyball players, track and field athletes, as well as soccer players. With repetitive jumping, small, often "microscopic" tearing and injury of the tendon can occur. The chronic injury and healing response results in inflammation and localized pain. Many well-known elite athletes, including Brandon Inge of the Tigers, Oliver Perez of the Mets, and tennis star Rafa Nadal have fought chronic battles with patellar tendonitis during their career. Rarely, an acute patellar tendonitis can develop in response to a single traumatic event and should raise concern regarding a partial or complete tendon rupture.

What are the symptoms of patellar tendonitis in athletes?

The diagnosis of patellar tendonitis is usually straightforward. Pain is usually reproduced with palpation of the area of inflammation and injury. This is most commonly at the inferior pole of the patella, but can occur anywhere along the course of the tendon. Compared to the opposite, normal knee, the tendon will often appear swollen and often warm to the touch. Depending on the severity, the athlete may have significant pain with jumping or kneeling. Walking up and down stairs can also place significant loads of the extensor mechanism and exacerbate the pain.

X-rays are sometimes useful to evaluate for other causes of knee pain, but are typically normal with patellar tendonitis. If the patellar tendon is ruptured, the kneecap will displace "upward" and the distance between the kneecap and shinbone is greater than normal ("patella alta"). Ultrasonography and MRI are both sensitive and specific in identifying patellar tendinitis and localizing the area of "micro-injury" to the tendon.

What may increase my risk of patellar tendonitis as an athlete?

The cause of patellar tendonitis in athletes is often multifactorial. However, some factors that may increase the risk of this injury include:

• Overuse, particularly with recurrent jumping activities.
• Inadequate conditioning or stretching - an abnormal length-tension relationship and compliance of the thigh and calf muscles can increase strain on the patellar tendon and increase the risk of injury.
• Obesity - small increases in weight place dramatically increased stress on the kneecap and extensor mechanism. In fact, a gain of one pound can manifest as 8 to 10 more pounds of force on the knee with certain activities.
• Patella alta - a "higher than normal" kneecap position may increase the strain and risk of injury to the patellar tendon.

Can athletes prevent patellar tendonitis?

Unfortunately, it is hard to anticipate the development of patellar tendonitis. However, as with most overuse injuries, routine stretching before strenuous competition can help to prevent injury. Stretching the quadriceps, hamstrings, and calf muscles help to minimize the risk of eccentric, injurious loads on the tendon during running or jumping activities.

How is patellar tendonitis treated in athletes?

The first line of treatment of patellar tendonitis in athletes is typically nonoperative. The fundamental tenets of treatment include: Rest

It is critical that the athlete avoid the provocative activities that are causing pain. Typically, this means a cessation of competition and period of rest from running and jumping activities. This will decrease the strain and prevent recurrent injury to the tendon.

Ice & Anti-Inflammatory Medications (NSAIDs)

Ice and nonsteroidal anti-inflammatory medications (NSAIDs) can certainly help to alleviate the pain, and may be a useful augment to physical therapy and stretching exercises during the healing and recovery phase.

Exercises and Physical Therapy

As the pain resolves after a period of rest, gentle stretching and strengthening exercises are initiated. These exercises help to restore the normal length-tension relationship or the muscles and tendons, and also play a crucial role in preventing a recurrence of patellar tendinitis. It is of tantamount importance to learn proper jumping and landing techniques, and to strengthen the muscles around the kneecap to reduce the forces on the tendon itself. Eccentric strengthening exercises of the quadriceps muscles have been shown to be particularly effective - these are exercises which involve muscle contraction while lengthening; for example, lowering a weight in a controlled fashion from a extended to flexed knee position.

Steroid injections are generally NOT recommended for the treatment of patellar tendonitis. While they can certainly decrease local inflammation at the site of injury, the injections must be approached caution as the steroid medication can weaken the tendon and increase the risk of patellar tendon rupture.

Is there a role for taping or bracing in the treatment of patellar tendonitis?

Taping or use of a patellar tendon "strap" brace has often provided significant relief to athletes, although the success is quite variable. The precise mechanism of action is unknown, but it is believed that taping or bracing alters the angle and direction of stress at the site of injury, effectively "unloading" this region and decreasing the pain by distributing forces away from the tendon. A Chopat strap has been specifically used to unload the patellar tendon for both patellar tendonitis and Osgood-Schlatter's Disease.

What other treatment options can be considered for patellar tendonitis short of surgery?

A number of other treatments have been used with variable success in the treatment of patellar tendinitis. These include:

Platelet-Rich Plasma (PRP): PRP injection has recently been used in the treatment of chronic, refractory tendonitis. PRP is derived from the patient's own blood and concentrates many important growth factors that have been shown to be important in the body's healing response following injury. Preliminary results have been encouraging, but long-term success remains unknown.

Extracorporeal Shock Wave Therapy (ECW): ECW uses sound waves to stimulate healing at the injured tendon. It has been used with modest success in the treatment of tendinitis and plantar fasciitis.

Laser & Electrical Stimulation: While the mechanism of action is unclear, laser and electrical stimulation techniques have been reported with good success in small case series.

Is there a role for surgery in the treatment of patellar tendonitis in athletes?

Surgery is indicated in severe cases of patellar tendonitis that fail to resolve with conservative measures. The operation is directed at repairing viable tendon tissue and debriding away severely damaged tendon, usually just below the kneecap. Many elite athletes, including Brandon Inge, Oliver Perez, and Carlos Beltran, have undergone this surgery and successfully returned to MLB competition.

Asheesh Bedi is a freelance writer for SportsMD. For more helpful information on sports injuries and issues please visit SportsMD, the most trusted resource for sports health and fitness information for people engaged in sports everywhere. We have assembled the sports industry's leading Doctors and health experts - each sharing valuable, practical advice to keep you playing injury-free.

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by EricT

By Asheesh Bedi, M.D.

What is a Sports Hernia?

A sports hernia also known as athletic pubalgia, Gilmore's groin, and slap shot gut, is an uncommon, but often missed cause of groin pain in high level athletes. It is poorly understood and poorly defined in the medical community. It is also very difficult to identify based on history and physical exam of an athlete with groin pain. The name sports hernia is a misnomer as well because there is no discernable hernia (or protrusion of abdominal cavity contents) present in this condition.

Who gets a Sports Hernia?

Sports hernia is a diagnosis almost exclusively of very high level male athletes. It is a common diagnosis in athletes with chronic longstanding groin pain that does not respond to a very long (often years) course of non-operative treatment. Typically athletes involved in repetitive twisting sports such as ice hockey, soccer, Australian rules football, and tennis. Recent well known athletes such as Donovan McNabb of the Philadelphia Eagles, Tomas Holmström of the Detroit Red Wings and Jeremy Shockey of the New Orlean's Saints have all had surgery to repair a sports hernia.

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Hockey player's syndrome otherwise known as "slap shot gut" is a variant of a sports hernia unique to high level ice hockey athletes. It is due to repetitive twisting motions of the torso common in hockey such as with taking a slap shot. The result is a tearing over time of the covering (fascia) lining the lower abdominal oblique muscles. It is most often seen on the side opposite the player's forehand slap shot. There may also be an associated inguinal nerve irritation. This may explain why the pain seen in hockey player's syndrome often travels to the scrotal region. The treatment involves a repair similar to that in many sports hernias.

This is in contradistinction to a typical hernia where there is a protrusion of abdominal contents such as fatty tissue or bowel through a well-defined defect in the inguinal canal of the groin. Despite this, the name sports hernia has persisted because many of the surgical treatments are similar to that of a typical hernia.

How does a Sports Hernia happen?

Repetitive twisting and shear forces encountered during high level athletics can lead to injury of the lower abdominal wall. This may be exacerbated by the typical strong thigh adductors (muscles that bring the thighs closer together) compared with often weaker lower abdominal muscles.

How is the diagnosis of a Sports Hernia made?

Athletes typically complain of a longstanding history of pain in the inguinal (groin) region. They often complain simply that their performance has deteriorated below a satisfactory level. Often the pain is not present during periods of inactivity, rest or periods away from athletic involvement. However, symptoms classically reappear with return to the athletic activities responsible for the injury in the first place. The pain may travel, or radiate, from the groin into other areas like the testes, lower abdominal musculature and the inner thigh region. The pain is often exacerbated by coughing or sneezing as well as by athletic movements like sit-ups and kicking motions.

On physical examination, there may be groin pain to palpation in the region of various structures along the wall of the lower abdomen. These may include anatomic regions like the inguinal ring and canal as well as the pubic symphysis (central fusion point of the 2 halves of the pelvis in the front/center of the pelvic region). There is however no classic inguinal hernia detectable on exam as there is no defect in the inguinal wall and no intra-abdominal contents that herniated through. Patients will have pain with a resisted abdominal contraction such as with a sit-up. This may be worsened by doing so with the thighs squeezed together (adduction).

What else can masquerade as a Sports Hernia?

There are many possible causes of groin pain in athletes. Sports hernia is a rarely confirmed diagnosis, and therefore it is extremely important to be sure that other conditions are not the source of an athlete's symptoms. Some conditions that can mimic a sports hernia include:

● Pulled Groin Muscle (Hip Flexor/Adductor Strain)
● Hip impingement
● Inguinal hernia
● Osteitis pubis (inflammation of the pubic symphysis: joint connecting the 2 halves of the pelvis)
● Stress fracture
● Snapping hip
● Labral tears
● Osteoarthritis
● Nerve entrapment
● Avulsion fractures in teenagers and children
● Non-orthopaedic causes of pain such as those involving the genitourinary system

How is a Sports Hernia treated?

Special emphasis should be given to core stabilization exercises as well as countering any imbalance between the various hip, pelvis and thigh musculature. An evaluation by a highly specialized physical therapist is necessary to help the athlete along with their rehab program and identify and treat these imbalances. A good example to improve this imbalance is Hip Abductor Strength

For more information on treatment including several other instructional core strength exercises as well as hip strengthening videos, please click the following link. Surgical information is also provided in this link: Sports Hernia & Athletic Pubalgia

What is the prognosis for recover?

About 90% of athletes who have surgery for a sports hernia are able to return to competition at the same level or higher to where they were prior to their injury. The timing of return to competition for laparoscopic surgery is typically within 6 weeks while for open surgery it is usually a few months to as long as 6 months.

Asheesh Bedi, MD - About the Author:

SportsMD is the most trusted resource for sports health and fitness information for people engaged in sports everywhere. We have assembled the sports industry's leading Doctors and health experts – each sharing valuable, practical advice to keep you playing injury-free.

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by EricT

By Asheesh Bedi, M.D.

Runner's knee is a term used to describe a constellation of symptoms of knee pain that is frequently encountered in running athletes. Other terms that have been used to describe this condition are "anterior knee pain", "chondromalacia patella", or "patellofemoral pain syndrome (PFPS)". Runner's knee involves the kneecap, quadriceps tendon, patellar tendon, and the associated soft tissues that are critical to extension of the knee. Historically, "runner's knee" was attributed to irritation and softening of the cartilage lining on the undersurface of the kneecap ("chondromalacia"). More recently, however, it has been recognized that overloading of the underlying ("subchondral") bone can be a substantial source of pain, as it has a rich nerve supply. The soft tissues and fat pad in the front knee can be causes of pain as well.

Who gets Runner's Knee?

While classically associated with long-distance running, any activity that places significant stresses on the front of the knee joint ("patellofemoral") can result "runner's knee". This includes repetitive jumping sports like basketball or volleyball, as well as skiing, cycling, and soccer. The repetitive pressure and stress between the femur and patella in these sports can result in softening of the cartilage and abnormal loading of the underlying bone.

How does Runner's Knee present?

Runner's knee presents as activity-related pain in the front of the knee and around the kneecap. While the pain develops during athletic activity, it can often be most pronounced afterwards during a period of rest. Pain is also felt after sitting for a long period of time with the knees bent - the bent position actually increases the pressure between the kneecap and femur. For the same reason, marathon runners will often paradoxically complain of greater difficulty running downhill rather than uphill. Kneeling, squatting, or direct pressure on the front of the knees may be uncomfortable as well.

What things might predispose me to Runner's Knee?

The kneecap and its cartilage is subject to very high forces with daily activities, and any injury to the cartilage or factors which result in increased pressure between it and the thigh bone ("femur") can increase the risk of "Runner's Knee". These include:

• Malalignment of the kneecap and/or leg
• Subluxation or dislocation of the kneecap
• Direct trauma to the kneecap
• Overuse with running and jumping activities
• Wide hips and/or "knock knees" (valgus) resulting in maltracking of the kneecap
• A weak quadriceps/vastus medialis muscle
• Flat feet ("pronated" feet)
• Direct trauma to the kneecap
• Overuse with running and jumping activities
• Wide hips and/or "knock knees" (valgus) resulting in maltracking of the kneecap
• A weak quadriceps/vastus medialis muscle
• Flat feet ("pronated" feet)

In certain cases, runner's knee results from irritation or injury to the soft tissue around the kneecap. For this reason, inadequate muscle strength and/or stretching of the thigh and calf muscles can predispose to "Runner's Knee" as well.

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What can I do to prevent Runner's Knee?

While certain predisposing factors such as kneecap and leg alignment are not in the control of an athlete, other preventative measures can be taken to minimize the risk of "runner's knee". These include:

• Quadriceps and vastus medialis strengthening - a strong quadriceps and, specifically, the vastus medialis muscle will improve the tracking of the kneecap and help to minimize contact pressures between the kneecap and thigh bone.
• Keep your weight down - the patellofemoral joint experiences forces that are 8 to 10 times our body weight, such that even small reductions in weight can significantly reduce the forces on the kneecap. Ten pounds of weight loss can be as much as 80 to 100 pounds less force of the kneecap when climbing or descending stairs.
• Stretch before running or jumping activities - Strains of the patellar tendon, quadriceps tendon, or other soft tissues that stabilize the patella can cause significant anterior knee pain. Warming up and stretching both before and after exercise can help to prevent strain injuries to these structures.
• Wear proper shoes and orthotics - Flat feet ("pronated" feet) can predispose to maltracking problems and knee pain. Orthotics to reconstitute the arch of the foot can help to alleviate these symptoms. High heels can also worsen anterior knee pain and should be avoided if you have "runner's knee" symptoms.
• Plan for a good running surface - Running on a flat surface without steep, downhill slopes can help to prevent significant stress on the knee cap. Even, padded surfaces and good running shoes can help as well.

How is Runner's Knee diagnosed in athletes?

Usually, the diagnosis of "runner's knee" can be made in athletes based on the history and physical examination of the knee by your sports medicine specialist. The exam will evaluate the stability of the kneecap as well as alignment of the leg. Signs of tenderness under the kneecap and/or instability will be assessed. Strength and tone of the quadriceps and hamstrings will also be determined. Flexibility of the feet and loss of the arch should also be noted as this will predispose to kneecap problems. X-rays, MRI, and CT scans can all be useful adjuncts depending on the examination findings and symptoms. Special views can show the position and alignment of the patella in its groove on the thigh bone ("trochlea"). Tilting of the patella that leads to abnormal contact pressures can be appreciated. If instability of the kneecap is suspected, CT scan can help to determine abnormalities in alignment and position. MRI is useful to evaluate for softening or injury to the cartilage on the kneecap and femur.

What is the treatment for Runner's Knee?

The first line of treatment for "runner's knee" is typically nonoperative. Recommendations include:

• Stop running, jumping, or any of the activities that cause pain in the knee. Even though it is difficult, the athlete must refrain from competition until he/she is pain-free. Fortunately, low-impact activities such as swimming or cycling can allow the athlete to maintain their aerobic fitness while protecting the patellofemoral joint.
• Avoid running down hills or down steep slopes or stairs that increase pressure on the kneecap.
• Ice and anti-inflammatory medications can certainly help to relieve the pain in the front of the knee.
• In certain cases, taping of the kneecap ("McConnell taping") or use of stabilizing braces for the kneecap can help. These are particularly useful in the setting of instability of the kneecap.
• If the athlete has flat feet ("pronation"), orthotic inserts to reconstitute the arch can be extremely useful to alleviate symptoms.
• When the knee is pain-free, a course of rehabilitation for range-of-motion of the knee and strengthening of the quadriceps and vastus medialis muscle may be useful.

However, exercises that are performed with the knee bent should be avoided, as the pressure beneath the kneecap is increased in this position. Instruction on preventative stretching exercises for the quadriceps, hamstring, and calf muscles is very important as well. In rare circumstances, the knee will continue to be painful and refractory to all of the nonoperative measures described above. When the pain of "Runner's Knee" prevents the athlete from returning to play, surgery may be considered.

The specific treatment will depend on the underlying cause for the pain. Arthroscopic ("minimally invasive" camera-based) surgery can be pursued to manage softening or damage of the articular cartilage of the kneecap and thigh bone. If there is accompanying instability of the knee cap, soft tissue reconstructive procedures or re-alignment of the leg ("osteotomy") may be performed to improve the tracking of the patella. These may also be performed to relieve abnormally high pressures between the kneecap and femur.

For additional information on runner's knee, check out this SportsMD video on "patellofemoral pain syndrome (PFPS)."

Dr. Bedi is a fellowship-trained orthopaedic surgeon specializing in Sports Medicine. He is currently the Assistant Professor for Sports Medicine and Shoulder Surgery, at the University of Michigan Health System. Dr. Bedi did a sports medicine fellowship at the Hospital for special Surgery and completed his residency at the Department of Orthopaedic Surgery University of Michigan Medical Center. He graduated from Northwestern University with a Major in Biochemistry/Biophysics Summa Cum Laude and graduated from the University of Michigan Medical with School Academic Honors and Research Distinction.

For more information on sports related injuries and issues please visit http://www.sportsmd.com. SportsMD is the most trusted resource for sports health and fitness information for people engaged in sports everywhere. We have assembled the sports industry's leading Doctors and health experts - each sharing valuable, practical advice to keep you playing injury-free.

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