Lots of trainees ask whether they can get a torn bicep from deadlifts. Actually there are three related questions which I will introduce one after the other:

Can I get a bicep tear from deadlifting?

Understanding the mechanisms of a muscle strain will help us figure out whether the deadlift is a culprit in biceps pulls. Most often, muscle strains happen when a muscle is actively lengthening against load - the eccentric action. Alternatively a strain can occur when the amount of tension developed in a muscle exceeds the tensile strength of the tissues. A muscle can be strained, of course, by the simple application of a mechanical stretch. Even then the muscle is developing tension.

When you deadlift, the biceps do not actively contract. They are at resting length and are not being stretched much beyond this length. In fact, they cannot be stretched much beyond resting length during the deadlift since to introduce this kind of stretch you would have to hyper-extend the shoulder. Even then the bicep cannot be stretched that much, relatively speaking. Since the bar is in front of you the shoulders cannot hyper-extend and the elbows are incapable of hyper-extension. So the bicep muscle is not contracting and iIt is not actively lengthening against a load. It is not developing a large degree of tension.

Will using an alternating grip be more likely to cause me to tear a bicep?

This question usually refers to the perception that the supinated arm¹ suffers a strained bicep or at least pain after deadlifting. One action of the biceps muscle IS to assist in supination of the forearm. So it would stand to reason that a bit more tension will be felt in the supinated versus the pronated arm.

However that does not translate to a bicep strain waiting to happen. The tension is not of the muscle shredding variety and there is no resistance to contraction. The forearm is being held in a suppinated position by the hand gripping the barbell and the elbows are not flexed. The biceps bracchi contribute to supination of the forearm but this action is much stronger if the elbow is flexed rather than extended as during the deadlift. You can check this for youself by turning your palm up with your arm straight and then with your arm bent to a ninety degree angle. When you supinate your arm with elbow bent you will notice a very strong biceps contraction as compared to supination with the arm straight.

Should I alternate the pronated and supinated hand for each rep when using the alternating grip in order to protect against bicep pulls?

You should alternate the supinated and pronated arms. But not to protect from a bicep pull, necessarily. Using an alternated grip changes slightly the position of the bar relative the body and the action of the shoulders and upper back. Alternate the grip position to create balance about the shoulders and upper back.

So Why This Talk about Deadlifts and Bicep Pulls?

Two likely answers come to mind. A foreshortened biceps is quite likely with many trainees owing to overindulging in biceps curls lacking full range of motion. Not to mention pullups done without full range of motion.

Many trainees habitually do bicep curls without allowing the elbow to completely extend at the bottom of the curl. Pullups and chinups are even more likely to be done this way and this is the origin of the so-called "deadhang" pullup whereby the elbow is allowed to completely extend at the bottom of the pullup, perhaps with a pause in this position to eliminate any "stretch reflex" or rebound. I would argue that there isn't really any other way to do a pullup but "deadhang". Anything else is either a partial pullup or some kind of gymnastics. That is personal opinion though and the fact is many trainees fail to use full range of motion in exercises that require elbow flexion.

The idea is that both electrical and tissue responses cause a muscle to become "foreshortened" relative to its normal resting length. The "fore" means the same as "pre". Repeated elbow flexion against heavy resistance without allowing the elbow to extend fully seems likely to cause one's biceps to become "short" or "tight". However it is unclear whether this is a true phenomenon especially through resistance training alone. We've all probably experienced the feeling of very tight and sore biceps after overzeolous curling. We may even have been unable to fully extend our elbows during these times. But we've also found that the normal resting length returns after a day or two.

Considering the normal resting length of the biceps muscle and the position of the arm during the deadlift it is not likely that a correctly performed deadlift should result in a biceps strain. It could be, then, that trainees who experience biceps strains during deadlifts are not performing them correctly. In fact one of the most common mistakes that trainees make is to slightly flex the elbows during the deadlift and most trainees are not conscious that they are doing so. This, undoubtedly, could produce a biceps strain! The biceps, if flexed during a deadlift, must resist lengthening against a very great resistance. The tensions that result can be large and although a major strain is not likely due to the range of motion this is probably the origin of the bicep strains that are reported by some trainees. The solution is quite simple. Never flex your elbows during the deadlift.

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by EricT

The last post about the concept of optimal strength training was more philosophical than practical. Even so, many practical ideas are derived from an underlying philosophy concerning training. However, I promised to get more technical and “sciency” in the next post so this one is about science itself being applied to strength training.

Throwing Out the Baby with the Bathwater

A prevailing habit of many trainees that I’ve had to contend with is something very much akin to “throwing out the baby with the bath water”. For example, a student of strength training learns something about technique and injury prevention and begins to focus exclusively on this one aspect of performance, forgetting all he or she has learned about various other performance parameters. We do not need to “unlearn” everything each time we discover something new! We simply need to incorporate.

Perhaps surprisingly, this habit is not the sole province of trainees. It happens in the professional strength training world as well! This brings us to one more important trend that students of strength training must be aware of and this is where the science comes in.

The Current Bias and Science

Science being applied to the improvement of human athletic performance is nothing new. The desire to train scientifically is not a recent development. Only our understanding has taken great leaps forward in modern times.

Nowadays we see many kinesiology majors becoming involved in strength training. We also see physical therapists from many different educational backgrounds or philosophies. Some of them are great up and coming coaches and some are just people with letters after their name.

The problem however is that many people with a bachelors degree in kinesiology or some similar major would like you to believe that they basically studied “deadlifting 101” and that their studies put them on the cutting edge of performance improvement. Nothing of the sort. They are ahead of those starting from scratch but most of the improvements and innovations in improving strength come from the “trenches” rather than research studies.

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No, no, this does not mean that some keyboard legend telling you that “the real studies are done under the bar” is right. That’s not science of course its just somebody repeating some tough guy rhetoric they’ve heard. I read another similar statement about nutrition on a comment post at Alan Aragon’s blog the other day to the effect that “real nutrition research is done at the table” or some such similar nonsense.

There is relatively little study directly concerned with improving performance compared to preventing injuries. The discipline of biomechanics tends to lag behind those developments. To perform studies you need funding. Well, ask yourself whether there is a lot of studies concerning lifting big old heavy things. Sounds like I’m kidding doesn’t it?

I’m not. “Strength training” research, when it is done, is not concerned with strength for the sake of strength. It’s concerned mostly with power or endurance athletes. The bulk of the research is about injury prevention, however, or something that is related in some way to injury prevention such as studying the effects of over-training.

Of course preventing injury is part of improving performance! Corrective exercise is all the rage right now and it’s got a right to its popularity because trainees are seeing vast improvements in their movement quality with quite simple interventions.

There is yet another backlash because strength coaches don’t want to be known as ‘soft corrective exercise types’ so we get “strength training is always corrective” and that sort of thing. In the past I’ve referred to this as a demonstration of the “is-ought” problem.

For instance, let’s say that I tell you “being stronger makes you better” and that I consider this a factual statement. Now let’s say I go a bit further. “Being stronger makes you better and therefore all strength training is corrective.” See, I have gone from a general statement of what IS to a statement about what I feel should be. There is nothing in the statement about being stronger making us better than leads to the conclusion that all strength training is corrective. Yet, upon first glance this leap in logic may be hardly detectable. Well, in the strength training world these kinds of logic leaps are the rule rather than the exception so be on guard for them.

"Being stronger makes you better" is itself a value statement since the word better speaks to values rather than an objective performance criteria. So here we have a value statement disguised as an objective statement of fact and then a leap to a baseless conclusion. Yet this statement is very much like more statements about strength training.

You can read more about the is-ought concept in my post about specificity and transfer of training effect.

Trainees are NOT Patients

We must prevent injuries and correct deficiencies in order to continue progressing in our strength training. However the pendulum seems to be swinging so far to the “prevention” side that trainees are being treated like patients. Strength coaches seem to be becoming apologists to physical therapists rather than performance specialists. I’ve spoken of tools many times before. The tools are the servants. Trainers and coaches should not be the servants of theory, assessments, corrective exercise, pre-hab, and the like. These things should be the servant of the coach.

It makes sense why such a servile attitude toward these things could emerge. Many coaches have a very firm foundation in biomechanics but the fact of the matter is there are few cut and dry answers and even little problems can be quite complex. There is just so very little data. Trainers are forced to experiment and innovate and there is a great desire for concrete information.

Enter the physical therapist or other professional armed and ready with the information that will save all the hapless coaches who are running their athletes to an early retirement. Ready and willing to take anything and everything they can to improve their athletes some of the strength community has forgotten that they are not therapists and their athletes are not patients or therapy clients!

Injury prevention and “prehabilatative” techniques are great. And technique IS crucial. But there are other factors that are routinely ignored. Just because your favorite guru only harps on form doesn’t mean that is the only factor in your weight lifting success.

There are Many Aspects of Performance

Sometimes we complain about quantity over quality. I myself base my training techniques on quality. But I also base them on success which means there are certain quantitative means I must use. And they can be quite aggressive. For instance, while we must maintain quality as much as possible we also need a certain tolerance to workload in order to see incremental improvements in our lifting range. I try to bridge that with quality which makes me stay away from simple volume loading protocols in favor of more more "creative" strategies, for lack of a better description. But the simple fact of the matter is there is a need for physiological changes as well as motor changes.

A great example is running, or in particular, sprinting. I am not extremely knowledgeable in this area but I can recognize fallacies when I see them because I understand performance. Log on to any running related forum and you will find pages and pages of discussion into technique. So much so that it seems as if the trainees think that they will be the fastest in the world if they can just make that one small and magical change in their technique.

But the simple fact is that in already accomplished sprinters technique changes have shown only very small improvements in studies. Running fast is mostly about physiology and training. You’ve got to run fast a lot to run fast. Perfecting technique can make that training more effective and efficient; it can help prevent injuries. It can do all sorts of things but another second is rarely about a little tweak in technique!

There are no hard answers and I am not trying to make any hard statements. I only wish for you to be aware of the current bias. I also wish for you to be aware of the population bias in the strength training literature. That is most of it is aimed at either the professional athlete (of any sport you can imagine) or the professional Powerlifter or Olympic weightlifter.

For those of us who train for absolute strength simply and solely for the sake of absolute strength, which are very few of us I know, there is not a whole lot of love out there! Information aimed at basketball players, baseball players, hockey players, or rugby players does not apply to us. Information aimed at a lifter who is concerned solely with his numbers on deadlifts, squats, and bench press may not apply to us if we don’t compete in these lifts.

Therapy won’t get you a 600 pound deadlift or a big squat. There is still a need for those who know how to train for strength and let’s not forget it.

Be that as it may many strength and performance coaches seem to take this as an excuse to ignore technique altogether. What’s even more disturbing is the teaching of corrective exercises with bad technique, let alone the primary movements. It’s becoming a mess with every Tom, Dick and Harry thinking they are qualified to not only train people but also to rehabilitate them. I have found many ridiculous practices being recommended in a wholesale way and qualified by simply labeling them with a ‘rehab’ tag.

The selling of strength training has made it a commodity much like fatloss and fitness and the experts are cashing in with watered down advice for the masses.

Tests Don't Move Weights

Be aware that there is no hard science attached to movement screens and functional evaluations much of the time. The testing is very subjective and depends on the administrator with the screens themselves often based on the opinion of one or two people. What’s more, many of these screens lack face validity, content validity, and reliability. Often they aim to predict that which is subjective rather than concrete. I discussed the overhead “deep squat” in the GUS Overhead Squat Book to demonstrate this. You can get that book by signing up for the Ground Up Strength newsletter in the box provided at the bottom of this page.

Please do not take any of this as simple opposition for the sake of opposition. I embrace many of the things I’ve discussed here. But I try not to let them become biases. You cannot make a bad strength training plan a good one by tacking on some mobility drills and external shoulder rotations!

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All posts in this series:

Training to Fail Series

by EricT

This is an older post from the GUStrength's Blog.

I noticed a post about a study at Male Pattern Fitness that I would like to have reacted to but for some reason the comments are always closed kinda quickly at this blog so I wanted to comment on it here.

I feel it may be a bit misleading.

Yes, I agree completely that most people train in a way that predisposes them to imbalances and injury. Such as the internal rotator dominance that was brought up in the post.

However, it is not likely that a study can prove what the study claims to prove:

The findings of this investigation suggest that RWT [recreational weight training] participants are predisposed to strength and mobility imbalances as a result of training. The imbalances identified have been associated with shoulder disorders in the general and athletic population; thus, these imbalances may place RWT participants at risk for injury.

- Shoulder Joint and Muscle Characteristics in the Recreational Weight Training Population

There are just WAY too many variables. The quote above about the findings of the invesigation is not even a logical statement since the authors basically say that the same imbalances are found in both the general AND athletic populations and that these imabalances are associated with shoulder injury. So what they are saying is that imbalalances place EVERYONE at risk for shoulder injuries, including athletes. This would lead me to believe that the point is that training does not "protect" us from injury or from the consequence of imbalances. That is not the same thing as saying that recreational lifters are more more predisposed to injury than the general population. Yet the opening sentance says that these lifters are more prone to injury as a result of training. Seeing that the following statements in no way back up the opening statement I would call the entire study into question without even reading it!

However the study simply finds that recreational lifters tend to have internal rotator dominance which these days most gym trainers could have told you. It's hardly "news". But yes, those same imbalances are found in the general population.

Here is the thing though and I want to make this very clear: Everybody has baggage. You can and likely do have imbalances regardless if you've ever hit the weights. Many occupations which require the constant repetition of certain movement patterns or the maintenance of certain positions cause huge postural distortions and do result in PAIN for many, many people who do NOT lift weights.

My side job is painting and I don't need a study to tell you that painters are prone to shoulder dysfunction.

In fact, what you do 23 hours a day probably has a much bigger impact than what you do one to two hours a day three to four times a week. That is not to say that you cannot do some serious harm with faulty training practices.

But hell, sleeping habitually in a bad position can lead to problems as well. Sleeping on my right shoulder almost constantly contributed to a bout with bursitis, for instance. Notice I didn't say "caused" but contributed.

Ask a physcial therapist. Or ask a body work person who does deep tissue therapy of some kind. If you think the majority of their clients are athletes (even "recreational") of some kind…think again.

That internal rotator problem..desk jockeys are prone to shortened pecs, pec minor, lats which dominate the scapular adductors leading to problems about the shoulder complex. Factory assembly workers…

Very often weight training is simply the straw that breaks the camel's back. Going too heavy too fast and not paying attention to all the factors mentioned in the post is just a tipping point that turns deficiencies into "injuries".

There are many problems with the thinking involved in separating groups of people into "trained and "untrained" or "trained" and "control". When it comes to lifestyle habits that may predispose someone to certain imbalances and injuries this "baggage" begins accumulating at an early age, at least around puperty.

One of the major fallacies here is the base rate fallacy¹. Separating groups into "trained" and "control" is essentially ignoring a great deal of information about the individuals in the 'trained' group, much of which could be pertinent in determing lifestyle habits that may predispose these individuals to injuries. Even the term "recreational weight training" suggests this.

Base rate information is information about the population or group a person comes from. If we take 100 individuals and separate them into a "training" and "non-training" population then we might consider the typical attributes of a weight training population to be base rate information. But what if we mix our training group in with 500 other people of a similar background but have no training history? Say our population has similar jobs involving manual labor, repetitive motions and sustained postures? Suddently the fact that "John" and "Ed" lift weights recreationally becomes information that is perhaps accacerbating but if we focused on this we would be ignoring the population that these two individuals come from which is our forementioned manual laborers.

So what this all means is that we cannot make broad sweeping conclusions from the conclusions of one controlled study and that we shouldn't assume that a person's injuries or chronic pain problems stem solely from their training habits.

None of this is to suggest that the points brought up in the article are untrue…simply a bit unfair and not the whole picture.

One thing I wholeheartedly agree with though: Your training should make you BETTER. Not just stronger but better in every way. It just so happens that those two things can go hand in hand.

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by EricT

Understanding acute ankle ligamentous sprain injury in sports

Daniel TP Fong¹, Yue-Yan Chan², Kam-Ming Mok³, Patrick SH Yung⁴ and Kai-Ming Chan⁵

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Sports Medicine, Arthroscopy

This paper summarizes the current understanding on acute ankle sprain injury, which is the most common acute sport trauma, accounting for about 14% of all sport-related injuries. Among, 80% are ligamentous sprains caused by explosive inversion or supination. The injury motion often happens at the subtalar joint and tears the anterior talofibular ligament (ATFL) which possesses the lowest ultimate load among the lateral ligaments at the ankle. For extrinsic risk factors to ankle sprain injury, prescribing orthosis decreases the risk while increased exercise intensity in soccer raises the risk. For intrinsic factors, a foot size with increased width, an increased ankle eversion to inversion strength, plantarflexion strength and ratio between dorsiflexion and plantarflexion strength, and limb dominance could increase the ankle sprain injury risk. Players with a previous sprain history, players wearing shoes with air cells, players who do not stretch before exercising, players with inferior single leg balance, and overweight players are 4.9, 4.3, 2.6, 2.4 and 3.9 times more likely to sustain an ankle sprain injury. The aetiology of most ankle sprain injuries is incorrect foot positioning at landing – a medially-deviated vertical ground reaction force causes an explosive supination or inversion moment at the subtalar joint in a short time (about 50 ms).

Another aetiology is the delayed reaction time of the peroneal muscles at the lateral aspect of the ankle (60–90 ms). The failure supination or inversion torque is about 41–45 Nm to cause ligamentous rupture in simulated spraining tests on cadaver. A previous case report revealed that the ankle joint reached 48 degrees inversion and 10 degrees internal rotation during an accidental grade I ankle ligamentous sprain injury during a dynamic cutting trial in laboratory. Diagnosis techniques and grading systems vary, but the management of ankle ligamentous sprain injury is mainly conservative. Immobilization should not be used as it results in joint stiffness, muscle atrophy and loss of proprioception. Traditional Chinese medicine such as herbs, massage and acupuncture were well applied in China in managing sports injuries, and was reported to be effective in relieving pain, reducing swelling and edema, and restoring normal ankle function. Finally, the best practice of sports medicine would be to prevent the injury. Different previous approaches, including designing prophylactice devices, introducing functional interventions, as well as change of games rules were highlighted. This paper allows the readers to catch up with the previous researches on ankle sprain injury, and facilitate the future research idea on sport-related ankle sprain injury.

Introduction

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Ankle ligamentous sprain injury is the most common single type of acute sport trauma [1]. Over the years, various preventive strategies have been implemented, however, a recent epidemiology revealed that ankle sprain injury still dominated in sport injury, as it accounted for 14% of all attendance in an accident and emergency department [2]. In the recent decade, the growing orthopaedic biomechanics techniques have enhanced a better understanding of injury mechanism, and the subsequent research in sports injury prevention and management [3]. This paper summarizes the current understanding in acute ankle ligementous sprain injury in sports, which facilitates the future research on ankle sprain prevention. Literature search of MEDLINE (from 1966) and PubMed (from 1950) was conducted in May 2008. The search keyword string was "ankle AND (injury OR injuries OR sprain)", which appeared in the title, abstract or keyword fields. The title and abstract of each entry was read to identify and exclude unrelated articles. Articles not written in English were also excluded. The information of the papers was summarized into the sub-topics in this article in the following paragraphs to form the current understanding on acute ankle ligamentous sprain injury in sports.

Sports participation and sports injury

All around the world, medical doctors and sports scientists were actively promoting regular physical exercises to gain health benefits and to prevent cardiovascular related disease [4]. People nowadays are more eager in participating in sports and exercises for personal interest, leisure, relaxation, health and fitness purposes. In Hong Kong, according to the annual survey of sports participation conducted by the Hong Kong Sports Institute [5], people in general were becoming more active in sports participation from 1996 to 2001. The increasing trend was found in youngster and elderly [6] as well as working population [7]. The increasing sports participation was also reflected by the number of participants in the annual marathon race. There were only 1,000 participants in the first marathon race in 1997. The number of participants increased every year, and reached 10,000 in 2001. The number of participants kept increasing in recent years and has dramatically increased to 50,000 in 2008 [8]. Most of the participants were recreational athletes, indicating a mass participation of sports among the population.

However, in contrary to the promotion of the health benefits from sports participation, sports often cause injuries [9]. A study in Sweden [10] reported that 17% of the 3,341 acute visits to a clinic due to accidents in a one-year prospective study were from sports. It was comparable to home accident (26%), work accident (19%) and was much higher than traffic accident (7%). In United Kingdom, there were 7.1% of the 2,432 new patients attending accident and emergency department in a 10-day period sustained trauma from sports [11]. In North Ireland, for adolescent of age 11–18 who actively participated in sports, as much as 51% of the attendees sustained sports injuries [12]. When the sports participation rate became high, the exposure to potential injury increased and thus the high incidence of sport injury [13].

Problem and outcome of sports injury

Sports injuries resulted in pain [14], loss of playing or working time [15], as well as medical expenditure [16]. Severe ankle injuries also occasionally resulted in bone fractures [17], functional instability [18], decreased muscle strength [19], inferior proprioception [20], limited mobility [21], disability [22], permanent cease or retirement of sports participation [23]. Without adequate treatment and rehabilitation, sports injuries may also cause significant susceptibility in developing osteoarthritis [24] and other kinds of permanent sequalae [25]. For world-class and commercial sports teams, absence of key players due to unexpected injuries may result in defeats in major games and huge economic loss.

Prevalence and patterns of ankle sprain injury

Previous studies reported that injury to the knee was the most common and injury to the ankle the next [9,26]. Ankle was the most common injured body site in 24 of 70 included sports [1]. Ankle ligament sprain were also reported to be the most common injury for college athletics in the United States [27]. In Hong Kong, a survey on 2,293 patients attending a sports injury clinic reported that the knee (27.3–50.5%) and the ankle (16.8–24.7%) were the most common sites of injury in soccer, basketball, volleyball and long-distance running sports [9]. In marathon racing, another study on 580 runners in a marathon race reported that 33.9% of the injuries were to the knee and 20.9% were to the ankle [28]. Among ankle injuries, ankle sprain injury accounts for more than 80%, and is also the most common single type of sport-related trauma among all body sites and types [29-31]. Among ankle sprain injuries, 77% were lateral sprains [22] and 73% involved isolated rupture or tear to the anterior talofibular ligament [32,33]. A local survey conducted on 380 athletes with 563 sprained ankles reported that the majority of these injured athletes were pursuing running and jogging activities (25%), racquet sports (20%), ball games (19%) and soccer (14%) [34]. The residual problem included pain (30.2%), instability (20.4%), crepitus (18.3%), weakness (16.5%), stiffness (14.6%) and swelling (13.9%).

Ankle anatomy and biomechanics

In human anatomy, the ankle joint is where the foot and the leg segments meet. It comprises of three major articulations: the talocrural joint, the subtalar joint, and the distal tibiofibular syndesmosis [18]. The talocrural joint is also termed the tibiotalar joint or the mortise joint, and is formed by the articulation of the dome of talus, the tibial plafond, the medial malleolus and the lateral malleolus. This joint, in isolation, behaves rather like a hinge joint that allows mainly plantarflexion and dorsiflexion. The fibula extends further to the lateral malleous than the tibia does to the medial malleolus, thus creating a block to eversion [35]. Such body feature mainly allows larger range of inversion than eversion, thus, inversion sprains are more common than eversion ones [36].

The talocrural joint is supported by several main ligaments, namely the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL) and the posterior talofibular ligament (PTFL) at the lateral aspect, and the deltoid ligament in the medial aspect of the ankle [37]. Among the lateral ligaments, the ATFL is the weakest as it has the lowest ultimate load, approximately 138.9N, which is about half of that of PTFL, that is, 261.2N, and one-third of that of CFL, that is, 345.7N [38]. These values were obtained from mechanical test on ligaments of fresh human ankles. ATFL is approximately 20–25 mm long, 7–10 mm wide and 2 mm thick [39,40]. It originates from the anterior-inferior border of the fibular and inserts to the neck of the talus [30]. It prevents anterior displacement and internal rotation of the talus, especially when the talocrural joint is plantarflexed [41-43]. Due to its low ultimate load and the anatomical positions of origins and insertions, the ATFL is most commonly injured in a lateral ankle sprain [30].

The subtalar joint is formed by the articulation between the bottom of the talus and the calcaneus [18]. It consists of two separate joint cavities. First, the anterior subtalar joint, or also termed the talocalcaneonavicular joint, is formed from the head of the talus, the anterior-superior facets, the sustentaculum tali of the calcaneus, and the concave proximal surface of the tarsal navicular [44]. Second, the posterior subtalar joint is formed between the inferior posterior facet of the talus and the superior posterior facet of the calcaneus [45]. The anterior and posterior subtalar joints behave like a single ball-and-socket joint and share a common oblique axis of rotation [46], which averages a 42-degree upward tilt and a 23-degree medial angulation from the perpendicular axes of the foot [47]. This articulation allows inversion and eversion, or supination and pronation as described as a triplanar motion [36]. The subtalar joint is supported by three groups of ligaments, namely the deep ligaments, the peripheral ligaments, and the retinacula [48]. Together these ligament groups stabilize the subtalar joint and form a barrier between the anterior and posterior joint capsules [18].

The distal tibiofibular syndesmosis is formed by the articulation between the distal tibia and fibula [49]. The joint is mainly stabilized by a thick interosseous membrane, with the anterior and posterior inferior tibiofibular ligaments, to form the stable roof for the mortise of the talocrural joint [18]. This joint allows limited translation and rotation during talocrural dorsiflexion and plantarflexion to accommodate the asymmetric talus while maintaining congruency [50]. Injury to this ligament group is rare, and is often termed ankle syndesmosis injury [49], syndesmotic ankle sprain [51], or high ankle sprain [52].

Risk factors for ankle sprain injury

Risk factors were commonly classified as extrinsic or intrinsic [53]. Extrinsic risk factors are those that come from outside of the body, while intrinsic factors are those from within the body. In 1997, Barker, Beynnon and Renstrom [54] did a comprehensive review on the ankle injury risk factors in sports as reported by about 20 prospective studies. For extrinsic factors, although they found some discrepancies among the included studies, they generally reported that the prescription of orthosis, but not high-top shoes, could help decreasing the risk of sustaining ankle sprain injury in players with previous sprain history. Increased exercise intensity in soccer raised the injury risk, but the player positions in soccer and basketball did not cause any difference.

For intrinsic factors, they reported that a previous sprain history, a foot size with increased width, an increased ankle eversion to inversion strength, plantarflexion strength and ratio between dorsiflexion and plantarflexion strength, and limb dominance could increase the ankle sprain injury risk. The foot type, indication of ankle instability, and high general joint laxity were identified not to be risk factors. In 2002, Beynnon, Murphy and Alosa [55] conducted another comprehensive literature review and reported a consensus that gender, general joint laxity and foot type were not risk factors for ankle sprain injury. In 2007, Morrison and Kaminski [56] suggested that the cavovarus deformity, increased foot width, and increased calcaneal eversion range of motion were related to the occurrence of lateral ankle sprain injury. However, significant discrepancies were found with regard to whether or not height, weight, limb dominance, ankle joint laxity, anatomical alignment, muscle strength, muscle reaction time, and postural sway are risk factors for ankle sprain injury.

Some recent studies reported that players with a history of ankle sprain, players wearing shoes with air cells in the heel, and players who did not stretch before exercising were 4.9, 4.3 and 2.6 times more likely to sustain an ankle sprain injury [57]. People with inferior single leg balance [58] and overweight [59] were 2.4 and 3.9 times more likely to have sprain injury respectively. Reduced ankle dorsiflexion range [60], the use of artificial turf for soccer [61] and having a posteriorly positioned fibula [62] were also reported as risk factors. In 2005, Willems and coworkers [63] investigated some dynamic risk factors during gait in related to ankle sprain injury. They reported that for subjects who were at risk of sustaining an inversion sprain, a laterally situated center of plantar pressure was found at initial contact during the stance phase. The same research group also reported the intrinsic risk factors for inversion ankle sprain for male and female.

For male, a slower running speed, less cardiorespiratory endurance, less balance ability, decreased dorsiflexion muscle strength, decreased dorsiflexion range of motion, less coordination ability, and faster reaction of the tibialis anterior and gastrocnemius muscles were the significant risk factors [64]. For female, a less accurate passive joint inversion position sense, a higher extension range of motion at the first metatarsophalangeal joint, and a less coordination of postural control were the major risk factors [65]. However, we have to be aware that these risk factors are only some correlations with ankle ligament sprain injury. They may not be the direct cause, or the aetiology of ankle ligament sprain.

Aetiology of ankle supination sprain injury

Fuller [66] suggested that most ankle sprain injuries were caused by an increased supination moment at subtalar joint, which was often a result of the position and the magnitude of the vertically projected ground reaction force at initial foot contact. If the center of plantar pressure deviated medially to the subtalar joint axis, a greater moment arm along the subtalar joint axis was achieved and thus the subsequent increased supination moment to initiate sudden explosive ankle supination. Wright and coworkers [67] conducted a computational forward dynamic simulation study and reported that increased touch down plantarflexion caused increased ankle sprain occurrences. When a foot was plantarflexed during touch down, the contact to the ground was made with the forefoot, thus increased the moment arm among the subtalar joint axis and also the resultant joint torque to cause sudden explosive twisting motion and ankle sprain injury. Therefore, foot positioning during touch down was identified as an aetiology of ankle sprain injury. This also supported the suggestion that ankle taping or bracing corrected ankle joint positioning at landing rather than provided mechanical support to the ankle joint [68-70].

Another aetiology of ankle sprain injury is the delayed reaction time of the peroneal muscles at the lateral aspect of the ankle. Ashton-Miller and coworkers [69] suggested that an ankle sprain injury occured in 40 milliseconds (ms), as the vertical ground reaction force peaked at about 40 ms when landing from a jump [69]. At the lateral aspect of the human ankle, the peroneal muscles, including the peroneal longus and peroneal brevis, function to initiate ankle pronation which opposes the ankle supination motion [70]. Numerous research groups reported the reaction time of the peroneal muscles to be 50 ms or more. For instance, in sudden inversion tests with healthy subjects in an initial standing position, the peroneal muscle reaction time was reported to be 57–58 ms [71], 57–60 ms [72], 58 ms [73], 65–69 ms [74], 67–69 ms [75] and 69 ms [76]. For patients with ankle instability, the peroneal reaction time is longer – it was reported to be 82–84 ms [77] and 85 ms [78]. In a sudden inversion in a dynamic walking trial, the reaction time is also longer, as reported to be about 74 ms [72]. After the reflex response, the eversion torque was generated at 135 ms [79] and the subsequent active eversion was achieved at about 176 ms [80]. Therefore, it is postulated that the human reflex response is not fast enough to accommodate the sudden explosive motion in a sprain injury.

Mechanism and biomechanics of ankle supination sprain injury

Understanding the injury mechanism is very important for the research of injury prevention [81,82]. In ankle supination sprain, there is ankle inversion plus an internal twisting of the foot [83], and plantarflexion with the subtalar joint adducting and inverting [84]. Sometimes there is also an external rotation of the lower leg in respect to the ankle joint [85]. Stormont and coworkers [86] suggested that most ankle sprains occurred during systematic loading and unloading, but not while the ankle was fully loaded due to articular restraints. When the foot is in plantarflexion, the anterior talofibular ligament is often injured; when the foot is in dorsiflexion, the calcaneofibular ligament is often injured [39]. In soccer, most ankle sprains were sustained during player contact (59%), but during non-contact situations for goalkeepers (79%) [32]. In a recent study to analyze the ankle supination sprain injury with video, Andersen and coworkers [87] reported that there were two major mechanisms: (1) impact by opponent on the medial aspect of the leg just before or at foot strike, resulting in a laterally directed force causing the player to land with the ankle in a vulnerable inverted position; (2) forced plantar flexion when the injured player hit the opponent's foot when attempting to shoot or clear the ball. Most of these mechanisms finally led to the rupture of the anterior talofibular ligament, as this ligament often sustained higher strain and strain rate values than the other ligaments at the lateral ankle [88].

The biomechanics of ankle supination sprain injury was seldom reported in the literature, as it is practically impossible and also unethical to conduct systematic dynamic ankle sprain test in the laboratory. Previous mechanism study only reported qualitative information. For quantitative evaluation, different research groups managed to conduct cadaver study to understand the ankle biomechanics during simulated spraining tests. In static cadaver study, Markolf, Schmalzried and Ferkel reported that a 41–45 Nm external rotatory torque would cause ankle failure [89], as defined by a major drop-off of the torque as the foot continued to rotate, indicating a bony fracture or ligamentous rupture. In dynamic cadaver study, Self, Harris and Greenwald [88] studied the ankle biomechanics during a drop test with cadaver ankles, to simulate the scenario in landing technique in sports [90]. For systematically evaluation, Wright and coworkers [67,91] conducted a computational forward dynamic simulation study to investigate the ankle biomechanics during landing on irregular surfaces. Yet there was only one quantitative investigation on the ankle biomechanics during a real ankle sprain injury scenario being reported [92]. An accidental supination sprain injury was analyzed, where the ankle sprain injury occurred in a laboratory under a high-speed video capturing setting. It reported that the ankle joint reached an inversion of 48 degrees and an internal rotation of 10 degrees.

Diagnosis of acute ankle sprain injury

It is not uncommon for primary care physicians to misdiagnose various ankle problems as simple ankle sprains [93], and thus it is important to have a good differential diagnosis system for every acute ankle sprain injury (Table 1). Lynam [94] presented a protocol for the nurse to assess acute foot and ankle sprain at the emergency room, while Harmon [36] presented a systematic approach that consists of five steps to avoid missing potentially serious injuries: (1) palpation of bony structures, (2) palpation of ligamentous structures, (3) assessment of range of motion of the ankle, (4) testing of ankle muscles, and (5) special tests. Firstly, the diagnosis of fracture injuries was important as these patients normally have to be admitted to wards for emergency operative treatments [95]. Ankle fracture injuries were commonly diagnosed with the use of radiography [96], or the Ottawa Ankle Rules [97] which had a nearly 100% sensitivity [98,99] – it could significantly reduce the routine use of radiography [100,101]. Secondly, palpating ligamentous structures gave an idea that which ligament is probably injured. This can also be done together with the range of motion test, especially in voluntary dorsiflexion and plantaflexion. By doing the range of motion test, the physician could at the same time examine the ankle muscles.

Table 1. Summary of assessments for ankle injury

When fracture is ruled out, specific special tests should be performed in order to correctly diagnose if the problem is a ligamentous injury. The anterior drawer test and the talar tilt test were the two common tests to assess the integrity of the anterior talofibular ligament, and could be useful in diagnosing the grading of the tear of the ligament [39,102]. To test the medial ligament, mainly the deltoid ligament at the medial aspect of the ankle, the eversion stress test was commonly performed [103]. This could be tested by the external rotation test and the squeeze test [49]. Sometimes these specific tests are performed together with radiography, that is, the stress radiography test [96]. There were also some other devices and techniques to assist the diagnosis: magnetic resonance imaging [104], arthrography [105], sonography [106], three-dimensional computed tomography [107], bone scintography [99], and arthroscopic diagnosis [108].

Beside ligamentous injuries, the problem could be a tendon rupture. The rupture of the Achilles tendon at the rear ankle could be examined by Thompson test [109], where the calf of the patient was squeezed with knee flexed. If the foot moved with the plantar flexion maneuver, the Achilles tendon was at least partially intact. Peroneal tendon rupture was less sensitive to the physical examination such as subluxation test and stress radiographic assessment, and may sometimes require tendonscopy [110] or surgical exploration [111,112] to confirm the diagnosis.

Grading systems for evaluating acute ankle ligamentous sprain

There were numerous grading systems to grade an acute ankle ligamentous sprain injury [113], as summarized in Table 2. The two most basic systems were the Anatomic System which grades the injury in three grades accordingly to the ligaments that have been damaged, and the American Medical Association Standard Nomenclature System which considers the severity of the injury to the ligaments [114]. There were also some three-grade systems that grade the injury according to combined clinical presentation from the anatomical damage, severity of injury, and associated injuries of the surrounding structures [115-117]. Davis and Trevino [118] presented a staging system which consisted of four grades with some sub-grading to grade an ankle injury accordingly to the pathology, that was the damage to the ligamentous structure, and also the instability as presented clinically. Mann and coworkers [113] devised a practical system for outpatient clinical use. It was based on three items – pain, swelling and inability to walk. Each item was rated with 0 to 3 points (0 = none, 1 = mild, 2 = moderate, 3 = severe), and a total score was summed up for the final grading: Grade I: 1–3 points, Grade II: 4–6 points, Grade III: 7–9 points.

Table 2. Summary of grading scales to classify ankle sprain injury.

For dynamic functional evaluation, Kaikkonen, Kannus and Jarvinen [119] devised a performance test protocol with scoring scale, which consisted of three questions on subjective assessment, two clinical measurements on the ankle, two muscle strength tests, one ankle functional stability test and one balancing test, for evaluating ankle injuries. The total score correlated very well with the isokinetic strength test of the ankle, the subjective opinion about the recovery, and also the subjective function assessment, and thus the protocol was practical for clinical evaluation of ankle sprain injury. de Bie and coworkers [120] derived an ankle functional scoring system which evaluated the pain, instability, weight bearing, swelling and gait pattern and added up to a score of 100. Clanton [114] devised another system that related to the treatment protocols requested. The system consisted of two main classes which categorized the injured ankle as a stable or unstable one. The stable group was suggested to receive symptomatic treatment for pain relief. For the unstable category, another sub-category classified the patient to be non-athletes or older patients, and young active athletes. Non-athletes and older patients were suggested to receive functional treatment. For the young active athletes group, there was one more layer to divide the patients to be with negative stress radiograph findings, with positive tibio-talar stress radiograph findings, and with subtalar instability. Those with positive tibio-talar instability were suggested to consider operative surgical repair of the ligament complex.

Management of acute ankle ligamentous sprain

When an acute ankle ligamentous sprain happened, it was often the team physician to give immediate on-field care to the injured athletes [121]. The aim was to remove the injured athlete from the field and protect the athlete from further injury, instead of to diagnose the injury immediately, as the accuracy of an on-field diagnosis was reported to be inadequate [122]. Table 3 shows the details of some common treatments. Most commonly, the RICE (Rest, Ice-cooling, Compression, Elevation) treatment was delivered to the patients both on-field [123] and at the accident and emergency department [124,125]. Cryotherapy, or ice-cooling, may help in reducing pain in the first week after the injury [126], however, compression and elevation could only decrease ankle swelling temporarily and the effect lasted for less than five minutes after the limb was returned to a gravity-dependent position [127], and may even lead to discomfort and the need for analgesia after the application of the double Tubigrip compression bandage [128].

Table 3. Summary of the treatment Methods for ankle sprain injury.

In five days after the initial injury, the sensitivity of physical examination to ankle injury improved gradually after the pain and swelling had diminished [129]. Appropriate treatments could be delivered accordingly to the diagnosis of the injured ankle. There was a general consensus to conservatively treat grade I and II ankle ligamentous injuries with functional exercises [130-132]. Trevino, Davis and Hecht [133] and Mattacola and Dwyer [134] presented some functional treatment protocols to manage ankle ligament injuries, which consisted of various modalities such as flexibility exercises, strength and balancing training, ankle joint proprioception and muscular strength training, isometric and isotonic strength training, and even exercises in water. Kerkhoffs and coworkers [135] conducted a systematic review and reported that functional exercises were more effective than immobilization in terms of return to sports, return to work, reduce persistent swelling, restore ankle stability, restore range of motion, and patient satisfaction.

The effect of other conservative treatments was reported by different research groups. Boyce, Quigley and Campbell [136] reported that the use of an Aircast ankle brace produced significant improvement in ankle joint function in 10 days and one month compared with an elastic support bandage. Madras and Barr [137] reported that ankle disk training on wobble board were effective in enhancing single leg balance and reducing recurrent sprain injury, while Osborne and coworkers [138] and Sheth and coworkers [139] reported the effect of ankle disk training in enhancing peroneal muscle reaction time. De Simoni and coworkers [140] suggested that a 12-week prescription of orthosis was effective in improving functional stability at the ankle joint. Recently, Christakou, Zervas and Lavallee [141] suggested that imagery may be effective in improving muscle endurance in the rehabilitation of grade II ankle sprain.

For grade III ankle sprain, the treatment was still controversial [131]. Some surgeons recommended surgical repair [142], and some favored non-operative conservative treatment [143]. In 2000, Pijnenburg and coworkers [144] conducted a meta-analysis and suggested that primary operative repair of lateral ankle ligaments led to better results concerning recurrent giving way and pain on activity when compared with conservative treatment. However, in 2002, the same research group [145] conducted another systematic review which concluded that there was still insufficient information to recommend surgery over conservative treatment, or vice versa. Lynch and Renstrom [130] commented that surgical treatment to ankle lateral complex may induce some serious, though infrequent complications. Functional conservative treatment was free of complications, and did not produce late symptoms than surgical repair and casting, therefore, there was a growing consensus to treat grade III sprains firstly with conservative functional treatment. If such treatment failed to enhance ankle function after a considerable period of time, surgical repair could be performed. Karlsson and Sancone [146] suggested that immobilization should never be used, not even in severe ankle sprain injury, as it may result in joint stiffness, muscle atrophy, and loss of proprioception.

For syndesmosis ligamentous sprains, the common treatment was to prescribe a walking boot for four to six weeks [147]. The walking boot provided resistance to avoid the distal tibia and fibula to separate apart – a motion that imposed stress on the interosseous tibiofibular ligament between the distal tibia and fibula. The prescription lasted for four to six weeks for the interosseous tibiafibular ligament to heal.

Lastly, traditional Chinese medicine methods, such as herbs, massage and acupuncture, were well applied in China or managing sports injuries. They were treated as a kind of effective alternative method, especially in treating ankle ligamentous sprain injury. The effect was already widely reported in the Chinese literature, and also in numerous studies in the English literature, on its analgesic effect to relieve pain [148], reduce swelling [149] and edema [150], restoring normal ankle function [151,152].

Sequela of ankle ligamentous sprain

Injuries to the lateral ligament of the ankle often led to ankle instability [153]. Previous studies reported that 74% of the patients who suffered from an inversion ankle sprain injury had persisting symptoms 1.5–4 years after the injury [154], in which 10–30% of patients may have chronic symptoms such as persistent synovitis or tendinitis, ankle stiffness, swelling, pain, muscle weakness and frequent giving-way [130]. Yeung and colleagues [34] conducted an epidemiology study and reported that for ankles sprained 1–4 times, the major residual problem was pain (24–28%), while for ankle sprained five times or more, instability problems arose and became the major sequela (38%). Chronic ankle instability was commonly divided into mechanical ankle instability and functional ankle instability [85,155]. Mechanical ankle instability referred to abnormal laxity of the ligementous restraints, while functional ankle instability referred to normal ligamentous restraint but abnormal function with recurrent episodes of ankle giving-way [130]. Hubbard and Hertel [156] suggested that mechanical ankle instability may lead to functional ankle instability, however, Birmingham and coworkers [157] reported that functional ankle instability could exist in the absence of mechanical ankle instability.

Chronic ankle instability could be diagnosed by various methods, including imaging [158], arthroscopic diagnosis [159], and some functional scoring system such as the Foot and Ankle Disability Index [160], Ankle Activity Score [161], and the Cumberland Ankle Instability Tool [162]. It could lead to a delayed peroneal muscle reaction time [163], an inferior ankle kinesthesia and joint position sense [164], inferior proprioception and evertor strength [19]. In dynamic motions, it caused significant ankle biomechanics changes in gait [165-167], in single leg drop jump [168], in hopping [169], in cutting maneuver [170], and in figure-of-eight running and side hopping [171]. Beside chronic ankle instability, injuries to the lateral ligament of the ankle may also occasionally lead to ankle osteoarthritis [172], sinus tarsi syndrome and subtalar joint instability [173], and osteochondral defect at the talar dome [174].

Prevention of sport-related ankle sprain injury

Garrick and Requa [175] were the first research group to attempt to prevent ankle sprain injury. They reported that high-top shoe and prophylactic ankle taping were effective in reducing the ankle sprain injury rate among a group of 2,562 basketball players during a one year study period. In 1987, van Mechelen, Hlobil and Kemper [176] proposed a "sequence of injury prevention" which described how sport injury-related studies came together to form the research framework. The first step was to identify the extent of the sports injury problem by epidemiology studies. The second step established the aetiology and mechanism of injuries and the third step designed and introduced preventive measures. Finally, the effectiveness of the preventive measures was assessed by repeating the original epidemiology study (step one). From that time, numerous studies had been conducted to evaluate different strategies for ankle sprain injury prevention. The strategies could be divided into prophylactic devices, functional training, technique training, change of game rules, and education. [177].

For prophylactic devices, most attempts were on taping, bracing, and orthosis. The similarity of these devices was to wrap the ankle joint from the foot segment to the shank segment. Some studies suggested that these devices provided a mechanical support to resist the ankle inversion moment [178,179], but some suggested that it instead improved the proprioception and joint position sense [180-182] and thus maintained a proper anatomical position during landing [68,183]. The effectiveness of these devices in reducing the ankle sprain injury rate was reported in numerous studies [70,184-186]. The role of shoe in ankle sprain prevention was less clear [186]. Barrett and Bilisko [187] suggested that high-top shoe limited extreme range of motion, reduced the external stress, and enhanced proprioception of the ankle joint, while Robbins, Waked and Rappel [182] argued that modern athletic footwear impaired proprioception. In a combination, Rovere and coworkers [188] suggested a low-top shoe with a laced ankle stabilizer was effective in reducing ankle sprain injury.

Most functional training protocols consisted of stability and postural control exercises [189]. For examples, wobble balance board or ankle disk were often used in stability training [190], and their effects was demonstrated in various studies [139,191,192]. Technique training was also prescribed by some research groups. For example, Stasinopoulos [193] devised a technical training program on take off and landing technique during attack and two man blocks for volleyball players which was effective in reducing ankle sprain occurrence. The aim was to coach the players to perform a quick and long final approach step and jump straight to avoid landing on the centre line under the net or on the feet of other players. Scase and coworkers [194] devised a program to coach a group of junior elite Australian football player with safe landing, falling, rolling, and recovery skills, to avoid the common injury mechanism which was to land badly. The program was evaluated to be successful in reducing the incidence of ankle sprain injury, especially landing-related injury.

Game rules also played significant contribute to the occurrence of injury. Andersen, Engebretsen and Bahr [195] reported that less than one-third of the injuries seen on video were called foul in a one-year prospective study on the Norwegian professional football league. They concluded that there may be a need for an improvement of the game rules to protect players from dangerous play. In volleyball, Reeser and coworkers [196] proposed a change of rule to make any centreline contact within the conflict zone between the attacker and blocker a fault, as they believed that the majority of ankle sprain injury in volleyball happened when the players collided near the net. In rugby, injuries were believed to have association with match speed and the impact forces during physical collision and tackles. Gabbett [197] introduced a limited interchange rule to the game, and found that the injury rate was significantly reduced in a one-year prospective study. It was suggested that the match speed and impact forces were reduced because the players got fatigued due to the limited interchange rule. Last but not the least, education to athletes was also important. In a three-day netball competition in New South Wales in Australia and 1995, Hume and Steele [198] reported that only 5.1% wore high-cut shoes even if this was advised before the competition. Furthermore, although players had been advised to seek immediate treatment when injured, 54.7% of players finished the game before seeking treatment. They suggested that compliance to advice from sports medicine specialists, together with the research into the effectiveness of different injury prevention strategies, were both important to the injury prevention and safety promotion in sports [199].

Conclusion

This paper summarizes the current understanding on acute ankle ligamentous sprain injury, which is the most common single type of sport-related trauma. As there is a global trend of mass participation in recreational sports, treating and preventing ankle sprain injury will become essential topics in sports medicine. Inadequate management to ankle sprain injury may lead to various sequelae and problems like functional instability and osteoarthritis. This article presents the ankle anatomy as the fundamentals, which is essential for understanding the injury and the subsequent research and improvement in treatment and prevention. Anterior talofibular ligament (ATFL) was the weakest ligament in the lateral ankle was most often getting injured in ligamentous sprain injury.

Risk factors, aetiology and mechanism of ankle sprain injury were presented from a summary of previous studies. Players with a history of ankle sprain, wearing shoes with air cells in the bell and players who did not stretch before exercising were 4.9, 4.3 and 2.6 times more likely to sprain their ankle. Foot positioning and the reaction time of the lateral peroneal muscles were identified as the aetiology of ankle sprain injury. While in ankle supination sprain, there was an ankle inversion plus internal twisting of the foot, plantarlfexion with the subtalar joint adducting and inverting, and sometimes external rotation of the lower leg. A 41–45 Nm external rotatory torque would cause ankle failure. For examining the injury, diagnostic techniques and grading systems are introduced.

Ankle fractures were commonly diagnosed with radiography or the Ottawa Ankle Rules. Anterior drawer test and talar tilt test were commonly used to identify ligamentous injury, while Thompson test, tendonscopy and radio graphic assessment were used to examine tendon rupture. Different grading system classify different injury level by the severity of injury to the ligaments, combined clinical presentation, the instability of ankle, and some consider multiple discipline with a scoring scale. The management, sequela and some suggestions of preventive strategies to be implemented are introduced. RICE treatment was commonly applied on-field, while Cryotherapy, ice-cooling were used in the first week after injury. Several functional treatment, braces and traditional Chinese medicine methods were usually applied after five days of injury. This review allows the reader to catch up with the previous researches on ankle sprain injury, and facilitate the future research idea on sport-related ankle sprain injury.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

DTPF conducted the revise and drafted the manuscript. YYC and KMM assisted in compiling the data and summary. PSHY interpreted the findings and critically revised the manuscript. KMC conceived and coordinated the study. All authors read and approved the final manuscript.
Acknowledgements

This study was made possible by equipment/resources donated by The Hong Kong Jockey Club Charities Trust.

© 2009 Fong 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.

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by EricT

Patellofemoral pain syndrome (PFPS): a systematic review of anatomy and potential risk factors

Gregory R Waryasz¹ and Ann Y McDermott²

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Dynamic Medicine 2008

Patellofemoral Pain Syndrome (PFPS), a common cause of anterior knee pain, is successfully treated in over 2/3 of patients through rehabilitation protocols designed to reduce pain and return function to the individual. Applying preventive medicine strategies, the majority of cases of PFPS may be avoided if a pre-diagnosis can be made by clinician or certified athletic trainer testing the current researched potential risk factors during a Preparticipation Screening Evaluation (PPSE). We provide a detailed and comprehensive review of the soft tissue, arterial system, and innervation to the patellofemoral joint in order to supply the clinician with the knowledge required to assess the anatomy and make recommendations to patients identified as potentially at risk. The purpose of this article is to review knee anatomy and the literature regarding potential risk factors associated with patellofemoral pain syndrome and prehabilitation strategies. A comprehensive review of knee anatomy will present the relationships of arterial collateralization, innervations, and soft tissue alignment to the possible multifactoral mechanism involved in PFPS, while attempting to advocate future use of different treatments aimed at non-soft tissue causes of PFPS.

A systematic database search of English language PubMed, SportDiscus, Ovid MEDLINE, Web of Science, LexisNexis, and EBM reviews, plus hand searching the reference lists of these retrieved articles was performed to determine possible risk factors for patellofemoral pain syndrome.

Positive potential risk factors identified included: weakness in functional testing; gastrocnemius, hamstring, quadriceps or iliotibial band tightness; generalized ligamentous laxity; deficient hamstring or quadriceps strength; hip musculature weakness; an excessive quadriceps (Q) angle; patellar compression or tilting; and an abnormal VMO/VL reflex timing. An evidence-based medicine model was utilized to report evaluation criteria to determine the at-risk individuals, then a defined prehabilitation program was proposed that begins with a dynamic warm-up followed by stretches, power and multi-joint exercises, and culminates with isolation exercises. The prehabilitation program is performed at lower intensity level ranges and can be conducted 3 days per week in conjunction with general strength training. Based on an objective one repetition maximum (1RM) test which determines the amount an individual can lift in good form through a full range of motion, prehabilitation exercises are performed at 50–60% intensity.

To reduce the likelihood of developing PFPS, any individual, especially those with positive potential risk factors, can perform the proposed prehabilitation program.

Background

Patellofemoral Pain Syndrome (PFPS) is a term for a variety of pathologies or anatomical abnormalities leading to a type of anterior knee pain [1]. Knowledge of the anatomy of the patellofemoral (PF) joint is essential to developing an understanding of the pathogenesis of PFPS. The symptom of anterior knee pain is associated with the conditions listed in Table 1. Pain may be caused by increased subcondral bone stress attributed to the stress of articulation or from cartilaginous lesions on the patella or distal femur [2-4]. Nearly 10% of all sports injury clinic visits by physically active individuals are attributed to PFPS [5], with more than 2/3 of patients being successfully treated through rehabilitation protocols [6-8].

Table 1. Common Pathologies Leading to Anterior Knee Pain (AKP)*

• Based on research presented by S. Dixit 2007, P. Brukner 2002, R.H. Miller 1998, J.P. Fulkerson 2000, W.E. Prentice 2001, T.A. Peters 2000, R. Khaund 2005, A. Haim 2006

Physical training including sport-specific cardiovascular training, plyometrics, sport cord drills, strength and flexibility training has been found in adolescent female soccer players to significantly reduce lower body injury incidence from 33.7% to 14.3%, allowing athletes to be game-ready [9]. Injuries cannot be prevented entirely, however practitioners can attempt to avoid some types and keep more severe injuries to a minimum [9]. Also, participating with injuries due to insufficient recovery time increases the risk of new injury [10]. Concern over the long term consequences of anterior knee pain in adolescence and young adulthood includes a predisposition to patellofemoral osteoarthritis in later life [11]. The goal of sports medicine should be to keep athletes and patients healthy, pain free, and able to enjoy their sport and physical activity for years to come.

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Physical rehabilitation programs to treat anterior knee pain have proven to be a highly effective non-operative option [6-8]. Results have ranged from an 82% success rate in decreasing the severity of symptoms in athletes with chondromalacia patella [7], to an 87% initial success rate for a combination physical therapy and NSAIDs intervention, with 68% maintaining improvements for a mean of 16 months post-rehabilitation [8]. In treating chronic patellofemoral pain syndrome, continuous rehabilitation conducted over seven years had a 67% success rate of complete subjective and functional recovery [6]. These high rehabilitation success rates for anterior knee pain due to either cartilaginous injury or anatomical abnormalities suggest the potential for the prevention of a majority of anterior knee pain using a prehabilitation approach.

PFPS is a condition of both malalignment and muscular dysfunction [1]. Unlike a surgical distal realignment procedure [12,13], rehabilitation exercises can restore PF joint homeostasis although the anatomical malalignment of PFPS may not be corrected [1]. In comparison, prehabilitation aims to optimize function and pain measures before a stressful event [14]. Because the symptoms of anterior knee pain are brought on by overuse stress [15], PFPS is an ideal condition for prehabilitation. It should be noted that the shape and size of the patella and trochlear groove are limiting factors in the outcome of a rehabilitation program [16], and therefore would likely limit the outcome of a prehabilitation program. Based on anatomical, functional, and biomechanical parameters known to occur in symptomatic athletes before overuse resulted in pain, prehabilitation involves a pre-diagnosis in asymptomatic individuals. The Preparticipation Screening Evaluation (PPSE) offers an opportune time to make a pre-diagnosis and initiate a prehabilitation protocol [17].

Anatomy of the Patellofemoral Region

The patella (Figure 1), the largest sesamoid bone in the human body [18], functions to improve flexion efficiency and to protect the tibiofemoral joint [18]. The combination of the quadriceps tendon, lateral retinaculum, medial retinaculum, and the patella tendon help stabilize the patella [19]. Because the patella is not completely engaged in the patellar groove during the first 0–30 degrees of flexion, instability and the potential for subluxation/dislocation injury increases if patellar stabilizers are weak or malaligned [19].

Figure 1. Cadaver Patellofemoral Computed Tomography Scan. P- Patella; LR- Lateral Retinaculum; MR- Medial Retinaculum; LFC- Lateral femoral condyle; MFC- Medial femoral condyle.

Arterial System

Arterial blood flow to the knee is accomplished by an intricate system of anastomoses between five major arteries: superior medial and lateral, the middle (posterior), and the inferior medial and lateral genicular arteries [20]. An anastomosis occurs between the anterior tibial recurrent artery and the descending genicular arteries [20]. The genicular arteries except for the middle genicular artery make a contribution to the circumpatellar anastomosis [20]. The cirumpatellar anastomosis extends into the superficial and deep structures of the bone, synovium, capsule, retinaculum, and subcutaneous fascia [20]. The arterial supply to the patella arises from the circumpatellar anastomosis [20].

Arising from the popliteal artery, the medial superior genicular artery lies anterior to the semimembranous and semitendinosus muscles, and the lateral superior genicular artery will then anastomose with the descending branch of the lateral collateral femoral artery to supply the vastus lateralis, vastus intermedius, and branches of the femoral nerve [20]. The middle genicular artery passes anterior to the joint line and into the posterior joint capsule to supply the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL) [20,21].

The medial inferior and lateral genicular arteries arise from the popliteal artery distal to the posterior joint line and proceed to the deep collateral ligaments [21]. The medial inferior genicular artery provides blood supply to the tibial (medial) collateral ligament, anastomoses with the saphenous branch of the descending genicular branch, and anastomoses with the anterior tibial recurrent artery [20]. The lateral inferior genicular artery forms an anastomosis with the anterior tibial recurrent artery and supplies the fibular (lateral) collateral ligament at the joint line [20].

Gross arterial anatomy is similar between adults and children, however on a microscopic level, there are childhood differences in blood supply to the epiphyseal plate [20]. The pathology of PFPS may be related to decreased pulsatile blood flow in skeletally mature individuals [22]. Tissue ischemia resulting from mechanical forces that reduce genicular arterial flow during passive flexion from 20 to 90 degrees may be a cause or consequence of the pain associated with PFPS [22]. Surgical disruption of the genicular arterial system has not been reported to cause permanent vascular abnormalities to the patella, because the arterial supply appears able to revascularize the patella adequately after a surgical insult during ligamentous reconstruction procedures involving the knee [23]. Such surgical disruption can occur during a lateral retinculum release of the patella [23], a common surgical procedure for the alleviation of PFPS pain. If ischemia is an issue in the pathogenesis of PFPS, an arteriogram or other sophisticated test may detect defects in the collateral flow that could warrant the use surgical or medical revascularization to treat PFPS.

Quadriceps Force Vector

The quadriceps force vector (Figure 2) includes forces from the fiber orientation of the vastus lateralis (VL), vastus intermedius (VI), rectus femoris (RF), and the vastus medialis (VM). The vastus lateralis is composed of two force vector components, the vastus lateralis longus (VLL) and vastus lateralis obliquus (VLO) [19]. The vastus medialis is composed of two force vector components, the vastus medialis longus (VML) and vastus medialis obliquus (VMO) [19]. In the coronal plane, the quadriceps force vector angles are made by the VLO at 35 degrees and the VLL at 14 degrees laterally, by the VI and RF at 0 deg, and medially by VMO at 47 degrees and VML at 15 degrees. Overall the quadriceps force has a posterior pull sagitally to keep the patella in proper articulation with the trochlear groove [19].

Figure 2. Quadriceps-Patellar Force Diagram.
VMO- Vastus medialis obliquus;
VML- Vastus medialis longus;
RF- Rectus femoris;
VI- Vastus intermedius;
VLL- Vastus lateralis longus;
VLO- Vastus lateralis obliquus;
P- Patella; TT- Tibial Tubercle;
T- Tibia; MR- Medial retinaculum;
LR- Lateral retinaculum.

The lateral retinaculum is two layers; the superficial oblique retinaculum and a deep transverse retinaculum. The superficial oblique retinaculum is the culmination of the interdigitating of the patellar tendon, the VL group, and the iliotibial (IT) band [16,21,24-26]. The IT band originates from the tensor fascia lata and the gluteus maximus [21], with its attachment on the lateral epicondyle of the femur [12] and Gerdy's Tubercle on the anterior promixal tibia [12,21].

The deep transverse retinaculum consists of three structures; the epicondylopatellar band or lateral patellofemoral ligament, the midportion, and the patellotibial band [26]. The epicondylopatellar band provides superolateral support, the midportion provides lateral support, and the patellotibial band provides inferolateral support to the patella [16,21,24-26]. The midportion originates from the IT band and attaches to the lateral patella [26].

The lateral retinaculum is often released arthroscopically to alleviate its lateral displacement force [27]. To avoid complications, the procedure involves an incision through the superficial oblique retinaculum and deep transverse retinaculum without violating the joint capsule [26].

The medial retinaculum is much thinner than the lateral retinaculum and consists of three ligaments beneath the retinaculum; the medial patellofemoral ligament (MPFL), medial patellomeniscal ligament (MPML), and medial patellotibial ligament (MPTL). The MPFL merges with the VMO forming the primary restrictive mechanism for excessive lateral patella deviation, especially during lower degrees of knee flexion approaching full extension [16], the time when the patella is at greater risk of dislocation/subluxation [19]. Acute lateral patellar dislocation can occur if the MPFL is torn away from the femur or if the VMO muscle is torn from the adductor magnus tendon [28]. There is controversy as to validity of the VMO as being anatomically distinct and functionally separate from the VML [29]. The VM muscle group is both a knee extensor and patellar stabilizer dependent on the task performed [30]. The MPML and MPTL are thought to be less important in PF joint stability than the MPFL [16,19,31,32].

A cadaveric study demonstrated that static medial stability contributions were 50% from the MPFL, 24% from the MPML, 13% from the MPTL, and 13% from the medial retinaculum [33]. Due to the interdigitation with the VMO, the MPFL contributes over 50% against lateral dislocation as it assists to maintain the patella in the trochlear groove during the initial 20–30 degrees of flexion [33].

Sensory Receptors

The patellofemoral joint contains a variety of sensory receptors not distinct to this specific joint including: bare nerve endings, Pacinian corpuscles, Ruffini endings, Golgi receptors, and muscle spindles [34]. The major sensory nerves supplying the knee joint are the posterior articular (PAN), lateral articular (LAN), medial articular (MAN), intramuscular, and muscle nerves [34]. PAN is a branch of the tibial nerve that supplies the posterior cruciate ligament, anterior cruciate ligament, posterior oblique ligament, insertion of the annular ligament at the mediolateral menisci, posterior fat pad, posterior capsule, fibular collateral ligament, and the tibial collateral ligament [34]. LAN is a branch of the common peroneal nerve that inconsistently innervates the tibiofibular joint capsule and the lateral knee tissues. MAN is a branch of the saphenous nerve that supplies the anterior and medial capsule, medial meniscus, tibial collateral ligrament, posterior capsule, patellar fat pad, and patellar tendon [34]. The intramuscular and muscle nerves include the golgi tendon organs and muscle spindles supplied by branches of the femoral, obturator, or sciatic nerve depending on the location of the myotome [21,34,35].

The lateral patellar nerve innervates the patella at the lateral anterior border at the 11 o'clock position [36]. The medial patellar nerve innervates the patella at the medial anterior border at the 2 o'clock position. Both the medial and lateral patellar nerves are distal branches of the femoral nerve [36]. The medial based neurovascular bundle is the primary interosseous innervation to the patella [37]. The medial and central portions of the patella are densely interosseosly innervated in comparison to the lateral patella [37].

The innervation to the skin in the anterior region of the knee is from the lateral and anterior cutaneous branches of the femoral nerve and the infrapatellar branch of the saphenous nerve [21,35]. Posterior skin overlying the knee is supplied by the posterior cutaneous nerve, and cutaneous branches of the obturator nerve [21,35].

There is substance-P in the soft tissue supports of the patella including the fat pad, retinaculum, and periosteum, which is evidence for the soft tissue role in anterior knee pain [38]. Substance-P is involved in nociceptive input to the spinal cord and functionis as a vasodilator producing inflammation [38]. Woijtys (1990) observed that substance-P fibers may be denser in the lateral than the medial retinaculum, however the study did not specifically quantify the observation [38]. Substance-P fibers have also been found in the patellar marrow cavity in degenerative knees [38]. Identifying possible nerve defects or increased sensitivity to pain could alter treatment to include corticosteroid injections through regional nerve block techniques that are highly specific to the region of pain.

Methods

A systematic database search of PubMed, SportDiscus, Ovid MEDLINE, Web of Science, LexisNexis, and EBM reviews, plus hand searching the reference lists of these retrieved articles was performed to determine potential risk factors for patellofemoral pain syndrome. Key words searched were "patellofemoral pain syndrome", "patellofemoral", "anterior knee pain", "chondromalacia patella", "knee", and "patella". Articles were included based upon availability through the Tufts Hirsch Health Science Library and Interlibrary Loan. Selection criteria were based on a subject population with PFPS or a description of anterior knee pain not consistent with other pathologies listed in Table 1 and based on inclusion criteria presented in the article. Articles included were prospective cohorts, case-control, and case series. The articles included were limited to the English language and published between January 1984 and July 2007. Excluded from analysis were articles involving a treatment intervention.

Results

A total of 24 articles were included in Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors. There are 3 prospective cohorts [39-41], 17 case-controls [42-58], and 4 case series articles [59-62] included in Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors. Two articles were included that did not report P values [51,59]. Seven articles were included that did not have a patient population described specifically as PFPS [40,51,55,56,59,63,64], however the articles met the review inclusion criteria presented in the methods section. The articles were included to present the extent of research into the potential risk factors of PFPS that has been performed from January 1984 to July 2007.

Additional file 1. Review of Potential Patellofemoral Pain Syndrome Risk Factors. Comprehensive table of the articles discussed in the results section of the manuscript that review the potential risk factors for Patellofemoral Pain Syndrome. Format: DOC Size: 107KB

Electromyography (EMG) Measured Neuro-Motor Dysfunction

Using electromyography (EMG) to measure neuro-motor dysfunction in PFPS has been analyzed in 5 studies. All 5 studies have determined that when comparing PFPS subjects to controls, there is significant neuro-motor dysfunction in PFPS. Thomee (1996) demonstrated that the vastus medialis muscle was less active on EMG in PFPS patients, while the rectus femoris was equally active to healthy controls while standing [45]. Cowan (2001) and Cowan (2002) determined that during activities of daily living there was a difference in EMG onset in PFPS compared to controls [42,43]. Witvrouw (2000) found VMO/VL reflex response time to be a significant finding in PFPS [39]. The VMO/VL reflex response time was determined by electromyography unit with skin electrodes over the VL and VMO muscle bellies. Readings were taken using the patellar tendon reflex with the test performed 10 times per knee [39]. The VMO/VL muscles responded faster in the PFPS group compared to the controls [39]. Although not statistically significant, the group noticed that the VMO fired earlier compared to the VL in the control group [39], which would equate to an earlier activation of the medial force vector preventing lateral patella displacement. The authors concluded that an altered VMO/VL response time was a risk factor for PFPS [39]. The authors found no statistical difference when the VL response time was subtracted from the VMO response time (VMO-VL) between the PFPS group and the control group [39]. Crossley (2004) states that although the magnitude differences measured by EMG may be small, but statistically significant detecting these differences may influence treatment [44].

Foot Abnormalities

The characteristics of genu varum, genu valgum, pes cavus, and pes planus have not been found to contribute to PFPS [39,48] or other related conditions [15,47,65]. Arch index was determined in one study to be significantly lower for only a discriminant analysis of anterior knee pain not specifically classified as PFPS [63]. The arch index was calculated by forming three equal foot sections (forefoot, midfoot, and rearfoot), then dividing the midfoot area by the total footprint area and serves as a marker that the anterior knee pain group had a higher arched foot (cavus) which may produce greater pressures during running on the PF joint [63]. Other literature does suggest an increased risk of running injuries may be due to genu varum, genu valgum, and foot postural abnormalities, including excessive pronation, valgus ankles, and lowered foot arches [12,66-68]. Additional research is needed to clarify the validity of these characteristics as potential risk factors for PFPS.

Functional Testing

Functional testing may show that PFPS patients have lower strength capacity [39] as demonstrated by decreased vertical jump performance [39,46], anteromedial lunge [49], step-down [49], single-leg press [49], and balance and reach tests [49]. No difference was appreciated between the PFPS patients and controls for Flamingo balance, standing broad jump, bent arm hang, shuttle run, plate tapping, arm pull, leg lifts, sit and reach, sit ups, and maximal oxygen uptake[39]. No research has definitively suggested that PFPS is due to the lower strength capacity or rather a result of lower strength capacity. For this reason, functional testing deficits are a potential risk factor until proven otherwise.

Gastrocnemius Tightness

Gastrocnemius and soleus tightness reduces the amount of dorsiflexion leading to excessive subtalar joint pronation and tibial internal rotation which will cause femoral internal rotation to increase the Q angle [50]. Therefore, one mechanism to PFPS pathogenesis is by increasing Q angle and increased PF joint stresses [50]. Gastrocnemius tightness was significant in two studies comparing PFPS patients to controls [39,50], but was not significant in another study comparing anterior knee pain subjects to controls [63].

Generalized Ligamentous/Joint Laxity

Generalized ligamentous laxity is proposed to increase the total patellar mobility which would alter patellar tracking and lead to symptoms [64]. Generalized ligamentous laxity was significantly increased in PFPS patients in two out of three studies. Al-Rawi (1997) found significant generalized ligamentous laxity in chondromalacie patella knees [64]. Witvrouw (2000) was only able to find significance in the thumb-forearm mobility exam, the rest of the exam was not significant [39]. Fairbank (1984) found the relationship between knee pain and generalized ligamentous laxity not to be significant [51].

Hamstring Strength

The mechanism behind hamstring strength and pathogenesis of PFPS is not well understood, however overall lower body strength is recommended for a runner's exercise program [63] and the hamstrings are involved in power activities such as the vertical jump [69]. Hamstring strength was examined in one study and determined that running athletes with a "syndrome complex" have an 81% absolute strength deficiency at 60 degrees per second and 73% had a deficiency at 240 degrees per second when using a Cybex dynamometer [59]. "Syndrome complex" refers to pain in the anterior aspect of the knee in the soft tissues or around the patellar tendon, pain upon running, mild retropatellar pain upon compression with minimal crepitus, and no clinical evidence of patellar subluxability, chondromalacia, plica, increased Q angle, or increased foot pronation [59]. The data however was not presented as a research article, and no P values were reported [59].

Hamstring Tightness

Hamstring tightness has been theorized to either cause slight knee flexion during activities or to necessitate higher quadriceps forces to overcome the passive resistance of the hamstring, both of which may increase PF joint reaction forces [50]. Hamstring tightness was evaluated in four articles [39,40,50,59]. Two of the four articles found hamstring tightness in anterior knee pain/PFPS athletes [40,50], one study found no significance [39], and one study stated that 23% of "syndrome complex" athletes had appreciable hamstring tightness [59].

Hip Musculature Weakness

The iliopsoas muscle, a hip flexor and secondary femoral external rotator, if weak de-stabilizes the pelvis [70,71]. The individual then compensates by developing an anterior pelvic tilt with an internally rotated femur [70,71], the Q angle is then increased, leading to increased PF joint stresses [50]. For the small number of patients who show asymmetrical hip rotation with diminished medial rotation and excessive lateral rotation, a program designed to create a balance in internal and external rotation hip strength is required [72]. A strong VMO with weak hip adductors results in the adductor magnus tendon being drawn to the patella; therefore, strong hip adductors serve as a stable origin for VMO contraction [73].

Two of three studies evaluating hip musculature found weakness [52,53]. Hip abductor strength was determined to be significantly decreased in both studies when comparing PFPS patients to control subjects [52,53]. Piva (2005) found hip external rotation strength and hip abduction strength not be significant [50].

Balanced hip strength is very important for PFPS prevention, as the IT band originates from the lateral hip musculature [12] and the VMO has a relationship to the adductor magnus tendon [28]. A 6-week treatment program designed to improve hip flexion, adduction, and abduction strengths in patients with PFPS (n = 35) led to a combination of improved hip flexion strength with a normalized Ober Test and Thomas Test in 93% of successfully treated PFPS cases defined by a decrease in VAS pain score [74].

Iliotibial (IT) Band Tightness

IT band tightness through anatomical correlations to the lateral retinaculum and patella will increase the lateral force vector on the patella during flexion to increase the lateral PF joint stresses [54,75]. Iliotibial band tightness was found in PFPS athletes in three articles evaluating the IT band [54,59,60]. An early study Kibler (1987) reported 67% of running athletes with "syndrome complex" had IT band tightness, although there was no P value reported [59]. Piva (2005) reported no tightness in the IT band/tensor fascia lata complex [50].

Quadriceps Angle (Q-Angle)

A greater Q angle is believed to change the location of contact and pressure in the PF joint, resulting in areas experiencing excessive stresses that are not physiologically manageable [63]. Huberti (1984) using cadaver knees and a special loading fixture found that both an increased and a decreased Q angle increased peak patellofemoral pressures [76]. These increased pressures may predispose an individual to degenerative pathological changes [76]. Increasing the Q angle is associated with increased lateral patellofemoral contact pressures and patellar dislocation, while decreasing the Q angle may not shift the patella medially, but rather increases the medial tibiofemoral contact pressure through increasing the varus orientation of the knee [77]. The effect of Q angle has been examined in a number of studies [39,47,48,55-57,63]. Three studies reported the Q-angle to be significantly increased in PFPS subjects against controls [48,55,57], while four studies reported no difference in Q angle [39,47,56,63].

Haim (2006) reported an abnormal Q angle of greater than 20 degrees was statistically associated with anterior knee pain [48]. Q angle has been believed to differ between males and females, however the slight difference of only 2.3 degrees appears to be related to height rather than pelvic dimensions [78]. Shorter statured individuals appear to have larger Q angles and therefore the slight difference between genders may be attributed to men being taller than women [78].

Quadriceps Tightness

Witvrouw (2000) states that the decreased quadriceps flexibility existed prior to developing the symptomatic syndrome, and therefore is not necessarily a result of PFPS [39]. Quadriceps tightness may cause high patellofemoral stresses that predispose individuals to developing symptoms [39,79]. The presence of quadriceps tightness was reported in all five studies that evaluated quadriceps tightness [39,40,50,59,63]. While Kibler (1987) reported 61% of "syndrome complex" patients had rectus femoris tightness, no P value was reported [59].

Quadriceps Weakness

Quadriceps weakness, specifically VMO weakness in comparison to the VL, can lead to lateral displacement of the patella causing the articulating pressure to be on the lateral facet [16,19]. The quadriceps force vector (Figure 2) explains how an imbalance in strength can lead to improper patella alignment as a weak VMO cannot adequately support medial patellar stability [16,19]. A total of six studies evaluated quadriceps weakness on anterior knee pain/PFPS. Two studies reported quadriceps weakness was a non-significant finding [41,57]. Three studies found weakness to be a significant finding [46,58,62]. Kibler (1987) reported that 39% of "syndrome complex" athletes had appreciable quadriceps weakness (no P value reported) [59].

Patellar Compression/Crepitus

Patellar compression/crepitus was examined in two studies [48,61]. Testing using the patellar tracking test was determined to be 56% sensitive and 55% specific as confirmed by arthroscopy [61]. The patellar tracking test is performed by compressing the patella in the trochlear groove while moving the patella up and down, with pain during the test indicating a positive result for chondromalacia [61]. Haim (2006) found patellofemoral crepitation significantly associated with reduced mobility in PFPS patients [48]. Crepitus alone may be a non-specific finding [75], and therefore may not be useful as a potential risk factor based on the current research.

Patellar Mediolateral Glide/Mobility

While two studies reported reduced patellar mobility in PFPS patients [48,60], Witvrouw (2000) reported that medial, lateral, and total patellar mobility were greater in PFPS, however the findings were not significant [39]. After assessment of the research of patellar glide/mobility as a risk for PFPS, data appears to be inconclusive at the current time.

Patellar Tilting

Excess patellar tilting laterally can lead to patellar medial hypomobility resulting in high stresses between the lateral facet of the patella and the lateral trochlea [75]. Excessive tightness of the lateral structures inhibits the patella from reentering the trochlear groove when the pathologic lateral tilt is in excess of 20 degrees when the knee is in extension as measured by CT scan [19]. Haim (2006) reported a positive patellar tilt was significant for PFPS subjects compared to controls with 92% specificity and 43% sensitivity [48].

Discussion

Recommendations for Pre-Diagnostic Physical Examination

A number of identifiable and diagnostically accurate risk factors exist that can be determined without radiographic imaging (Table 2) [75]. General visualization of the patellar movement through flexion extension may be helpful in detecting malalignment if there is a "J sign" [80,81] as result of lateral retinacular tightness or medial retinacular weakness. Decreased quadriceps flexibility, specifically rectus femoris tightness, can be assessed by using the Ely Test [82].

Decreased IT band flexibility is evaluated using the Ober Test [74,79]. Decreased hip flexor flexibility is assessed using the Thomas Test [74,83-85]. Weak hip abductors are evaluated using the Trendelenburg Test [86].

A Q angle measurement in excess of 20 degrees may increase PFPS risk [48], however studies have demonstrated slight differences in Q angle between PFPS and control at lower Q angle values [55,57].

Weak quadriceps or quadriceps atrophy can be determined visually or by using a tape-measure to check for asymmetry between sides. Quadriceps circumference is measured proximal to the patella. The diagnostic parameters have not been well-defined, as the level of atrophy may be minimal [58], however athletes should have near bilateral symmetry. Utilizing the quadriceps atrophy criteria may be left to the opinion of the clinician as to whether there is enough quadriceps tone or if the asymmetry warrants a prehabilitation program prescription.

Altered VMO muscle reflex time compared to VL is assessed by simultaneous VMO and VL palpation during knee extension. In normal patients, no timing difference between the contraction of the VMO and VL exists. In some patients, a marked delayed onset of VMO is evident on palpation [1]. Electromyography using skin electrodes over the VMO and VL could be used to more accurately ascertain the reflex time difference during an elicited patellar tendon reflex using a reflex hammer [39], however this may not be feasible financially for most clinicians.

Decreased vertical jump is assessed by direct measurement, preferably using a Vertec device, however the criteria for jump height, type of jump surface, and specific testing technique are not developed well enough for pre-diagnostic use. Rather, comparison with previous vertical jump testing and a decrease in performance may indicate decreased power production which may translates to an increased risk for developing PFPS [39]. Other functional tests can be performed (see Additional File 1: Review of Potential Patellofemoral Pain Syndrome Risk Factors), however the vertical jump test is a practical way to track athletic progress as a prehabilitation is initiated.

Generalized ligamentous laxity is determined by a variety of tests listed in Table 2. Having any generalized ligamentous laxity characteristics may be a positive indication for PFPS prehabilitation, as studies have showed a significant correlation with generalized ligamentous laxity tests and symptomatic PFPS [39,64,75].

A patellar tilt test can also show lateral retinacular tightness if the lateral patella cannot be raised to horizontal while compressing the medial patella posteriorly [39,80]. There is still the clinician's opinion as to whether or not the athlete has a hypomobile patella even if the criteria are not met. Other pre-diagnostic criteria may be developed or the current criteria altered as larger prospective PFPS studies are conducted and more information is learned. Radiographic measurements are more accurate, but cost effectiveness is a concern.

Proposed Prehabilitation Intervention

The prehabilitation program is derived from common practices in PFPS rehabilitation and from strength and conditioning trends designed to increase power output, create balanced strength, and reduce overuse injuries associated with symptomatic PFPS (Tables 3 and Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions). As with diagnosis, it is important to consider factors in a joint proximal and in a joint distal to the joint of interest. The program consists of a general dynamic warm-up, stretching (13 total), power exercises (1 total), multi-joint exercises (2 total), and isolation exercises (1 total) for each of the defined muscle groups.

Isolation exercises described have a major effect on a single muscle group, although have minor effects on other muscle groups as a true isolation is difficult to achieve during exercise. Athletes are encouraged to incorporate this program 3 days per week at rehabilitation intensity levels [light (50% intensity of 1 repetition maximum (1 RM)/heavy (60% intensity of 1 RM)/moderate (55% intensity of 1 RM)], as a supplement to general weight lifting and stretching activities. This intensity is in contrast to "heavy week" training in which the strength and conditioning professional or certified athletic trainer prescribed intensity levels reach up to or near a 1 RM.

A variety of general weight lifting programs are outlined by the National Strength and Conditioning Association (NSCA) [69] and should be the primary program of the athlete, with the PFPS prehabilitation program serving as additional, less intense exercises performed to develop symmetrical lower body strength and flexibility. The proposed program is based on a non-linear periodization model and can be made flexible based on athletic training demands. A 1 RM can be determined by a formal maximal weight lift if the athlete demonstrates proper form for a back squat and leg press. The athlete should not experience pain during the 1 RM lift. Other exercises listed in Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions require the athlete and fitness practitioner to determine an appropriate weight that pushes the athlete at a targeted rate of perceived exertion (Borg RPE scale) [87]. The 1 RM lift for exercises such as lunges, resistance band training, Romanian Dead Lift (RDL), and box jumps also involve RPE, rather than by actual maximal lift.

Additional file 2. Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions. Table of recommendations and instructions for exercises and stretches suggested to possibly prevent Patellofemoral Pain Syndrome. Format: DOC Size: 99KB

Once identified as "at risk for developing symptomatic PFPS", the athlete should 1) continually perform the prehabilitation program as long as the athlete wishes to remain physically active, with 2) periodic vertical jump testing to ensure there is no decrease in power production. Due to bone growth changing the lower leg moment of inertia in children [88], the prehabilitation program may not be necessary or appropriate for anterior knee pain prevention in skeletally immature individuals.

Dynamic and static methods of stretching increase both ROM and flexibility for injury prevention, and are both incorporated in rehabilitation [89]. Dynamic stretching is performed during the general dynamic warm-up (Table 3) taught by the certified athletic trainer or strength and conditioning specialist [69]. Dynamic stretching involves controlled movements that gradually increase in speed and range of motion, mimicking the athletic activity to follow so as to increase muscle memory [69]. This is in contrast to ballistic stretching which uses the momentum of a moving limb in a spring-like manner, attempting to force it beyond its normal range of motion [69]. The dynamic warm-up does not include any ballistic stretching, as ballistic stretching has been associated with injury [69]. Static stretching and Active Isolated Stretching (AIS) are performed after the dynamic warm-up [69,90]. Stretching the IT Band, hamstrings, quadriceps, hip adductors, hip abductors, hip external rotators, hip internal rotators, quadriceps, gastrocnemius/soleus, and hip flexors is prescribed for PFPS rehabilitation and therefore is appropriate for prehabilitation [16,74,79,89,91,92].

Power exercises, such as the power clean, snatch, or push jerk, can increase power production if the athlete has the proper instruction and equipment available [69]. The power clean is an Olympic style lift that involves a quick and forceful lift of a bar off the ground to the final position in front of the shoulders through one movement [69]. The snatch is an Olympic style lift that involves quickly and forcefully lifting a bar off the floor to an overhead position in one uninterrupted motion, ending with the elbows in full extension [69]. The push jerk involves rapidly moving the bar from the shoulders to an overhead position using an explosive extension of the hips and knees to accelerate the bar to its final overhead position ending with elbows extended. [69]. Due to the potential for injury from improperly performing Olympic lifting exercises, the box jump and resisted squat jump are included in the supplemental program to improve power output [69]. It is recommended these exercises be performed on an Olympic-style platform with hard-soled shoes, preferably Olympic-style weight lifting shoes.

Rehabilitation protocols have determined that both closed kinetic chain (CKC) and open kinetic chain (OKC) do not create supraphysiologic stresses and are advantageous to the individual with PFPS [28,91,93]. Lower body CKC exercises involve many muscle groups, are typically weight bearing and involve the foot remaining in a fixed position without movement. Examples include the back squat and leg press. CKC exercises are considered superior for athletic purposes [93] based on mimicking functional movements in sport and involving many muscle groups.

In comparison, lower body OKC exercises isolate a specific muscle, are typically non-weight bearing and involve free movement of the foot. Examples include straight leg raises and knee extensions. Both CKC and OKC are included in PFPS rehabilitation programs [91,92,94], with adjusted ranges of motion on traditional exercises (Additional File 2: Patellofemoral Pain Syndrome (PFPS) Exercises and Prescription Recommendations and Instructions).

VMO training is important to improve VL and VMO onset timing differences [95]. Retraining the vasti with eccentric exercises such as squats has been noted to improve PFPS rehabilitation outcomes [96]. VMO muscle isolation has been difficult to prove possible without the use of electrode stimulation [97], however it is generally believed that VMO activity is greater with the hip in external rotation [97]. Hip external rotators have been determined to be weaker in PFPS patients as diagnosed by the single-leg squat test, therefore loading in external rotation is beneficial [13], even if there is no added benefit to the VMO. Many protocols have successfully emphasized the use of a 10 o'clock and 2 o'clock (between 30–45 degrees) position of femoral external rotation [98].

The hip's external/internal rotation, flexion/extension, and abduction/adduction groups need to be both stretched and strengthened [74,79,89,91,99,100]. Isolation exercises for these groups, as well as multi-joint exercises that focus on eccentric loading and isometric contraction, are important [99].

Historically, patellar taping has been advocated in treating PFPS patients to increase VMO activity and decrease VL activity [101]. In asymptomatic individuals the data are limited and conflicting, with patellar taping noted to be effective [102] or detrimental [101], therefore the prehabilitation program does not promote use of patellar taping until supported by additional research.

Summary

In skeletally mature patients, anatomical abnormalities may be pre-diagnosed during the Preparticipation Screening Evaluation (PPSE) by using the evidence-based criteria for potential PFPS risk factors. The clinician with a proper knowledge of the neurovascular, bony, and muscular anatomy has the knowledge to appropriately assess malalignment of the PF joint and therefore perform a screening physical examination for PFPS based on potential risk factors. The anatomy section also serves as a reference point to 1) explain exactly how anatomical deviations can potentiate PFPS pathogenesis and 2) stimulate thought about other possible therapies, including addressing vascular insufficiency and neuropathic pain.

In an effort to prevent the onset of debilitating knee pain, a positive finding in any pre-diagnostic category or asymptomatic PFPS that concerns the physician results in prophylactic treatment prescribing a prehabilitation exercise protocol based upon proven, successful rehabilitation techniques that create balanced lower body strength, increased flexibility, and increased power production. As more research is conducted on PFPS risk factors and potential risk factors, the pre-diagnostic criteria should be updated and changes made to the supplemental prehabilitation program. By conducting prospective cohort studies in healthy individuals, research could determine whether the risk factors listed in this article serve to initiate or contribute to PFPS, or rather result from PFPS development. The proposed supplemental prehabilitation program offers a safe and effective means to develop balanced lower body strength and flexibility in any individual and should be considered along with a more intense strength training program as necessary for injury prevention and performance enhancement. The proposed program is to be understood as an example of a possible program, other programs can be made that accomplish a similar task of attempting to prevent PFPS. Practitioners are encouraged to alter the program to make it more specific to the athlete and utilize available resources.

Abbreviations

AIS: Active isolated stretch; Deg: degree(s); MR: Manual resistance; RDL: Romanian dead lift; Yd: Yard

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

GRW conceptualized the idea of the pre-diagnostic criteria, prehabilitation exercise protocol, and was the principal author of the manuscript, AYM was responsible for significant reviewing and assistance with the writing and final formatting of the article.

Acknowledgements

The authors would like to acknowledge Dr. Stanley Jacobson, PhD of the Tufts University School of Medicine, Department of Anatomy and Cellular Biology for the Cadaver Patellofemoral Computed Tomography Scan and the VolView cadaver image.

© 2008 Waryasz and McDermott; 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.

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© 1999-2010 BioMed Central Ltd unless otherwise stated. Part of Springer Scien

by EricT

Ho-Joong Jung¹, Matthew B Fisher² and Savio L-Y Woo³

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Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology 2009

Ligaments and tendons are soft connective tissues which serve essential roles for biomechanical function of the musculoskeletal system by stabilizing and guiding the motion of diarthrodial joints. Nevertheless, these tissues are frequently injured due to repetition and overuse as well as quick cutting motions that involve acceleration and deceleration. These injuries often upset this balance between mobility and stability of the joint which causes damage to other soft tissues manifested as pain and other morbidity, such as osteoarthritis.

The healing of ligament and tendon injuries varies from tissue to tissue. Tendinopathies are ubiquitous and can take up to 12 months for the pain to subside before one could return to normal activity. A ruptured medial collateral ligament (MCL) can generally heal spontaneously; however, its remodeling process takes years and its biomechanical properties remain inferior when compared to the normal MCL. It is also known that a midsubstance anterior cruciate ligament (ACL) tear has limited healing capability, and reconstruction by soft tissue grafts has been regularly performed to regain knee function. However, long term follow-up studies have revealed that 20–25% of patients experience unsatisfactory results. Thus, a better understanding of the function of ligaments and tendons, together with knowledge on their healing potential, may help investigators to develop novel strategies to accelerate and improve the healing process of ligaments and tendons.

With thousands of new papers published in the last ten years that involve biomechanics of ligaments and tendons, there is an increasing appreciation of this subject area. Such attention has positively impacted clinical practice. On the other hand, biomechanical data are complex in nature, and there is a danger of misinterpreting them. Thus, in these review, we will provide the readers with a brief overview of ligaments and tendons and refer them to appropriate methodologies used to obtain their biomechanical properties. Specifically, we hope the reader will pay attention to how the properties of these tissues can be altered due to various experimental and biologic factors. Following this background material, we will present how biomechanics can be applied to gain an understanding of the mechanisms as well as clinical management of various ligament and tendon ailments. To conclude, new technology, including imaging and robotics as well as functional tissue engineering, that could form novel treatment strategies to enhance healing of ligament and tendon are presented.

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Introduction

Ligaments and tendons are soft connective tissues which transmit forces from bone to bone and muscle to bone, respectively. These unique tissues serve essential roles for biomechanical function of the musculoskeletal system by stabilizing and guiding the motion of diarthrodial joints. To accomplish this, ligaments and tendons have a hierarchy of highly aligned collagen composed of fibrils, fascicles, fibers, and the tissue itself, to form one of the strongest tissues in the body. Nevertheless, these tissues are frequently injured due to repetition and overuse, eccentric activities, and quick cutting motions that involve acceleration and deceleration. These injuries often upset this balance between mobility and stability of the joint which results in abnormal loading that could damage other soft tissues in and around the joint manifested as pain and other morbidity, such as osteoarthritis [1-6].

The numbers on incidence of ligament and tendon injuries are huge. For example, it is estimated that tendinopathy accounts for 30% to 50% of all injuries related to sports, plus over 48% in occupational maladies [6-8]. Achilles tendinopathy accounts for 7–11% of all running injuries [9-11]. Similarly, the incidence of knee ligament ruptures, primarily involving the anterior cruciate ligament (ACL) and the medial collateral ligament (MCL), is estimated to be 2 per 1,000 people per year in the general population [12,13]. In the shoulder, injuries to the ligaments and capsule results in approximately 34,000 dislocations occur per year in the young adult population [14,15], and rotator cuff tears in more than 30% of people over 60 years of age [16,17].

The healing of ligament and tendon injuries, if it takes place, is usually slow. Tendinopathies, including tendinosis, tendonitis, and paratenonitis, are ubiquitous, occurring in the Achilles, patellar, quadriceps, hamstrings, and rotator cuff tendons as well as in the elbow, wrist and hand joints. These detrimental injuries can take up to 12 months for the pain to subside before one could return to physical and sports activity [6]. Further, although a ruptured MCL can generally heal spontaneously and sufficiently well such that nonsurgical management has become the treatment of choice [18-25], its remodeling process takes years, and its mechanical properties remain inferior to those for the normal MCL [18,23,24,26-30]. It is also known that a midsubstance ACL tear has limited healing capability [20,31-33] and reconstruction by replacement grafts has been regularly performed in order to regain knee function [34-37].

Well over 100,000 of these procedures are done per year in the U.S. alone [13]. However, long term follow-up studies have revealed that 20–25% of patients experience unsatisfactory results at 7 to 10 years following ACL reconstruction [1-5]. Thus, it is clear that a better understanding of the function of ligaments and tendons, together with knowledge on their biology and healing potential, is needed for investigators to develop novel strategies to accelerate and improve the process of healing of ligaments and tendons. Well over 4000 new papers have been published in the last ten years that involve biomechanics of ligaments and tendons. As a result, orthopaedic surgeons and other health related professionals have an increasing appreciation of the importance of this subject area and have use for biomechanical findings to help their clinical practice. On the other hand, biomechanical data are complex in nature, and there is a danger of misinterpreting them. Thus, we wish to provide the readers with a brief overview of ligaments and tendons and point them to appropriate methodologies used to obtain the biomechanical properties of these soft tissues [38-43]. More importantly, how the properties of these tissues can be altered due to various experimental and biologic factors will be discussed [44-52]. Following this background material, we will present how biomechanics can be applied to gain an understanding of the mechanisms and management of various ligament and tendon injuries. Examples given will include tendinopathy, as well as MCL and ACL tears. To conclude, new technology, including imaging and robotics as well as functional tissue engineering, that could form novel treatment strategies to enhance ligament and tendon healing will be presented [53-61].

Basic biomechanics on ligaments and tendons

Definition of biomechanical properties

Because the primary function of ligaments and tendons is to transmit tensile forces, experimental studies of the biomechanical properties of these tissues are generally performed in uniaxial tension. Testing isolated ligament and tendon tissue is inherently difficult for several reasons (i.e., slipping of the specimen from the clamp, stress concentrations, shortness of substance of ligaments). As a result, tensile tests have been performed with the ligament or tendon insertions to bone left anatomically intact (e.g., the entire bone-ligament-bone complex). From this test, a nonlinear (concave upwards) load-elongation curve for the bone-ligament-bone complex or muscle-tendon-bone complex can be obtained (Figure 1A). Parameters obtained from this curve, representing the structural properties of the complex, include stiffness, ultimate load, ultimate elongation, and energy absorbed at failure.

Figure 1. A: A representative load-elongation curve of the bone-ligament-bone or muscle-tendon-bone complex. B: A stress-strain curve representing the mechanical properties of a ligament or tendon substance.

From the same uniaxial tensile test, a stress-strain curve of the ligament or tendon substance (from which its mechanical properties are determined) can also be obtained. This is done by normalizing the tensile load by the cross-sectional area (i.e., stress) and by normalizing the change in elongation in a defined region of the tissue midsubstance by the initial length (i.e., strain) (Figure 1B). One assumption in this test is that of a uniform stress distribution throughout the specimen. By engineering standards, this requires an aspect ratio (ratio of length to width) of greater than 10 to 1. However, for biological tissues, a ratio of greater than 4 to 1 is generally accepted due to anatomical limitations. Parameters obtained from this curve, representing the mechanical properties, or quality, of the tissue substance include the tangent modulus, ultimate tensile stress (or tensile strength), ultimate strain, and strain energy density of the ligament or tendon substance.

Methods to determine stress and strain

As a specimen's cross-sectional area is required for stress calculations, methods to accurately measure it are important. However, the irregular, complex geometry presents challenges, and in some cases, can introduce very large errors. The literature has presented us with a long list of techniques [62-65]. In general, they can be divided into contact or noncontact approaches [42,66]. Contact methods include molding techniques, digital vernier calipers, and area micrometers [67]. We, as well as many others, have advocated the use of noncontact methods, so as not to disturb the natural shape of these soft tissues. These techniques include the shadow amplitude method [62], the profile method [64], and the use of a light source [63]. In our research center, laser micrometer systems have been developed to measure both the cross-sectional area and the shape of soft tissues with high accuracy and precision [42]. For those tissues that contain concavities, we have developed a more advanced laser reflectance system to accurately measure cross-sectional shape and area of these soft tissues [66].

Accurate experimental measurement of tissue strains also poses a number of hurdles. Methods, such as video tracking systems, have been developed to avoid possible errors of elongation from contribution of connecting structures [68-71]. Two or more reference markers are placed on the surface of the tendon or ligament substance, by means of Verhoeff's stain, elastin stain, or reflective tape, to serve as gauge lengths [23,50]. Then, a camera system could record the motion of the markers during tensile stretch, and the percentage strain of the tissue could be calculated [70]. Additionally, it must be noted that under tension, the strain along the ligaments and tendons can vary considerably. We have found that higher strains occur near the insertion sites [72]. To measure tissue elongation in-vivo, contact techniques such as the use of a differential variable reluctance transducer have been employed to obtain in-vivo strain of the ACL during physiologic motions [73].

The range of mechanical properties of various ligaments and tendons is very large as these tissues are designed specifically to function in different joints (Table 1) [67,74-85]. For the human MCL, the tangent modulus and the tensile strength were found to be 332.2 ± 58.3 MPa and 38.6 ± 4.8 MPa, respectively [74]. In comparison, values for the inferior glenohumeral ligament were found to be many folds lower than those for the MCL, ranging from 5 to 42 MPa and 1 to 6 MPa, respectively [83]. The large range of motion and flexibility of the glenohumeral joint dictate such lower values.

Additionally, since ligaments and tendons are highly organized fibrous tissues, their mechanical properties are directionally dependent (anisotropic). For example, the human MCL has mechanical properties that are 30 times higher along its longitudinal direction compared to its transverse direction [74].

Table 1. Mechanical properties of human ligaments and tendons

Determination of viscoelastic properties

Ligaments and tendons display time- and history-dependent viscoelastic properties that reflect the complex interactions between proteins (e.g. type I, III, V collagen, elastin), ground substance (e.g. proteoglycans and glycolipids), and water. The loading and unloading curves of these tissues do not follow the same path but instead form a hysteresis loop representing internal energy dissipation during each cycle. Additional important viscoelastic characteristics of ligaments and tendons are creep (i.e., an increase in deformation over time under a constant load) and stress relaxation (i.e., a decline in stress over time under a constant deformation). These viscoelastic behaviors for ligaments and tendons have important clinical significance as they help to prevent fatigue failure of ligaments and tendons. For example, during walking or jogging, cyclic stress relaxation occurs, in which the peak stress in the tissue substance decreases with each cycle [7,86].

Mathematical models have been made to describe the viscoelastic properties of ligaments and tendons. The quasi-linear viscoelastic (QLV) theory originally formulated by Fung (1972) has been modified and adopted to describe the viscoelastic properties of the normal and healing MCL and ACL [87-96]. For ligaments and tendons undergoing larger deformations, a single integral finite strain (SIFS) theory has been implemented and used for the patellar tendon and ACL [97]. The interested readers are referred to others research articles and reviews for a more in-depth treatment of this subject area [88-90].

Factors influencing tensile properties of ligaments and tendons

When tensile testing ligaments and tendons many factors can impact the outcome of their biomechanical properties. Those factors can be divided into 1) experimental factors, and 2) biological factors and can help the readers to identify why the findings on the same tissue can differ from study to study.

Specimen orientation during tensile testing, e.g. for the human femur-ACL-tibia complex (FATC), can alter its structural properties significantly because of its geometric complexity [48,98]. When tested in an anatomic orientation, by maintaining its natural insertion angles, the results became significantly differ from those tested in an orientation along the tibia [48]. For example, the ultimate load of specimens in the anatomic orientation was 35% higher than those in the tibial orientation in young donors.

Considerable attention has also been given to the effects of the strain rate on the mechanical properties of ligaments and tendons [98-100]. Using skeletally mature rabbits, we could demonstrate little rate sensitivity over a range of four and a half decades of strain rates [98,101]. Other environmental conditions, including temperature and hydration, however, were found to have significant influence on the mechanical properties of ligaments and tendons [49,102]. Finally, appropriate storage by freezing with the muscles and joint intact were found to have little or no significant differences on its biomechanical properties after one or two freeze-thaw cycles. It should be cautioned that special care still must be taken in tissue sample storage, especially relating to protecting tissue before and after freezing from a lack of hydration [50,103,104].

Age-related changes are one biological factor worth discussing. Skeletal maturity has been shown to play a major role in the biomechanical properties of tendons and ligaments, because of the development at their insertions. For New Zealand white rabbits, the structural properties of the femur-MCL-tibia complex (FMTC) increased dramatically with skeletal maturity. For example, the stiffness in the skeletally mature group (12–15 months of age) were 40% higher than skeletally immature animals (4–6 months of age). Similar results were obtained for the mechanical properties of the ligament substance, as up to 90% increases in modulus were observed with skeletal maturity [51,105].

All skeletally immature FMTCs failed by tibial avulsion; whereas, the majority of skeletally mature animals failed at the tissue substance indicating that there is an asynchronous maturation process between the bone-ligament-bone complex and ligament midsubstance [51] (Figure 2). Prior to skeletal maturity, the strength of the MCL substance reached near its peak value, while the bone-ligament junction, especially at the proximal tibial insertion site, was still maturing, causing failure by tibial avulsion. Once skeletal maturity was reached, the proximal tibial insertion site became stronger, and the FMTC failed in the ligament substance.

Figure 2. A schematic diagram depicting the relationship between failure mode and age, hypothesizing the asynchronous rates of maturation between the bone-ligament-bone complex and the ligament substance.

The properties of ligaments and tendons also can change with advancing age as well as with activity level [83,106,107]. For example, in the human FATC, the mean stiffness and ultimate load of younger specimens (22–41 years) was 1.3 and 3.3 times higher, respectively, than those obtained from older specimens (60–97 years) [48].

Ligaments and tendons are also known to remodel according to applied motion and stress. Studies using rabbit hind limbs have shown that a few weeks of immobilization can severely increase joint stiffness as well as significantly decrease the structural properties of the FMTC and the mechanical properties of the MCL tissue [47]. Remobilization could reverse these negative changes, but would require up to one year before these biomechanical properties could return to near normal levels [47]. On the other hand, exercise and training could only result in marginal increases in the biomechanical properties of ligaments (e.g. MCL of the knee) and tendons (e.g. extensor and flexor tendons of the hand) [45,52,109]. Based on these studies, a highly nonlinear curve could be drawn to represent the relationship between levels of stress and motion with the changes in properties for ligaments and tendons (Figure 3). Following immobilization, there would be a rapid reduction in tissue properties and mass from those for the normal range of physiological activities- as represented by the middle of the curve. In contrast, the positive gains following long-term exercise and training are much more moderate.

Figure 3. A schematic diagram describing the homeostatic responses of ligaments and tendons in response to different levels of stress and motion.

Biomechanics and tendinopathy

Tendinopathy, including tendinosis, tendonitis, and paratenonitis, is a work related and/or sports-induced ailment that involves severe discomfort and pain [9,110-115]. In general, tendons, after being subjected to repetitive loading of varying levels and for a prolonged period of time, could exhibit chronic pathology. Nevertheless, the etiology of tendinopathy is still unclear and hotly debated. Many years of research suggest that the problem is likely multifactorial [6,116-118]. Biomechanically, it is thought that microtrauma first occurs in the tendon, causing rupture of a small number of collagen fibrils while increasing the loading of the remainder [117-121]. The initial insult could be either due to one abnormal loading cycle of high (but subfailure) strain or a series of lower subfailure strains [70,110,122-129]. A number of in-vitro studies have shown that both loading regimens can induce such injury and the ensuing degeneration of tendons, is characterized by a reduction in their biomechanical properties [130-132].

A mechanism by which the trauma spreads to the remaining intact tendon until the symptoms of tendinopathy are presented has been suggested by a number of in-vitro experiments [110,116,119,128,133-136]. These studies have shown that high strains (or long duty cycles) applied by stretching bioreactors can cause tenocytes to produce abnormal levels of matrix metalloproteases (MMPs), which would in turn degrade the collagen and cause degeneration [131,137-144]. However, other studies have shown that loading protocols consisting of large strains were well-tolerated by tendon fibroblasts [6]. Whether these in-vitro strain levels simulate the physiological condition, and whether tensile loads that are within or slightly above the normal physiological range would cause any damage to the tendon fibroblasts are hotly debated [117]. Further, imaging studies of common sites of tendinopathy, e.g. for the supraspinatus tendon, patellar tendon, and Achilles tendon, were found to be in relatively lower levels of tensile strains than other parts of the tendon, suggesting that high tensile strains may not be the only major etiologic factor [116,145,146].

Recently, in-vitro studies have demonstrated that understimulation of tenocytes can also lead to altered MMP expression and apoptosis, followed by tendon degeneration [147-152]. Others hypothesized that it is the compressive loading that leads to altered cellular morphology and degenerative changes [116,120,153-156]. Additionally, internal shear forces and heat have been postulated to be causes of intratendinous degeneration [6]. New finite element models of tendons may be useful tools to predict the response of these various loads on tendon cells and the resulting changes in extracellular matrix [157]. The literature has also shown other etiological factors, such as age, and gender, in the development of tendinopathy. Interested readers are referred to the International Olympic Committee Medal Commission publication Tendinopathy in Athletes edited by Woo, Renström, and Arnoczky for additional details [6]. Overall, it is clear that tendinopathies are complex biomechanical and biochemical problems.

Management of tendinopathy

Clinical management of tendinopathies are frequently empirically-based, and as such, the recommended treatment strategies by different clinicians can vary greatly. Although excessive exercise may be a cause of tendinopathy, eccentric exercise has been shown to work well in a number of studies to treat tendinopathy [112,158,159]. More than 80% of patients were satisfied with the treatment and were able to return to previous activity levels [159-161]. Others have used traditional Chinese exercises, such as Tai Chi, to enhance body functions in promoting muscle performance, increasing flexibility and proprioception while weight bearing to stimulate bone and soft tissue [6]. These treatment strategies are supported by previous animal studies which have shown that moderate, prolonged exercise is effective and results in an increase in the cross-sectional area of swine extensor tendons as well as its mechanical properties, indicating improved tissue quality [109], as shown in Figure 3[162,163]. These changes contribute to the training-induced adaptation in mechanical properties, whereby exercise could improve tolerance toward strenuous exercise to avoid injury.

Additional modalities such as ultrasound, laser photostimulation, deep heat, pulsed magnetic and electromagnetic fields, and electrical stimulation are also used to treat tendinopathy [164-167]. Application of these modalities is intended to affect the stiffness of newly formed scar tissue inside the tendon. Yet other investigators use intratendinous injections of corticosteroids to relieve pain, but these injections may lead to negative effects on the mechanical properties [168-171].

When conservative treatment has failed, surgeons have used many techniques including needling, coblation, percutaneous tenotomy, arthroscopic debridement, percutaneous paratenon stripping, open tenotomy, paratenon stripping, and tendon grafting to treat tendinopathy [172]. In general, a return to sports after surgery has been reported in 60–85% of cases, although some have questioned these findings [173]. It has been suggested that first time ailments may require 2–3 months to recover but chronic cases may take 4–12 months [174]. As the physiologic, biomechanical, and biologic mechanisms of this ailment are not clearly understood, the general clinical advice remains that one must be patient as there is no "quick fix."

Biomechanics and ACL reconstruction

For the ACL, it is well known that there is limited capacity for healing after its injury [36,175-177]. Unlike extraarticular ligaments, there exist several well known factors that limit the ACL from healing [178,179]. The thin synovium surrounding the ACL, which has been shown to play an important role in providing a vascular supply to the relatively avascular ACL as well as to protect it from the harsh synovial fluid [180], is disrupted and not regenerated until 1 to 2 months following ACL injury [175,181-183]. Histological examination of the human ACL reveals that it is also retracted following rupture and that clots formed are insufficient to fill the open gap [175]. In addition, a number of studies have also documented that the intrinsic healing capacities, cellular proliferation, and extracellular matrix (ECM) production of the ACL are also lower compared to the MCL [24,178,179,181,184-188].

Most studies show unfavorable results after conservative treatment of an ACL rupture, particularly in patients with high levels of activity [189-193]. Overall success rate of conservative treatment for ACL has been about 30 to 50% [37,189,194,195]. Surgical replacements have been done for a large percentage of patients to help maintain knee stability [196-200]. Autografts, such as the bone-patellar tendon-bone (BPTB) and hamstring tendons, and allografts are the graft of choice. However, long-term follow-up studies (10+ years) of patients with ACL reconstruction showed 20–25% unsatisfactory results, with complaints such as knee pain and extension deficits [78,201-204], and most concerning, many of these cases had progressed to knee osteoarthritis [205-217]. Much effort is being made to improve the clinical outcome. Biomechanical studies can be used to lead to better understanding of the kinematics of the knee and the function of the intact ACL and ACL replacement grafts in order to improve surgical decision making.

Complex anatomy of the ACL and its role in knee function

In the human knee, the ACL can be represented by two bundles: the anteromedial (AM) and the posterolateral (PL) bundle. The anatomic division of these bundles is based on the gross tensioning pattern of the ACL during passive flexion-extension of the knee, with the AM bundle tauter in flexion and the PL bundle tauter in extension. With these two bundles, the ACL is well designed to stabilize the knee throughout knee flexion under various loading conditions.

To assess the function of the ACL under multiple degree of freedom (DOF) knee motion, our research center has developed a robotic/universal force moment sensor (UFS) testing system since 1993 (Figure 4) [218]. This novel testing system can control and reproduce the multiple DOF knee motion [38,40,41,219-221] and is also capable of applying external loads to knees. By operating in both force and position control modes, the robot can apply a pre-determined external load to the specimen, such as those used for the diagnosis of ACL deficiency [222-224], and the corresponding kinematics can be obtained. For example, an 134-N anterior tibial load can be applied to simulate the Lachman and anterior drawer tests, or a combined 10 N·m of valgus torque and 5 N·m of internal-external tibial torque can be applied to statically simulate the pivot-shift test. Then, the ACL can be transected. Subsequently, the specimen is moved along a previously recorded path of motion while the UFS records a new set of force and moment data [38]. Since the path of motion can be precisely repeated, the in-situ force in the ligament can be calculated by determining the changes in forces after cutting the ACL, based on the principle of superposition [41].

Figure 4. Schematic drawing illustrating a robotic/universal force-moment testing system and the six degrees of freedom of motion of the human knee joint (permission requested from [218]).

Most importantly, this advanced methodology has the advantage of collecting experimental data from the same cadaveric knee specimen under different experimental conditions (such as ACL intact, and ACL-reconstructed knee conditions), eliminating the effect of interspecimen variation. Thus, the robotic/UFS testing system has been used to quantitatively determine the data on motions of the intact, ligament deficient, and reconstructed knee with respect to the same reference position while the in-situ forces in ligaments and replacement grafts were calculated. As a result, the analysis of data through repeated-measures analysis of variance significantly increases the statistical power. To date, over 80 studies have been published using this technology, and it has been adopted by many laboratories around the world [225,226].

We have found that the two anatomical bundles of the ACL have different functions even under the simplest external loading conditions [220]. For instance, it has been found that under an anterior tibial load, the PL bundle carried a higher load than the AM bundle with the knee near extension, and the AM bundle carried a higher load with the knee flexion angle larger than 30 degrees. It was also found that when the knee was subjected to combined rotatory loads of valgus and internal tibial torques to statically simulate the pivot shift test, the AM and PL bundles almost evenly shared the load at 15 degrees of knee flexion. Thus, the fact that both bundles play significant roles in controlling knee stability is well illustrated.

Computational finite element models are also valuable for studying for the complex function of the ACL and its bundles. Once such models are validated with experimental data (e.g., knee kinematics or in-situ forces as determined using the robotic/UFS testing system [227,228]), they can be used to calculate the stress and strain distribution in the ACL, by incorporating its non-uniform geometry (in which the midsubstance cross-sectional area is one-third that of the insertions) and its twisting fiber orientation. For example, it could be shown that the peak stresses in the ACL were seen near the femoral insertion sites, suggesting this area could be susceptible to injury (Figure 5). These results are consistent with clinical reports in which most ACL tears occur near the femoral insertion site [229].

Figure 5. A) Finite element model of the knee joint and B) Cauchy stress distribution within the AM and PL bundles under a 134 N anterior tibial load with the knee at full extension (lateral view).

Choice of autograft

As the majority of autografts for ACL reconstruction procedures are either bone-patellar tendon-bone or hamstrings tendon autografts, it is of interest to compare their biomechanical effectiveness to restore knee stability. To accomplish this goal, human cadaveric knees were tested using the robotic/UFS testing system following ACL reconstruction using a hamstrings tendon graft or bone-patellar tendon-bone graft [54]. Due to this unique system, both reconstructions were performed in the same knees and could be quantitatively compared. When an anterior tibial load was applied, both reconstructions were found to be successful in limiting excessive anterior tibial translation, and the in-situ forces in the grafts were near those of the intact ACL from full extension to 90° of flexion. However, when a combined 10 N-m valgus and 5 N-m internal tibial torque was applied, both reconstructions were insufficient to reduce coupled anterior tibial translation. This insufficiency was further revealed by the significantly lower in-situ forces in the grafts, which ranged from 45% to 65% of that in the intact ACL. Thus, our data suggest better graft placement, i.e. the location of the femoral tunnel such that the graft could resist rotatory loads applied to knee, would be needed.

Femoral tunnel location

To investigate the effect of femoral tunnel location for ACL reconstruction grafts, a series of biomechanically based experiments have been performed in our research center [54,55,230]. First, we studied how well a bone-patellar tendon-bone autograft placed at the PL or AM insertion site in the femur (equivalent to the 10 and 11 o'clock positions in the frontal view) could restore knee function [231]. In response to an anterior tibial load, both the single PL-bundle and single AM-bundle reconstructions were able to restore anterior tibial translation to a level similar to that of the intact knee, except at deep knee flexion angles for the single PL-bundle reconstruction. Under combined rotatory loads, however, the single PL-bundle reconstruction could better restore the coupled anterior tibial translation and in-situ force in the graft to those of the intact knee at 15° and 30° of knee flexion. Thus, although the grafts are similarly effective under an anterior tibial load, the more laterally placed single PL-bundle reconstruction could more effectively resist rotatory loads, particularly when the knee is near full extension.

We then considered a double bundle reconstruction by replacing both the AM and PL bundles so that it would better approximate the anatomy of the ACL, and compared it to a single AM bundle reconstruction. The double bundle reconstruction could not only better restore knee kinematics and in-situ force under anterior tibial loading but also under the combined rotatory loading. Additionally, the in-situ force at 30° of flexion was 91% ± 35% of the intact ACL, compared to only 66% ± 40% for the single AM bundle reconstruction under the rotatory loads.

A similar study was also done to compare the anatomic double bundle reconstruction to a more laterally placed single PL bundle reconstruction [232]. In this case, in response to anterior tibial and combined rotatory loads, both reconstructions were able to restore anterior tibial translation and in-situ force in the ACL graft near those for the intact knee at flexion angles less than 90° of knee flexion. Moreover, there were no significant differences between the two reconstruction procedures at 15° and 30° of knee flexion under either loading condition (Figure 6, p < 0.05). Thus, to reproduce the complex function of the ACL throughout the range of knee flexion, reproducing both bundles of the ACL may have some biomechanical advantages. On the other hand, a more laterally placed reconstruction, such as the single PL bundle reconstruction, may also work well, especially with the knee near extension where the function of the ACL is most critical.

Figure 6. Anterior tibial translation (mean ± SD) in the intact, anterior cruciate ligament (ACL)-deficient, and anatomic double bundle and single posterolateral (PL) bundle ACL-reconstructed (ACL-R) knees in response to an anterior tibial load and combined rotational load at 15° of knee flexion. An asterisk indicates a statistically significant difference.

Biomechanics and ligament healing of the MCL

Laboratory research has discovered that the injured MCL of the knee can heal spontaneously [24]. Conservative treatment of an isolated MCL injury has produced better or similar results to those with surgical repair either with or without immobilization, in terms of restoring varus-valgus knee stability and its biomechanical properties [24,34]. Immobilization after ligament injury was shown to lead to a greater percentage of disorganized collagen fibrils, decreased structural properties of the FMTC, decreased mechanical properties of the ligament substance, and slower recovery of the resorbed insertion sites [47]. As a result, for the last twenty-five years the paradigm of clinical management of MCL tears has shifted from surgical repair with immobilization to functional management with early controlled motion [186,233].

The MCL has been an excellent experimental model to help understand the rate, quality, and composition of healing ligaments and tendons as well as treatment modalities [24,234]. It has brought better understanding of the continuous process of healing. Roughly, it can be divided into three overlapping phases [24,72]. The inflammatory phase is marked by hematoma formation which starts immediately after injury and lasts for a few weeks. It is followed by the reparative phase where fibroblasts proliferate and produce a matrix of proteoglycan and collagen, especially type III collagen, to bridge between the torn ends. Over the next 6 weeks, an increasingly organized ECM formation, predominantly type I collagen, and cellular proliferation occur. Finally, the remodeling phase, which is marked by alignment of collagen fibers and increased collagen matrix maturation, can continue for years [72].

These changes are reflected in the structural properties of the healing FMTC which are inferior to controls at 12 weeks after injury [24]. However, by 52 weeks post-injury the stiffness of the injured FMTC recovered, but the ultimate load remained lower than those for the sham-operated MCL [22,235,236]. This return to normal is largely due to an increase in the cross-sectional area of the healing ligament to as much as 2 1/2 times its normal size [237]. Thus, the recovery of the stiffness of the FMTC is largely the result of an increase in tissue quantity. On the other hand, the mechanical properties of the healing MCL midsubstance remain consistently inferior to those of the normal ligament and do not change with time up to one year [24,237] (Figure 7). This means the healing process involves a larger quantity of lesser quality ligamentous tissue.

Figure 7.Stress-strain curves representing the mechanical properties of the medial collateral ligament substance for sham-operated and healing MCLs at time periods of 6 (n = 6), 12 (n = 6), and 52 (n = 4) weeks.

Clinical management of combined ligamentous injuries to the knee is obviously more difficult and remains controversial [20,186,238,239]. In the case of a combined ACL/MCL injury, our research center has utilized basic science studies to elucidate suitable treatments. As a first step, it is important to understand the contribution of each ligament to knee stability. For example, under a valgus torque, there was a 123% increase in valgus rotation of the knee after the ACL was transected in contrast to only a 21% increase when the MCL was transected, when the knee was allowed to move freely in 5 DOF (varus-valgus and internal-external tibial rotation, proximal–distal, anteroposterior, and medial–lateral translations) [240]. The MCL was only found to be the "primary" restraint to valgus rotation when the knee joint was artificially restrained to 3 DOF, i.e. axial tibial rotation and anteroposterior translation. As a result, after a MCL injury, the functional deficit in valgus rotation can be compensated for by the remaining structures, especially the ACL.

In a combined ACL/MCL injury model in the rabbit, it was demonstrated that MCL repair combined with ACL reconstruction restored valgus laxity and improved the structural properties of the FMTC over those with ACL reconstruction alone in the short term (12 weeks). However, at longer term (52 weeks), the advantages of the MCL repair on the biomechanical properties of the FMTC disappeared [30,237]. Therefore, it is apparent that only reconstruction of the ACL is necessary after a combined injury due to the important role the ACL plays in maintaining valgus instability.

Further studies of combined ACL/MCL injuries in the goat model using our robotic/UFS testing system have shown that the initially high in-situ force in the ACL graft was transferred to the healing MCL during the early stages of healing (i.e. from time zero to 6 weeks). These excessively high loads likely contributed to the observed decrease in the structural properties of the FMTC and tangent modulus of the MCL substance when compared to an isolated MCL injury [23,241]. Thus, future work is still needed to optimize treatment strategies following combined ligamentous injuries.
Summary and future directions

During the past four decades, significant advances have been made in characterizing the biomechanical properties of normal and injured ligaments and tendons. Data on the tensile and viscoelastic properties of ligaments and tendons, as well as knowledge on their contribution to joint kinematics and function, have significantly helped to move the field forward. Further, new findings on the healing process have led to improved treatment of ruptured ligaments and tendons, making it an exciting period for ligament and tendon research.

The new field of functional tissue engineering offers yet many new possibilities. The use of growth factors, gene therapy, cell therapy, and biological scaffolds to enhance healing certainly will result in improved outcomes [61,242-247]. We believe the ECM-derived bioscaffolds will play a significant role because it could accelerate the healing process and establish a bridge between the torn ends. ECM bioscaffolds have been successfully applied to improve MCL and PT healing, because their chemoattractant degradation products and bioactive agents allow aligned matrix formation with a concomitant improvement in biomechanical properties closer to normal values [58,248-250]. Efforts to healing of the ACL, which has long been considered as a "holy grail" for orthopaedics are now being made [251,252]. Additionally, it is possible to further improve the properties of these biological scaffolds by seeding bone marrow-derived cells (BMDCs) in-vitro followed by mechanical cyclic stretching to achieve better fiber alignment, thus making them to better suited to accelerate the healing process when used in-vivo [253].

While in-vitro testing has contributed significant advances, it is time to move on to in-vivo studies. To do this, we have developed a new higher payload robotic/UFS testing system capable of handling levels of applied loads during activities of daily living (Figure 8). This system has also been shown to be highly accurate to 0.1 mm and 0.1°, which is needed to obtain meaningful data. Additionally, our collaborators at the Steadman-Hawkins Research Foundation have constructed a new biplanar fluoroscopy system, designed to measure in-vivo joint kinematics. It could measure the knee motion to within an accuracy of less than 0.2 mm and 0.3° [253]. These accurate in-vivo kinematics data can then be reproduced on cadaveric knees utilizing the robotic/UFS testing system and the in-situ forces in the ACL can be obtained. Thus, the combined technology will allow us to identify mechanisms of ACL (as well as other ligament and tendon) injuries and to design and optimize reconstruction procedures and rehabilitation protocols leading to improved patient outcomes as well as to help athletes successfully return to sports.

Moreover, in-vivo kinematics can be used as inputs for a three-dimensional finite element model of the knee. The predicted results from the model must be first validated with experimental data such as those obtained from the robotics/UFS testing system. With a validated finite element model, it will be possible to calculate stress and strain distributions in the ACL and ACL grafts, as well as to develop a database of the in-situ forces for patients of different ages, genders, and sizes. These data are important for one to design preventative programs as well as surgical planning and rehabilitation protocols.

Nevertheless, ligament and tendon research will continue to present many challenges, including the prevention and treatment of tendinopathy as well as ligamentous injuries in addition to the reducing osteoarthritis following ACL injury. Solving these problems will require interdisciplinary and multidisciplinary collaborative research that involves biomedical engineers, biologists, clinicians, plus investigators from many other disciplines (i.e. mathematicians, statisticians and immunologists) to be working together to develop better therapeutic strategies. Ultimately, it is our hope to be able to make ligaments and tendons heal more completely with better tissue quality so that patients can return to both normal daily activities as well as sports.

thumbnailFigure 8. Flow chart showing the utilization of in-vivo kinematics data to drive experimental and computational methodologies leading to improved patient outcome (permission requested from [221]).

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

HJ, MF and SW all participated in drafting, editing, completion of the manuscript.

Acknowledgements

The authors acknowledge the financial support provided by the National Institute of Health (AR41820 and AR39683) and National Science Foundation (Engineering Research Center, #0812348). We also wish to acknowledge the research contributions of past and present members of the Musculoskeletal Research Center as well as our collaborators, Dr. Michael Torry and Dr. Richard Steadman, of the Steadman-Hawkins Research Foundation.

© 2009 Jung 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.

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253. Giphart JE, Shelburne KB, Anstett K, Brunkhorst JP, Pault JD, Woo SL-Y, Steadman JR, Torry MR: Measurement of 3D In Vivo Knee Motion Using Biplane Fluoroscopy: Investigation of Non-contact ACL Injuries. XVIth International Conference on Mechanics in Medicine and Biology; July 23–25; Pittsburgh, PA 2008.

by EricT

This video was filmed at Body Worlds, Edmonton science Center with Dr. Brian Abelson and Dr. Tarveen Ahluwalia.

Brian Abelson is the author of Release Your Pain: Resolving Repetitive Strain Injuries with Active Release Techniques®.

The figures used in this video are not sculptures, they are actual "plastinated" cadavers. So if you are squeamish about such things, don't watch the video.

Dr. Tarveen Ahluwalia, Kinetic Health Calgary

Dr. Ahluwalia opens the video with a discussion of whiplash which is a trauma related condition resulting from the head being forced back (hyperextension) and then forward again (hyperflexion) very quicky, or vice versa, as in a car accident.

She then explains some of the symptoms or complaints associated with neck pain, including pain at the base of the skull, or even in the shoulder or upper back area. Neurological signs may also be present, such as numbness and tingling which runs down the arm or upper back.

Due to the interconnected nature of the cerivical, thoracic, and lumbar spine areas, neck pain can be due to due to a problem lower down the kinetic chain. Treatment must start with a thorough evaluation of the entire kinetic chain.

Later on she discusses some treatment options which of course include soft-tissue techniques such as ART® or Graston to relieve adhesions (scar tissue), and at home exercises such as postural correction, stretches and of course strength training.

She mentions particularly the area of the pecoralis minor in regards to stretching.

Dr. Abelson

Dr. Abelson explains how restrictions in the area of the sternocleidomastoid (SCM) put pressure on a netword of nerves called the bracial plexus (which pass throught the scalenes) which results in numbness, pain, and tingling down the arm. Compression in this area causes a condition known as thoracic outlet syndrome. This is related to forward posture in which the shoulders are hunched forward the the pectoral muscles are tight and shortened.

Associated Neck Pain Symptoms

• Muscle Spasms

• Swelling

• TMJ

• Visual Problems

• Hearing Problems

• Dizziness, Nausea

• Pain down arms

• Neurological symptoms

• Numbness

• Tingling

• Muscle Weakness

Commonly Affected Posterior (Back of Body) Muscles

• Trapezius

• Semispinalis Capitis

• Splenius Capitis

• Rectus Capitis (Minor/Major)

• Superior/Inferior Obliques

• Rhomboids

• Serratus Posterior Superior

• Levator Scapulae

Commonly Affected Anterior (Front of Body) Muscles

• Platysma

• Sternocleidomastoid

• Longus Colli

• Scalenes

• Omoyiod

• Pectoralis Major/Minor

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by EricT

by Kai-Ming Chan and Sai-Chuen Fu¹

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Tendon Injuries and Anti-inflammatory Treatment

Acute and chronic tendon injuries are very common among athletes and in sedentary population. Most physicians prescribe anti-inflammatory managements to relieve the worst symptoms of swelling and pain, including non-steroidal anti-inflammatory drugs, corticosteroids and physical therapies. However, experimental research shows that pro-inflammatory mediators such as prostaglandins may play important regulatory roles in tendon healing. Noticeably nearly all cases of chronic tendon injuries we treat as specialists have received non-steroidal anti-inflammatory drugs by their physician, suggesting that there might be a potential interaction in some of these cases turning a mild inflammatory tendon injury into chronic tendinopathy in predisposed individuals. We are aware of the fact that non-steroidal anti-inflammatory drugs and corticosteroids may well have a positive effect on the pain control in the clinical situation whilst negatively affect the structural healing. It follows that a comprehensive evaluation of anti-inflammatory management for tendon injuries is needed and any such data would have profound clinical and health economic importance.

Commentary

Sporting injuries, including both acute trauma and chronic overuse, are usually presented with clinical signs of swelling and pain. Most sport medicine physicians prescribe anti-inflammatory managements to control the pain. However, there are increasing evidences about the unfavorable side effects on the use of various anti-inflammatory agents for tendon injuries.

Do we need to re-visit the rationale of anti-inflammatory drugs for tendon injuries?

In cases of chronic tendinopathy, a lack of inflammatory infiltration in the biopsies has challenged the status of "tendinitis". However, it did not rule out the possibility of an inflammatory response in the early development of tendinopathy. Overuse or repetitive stretching on tendons triggered the release of pro-inflammatory mediators, which can induce expression of metalloproteinases and leads to collagen degradation. These findings suggest that inflammatory responses play a key role in the development of degenerative overuse tendon injuries. Together with the fact that all chronic tendinopathy cases received anti-inflammatory management, it is logical to assume that suppression of inflammatory responses may interact with the failed healing of degenerative tendon injuries.

We coined the term failed healing to describe the histopathological characteristics of tendinopathy samples, which exhibited traits of both active repair and degenerative injuries. The development of overuse animal model clearly demonstrated the casual relationship of overuse and degenerative tendon injuries through activation of inflammatory mediators [1], but whether the injured tendons failed to heal in these models were not adequately described. On the other hand, animal models of collagenase-induced degenerative injuries revealed failed healing [2] and longstanding pain [3]. We believe that chronic tendinopathy is a result of failed healing of degenerative injuries (Figure 1). The reasons why the degenerative injuries fail to heal might be the core of the mystery. Since pro-inflammatory mediators affect various cellular activities related to tendon healing, it is possible that anti-inflammatory agents might negatively affect tendon healing and contribute to the development of tendinopathy.

Overuse or excessive mechanical stimulation to tendons can lead to elevation of metalloproteinases (MMPs) which mediate collagen degradation and hence degenerative tendon injuries. Healing responses are activated but failed to repair the degenerative injuries, resulting in tendinopathy. It is possible that anti-inflammatory management may affect the development of degenerative injuries as well as the pathological processes of failed healing in tendinopathy.

Non-steroidal anti-inflammatory drugs (NSAIDs)

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It is still a common practice to prescribe non-steroidal anti-inflammatory drugs (NSAIDs) which primarily work by inhibiting the production of pro-inflammatory prostaglandins. Interestingly, both beneficial and deleterious effects of NSAIDs on tendon healing were reported. It appears that NSAIDs exerted beneficial effects, if any, by influencing the remodeling of collagen matrix, resulting in reduction of cross-sectional area of the healing tendons but tensile strength may or may not be affected. NSAID may also negatively affect early tendon healing, as prostaglandin E2 (PGE2) is essential for early tendon healing such as control of vascular flow. We doubt that the unchecked use of NSAIDs may exert negative effects when prescribed to tendinopathy patients. As increased expression of cyclooxygenase 2 (COX-2) and increased production of PGE2 were found in chronic tendinopathy samples [4], the involvement of PGE2 for the development of chronic tendinopathy was implied. As PGE2 may mediate the development of overuse tendon injury by induction of metalloproteinases, it is possible that suppression of PGE2 may have reduced the extent of degenerative injuries but the normal matrix remodeling would also be affected, which may contribute to the failed tendon healing. Further investigation is urgently needed to disseminate the double-edged properties of prostaglandins in tendon healing before we could advocate the use of NSAIDs for chronic or acute tendon injuries.

Corticosteroids

Corticosteroids are strong anti-inflammatory agents and peri-tendinous injection of corticosteroid is commonly used to treat the chronic pain in tendinopathy. However, the use of corticosteroid may increase risk of spontaneous ruptures and the deleterious effects of corticosteroid were demonstrated on culture human tendon fibroblasts, including cell viability, proliferation and matrix synthesis [5]. In spite of its potential hazards, corticosteroid injections are still given indiscriminately in many sport clinics!! There is no doubt that the adverse effect of corticosteroids on tendon cells would affect the healing responses to degenerative injuries, corticosteroid injection should be considered as a last resort with careful control on the dosages.

Other anti-inflammatory modalities

Apart from NSAIDs and corticosteroids, the use of physical therapies to reduce inflammatory signs in tendon injuries is common, but rigorous scientific studies on the efficacy and the underlying mechanisms are not available. Pulsed electromagnetic fields and low level laser treatments may reduce inflammation, probably by suppressing PGE2 production. The therapeutic effect of extracorporeal shockwave therapy may be attributed to its anti-inflammatory actions through modulation of nitric oxide production. It appears that these biophysical interventions also exerted anti-inflammatory actions through modulation of pro-inflammatory mediators. As they are relatively safe, further exploration to consolidate their efficacies may yield a better clinical practice for anti-inflammatory management for tendon injuries.

It would be a breakthrough if we could identify disturbed prostaglandin levels as one of the causes of failed healing in tendinopathy, which will certainly guide the development of effective treatment strategies for overuse tendon injuries. In most clinical practice, it is very difficult to monitor the use of anti-inflammatory management for chronic tendinopathy, let alone restricting it in a rigid protocol.

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References

1. Millar NL, Wei AQ, Molloy TJ, Bonar F, Murrell GA: Cytokines and apoptosis in supraspinatus tendinopathy. J Bone Joint Surg Br 2009, 91(3):417-24.

2. Lui PP, Fu SC, Chan LS, Hung LK, Chan KM: Chondrocyte phenotype and ectopic ossification in collagenase-induced tendon degeneration. J Histochem Cytochem 2009, 57(2):91-100.

3. Fu SC, Chan KM, Chan LS, Fong DT, Lui PY: The use of motion analysis to measure pain-related behaviour in a rat model of degenerative tendon injuries. J Neurosci Methods 2009, 179(2):309-18.

4. Fu SC, Wang W, Pau HM, Wong YP, Chan KM, Rolf CG: Increased expression of transforming growth factor-β1 in patellar tendinosis. Clin Orthop Rel Res 2002, 400:174-183.

5. Wong MWN, Tang YN, Fu SC, Lee KM, Chan KM: Triamcinolone Suppresses Human Tenocyte Cellular Activity and Collagen Synthesis. Clin Orthop Rel Res 2004, 421:277-281.

by EricT

Men Versus Women Athletes: What's really Different anatomically, physiologically and psychologically?¹

by Alan Ivković², Miljenko Franić³, Ivan Bojanić, and Marko Pećina⁴

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The last three decades have witnessed a tremendous increase in female sports participation at all levels. However, increased sports participation of female athletes has also increased the incidence of sport-related injuries, which can be either acute trauma or overuse injuries. Overuse injuries may be defined as an imbalance caused by overly intensive training and inadequate recovery, which subsequently leads to a breakdown in tissue reparative mechanisms. This article will review the most frequent overuse injuries in female athletes in the context of anatomical, physiological, and psychological differences between genders.

The ancient Greeks barred women from participating at the ancient Olympics, even as spectators (1). Baron Pierre de Coubertin, the man credited for the birth of the modern Olympics, regarded women’s taking part in sports as being “against the laws of nature.” To cite his words: “Olympics are solemn and periodic exaltation of male athleticism, with internationalism as a base, loyalty as a means for its setting and female applause as a reward” (2). As a result of this attitude, women did not participate at the first modern Olympic games in Athens in 1896. However, a century later at the same place – during the 2004 Olympics, 4329 women from all over the world competed in the majority of 300 official events. Nowadays, taking part in sports is seen a positive experience for women, since it improves physical fitness, enhances self-esteem, and contributes to better physical and mental health. Apart from professional sport, there has also been a dramatic increase in women’s sports participation on recreational and amateur level.

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Injuries are an integral part of any sporting activity and they can be divided into two main groups: acute trauma and overuse injuries. Overuse injuries, otherwise known as cumulative trauma disorders, may be defined as tissue damage that is a result of repetitive demand over the course of time (3). It is not exclusively related to professional sports, but the term also refers to a vast array of diagnoses, including occupational, recreational, and habitual activities. Although injuries tend to be sport-related rather than gender-related, it has been noted that certain conditions, such as patellofemoral pain syndrome, stress fractures, or lateral epicondylitis are especially prevalent in female athletes (4).

Tremendous increase in female sport participation during the last three decades has offered scientists and clinicians valuable data on the physiologic and pathologic issues of the exercising female. This article will provide basic information on the most frequent overuse injuries in female athletes in the context of anatomical, physiological, and psychological differences between genders.

Special characteristics of female athlete

Anatomical considerations

Bones and joints: Compared with men, women have shorter and smaller limbs relative to body length. The length of lower extremities comprises 56% of the total height in men, compared with 51.2% in women (5). In the athletic disciplines where balance control is very important (eg, gymnastics), shorter stature and wider pelvis give women lower center of gravity, which gives them substantial advantage. Additionally, wider pelvis can produce varus of the hips, increased femoral anteversion, and genu valgum resulting in an increased Q angle, which is known to be a predisposing factor for patellofemoral problems (6) (Figure 1).

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Figure 1

Lower extremity anatomic differences between genders that may predispose women to certain overuse injuries. (A) 1 – less muscular thigh development, 2 – increased flexibility, 3 – less developed musculus vastus obliquus, 4 – genu valgum, 5 – wider pelvis, 6 – femoral anteversion, 7 – narrow femoral notch, and 8 – external tibial rotation; (B) 1 – more developed thigh musculature, 2 – less flexibility, 3 – vastus medialis obliquus hypertrophy, 4 – genu varum, 5 – narrower pelvis, 6 – wider femoral notch, and 7 – internal or neutral tibial torsion.
Croat Med J. 2007 December; 48(6): 767–778.
doi: 10.3325/cmj.2007.6.767.
Copyright © 2007 by the Croatian Medical Journal. All rights reserved.

Muscles:

During prepubertal years, there is not much difference in muscle mass between boys and girls. During the puberty, however, because of the influence of the testosterone boys accumulate greater muscle mass. In adults, total cross-sectional area of muscles in women is 60%, compared with 80% in men (7). As a result, maximal strength measures and maximal power measures are reduced. Various other studies have shown that when only muscle quality is concerned, male and female muscle is not different. It appears, however, that the strength and power differences between the sexes are a function of muscle quantity and not only of their quality (8). Studies also showed that female athletes have increased hamstrings flexibility which could be responsible for increased anterior cruciate ligament (ACL) injury risk (9).

Ligaments and joints:

Female athletes have increased general joint laxity than their male counterparts. It can be attributed to the more abundant joint capsule, as well as to the lower muscle mass that restrains the excessive joint movement in men (10). These observations are particularly true for the knee, ankle, and elbow joint. Several studies showed that joint laxity and hyperextension significantly increase the risk of ACL injury in female subjects (11).

Physiological considerations

Before puberty boys and girls do not differ much in terms of height, weight, heart size, or aerobic capability. After the stabilization of hormonal axis during the pubertal years, principal gender differences start to be more obvious. Proper estrogen serum levels are necessary for women to obtain maximum peak bone mass during the second and third decade (12).

Percentage of body fat is another variable that is different in men and women. It is known that adult women have 22 to 26% body fat levels and men have 12 to 16% (13). Androgens are responsible for greater lean body weight in men and estrogens are responsible for greater amount of fat weight. There was some speculation in the past that there is a critical level of body fat necessary to maintain normal menstrual function (14). Although this theory was not supported in the literature, it should be kept in mind that there is an individual threshold of body fat necessary for normal menstrual cycle.

For the same body weight, female athletes have smaller heart size than male athletes, lower diastolic and systolic pressures, and smaller lungs. This decreases female athlete effectiveness in both aerobic and anaerobic activities. Maximum oxygen consumption (VO2max) reflects body’s ability to extract and utilize oxygen, and is used as a measure for aerobic metabolism. It is known that VO2max is substantially lower in women than men, and even after accounting for differences in bodyweight and body fat percentage, there remains a gap of roughly 10%-15%. Recent evidence suggests that during heavy exercise, women demonstrate greater expiratory flow limitation, an increased work of breathing, and perhaps greater exercise-induced arterial hypoxemia than men (15).

Psychological considerations

Clinical observation has long suggested a link between the athlete’s personality and eating disorders. Anorexia and bulimia have thus been linked to personality traits such as introversion, conformity, perfectionism, rigidity, and obsessive-compulsive features (16). Furthermore, it should be noted that in most of the Western cultures athletic participation was always considered to be a man’s thing. Achievement, aggressiveness, and desire to win and conquer were traditionally considered as masculine, not feminine qualities. The widespread belief is that “the winning male athlete has just proved his masculinity, whereas the winning female often needs to justify her femininity” (17). This kind of prejudice, in combination with personality traits, may lead to depression and anxiety episodes because a female athlete may feel she is not up to the perceived expectations of her sex.

Female athletes have lower scores on dominance and confidence and higher on impulsiveness, tension, and general anxiety than male athletes (18). It should be noted that pressure to “win at all costs,” an overly controlling parent or coach, and social isolation caused by intensive involvement in sports may also increase the athlete’s risk for developing certain problems, such as eating disorders (19). These characteristics are known to be contributing factors in the development of eating disorders as an essential part of the female athlete triad syndrome which consists of eating disorders, menstrual dysfunction and osteoporosis.

Overview of most frequent overuse injuries in female athletes

Stress fractures

Stress fractures are relatively common overuse injuries, especially in athletes or military personnel. Although they are not exclusive to female athletes, this issue deserves a more detailed insight. There are two reasons for this: first, women in general have a higher incidence of stress fractures and, second, distribution of stress fracture sites seems to differ between genders. Stress fractures result from cumulative repetitive forces insufficient to cause an acute fracture. It has been noted previously that stress fractures occur more frequently in amenorrheic than normally-menstruating women (20,21). The exact mechanism of the development of stress fractures in amenorrheic women is uncertain and may not necessarily be related to low bone density. Menstrual status should be assessed in all female athletes who present with stress fractures.

Various studies have found that women have a higher incidence of stress fractures than men (22,23). Further studies consistently confirmed the fact that female recruits have a greater risk of stress fractures than their male counterparts, with the relative risk ranging from 1.2 to 10.0 (24). In the athletic population the risk ranges from 1.5 to 3.5.

Figure 2: Stress fracture of the second metatarsal bone.

Lower-extremity bones are most commonly affected, but stress fractures also occur in non-weight-bearing bones such as upper extremities and ribs. The tibia is the most commonly involved site for both men and women, but the fractures of the femoral neck, tarsal navicular, metatarsal, and pelvis are seen more commonly in the female athlete (25) (Figure 2Figure 2). Evidence shows that certain stress fracture sites are reported more often in some athletes, eg, medial malleolus of the tibia and tarsal navicular stress fracture in high jumpers (26). The athlete with stress fracture presents with gradual onset of pain, aggravated by exercise.

The hallmark of stress fracture is localized tenderness to palpation at the fracture site. Point tenderness may be best provoked over bones that can be easily palpated, such as the metatarsal bones or fibula. For bones that are deep, such as the pelvis or femoral neck and shaft, pain may be elicited through gentle range of motion or specific diagnostic tests. The combination of clinical picture and either bone scan or magnetic resonance imaging is sufficient for the diagnosis. The main treatment of stress fractures is rest from the offending athletic activity, a concept known as “relative rest,” and it is usually conducted as a step by step treatment algorithm (27).

There is a group of stress fractures, called high-risk stress fractures, that requires additional treatment to “relative rest.” High-risk stress fractures include those in the femoral neck, patella, anterior cortex of the tibia, medial malleolus, talus, tarsal navicular, fifth metatarsal, and great toe sesamoids. General conditioning is maintained by exercising other areas of body and partaking alternative training, such as water running, swimming, or cycling. When patients do not respond to conservative treatment, surgical procedure should be advised.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is a term used to describe painful but stable patella. It is a very common problem among female athletes, and the diagnosis of PFPS is made by exclusion of intra-articular pathologies, patellar tendinopathy, peripatellar bursitis, the plica syndrome, Sinding-Larsen-Johansson, and Osgood-Schlatter lesions (28). Anterior knee pain is possibly the most common symptom presenting in sports medicine. Other terms used in literature to describe pain-related problems in the anterior portion of the knee include patellofemoral arthralgia, patellar pain, patellar pain syndrome, and patellofemoral stress syndrome. Incidence of the PFPS in women is 20%, compared with 7.4% in men (29).

Radiological examinations are of great assistance in discovering anatomical deviations and irregularities in the patellofemoral joint. The increased incidence of PFPS in women compared with male athletes is thought to be related to structural, biomechanical, sociological, and hormonal differences between genders (30). Despite high incidence, etiology of PFPS still remains unclear. It still is unanswered what the cause of pain in PFPS is and which structure is involved. The causes of PFPS are usually classified as extrinsic and intrinsic, and three major factors contributing to the development of PFPS are lower extremity and patellofemoral malalignment, quadriceps muscle imbalance and/or weakness, and physical overload of patellofemoral joint (31). Many patients with marked patellar malalignment never experience pain, while others, with apparently no malalignment, experience problems.

Conservative treatment is effective in most patients. Quadriceps muscle stretches, balanced strengthening, proprioceptive training, hip external rotator strengthening, orthotic devices, and effective bracing will relieve the pain in most of the patients (32). If a comprehensive rehabilitation program of at least 6-month duration fails, surgical treatment should be suggested to the patient. There are several surgical procedures, such as lateral release, proximal patellar realignment, or medial/anteromedial tibial tubercle transposition, that can be used for realignment of the patella in the trochlear groove and reduction of the patellofemoral pressure (33).

Patellar tendinitis – jumper’s knee

Patellar tendinitis (jumper’s knee) is a clinical entity characterized with anterior knee pain. Pain is aggravated by excessive strain on the extensor system of the knees after numerous jumps or long periods of running. Important causative factor was found to be the amount of training (both the amount of time and the amount of mechanical strain placed on the knee) that the athlete habitually carries out. The development of jumper’s knee also to a large degree depends on anatomical characteristics of the athlete, particularly of the lower extremities.

Pain as the basic symptom and a decreased functional ability of the afflicted lower extremity is a characteristic clinical picture of the jumper’s knee. The functional inability of the afflicted lower extremity is accompanied by intense pain and shows a range from slight to complete inability to participate in athletic activities. The most common site of tendinitis is around inferior pole of patella (34). Pećina et al (35) reported the appearance of pain at the insertion site of the patellar tendon at the tip of the patella in 80% of athletes suffering from jumper’s knee (Figure 3Figure 3). In very rare cases, continuation of intensive athletic activities, despite the presence of evident symptoms of the disease, leads to a complete rupture of the patellar tendon. Kujala et al (36) reported that during a 5-year interval in a test sample of 2672 ambulatory patients with various knee injuries, 26.4% suffered from complications related to jumper’s knee. These findings led them to believe that jumper’s knee is the most common athletic injury to the knee.

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Figure 3

Magnetic resonance image of the female volleyball player diagnosed with jumper’s knee.
Croat Med J. 2007 December; 48(6): 767–778.
doi: 10.3325/cmj.2007.6.767.
Copyright © 2007 by the Croatian Medical Journal. All rights reserved.

Patellar tendinitis is relatively easy to diagnose, but its treatment is more difficult. Of the numerous treatments available, physiotherapy and correction of technical errors are often efficient. Surgical treatment is indicated if a prolonged and well-supervised conservative treatment program fails. Sclerosing injections or radical removal of the area with neovessels and nerves by arthroscopic shaving under ultrasound control has potential to reduce the tendon pain and allow the majority of patients to go back to full tendon loading activity within 2-month after surgery (37).

Lateral epicondylitis

A chronic overuse of the tendons at their insertion at the lateral humeral epicondyle is commonly called tennis elbow. The origin of the extensor carpi radialis brevis is always afflicted in the first 1-2 cm distal to its attachment to the extensor origin, and the origins of the other extensors are involved occasionally. It usually manifests between 30 and 50 years (but this condition may affect any age group) and women are more at risk than men. Lateral epicondylitis occurs in association with any activity involving repeated wrist extension against resistance. The main symptoms consist of pain and tenderness over the lateral humeral epicondyle. No single treatment has proven to be totally effective in the treatment of this condition. The treatment is usually non-operative and consists of pain relief and activity monitoring. Surgical treatment is required in 5% to 10% of all patients and it can be performed either as an open procedure or arthroscopic procedure (38).

Iliotibial band friction syndrome

Iliotibial band friction syndrome (ITBFS) is one of the most common overuse injuries in runners, not only professional athletes, but also recreational joggers and other athletes whose activities entail a lot of running.

ITBFS is caused by many repetitive flexion and extension movements of the knee, during which rubbing of the band against lateral femoral epicondyle occurs (39). Friction occurs near foot strike, predominantly in the foot contact phase, between the posterior edge of the iliotibial band and the underlying lateral femoral epicondyle.

Sutker et al (40) reported ITBFS prevalence of 4.7% in 4173 injured runners, as well as a higher incidence of ITBFS in long-distance runners than middle-distance runners and sprinters. The dominant symptom is pain at the lateral side of the knee, aggravated by running. Pain is stinging in nature, and is located at the lateral femoral condyle 2 cm above the joint line. The treatment is usually non-operative and is based on modification of athletic activity, stretching exercises, and correction of predisposing factors. In recalcitrant cases of ITBFS, surgery has been advocated.

Spondylolysis

Spondylolysis is a common cause of back pain in female athletes. The most common localization of spondylolysis is fourth and fifth lumbar vertebra (41). The lesion usually occurs in the pars interarticularis (junction between the superior and inferior processus articularis) and may be unilateral and bilateral. Women who participate in sports such as gymnastics, figure skating, and dance may have additional risks (42). It is more common in sports that require episodes of hyperextension, especially combined with rotation. The fracture usually occurs on the side opposite to the one performing the activity. The athletes complain of unilateral low back pain, occasionally associated with some pain in the gluteal region. The pain is aggravated by movements involving lumbar extension. Occasionally, stress fractures to the pars interarticularis are asymptomatic.

In cases with a recent onset of pain, x-ray may not demonstrate the fracture. In longer standing cases, special slanted oblique projections of the spine are taken, which, in positive cases form the shape of “Scottish terrier,” with an abnormally extended neck, indicating a defect in isthmus of the vertebral arch. When a spondylolysis is suspected clinically but plain x-ray is normal, isotopic bone scan or a single photon emission computed tomography (SPECT) scan should be performed (43). Patients with a positive SPECT scan result should then undergo CT scanning to image the fracture. The treatment is conservative and surgical fixation is very rarely indicated.

Female athlete triad

The female athlete triad was described and termed in 1992 by the American College of Sports Medicine, and consists of three inter-related disorders – eating disorders, menstrual disorders, and osteoporosis (44). The syndrome usually begins with disordered eating, and over the time low energy intake shuts down the hypothalamic-pituitary-ovarian (HPO) axis, leading to menstrual disorders and hypoestrogenism, which is ultimately responsible for decreased bone mineral density and osteoporosis (45). The obvious consequence of this cascade of interrelated pathophysiological events is greater risk of stress fractures.

Eating disorders

Eating disorders comprise a wide spectrum of disorders, ranging from occasional meal skipping and calorie avoiding to anorexia and bulimia nervosa. The term “anorexia athletica” has been used to distinguish between true anorexia nervosa and disordered eating associated with training and sports performance (46). Risk factors for the development of disordered eating include western sociocultural norms, which attribute thinness to beauty, power, and control; psychologic factors such as poor coping skills, low self esteem, general anxiety, and depression; and gender factors – 90% of patients suffering from disordered eating are women (47). Another important risk factor is participation in certain athletic disciplines, such as ballet, figure skating, gymnastics, or distance running, which demand low body-weight and thinness of the competitors (Box 1). Engaging in severely limiting food intake, constantly weighing the foods, eating secretly, refusing to eat in front of others, and abusing laxatives impairs athletic performance and increases the risk of injury. Furthermore, it results in dehydration, malnourishment, and unhealthy weight loss, as well as psychological difficulties such as food/weight obsession, depression, and anxiety. The prevalence of eating disorders among female athletes is between 15% and 62% (48). In contrast, incidence in the general population is 1% (49).

Menstrual dysfunction

Eumenorrhea or normal menstrual function is dependent on the intact function of the pituitary gland, hypothalamus, ovaries, and endometrium. Cyclic nature of the process is maintained by precise secretion of both luteinizing hormone and follicle-stimulating hormone from the anterior pituitary, as a response to gonadotropin-releasing hormone arising in hypothalamus. Normal menstrual cycle lasts 25-35 days and may be divided into two phases. The first half of the cycle is the follicular phase, characterized by gradually increasing levels of estrogen, and the second half is the luteal phase, characterized by high concentrations of estrogen and progesterone.

The average age of menarche is 12.7 years in the USA and 13.5 years in some parts of Europe. It is known that female athletes who begin strenuous training before menarche occurs may experience a later menarche and have increased incidence of menstrual dysfunction than athletes who begin their training after menarche (50). This is very important because bone mass accumulation is the most intensive during puberty and the athletes with delayed menarche will have lower bone mineral density (BMD) and increased risk of scoliosis and stress fractures in the years to follow (51).

Amenorrhea is the most frequent type of dysfunction found in athletes and its prevalence varies from 3.4% to 66%, compared with 2% to 5% in the general population (44). Primary amenorrhea is defined as the absence of a menstrual cycle by the age of 14 without associated secondary sexual characteristics or by the age of 16 with these characteristics, whereas secondary amenorrhea is defined as the absence of menstruation for three consecutive months. Exercise-associated amenorrhea (EAA) is a subset of hypothalamic amenorrhea and is usually induced by synergism of low caloric intakes and intense training (52).

Other factors such as weight, body composition, fat distribution, and mental stress must be considered as well. It is speculated that suppression and disorganization of pulsatile luteinizing hormone release and complete suppression of leptin diurnal rhythm are underlying pathophysiologic mechanisms of EEA (53). It is thought that low-energy availability, combined with high levels of athletic activity, induces the hormonal changes, and the menstrual cycle is suppressed in order to conserve energy. EEA is a diagnosis of exclusion, and all the necessary diagnostic steps must be undertaken before it is made.

Estrogen protects the skeleton form bone resorption, and because of resulting hypoestrogenic state, amenorrhea is associated with premature bone loss and increased risk of both acute and stress fractures. Although the exact mechanism is still not fully understood, it is known that estrogen receptors are present on bone cells and directly increase osteoblastic activity (54).

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Osteoporosis

Osteoporosis is defined by the World Health Organization (WHO) as inadequate bone formation and/or premature bone loss o more than 2.5 standard deviations bellow the average for young adults, resulting in low bone mass and an increased risk of fracture. However, it should be noted that International Society for Clinical Densitometry has published a position statement that the WHO guidelines should not be used for healthy premenopausal women (55). They also state that age-appropriate comparison scores (Z-scores) should be used instead of T-scores in the process of diagnosing osteoporosis in this population. Most of the bone mass is acquired during the adolescent years (especially during the pubertal growth spurt), and by the age of 18 most women have reached 95% of their peak bone mass. After peak mass is achieved, both men and women lose bone at a rate of 0.3% to 0.5% per year. It is known that bone tissue responds well to mechanical stress, and therefore, exercise combined with adequate nutritional intake is essential to attain peak bone mass in the adolescent female.

Amenorrheic young athletes may have failed to lay down sufficient bone mass or may have lost already accumulated bone mass (56). It is known that amenorrheic athlete may lose 2%-6% of bone mass per year, and develop the bone structure profile similar to that of the 60-year-old woman (57). Several studies showed that, amenorrheic athletes have significantly lower BMD at the lumbar spine, femoral neck, greater trochanter, Ward triangle, intertrochanteric region, femoral shaft, and tibia than healthy athletes (58). This kind of weakened bone puts her at 3-fold risk of stress fracture (59). Although BMD can be partially restored upon resumption of menstruation, studies showed that it still remains lower than in healthy athletes (60). Because of this partial irreversibility, it is crucial to identify all the athletes at risk as earlier as possible.

Clinical evaluation and treatment of female athlete triad

It is of utmost importance to educate athletes, coaches, physicians, and parents about the female athlete triad, so that they can readily recognize the symptoms and potential risks associated with this condition. The ideal time to screen for the triad is during the physical evaluation before sports participation, or at the beginning of the season in case of professional athletes (61).

An early diagnosis is the critical step in the prevention of immediate and long-term harmful health consequences. History should be detailed, and focus should be put on menstrual, nutritional, and body-weight history (62). General physical examination including basic anthropometrics measures such as weight, height, and subcutaneous fat thickness should be taken. Inspection should be focused on external signs of androgen excess, thyroid deficiency, and chromosomal abnormalities. The most precise tool for determination of BMD is dual energy x-ray absorptiometry (63). It should be used in determining the amount of bone loss, but also in measuring the success of therapy.

Treatment should be based on a multidisciplinary approach (physician, registered dietitian, and mental health practitioner) and should be focused on weight control and menstrual restoration. The first step of the treatment is to establish open and honest communication with the athlete, followed by setting common goals which include increase in the caloric intake and decrease in energy expenditure. This would restore normal menstruation and serum estrogen concentrations, and it would prevent further loss of bone mineral content. One of possible treatment schemes is the following: decrease training by 10% to 20%, increase the caloric intake, gain 2% to 3% of body weight, add resistance training, supplement calcium (1500 mg/d), and monitor using bone density scans (64). The use of hormone replacement therapy and oral contraceptive pills is not recommended in athletes with functional hypothalamic amenorrhea, since the increase in BMD is more closely associated with increase in weight than with hormone replacement therapy/oral contraceptive pills administration (65).

Conclusion

Female sports have come a long way. Women’s success in professional sports and the development of women’s professional sport teams is the evidence of the closing gender gap in athletics. Also, regular exercise is very important for obtaining general health, positive lifestyle behavior, and positive self-image, as well as learning such skills as teamwork, commitment, and goal setting. Combination of low energy intake, functional hypothalamic amenorrhea, and osteoporosis are the main constituents of the female athlete triad, which poses significant health risk to female athletes. If the symptoms of triad exist, early diagnosis and multidisciplinary approach are the essential aspects of the treatment of this disorder. It is of utmost importance that anyone involved in the training process of the young female athletes learns to recognize the signs and symptoms of this syndrome. Education remains the most important tool of prevention. In addition, preparticipation physical evaluation is the ideal time to identify athletes at risk and screen for any problems that may predispose the athlete to an overuse injury.

Acknowledgment

The authors thank Hrvoje Klobučar, MD, MSc from the Department of Orthopaedic Surgery, Medical School University of Zagreb for providing the figure of anatomic differences between genders.

Comments

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PubMEd article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.[[/footnote]]

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