gulf injuries, tendinitis vs tendinosis, gluteus medius, foot pain, & cartilage injuries

In this issue

Golf: the cause of low back pain 1

Tendon problems: inflammation v degeneration 5

Muscles: the gluteus medius 8

Foot pain: the kinetic chain 11

Rehab: chondral injuries in the knee 14

From the editorAndrew Hamilton’s opening article about golfing injuries is a must-read, looking at how this low-impact sport can create physical problems.

Alicia Filley, assesses the definitional differences between tendinosis and tendonitis – and how tendon problems are best diagnosed and treated.

Chris Mallac takes a look at fixing dysfunctions in the glutes and also how to diagnose chondral injuries in the knee.

And Tracy Ward rounds up some of the most common foot injuries that athletes

might encounter – and how they can be prevented altogether.

It’s 15 years since I helped launch SIB and in that time I hope we have helped promote a better understanding of sports injuries among the physical therapy community. I’m now handing over to a new team and would like to thank all who have contributed to SIB over the years for their exceptional work and loyalty. All the best.

Jonathan PyeEmail: [email protected]

The leisurely nature of golf makes it popular with older adults who may be unwilling or unable to take up a more punishing sport, where the risks of injury are perceived as much greater. However, the amount of physical activity required to play golf is still sufficient to provide health benefits.

Surprisingly, however, the reality of golf and injury risk is somewhat different. While a properly executed golf swing may not appear particularly stressful, a number of biomechanical studies have demonstrated that many joints and limbs are actually moving at high velocity and through extreme ranges of motion (ROM)(1-3), making them vulnerable to injury. To make matters worse, the successful execution of the golf swing requires a high degree of coordination, requiring many hours of practice during which these powerful movements are repeated hundreds of times. Add the fact that faulty swing mechanics are more likely to lead to an injury and that the golfers with poor swing actions are the most likely to be practising and you have a recipe for injury.

Prevalence of injuryPutting aside the risks of being struck by a golf club, ball, a golf cart or even lightning(!),

injuries related to golf practice are most likely to afflict the trunk and upper body. Studies show that hand/wrist injuries and elbow injuries are quite common, affecting around 13-20% and 25-30% of amateur golfers respectively. Shoulder injuries are also quite common, affecting around 8-18% of amateur golfers. The corresponding figures for professional golfers tend to be significantly lower, however(4-7).

The incidence of low back pain (LBP) among golfers by contrast is a rather more common, and is known to affect amateurs and professionals alike, regardless of skill levels(8). Epidemiological studies have shown that low back conditions account for approximately 25% of all golf injuries(9,10) although incidence rates as high as 54% (28) have been reported(11). Moreover, in a 2009 literature review, Cabri and colleagues reported that injury to the lower back r e p r e s e n t e d t h e m o s t c o m m o n musculoskeletal complaint experienced by both amateur and professional golf players.

Another study meanwhile surveyed 196 golfers who had just taken up the sport(12). While 25% suffered back pain during the one-year study period, the vast majority of these participants were unaware that playing golf was linked to their LBP. The

authors concluded that golf may aggravate pre-existing back pain due to the forceful nature of the movements associated with playing and practising.

The demands of the swingTo understand how something as apparently benign as golf can lead to a high incidence of lower back pain, it helps to appreciate the biomechanics of the swing (see Figure 1). The golf swing involves a slow deliberate rotation of the trunk away from the target (the backswing) followed by a powerful rotation of the trunk towards the target on the downswing. Although there are other spinal motions present during the swing movement, the axial twisting forces are especially noteworthy because this type of twisting has been identified as a significant risk factor for low back injury disorders in occupational settings(13).

Studies investigating the axial forces at play during the swing motion have come up with some startling findings. One of the first studies looked at forces on the lower back during a full golf swing while using a five iron – specifically the compressive, shear, lateral-bending and rotational loads on the L3/4 segment of the lumbar spine(14). Kinetic, kinematic and surface EMG data was

£17.99 Issue 149 November 2015

Golf

Golf: a gentle game that leads to painAlthough golf is regarded by many as a ‘gentle’ sport, the risk of lower back pain among its practitioners is surprisingly high. Andrew Hamilton explains the kinematics leading to back pain in golfers...

2 SPORTS INJURY BULLETIN No 149

collected from four amateur and four pro golfers. Shear loads were high in both groups but were higher in the amateurs, averaging 596 Newtons of force versus 329 Newtons in the pros. Compressive loading on the other hand was higher in the pros, averaging nearly 7,600 Newtonsversus 6,100 Newtons in the amateurs.

To put these compressive loads in perspective, consider that the swing of a pro golfer generates compressive forces around eight times his/her bodyweight and that of an amateur around six times bodyweight. Now consider that spinal compression forces in a runner are around three times body weight, and you can begin to appreciate the problem. It is also worth noting that cadaveric studies have shown disc prolapse to occur with compressive loads of around 5,500 Newtons, which explains why the swing motion can increase the risk of an acute low back injury(15).

Despite the risk of acute low back injury as a result of the swing, many golfers report the insidious onset of LBP.

Insidious LBP is thought to occur as a result of cumulative loading as a result of the combination of large magnitude spinal forces combined with a high frequency of swing repetitions. Studies show that elite golfers who consistently suffer LBP during golfing activities tend to have a higher frequency of swing repetitions (ie spend more time playing and practising) than symptom-free golfers(16). Cumulative loading also likely explains why elite players identify overuse rather than a traumatic event as the cause of their LBP(17).

Asymmetry and LBPAs we can see in Figure 1, a relatively slow backswing followed by a powerful downswing and follow-through produces an asymmetrical trunk rotational velocity, leading to differences in spinal loading patterns between the lead and trail sides of the lumbar spine. Indeed, studies show that LBP predominantly occurs on the trail side – ie the right side of a right-handed golfer and radiological investigations of elite

players have demonstrated a significantly higher rate of trail side vertebral body and facet jo int ar thr i t ic change than age-matched control subjects(11).

Other researchers have also noted that both left axial rotation velocity and right side-bending angles on the downswing r e a c h e d p e a k v a l u e s a l m o s t simultaneously and just after ball impact, coinciding with the point at which the majority of players in their study report experiencing LBP(18). The implication is that a large amount of side bend angle combined with trunk rotation through the impact phase damages the lumbar spine by creating excessive intervertebral lateral shear. This shearing motion is potentially harmful since it is resisted primarily by d i s c s t r e n g t h r a t h e r t h a n b o n y architecture, thereby resulting in injury and pain, particularly on the trail side.

One way to reduce lateral shear is to decrease right-side bending (in a right-handed golfer). Studies show that elite players with LBP tend to address the ball with more spinal flexion – ie they slouch

Figure 1: the golf swing (right-handed golfer)

Shows the large amplitude movements of the trunk, both shoulders and the lead hip as the body rotates from the top of the backswing into the finish position.


Exercises that improve transverse abdominis and multifidus strength and endurance are especially recommended. Of particular importance is ensuring any side-to-side asymmetry is minimised – something that should be emphasised to clients.

more and use more side-bend during the swing than healthy golfers(19). The good news for golfers is that decreasing the amount of right side-bend on the downswing may be as simple as using better posture when setting up over the ball. It’s also important to note that the use of shorter clubs encourages right-side bending and that longer clubs may help in this respect.

The ‘X’ factorIn an effort to hit the ball harder and fur ther , many go l fe rs deve lop a pronounced backswing, which in theory at least allows more time for maximal force to be generated before ball contact. More backswing generates higher axial loading in the spine. This is especially the case during the initial stage of the downswing when the pelvis starts rotating towards the target a fraction before the shoulder or acromion line. The idea is to generate the

maximum ‘X’ factor stretch – defined as separation in the transverse plane between a line connecting the left and right anterior superior iliac spines and a second line drawn through the acromion processes. A skilled player can increase this ‘X’ factor stretch by as much as 19% during the initial phase of the downswing.

The problem, of course, is that this additional stretch presents even higher loadings to the spine. An over-rotation or supra-maximal twisting of the trunk while performing the golf swing increases the risk of spinal irritation and subsequent LBP. Moreover, many golfers are unable to replicate this degree of rotational stretch in the clinic when asked to do so from a neutral posture at a moderate speed. This has led some researchers to question whether the X-factor loading can be reduced.

One study found that reducing the relative amount of spinal rotation or torsion by increasing the range of hip turn

during the backswing could help in cases of golfing-related LBP(20). In another study, researchers questioned whether an extreme backswing was even necessary(21). The researchers investigated the effects of using a shortened backswing on ball-contact accuracy and club-head speed. The results showed that restricting the backswing by almost 20% (thereby reducing spinal loading) had no negative effect on overall swing performance.

Together, these and other results have led some researchers to suggest that golfers with LBP adopt a more ‘classic’ golf swing – as used in an earlier era of the game. The classic swing incorporates a reduced X factor, which decreases the torque and subsequent stress on the lumbar spine. This is achieved by allowing the lead heel (ie left heel in a right-handed golfer) to lift during the backswing to allow the pelvis (and not just the shoulders) to turn away from the target.

Box 1: Core stabilisation training suggestions for golfers

Plank (with extension shown in B) Opposite arm/leg extensions

Side bridging

Resisted trunk rotation


Getting to the core of itGiven the role of trunk musculature in generating the swing movement (both downswing and backswing) , i t ’ s unsurprising that researchers have investigated whether core muscle dysfunction is implicated in golf-related LBP. Some studies do indeed suggest that golfers with LBP appear to activate their trunk muscles differently to symptom-free golfers, and it’s possible that over time, these differences contribute to reduced trunk muscle strength and endurance.

For example, one study found that the onset times of major bursts of activity from some of the abdominal muscles were delayed in the golfers suffering LBP(22). In particular, the lead external oblique (left in right-handed golfers) was activated significantly later during the backswing in the golfers with LBP when compared to asymptomatic controls. Another study looked at EMG activity in the abdominal and trunk muscles of golfers with and without LBP, and found that highly skilled players tended to demonstrate reduced erector spinae activity at the top of the backswing and at ball impact(23).

A small number of studies have compared trunk muscle endurance in golfers with and without LBP. For example one study (51) investigated the total time golfers with and without LBP could maintain an isometric transverse abdominis contraction and found that healthy golfers were able to maintain the static contraction for significantly longer than the golfers with LBP(24). This is relevant because transverse abdominis is known to be very important for protecting the lumbar spine by tensioning the thoracolumbar fascia(25).

Another study found that isometric trunk extensor (eg erector spinae) holding t i m e s f o r g o l f e r s w i t h L B P w a s significantly lower than values reported from heal thy subjects (26), and an Austra l ian s tudy on t ra inee gol f professionals found that golfers with a trail side (ie right side for a right-handed golfer) deficit of 12.5 seconds on the static side-bridge endurance test reported more frequent episodes of moderate to severe LBP(27). Further evidence indicates that elite golfers tend to have greater axial rotation strength in the direction they normally swing a golf club (ie to the left for a right-handed player) and that this asymmetry or imbalance is likely to be more pronounced in golfers with LBP(28). Together, these findings suggest that all

golfers, but especially those prone to LBP should perform some regular core stabilisation training exercise (see Box 1).

Summary and recommendationsWhen a golfer presents with low back pain, it’s more than likely that the regular practice of his/her sport will be a major contributing factor. In addition to the usual treatment modalities for LBP, it is useful for clinicians to understand how the kinematics of golf can result in LBP and what practical recommendations regarding golf practice can be made to patients in order to speed recovery and reduce the risk of re-injury. Box 2 summarises these recommendations.

References1. J Appl Biomech. 2002;18:366–73

2. Sports Med.2005;35(5):429–49

3. J Appl Biomech. 2011;27(3):242–51

4. Am J Sp Med. 2003;31:438–443

5. Phys Sports Med. 1990;18:122–26

6. Br J Sports Med. 1992;26:63–5

7. Phys Sports Med. 1982;10:64–70

8. Clin Sports Med.1996;15(1):1–7

9. Br J Sports Med. 1992;26(1):63–5

10. McNicholas MJ, Neilsen A, Knill-Jones RP.

Golf injuries in Scotland. Human Kinetics; 1999

11. Low back injury in elite and professional

golfers: an epidemiologic and radiographic

study. Champaign, IL: Human Kinetics; 1999

12. Am J Sports Med. 1996;24(5):659–64

13. Ergonomics. 1995;38(2):377–410

14. Biomechanical analysis of the golfer’s back.

Cochran AJ editor. London: E and FN SPON;

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15. Mechanics of the intervertebral disc. Ghosh

P editor. Boca Raton (FL): CRC Press; 1988

16. J Sports Sci. 2002;20(8):599–605

17. Phys Sportsmed. 1982;10:64–70

18. Morgan D, Sugaya H, Banks S. A new twist

on golf kinematics and low back injuries. South

Carolina: Clemson University; 1997

19. J Sports Sci. 2002;20(8):599–605

20. Med Sci Sports Exerc. 2000;32(10):1667–73

21. J Manipulative Physiol Ther.

2001;24(9):569–75

22. Med Sci Sports Exerc. 2001;33(10):1647–54

23. J Sci Med Sport. 2008;11(2):174–81

24. J Man Manip Ther . 2000;8:162–74

25. Phys Ther. 1997;77(2):132–42

26. Spine (Phila Pa 1976). 2001;26(16):E361–6

27. Phys Ther Sport . 2005;6:122–30

28. N Am J Sports Phys Ther. 2006;1(2):80–9

In the light of the evidence above, the following suggestions are likely to benefit all golfers, but particularly those who are prone to low back pain:

Encourage patients to adopt a common sense approach to play/practice volume; while playing and practising improves performance, players need to be aware of the spinal stresses that golf practice produces and find a balance between participation volume and recovery from LBP.

Address asymmetries in trunk musculature/strength between the lead and trail sides produced by high-volume, repetitive practice of golf swings. Perform bilateral strengthening exercise and encourage golfers to take left and right-handed practice swings.

Improve trunk rotation flexibility, which helps control the relative over-rotation of the spine during the golf backswing. Explain to golfers the importance of lifting the lead heel at the completion of the backswing, which allows more pelvic rotation, in turn reducing spinal torsion.

Improve the strength and endurance of the spinal stability musculature using a variety of core exercises.

Work on improving hip rotation and range of movement, especially on the lead side. During the swing, the body pivots onto the lead side; a reduction in the amount of hip rotation on the lead side can cause increased movement and force to be transmitted to the lumbar spine resulting in LBP.

Explain the importance of a thorough warm-up prior to playing/practicing and advise patients not to carry golf clubs on their shoulders when playing (push carts are preferable).

Last but not least, encourage patients to seek professional assistance from a properly qualified golf coach to assess swing mechanics and determine if there is a need to decrease the amount of spinal side bend on the downswing and through impact. Improving posture over the ball is an example of the way this can be achieved.

Box 2: Practical ‘on and off the course’ suggestions for reducing LBP in golfers


Tendons are bands of tough connective tissue that connect muscles to bones. They conduct the force generated by the muscle to move the bone; therefore they must be strong enough to endure the transmission of forces, yet flexible enough to, in some instances, act as pulleys around bony prominences. Collagen, a protein found in the extracellular matrix (ECM) of connective tissue, gives tendons their tensile strength and allows them to be stretched without breaking. Collagen molecules bind together to form a microfibril, and microfibrils join one another to form a collagen fibre (see Figure 1). Many collagen fibres make up a fibre bundle, and many fibre bundles joined together are called a tendon fascicle.

The fibre bundles and tendon fascicles are sheathed in a thin layer of loose connective tissue called the endotenon. The endotenon enables the bundles and fascicles to move independently of one another, sliding against each other as needed to adjust to the angle and force between the muscle and the bone. The endotenon is a continuation of the connective tissue that surrounds the entire tendon, called the epitenon. Some tendons have an additional sheath-like covering called the peratenon, which, while functioning with the tendon, is a distinct structure.

The tenocyte, the regulatory cell within the tendon, modulates the secretion of the extracellular matrix and the assembly of the collagen within the tendon. Tenocytes lie in long rows along the collagen fibres and are also found in the endotenon and epitenon of the tendon. The tenocytes form a connective web of finger-like projections that allows the cells to communicate with each other as to the need for synthesis or degradation of collagen fibres. They trigger the formation of more col lagen cel ls when they experience stresses of short duration. Prolonged tension, however, results in collagen inhibition.

The blood supply to tendons is markedly less than that of the muscle to which they are attached. The vessels that do exist within the tendon are quite small,

and run alongside the fascicles within the endotenon sheath. Some areas of tendon lack a blood supply altogether. As one might suspect, these areas are especially vulnerable to degeneration and rupture.

Tendon injuryAthletes frequently injure their tendons due to either overuse or trauma. Of the 32 mil l ion musculoskeletal injuries documented in the United States annually, 45% of them are injuries to tendons, ligaments, or joint capsules(1). The tendons most commonly injured by athletes are the tendons of the rotator cuff of the shoulder, the Achilles tendon, patellar tendon, and elbow extensor tendon.

Factors that place a strain on the tendon and contribute to overuse injuries include:

Abnormal direction of pull due to skeletal misalignment; Differences in limb lengths;

Muscle weakness or imbalances; Hypermobile joints; Inflexible muscles; Training errors; Faulty or improperly fitted equipment and shoes.

Notoriously difficult to treat, tendon injury was historical ly thought of as an inflammatory condition, and thus termed tendonitis. Treatment was aimed at reducing the inflammation through traditional anti-inflammatory medications and moda l i t i es , and was l a rge ly unsuccessful. Further study revealed that acute inflammatory cells were absent despite a disruption to the collagen formation within an injured tendon. A new term, tendinosis, was heralded to describe the degenerative lesions observed in the tendon tissue, and the absence of i n f l a m m a t i o n . D e s p i t e t h e n e w

Tendons

Tendonitis vs tendinosis: the inflammation vs degeneration debateAlicia Filley looks at tendon injury – and the ways in which these conditions have been diagnosed and treated…

Figure 1: The anatomic structure of a tendon

Tendons are comprised of groupings of building blocks beginning with collagen molecules which join to form collagen microfibrils, then tendon fibroblasts, then fibres, fibre bundles, and fascicles. Fascicles are surrounded by the endotenon and grouped together to form the tendon itself.


nomenclature and the addition of therapies to address the degeneration of the tendon rather than the inflammation, successful treatment of tendon dysfunction, which we shall call tendinopathy, has been elusive.

Inflammation plays a roleAdvances in histology allow scientists to now take a closer look at the process of tendinopathy. Studies of injured human tendon are difficult because by the time a person seeks medical help the injury is usually chronic. Therefore, animal models are studied to reveal acute tendon changes. Scientists from Queen Mary University in London examined the response of the tenocytes of horse tendons to cyclic loading(2). Fascicle bundles from six horses were divided into treatment and control groups. Treatment samples underwent repeated loading strain, while controls remained unloaded.

Twenty-four hours after a cyclic loading protocol, the collagen cells within the fascicles of the treated tendons appeared rounded and unorganised, while the control cells were long, thin, and aligned longitudinal ly a long the fascic le . Inflammatory markers were found in the treated samples after their loading cycle, while the control samples exhibited few if a n y m a r k e r s f o r i n f l a m m a t i o n . Researchers concluded that tendon cells respond to high levels of stress with an inflammatory reaction, especially in the acute period following injury.

These findings are consistent with other animal studies, which find both an increase in inflammatory markers after episodes of loading or tendon damage, as well as an increase in the number and size of the tenocytes(2). The proliferation of tenocytes is known to occur in the presence of inflammation; therefore, this reaction is seen as an ar te fac t o f a prev ious i n f l a m m a t o r y c a s c a d e ( 3 ) . W h i l e degeneration is seen in chronic tendon injury, inflammation may be the instigator of those changes within the tendon during the acute period of tendon disease.

Further evidenceUltrasound examination of symptomatic tendons shows an increase in blood flow to the tendons. Healthy tendons are characteristically lacking in blood supply, therefore, to achieve this increased circulation, new blood vessels infiltrate the tendon. This neovascularisation typically o c c u r s i n c o n j u n c t i o n w i t h a n accompanying nerve alongside the blood vessel. The sprouting of new nerves within

A continuum model of degenerative tendinopathy proposes that tendons that experience a continuous normal load (overuse) or a sudden excessive load (changes in training or equipment) may react in an abnormal way and begin a cascade toward degeneration. If the load is modified, then healing may take place during the reactive or disrepair stages. However, degeneration is irreversible. (Reproduced form British Journal of Sports Medicine. J. L. Cook, C.R. Purdam, vol 43, pg 410, 2009, with permission from BMJ Publishing Group Ltd.)

Figure 2: A model of degenerative tendinopathy

Degenerative tendinopathy

Normal tendon Adaptation

OptimisedUnloaded

Excessive load +

individual factors

Appropriate modified

load

the injured tendon is thought to be the source of pain in tendinopathy.

The influx of blood flow is assumed to be evidence of degeneration within the tendon and an attempt at healing the damaged t i s sue . However , such neovascularization and neoinnervation could likely not occur without the presence of inflammatory mediators at some point (4). Researchers at Cambridge University point to the fact that the appearance of the tendon body of patients with tendinopathy due to overload or injury is indistinguishable on ultrasound from those of patients with known inf lammatory d iagnoses such as rheumatoid arthritis3.

Biochemical influencesCyclooxygenase-2 (COX-2) is an enzyme, which in the presence of arachidonic acid stimulates the production of prostanoids and produces inflammation. Studies show that levels of prostanoids are increased in

animal tendons subjected to repeated loading(4). In tendons subjected to injected prostanoids, changes observed within the tendon are consistent with tendinopathy(3). Therefore, the presence of greater levels of prostanoids in diseased tendons is evidence of an inflammatory process within the tendon.

Substance P is a peptide secreted by nerves and inflammatory cells. The presence of substance P in significant amounts in chronic tendinopathy is thought to be the result of an inflammatory process within the tendon. Substance P causes an increase in the number of tenocytes in a tendon. Therefore, the increased number of tenocytes observed in an injured tendon may be the result of inflammatory mediators such as substance P. Substance P also increases the ratio of collagen III to collagen I molecules in the extra cellular matrix (ECM). In a healthy tendon, collagen I is the predominant type found within the ECM. This change in the

Optimisedload

Strengthen

Reactive tendinopathy

Tendon dysrepair

Normal or excessive load +/-

individual factors

Stress shielded


composition of the collagen in the ECM may well account for the difference in the shape and size of the collagen and simultaneous disorganisation observed in the London study(3).

Degeneration theoryResearchers in Melbourne, Australia, developed a multi-stage model of tendon injury that encompasses the current thinking on tendinosis (see Figure 2)(4). When a healthy tendon experiences an increased load, it responds by increasing its stiffness to handle the greater force demand and increasing the production of collagen cells. The Australian researchers propose that this short-term proliferative but non-inflammatory cell response, is a reactive tendinopathy. Their thought is that the increase in cells is an attempt by the tendon to increase the cross-sectional area and therefore, better handle the load. This short-term adaptation is reversible if the load is diminished or the tendon has a chance to rest before the next stress is applied. A healthy tendon adapts to the stress by growing larger and thus stronger. A diseased tendon does not recover from the stress and progresses to stage two.

In the second stage, termed tendon disrepair, the tendon attempts to heal itself by adding more cells to the ECM, which increases the protein production of proteoglycans and collagen. They propose that it is the increase in the number of proteoglycans that changes the collagen composition and appearance and gives the ECM a more disorganised appearance. They note the increased vascularity at this stage. Their posit ion is that with modification of the load applied to the tendon, the composition of the ECM can be altered and healing may still take place at this stage.

The f inal stage is degenerative tendinopathy. The hallmark of this stage is cell death, with areas of tendon completely devoid of healthy cells and an ECM filled with vessels, metabolic by-products, and little else. This stage is considered irreversible. Degenerative tendinopathy is found as distinct lesions within a tendon. The injured tendon may exhibit varying stages of degeneration throughout the tendon.

Two sides of the same coinWhat histology reveals about injured tendons, in fact, is that inflammatory changes and degenerative changes are both found within the same tendon(5). A group of scientists from Italy and Sweden

p r o p o s e d a d i f f e r e n t m o d e l f o r tendinopathy, encompassing both the in f l ammatory and degenera t i ve observations. Termed the “iceberg theory”, this model begins with the assumption that normal exercise stimulates the production of new collagen within a tendon (see Figure 3)(5). At the same time, collagen degradation also occurs, likely as a means of remodelling the tendon to accommodate the new load(6). Exercise therefore stimulates the production of inflammatory markers and growth substances, both needed for stimulation of the healthy tendon response of proliferation and degradation. In healthy tendons, collagen synthesis wins out in this equation and the tendon becomes larger and stronger.

When a tendon experiences repeated strain or overload, the collagen fibres within the tendon begin to slide past one another, breaking their connective bonds and causing a denaturation of the collagen. This micro-trauma is hypothesised to weaken the tendon, and affects both the ECM and the blood supply(5). Vigorous or repeated exercise also increases the temperature within the tendon tissue. The dissipation of heat is difficult in tendons, due to their sparse vascularity. The

scientists theorise that it may be the hyperthermia within the tendon that causes the degeneration of cells rather than hypoxia.

Cessation of loading, rest, and adequate blood supply are needed for the tendon to heal from excessive strain. If the tendon does not have the required blood supply, factors are produced which stimulate angiogenesis. The appearance of new vessels, which typically include nerves alongside the blood vessels, is thought to weaken the structure of the tendon(5). The secretion of both glutamate and substance P by the sprouting nerves contributes to a neurogenic inflammation as well as tendon cell death. It is at this point in the continuum that athletes may complain of pain and seek medical attention.

Clinical relevanceUnderstanding that there may be both inflammatory and degenerative processes in chronic tendinopathy may improve treatment outcomes. Since inflammation occurs early in the course of tendinopathy, non-steroidal anti-inflammatory drugs (NSAIDS) and steroid injections may be most effective at the onset of pain or when the athlete first notices a ‘tweaking’ or strain of the tendon. Sclerosing therapy

Figure 3: The iceberg theorisation of tendinopathy

The iceberg theory maintains that there are distinct phases of tendinopathy that include both inflammation and degeneration. By the time an athlete experiences a painful tendon, significant damage may have already occurred within the tendon. This may explain why previously asymptomatic tendons rupture and why symptomatic tendinopathy is so difficult to treat successfully. (Reproduced from Arthritis Research and Therapy, M. Abate, K. G. Silbernagel, vol 11, pg 235, 2009, with permission from BioMed Central.)

Iceberg theory

Pain

Neoangiogenesis nerve proliferation

Relative overload

Healthy exercise

Microruptures

Physiological adaptations

Neurogenic inflammation


IntroductionThe Gluteus Medius (GMed) is a muscle that has received a significant amount of interest amongst the correctional exercise fraternity and physical therapy world. It is a muscle that is often implicated in playing a crucial role in stabilising the pelvis during stance phase of gait and controlling the sagittal, frontal and coronal planes of movement of the lower limb during stance phase. Dysfunction in the GMed has often been associated with a range of musculoskeletal pain syndromes including knee, back and hip problems.

Relevant anatomy and biomechanicsDuring single-limb weight bearing movements such as stance phase of walking/running, lunging, landing from a jump amongst others, the natural tendency for the lower limb joints is to absorb the impact of gravity on the body. The force of gravity will generate joint moments into certain directions and muscles are required to work to counteract these forces (usually these muscles work isometrically and/or eccentrically). Table 1 describes the ‘absorbing’ joint movments and which muscles control these joint moments.

The GMed is a proximal hip muscle that is purported as one of the muscles that controls proximal pelvic/hip joint motion that in turn controls lower limb kinetics around the knee and ankle. Most anatomy textbooks will describe the GMed as attaching to the iliac crest and inserting onto the greater trochanter. Its function is often described as being a hip abductor,

hip external rotator and stabilising the pelvis on the femur during stance phase of gait. However, as Gottschalk et al (1989) suggest, its most significant role may in fact be to compress the femoral head into the acetabulum during the stance phase of gait(9). The muscle is divided into three equal components: anterior, middle and posterior.

The fibres of the posterior portion run almost parallel with the neck of the femur, while the middle and anterior parts run vertically from the iliac crest to the anterosuperior aspect of the greater trochanter. Each of the three parts of GMed has its own nerve supply running from the superior g lutea l nerve , suggesting that the muscle actions of the three heads are independent of each other.

Gottschalk et al (1989)(9) also conducted EMG studies and they found that the GMed is not all that active in isolated

abduction of the hip. This finding may well surprise most readers, as it is contrary to what has been taught for years in anatomy and biomechanics lectures and textbooks. They observed that the tensor fascia lata (TFL) is significantly more active in isolated hip abduction. They went on to suggest that the three heads of the GMed have a phasic muscle action during stance phase of gait. The posterior directed fibres are more active at heel strike, and then the muscle becomes progressively recruited from posterior to anterior as movement occurs from early stance to late stance of gait. In other words, the front portion of the muscle (which is anatomically similar to the TFL) is most active at full stance and single-leg support phase, while the rear fibres fire strongly at initial heel strike.

Gottschalk et al suggested that the main role of the GMed is to compress the head of the femur into the acetabulum (hip

muscle series

The Gluteus MediusChris Mallac looks at the gluteus medius – and the most common dysfunctions and how they’re best rehabilitated…

and eccentric exercise both function to destroy or reduce the number of new blood vessels and nerves in the tendon. In theory, by reducing the number of new vessels, the tendon returns to normal and pain decreases. Eccentric exercise has the added benefit of stimulating collagen production(4). Manual therapies, such as augmented soft tissue mobilisation, are thought to also stimulate collagen production and return the ratio of type III collagen to type I collagen within the ECM to normal.

This new paradigm of tendon disease stimulates new ideas for treatments. Treatments currently under investigation include biologic therapy, nitrous oxide, biochemical scaffolding, exogenous growth factor, platelet rich plasma injection, stem cell injection, and tissue engineering. More research is needed to isolate which tendons, in what stage of disease, respond best to which therapy. In the meantime, the best recommendation is to treat any twinge or suspicion of tendinopathy early when the anti-

inflammatory methods are most effective and the chance for healing is greatest.

References1. Birth Defects Res C Embryo Today. 2013

Sept;99(3):203-22

2. Scand J Med Sci Sports. 2014:1-11

3. Br J Sports Med. 2014;48:1553-7

4. Br J Sports Med. 2009;43:409-16

5. Arthritis Res Ther. 2009;11(3):235

6. J Anat. 2008;212:211-28

Table 1

Absorption movement Controlling muscles

Pelvic lateral tilt (Trendelenburg Sign)

Hip abductors (TFL, GMed, Glute Min, Glute Max – superior fibres)

Anterior pelvic tilt Pelvic posterior tilters such as gluteals and hamstrings.

Hip joint flexion, adduction, internal rotation

Controlled by gluteus medius and other hip joint external rotators such as the gemellus muscles, quadrutus femoris, obturator muscles and piriformis.

Knee joint flexion Quadriceps

Ankle dorsiflexion Soleus

Midfoot pronation Tibialis Posterior, FHL, FDL.


socket) during locomotion and to assist in stabilising the pelvis on the femur in single leg stance. They then put forward the notion that each of the three distinct heads of the muscle performs a unique role in locomotion:

The posterior fibres contract at early stance phase to lock the ball into the socket. This idea is supported by the observation that the posterior fibres have an almost parallel fibre alignment with the neck of the femur. The posterior fibres therefore essentially perform a stabilising or compressing function for the hip joint.

The middle/anterior fibres, which run in a vertical direction, help to initiate hip abduction, which is then completed by the TFL. These fibres work synergistically with TFL in stabilising the pelvis on the femur, to prevent the other side dropping (or Trendelenburg). The researchers point out that the TFL has the more important role in stabilising the pelvis on the supporting hip; the GMed simply assists this action, analogous to how the supraspinatus in the shoulder assists the more powerful deltoid in shoulder abduction. The anterior fibres allow the femur to internally rotate in relation to the hip joint at mid-to-end stance phase. This is essential for pelvic rotation, so that the opposite side leg can swing forward during gait. The anterior fibres perform this role with TFL. So Gottschalk et al postulated that the primary functions of the GMed are:1. To stabilise the femur on the ilium (pelvic stability)2. To act as hip rotators 3. To approximate the head of the femur into the acetabulum, in effect creating a very tight and stable hip joint during gait.

Other researchers have found on cadaver studies that GMed has a large physiological cross-sectional area and short fibre lengths and therefore is able to generate large forces over a narrow range of lengths(16). They

postulate the GMed really only works in neutral hip/pelvic postures as it would when stabilising the pelvis and hip during single leg stance. Exercises that force the GMed into lengthened or overly shortened positions may in fact not target the GMed but other hip abductors/external rotators. GMed has the largest CSA of the hip abductors so it should be the more dominant of the hip abductors. It can produce a lot of force for its size as it has short fibres which are packed tightly together. But is does not produce large forces over a wide range of lengths. It is designed to work isometrically and stabilise the hip on the femur and vice versa.

Injuries to the Gluteus MediusDysfunction in the GMed has often been associated with a range of musculoskeletal pain syndromes. It is believed that these injuries are a result of the inability of the GMed to control movement and alignment at the pelvis, femur and tibia. These injuries include but are not limited to:1. Patellofemoral pain syndromes(15)

2. Lumbar spine problems(11)

3. ITB friction syndromes(8)

4. Hip joint pathology(10).

It has been assumed for some time that hip internal rotation is an unwanted pathomechanic of the hip joint as hip joint rotation will allow the femur to migrate inwards and create valgus collapse at the knee. The assumption has then been further extrapolated to suggest that this unwanted hip internal rotation is a consequence of weak GMed and other hip joint external rotators. However, the work by Ward et al (2011)(16) suggest that in fact the GMed seems to work be t t e r physiologically if the hip is placed in some internal rotation. Therefore is this hip internal rotation a compensation to allow the GMed to be recruited better in the presence of weakness of other hip muscles such as the gluteus maximus and other deep hip rotators?

Direct injuries to the GMed such as trigger points, strain injuries, tendon tears and associated trochanteric bursitis have also been attributed to having weak GMeds(3,12,13).

Rehabilitation Exercises for the Gluteus MediusA wide range of studies have examined the funct ion of the GMed whi ls t performing a variety of lower limb exercises(1,2,4,5,6,7). These studies base their conclusions on relative electromyographic (EMG) data during certain exercises. The top five exercises in each study are presented in Table 2 and readers can be directed to the reference l is t for clarification on the exact exercises used in the respective studies. The % displayed alongside the exercise is the % of Maximal Voluntary Contraction (MVC) of the GMed. It needs to be pointed out that differences in activity between authors may be different due to a number of factors such as:1. EMG placement2. Electrical interference from other muscles3. Differences in the exact mechanics of the chosen exercises.

Also the EMG data does not necessarily tell us if the GMed is creating the action or simply stabilising the hip joint and pelvis whilst other muscles are working, similar to how the rotator cuff muscles work during active shoulder abduction and flexion movements.

In a more recent study, researchers looked at the relative contribution between the GMedand the TFL and identified these five exercises that best used GMed with minimal TFL(14):1. Clam with theraband2. Sidestep with theraband3. Unilateral bridge4. Quadruped hip extension, knee extending5. Quadruped hip extension, knee flexing.

Table 2: Rehabilitaion exercises for the Gluteus Medius

Distefano et al (2009)(7) Bolga and Uhl (2005)(4) Ayotte et al (2007)(2) Boren et al (2018)(5)

Sideways hip abduction 81% Pelvic drop 57% Wall squats 52% Side plank abduction with dominant leg on bottom 103%

Single limb squat 64% WB with flexion left hip abduction 46% Front step ups 44% Side plank abduction with dominant leg on top 89%

Lateral band walk 61% WB left hip abduction 42% Lateral step-ups 38% Single limb squat 82%

Single-limb deadlift 58% NWB side lie hip abduction 42% Retro step-ups 37% Clamshell (hip clam) 77%

Sideways hop 57% NWB standing hip abduction 33% Mini squat 36% Front plank with hip extension 75%


With so many variations in the possible beneficial exercises that may be used to strengthen the GMed, often the choice of exercise used by the therapist may simply be a ‘horses for courses’ approach. If the individual feels pain on weight bearing movements then non-weight bearing variations may be used. Often the client simply may not ‘feel’ the movement required therefore other exercises need to be chosen. Often it may simply be the therapist’s personal choice as to what they perceive to be the most effective GMed exercise. Furthermore, it could be argued that what a client feels in and around their postero-lateral hip may be GMed and/or other hip abductors such as gluteus minimus and/or other deep hip rotators such as piriformis, the obturator group, quadrutus femoris and gemellus muscles. Studies are needed using both surface EMG and fine wire EMG on deep muscles to truly elucidate the contribution of the complex interactions between these muscles.

The three exercises shown below are variations on other exercises listed in Table 2. The reason they have been included is to satisfy the work by Gottschalk et al(9) that shows that GMed works in varying ways during hip flexion to extension as demonstrated in the gait cycle, and also the work by Ward et al(10) that suggests the muscle works through very neutral hip/pelvic positions and works essentially isometrically or through very short ranges of movement. Furthermore, the three exercises attempt to either directly weight bear through the hip joint or simulate weight bearing through the hip joint, making them more functional in terms of activation in weight bearing positions.

1. Standing short range hip abduction.This exercise works both the stance limb ( isometr ic ) and non-s tance l imb (concentrically). a. Stand with a band around the foot and the hand on the same side supported by a broomstick for balance. b. Gently move the banded leg into abduction/external rotation/extension. c. The stance limb is in slight hip flexion and remains in this position. d. Perform 8-10 repetitions of slow hip abduction/external rotation/extension.e. This will be felt in both the stance side GMed (in slight hip flexion) as well as the abducting side GMed (into slight hip extension).

2. Kneeling clam. This is one variation on the ever popular clam exercise that has been shown in numerous studies to activate the GMed muscle. Again this is performed in weight bearing as the limb accepts axial load via kneeling. a. Kneel on a bench with a band wrapped around the knees. Feet are kept together.b. Hold onto a broomstick for balance.c. Gently move the knees apart whilst maintaining the foot contact. This moves the hip into slight abduction/external rotation. d. Perform sets of 10-15 repetitions and ensure the movement is kept small (2-3 inches only).

3. Modified clam. This is another variation on the clam exercise that resembles the traditional clam except with some variations. The first important difference is that the heels push into a wall or box to simulate weight bearing through the limb. Next the exercise is performed as an isometric hold and not an active abduction/adduction movement. Finally the exercise is performed in two positions: 1. Slight hip flexion and 2. Slight hip extension. A light weight is placed on the knee to act as external resistance. The aim is to hold the limb static for a prescribed period of time.

Standing short range hip abduction (finish)

Kneeling clam – start. Notice feet together and knees together

Kneeling clam – finish. Notice feet together and knees apart

Standing short range hip abduction (start)

Modified clam – hip in slight flexion

Modified clam – hip in slight extension. Note the contralateral hip is flexed to assist the pelvis to maintain a neutral tilt. If the knees are kept together, this encourages unwanted anterior pelvic tilt


The foot is the most complex region of the lower limb, and probably the most intricate area in the body. It serves as a launching pad of the athlete; being the first part to contact the ground, absorbing the ground’s forces (which can exceed more than four times your body weight running or up to 12 times with jumping and impact) and propelling the athlete forwards, or in to any direction they desire(1). It is therefore not surprising that the foot can become overused and subject to numerous localised injuries. However, the problems can also originate from further up the kinetic chain (further up the leg) such as the pelvis/hips, knee and/or ankle. Injuries or bio-mechanical problems more proximally up the leg can have a subsequent, indirect effect on the foot mechanics(2). Directly or indirectly, foot problems can therefore be a huge burden on the athlete. Here we present the issues to consider and how to address them.

Collectively the foot and ankle structure hosts 26 small bones that form 33 joints to allow the dynamic nature the foot provides to meet the athlete’s demands. Over 100 muscles, ligaments and tendons connect these joints together. Additional structures then connect the foot to the lower leg. The Achilles tendon connects the calcaneus (heel) to the calf muscles and provides major ankle stability. The front of the leg is supported by the tibialis anterior, which provides the upward motion to the foot, and the back of the leg is supported by tibialis posterior, which supports the foot arch. The peroneal muscles are located on the outside of the leg and ankle and provide

lateral stability. These intricate connections depict how a foot imbalance can affect the rest of the lower leg, and vice versa.

Ankle sprains are damage to the ligaments, and are reportedly the most common trauma ankle/foot injury in

athletes (4). Approximately 30% of ankle sprains then go on to develop chronic ankle instability, giving a less stable base at the bottom of the leg to impact the ground. This then affects the whole lower limb as the alignment of the leg will be imbalanced and

Foot injuries

Foot pain: looking up the kinetic chain

Foot injuries among athletes can originate from many sources. Tracy Ward explores the common problems, what may cause them and how you can prevent yours by looking further afield.

ConclusionThe GMed is a muscle that has received a lot of research and attention in the last few decades. Research into the GMed using EMG, biomechanical modelling and cadaveric studies have concluded that it is an important muscle that needs to be strengthened to assist in pelvic control, hip joint stability and lower limb kinetic control. This article presents the relevant and up-to-date anatomy and biomechanical knowledge on the muscle, the existing research on activation in exercise and also

the author’s suggestions on some new exercises that can work the GMed muscle.

References1. Arch Phys Med Rehabil; 1999. 80:842-850.

2. J Orthop Sports Phys Ther; 2007. 37: 48-55.

3. The Iowa Orthopedic journal. 2003. 23; pp57-

60.

4. J Orthop Sports Phyl Ther; 2005. 35: 488-494.

5. International Journal of Sports Physical

Therapy. 2011. 6(3). 206-223.

6. J Sport Rehabil; 2009. 18:91-103.

7. J Orthop Sports Phys Ther; 2009. 39: 532-

540.

8. J Orthop Sports Phys Ther; 2010. 40:52-58.

9. Journal of Anatomy. 1989. 166: 179-189.

10. Man Ther. 2009;14:611-617.

11. Arch Phys Med Rehabil; 1998. 79:412-417.

12. AJR. 173(4); 1123-1126.

13. Eur Radiol. 2006. 17(7); pp 1172-83.

14. Journal of Orthopaedic and Sports Physical

Therapy. 2013. 43(2); 54-65.

15. J Orthop Sports Phys Ther. 2009. 39:12-19.

16. Journal of Orthopaedic and Sports Physical

Therapy. 2011. 40(2); 95-102.

Foot anatomy

The sections of the foot are shown as the forefoot, midfoot and rearfoot. Within these sections the main bones are labelled.

The forefoot consists of the toes (phalanges) and these are connected to the midfoot by the metatarsals. The midfoot region is the shock-absorbing section and is formed by the cuneiform, navicular and three cuneiform bones. The rearfoot houses the talus and calcaneus (heel bone) and together these form the subtalar joint. The subtalar joint provides approximately 40 degrees of inversion and 20 degrees eversion of the ankle. The talus then meets with the ends of the tibia and fibula to form the ankle joint (talocrural joint) and is responsible for 20-30 degrees ankle dorsiflexion and 30-50 degrees plantarflexion.


stress the joints and muscles incorrectly. Achilles tendonitis and plantar fasciitis are the two most common overuse injuries, resulting in inflammation of the Achilles tendon and plantar fascia (ligament along the sole of the foot) respectively (5, 6).

Stress fractures can occur to any of the foot bones (see Figure 1). These are likely found where the athlete is heavier weight bearing and will depend on how they strike the ground. Finally, tendon strains can occur to the anterior or posterior tibialis muscles, or to any of the tendons associated with the foot and ankle. How these structures become impaired can be the result of the athlete’s biomechanics. This is simply how they move; how their foot strikes the ground and how all the muscles and joints respond to this further up the limb.

BiomechanicsRunning pattern is difficult to analyse for every sport and every individual within this one discussion, as how the athlete contacts the ground will depend on what they intend to do next. Distance runners will impact the ground usually with their heel first (see Figure 2); however, those who are sprinting or rapidly changing direction may utilise the forefoot initially. How the foot plants the ground can have substantial consequences thereafter.

The foot usually strikes the ground initially with supination at the subtalar joint; this is where the sole of the foot is angled slightly upwards. As the weight loads through the foot, it then rolls inwards in to pronation, with more weight on the inner edge of the foot. The position of the

foot controls the alignment of the rest of the leg as they work in coordination. Figure 2 shows the different positions of the knees and hips at the different phases of foot strike. Too much rotation of the foot, however, can then be detrimental as it impairs these other positions.

If the foot strikes in an excess pattern of increased pronation or supination, research has shown that the athlete is subject to greater ground reaction forces and rate of loading; this is the force returned from the ground, and the speed at which the load transmits through the foot(1). If the foot presents more in to pronation, there is excess internal rotation of the lower limb. This causes increased pressure to the medial structures, such as the big toe and plantar fascia. The calf muscles and peroneal muscles then work harder to control the foot angle and prevent further rotation. This creates an imbalance of forces at the patella (knee cap) and can strain the quadriceps and iliotibial band. Conversely, a more supinated foot strike has less mobility at the foot and ankle because they cannot roll in their natural movement pattern(2). Less mobility leads to less shock absorption so a greater force is transmitted through the foot, ankle up to the knee and hip. Ankle sprains are also more common with supination and inversion, as this places the lateral ankle ligaments on full stretch and strain.

Problems not to missIn addition to the common local foot and ankle injuries mentioned earlier on, there are other sources of foot pain, not

originating from the foot, that should not be overlooked: ankle impingement, gluteal weakness, and core instability.

1) Ankle impingement Ankle impingement can occur anteriorly or posteriorly. Both types involve the pinching of structures which restrict the ankle and foot movements and can be severely disabling. Dancing, athletics and soccer are the most commonly reported affected sports(8). Ankle impingement can be the result of ankle instability. Lax ankle ligaments allows greater translation of the joints and small bones, allowing gliding of the bones and can impinge on the surrounding soft tissues and tendons(8). This painful condition can refer pain throughout the foot and ankle. This is a complex problem to diagnose and must be considered if other injuries are ruled out.

2) Gluteal weakness Gluteal weakness is often due to an asymmetry at the pelvis. This can occur naturally as we weight bear more favourably through our dominant leg and cause it to be stronger and more stable. Furthermore, the gluteals often are not brought to full activation during everyday activities, as this requires proper squatting or deadlift manoeuvres, and therefore a lack of activation means they will eventually inhibit their function. Any injury that causes pain will also cause a pain inhibition effect on the gluteals. This is because of the powerful and propulsive role the gluteal muscles have, that if you have injured any lower limb structure, the

Figure 2: The phases of a running pattern (7)

The runner strikes with the heel, then plants the foot in mid-stance, before pushing off with the toes.


body inhibits the gluteals to slow you down. This will reduce the ability of the athlete to push harder(9). This is why regular gluteal training is essential to all athletes whether they are injured, or not.

3) Core instability The core muscles are enclosed within your trunk region and work endlessly to maintain posture and keep the body in correct alignment. This ensures the forces are distributed correctly throughout the body and that one limb, joint or structure is not overloaded. The core muscles respond to changing dynamics and as you change position they transfer the weight as re-quired, and bridge the space, and load between the upper and lower limbs (10).

Treat from above Once the local injury has been treated directly, the therapist should then explore the additional intrinsic factors that may have contributed to the problem. These are the problems within the body including muscle weakness and imbalances. The main areas are the gluteal muscles and

core stability. Balance is also a huge factor, incorporating all muscles and core work.

1) Gluteal strengtheningThese should be performed for the weak side initially to make up the discrepancy, and thereafter completed on both sides for bilateral stability and balance. Up to 3 sets of 10 can be instructed; however, it is more about quality of the movement and control than numerous repetitions.

2) Core stability and balanceThese should be performed on both sides to encompass the whole core region. These exercises are all done on a mat, on the stable floor surface. There is great speculation that performing core exercises on an unstable surface such as a Bosu ball, gym ball, wobble cushion etc provides greater core demand. Whilst this does provide an added challenge to the athlete, a recent study showed that performing core exercises on the unstable surfaces had no further advantage to physical fitness than the same exercises performed on the stable ground(11). So whilst they may be more core intensive, they do not

transfer to greater fitness benefits and perhaps executing the exercise with good technique is more important here than trying to achieve the hardest version.

Exercise Picture Description

Clam Lying on one side with shoulders and hips stacked on top of each other and knees bent. Keeping the feet together, open the top knee upwards as high as you can. Ensure the hips do not rotate backwards.

Side kick in kneeling

Place yourself on one side, resting on one arm and one knee. Keep the trunk lengthened and rigid. Extend the top leg and lift it up to hip height, then lower back to the mat. As an extra modification, bring the top leg forwards and backwards whilst keeping it at hip height.

Supine leg pull

Sit on the mat with legs extended and together. Squeeze through the buttocks and raise the body upwards as high as possible. Hold for 5 seconds and return. Try to keep the weight light on the arms.

Side plank

Leg bridge


3) Single-leg balancingBalance exercises on one leg are important to allow the whole kinetic chain to work together and coordinate, because most of the above exercises work muscle groups in isolation. These can also be tailored to the athlete by mimicking positions they may encounter during play. Single-leg balancing also strengthens the intrinsic foot muscles (small muscles between the foot bones) by encouraging them to function as they grip the surface for stability.

Treat outside the box Once the intrinsic factors have been addressed, the therapist should also consider the extrinsic influences. These are the external, environmental factors that may contribute to injury such as type and support of footwear, training plans, and training surfaces.

1) Footwear selectionFootwear is a hugely individual preference, and will also come down to the type of sport being played. Once the foot strike pattern has been identified the correct footwear can be selected. Those who overpronate will require a shoe with extra stability and control, and this usually consists of a medial arch support within the shoe. Those who have excess supination will require a trainer that provides extra cushioning and padding to absorb more shock.

Trainers gradually lose their support and shock absorption capacity and, for the

amateur, after 250 miles they will have depleted approximately 30-50% of their support. By 500 miles the athlete should be looking to replace their trainers to maintain good support(12). For the serious athlete the mileages could be much less. Having two pairs to alternate will also accustom the foot to different supports and minimise the wearing down of one trainer. More frequent change than this is not recommended, however, because new footwear will be more rigid, and research has shown that this causes an increase in the plantar pressure; this is the pressure the athlete places through the foot when running and could place extra strain through the foot structures(12).

2) Modified training plans/groundsThe surface by which an athlete plays on can be attributed to injury, although the evidence for this is not outstanding. In general, harder, drier surfaces can cause overuse injuries such as stress fractures and tendinopathy, as there is less shock absorption and more impact through the joints. Artificial grounds generally have a higher shoe-surface friction and are related to higher injury rates(13). If an athlete is recovering from injury, return to sport should be guided through suitable surfaces/softer grounds initially before return to normal surfaces.

Summary The foot is responsible for all weight

bearing activities, absorbing the ground’s

reaction forces, and propelling the athlete in movement;

The position the foot strikes the ground can influence injury, particularly if the foot is over-pronated or supinated;

The stability and alignment of the hips and knees can affect the angle the foot is positioned at, and impacts the ground;

Local foot positioning and patterns should be assessed first, followed by correction of abnormal foot strike, altered arches, knee position and pelvic position.

Strengthening exercises should work the gluteal muscles, core stability, alignment of the lower limb, and balance work;

Other factors to consider include the type of trainer or footwear, insoles, training grounds, and training plans.

References1. Annals of Biolog Research. 2011; 2(6): 102-108.

2. Clin Sports Med. 2010; January 29(1), 157-167.

3. Clinical Sports Medicine (2009). 3rd Ed.

Australia: McGraw-Hill Professional. pp. 646.

4. J Athl Train. 2007; 42(2):311-319.

5. Foot ankle Int. 2008;29(7):671-676.

6. Sports Med. 2006; 36(7):585-611.

7. Clinical Sports Medicine (2009). 3rd Ed.

Australia: McGraw-Hill Professional. pp.48.

8. Foot and ankle surgery. 2015;21:1-10.

9. Br J Sports Med. 2014; 48: Suppl 2: A6-A7.

10. J of Sports Rehab. 2013; 22: 264-271.

11. BMC Sports Sci, Med and Rehabil. 2014; 6:40.

12. BMC Research Notes. 2011; 4:307.

13. Scand J Med Sci Sports. 2003; 13(5): 299-304.

rehabilitation

Rehab Series: microfracture procedures for chondral defects of the knee (part 1)Chris Mallac discusses the pathophysiology behind chondral injuries in the knee, the usual mechanism of injury and presenting signs and symptoms – and focuses on the microfracture procedure…

IntroductionChondral surface defects in the knee are common in the athlete (2,3,7,14). It has been shown that around 63-66% of knees that are investigated under routine arthroscopy will have some manner of chondral defect either on the femoral condyles, posterior patella, trochlear groove or even the tibial plateau (in some cases more than one chondral defect). Furthermore, in 11% - 19% of the knees they are full thickness osteochondral defects of the articular hyaline cartilage(1,5,9).

Chondral surface injuries can affect all

types of athletes from runners to athletes in the more aggressive cutting and pivoting sports such as football, tennis and court sports such as netball and basketball. Injury to the articular cartilage between the femur and the tibia and the cartilage between the patella and femur can occur due to sudden load such as twisting on the knee in a lunge position, or it may result from repetitive trauma due to small loaded knee flexion movements that breakdown the cartilage over time.

The majority of these chondral injuries are low grade cartilage fissuring that can be

managed conservatively and do not need surgical intervention. However, a cartilage injury in a knee can progress to more serious osteoarthritic changes if not managed properly and this can lead to more serious functional impairments as the athlete gets older (3,6,13). Because articular cartilage is avascular, the transport of inflammatory mediators and cells to the site of tissue injury is limited; thus, cartilage has no intrinsic capacity to heal itself (12). Therefore managing cartilage defects in athletes is gaining more widespread attention in the literature.


Relevant pathophysiology of chondral lesionsArticular cartilage is the white, shiny covering tissue that covers the end of long bones and consists of chondrocytes (ar t icular car t i lage ce l ls ) , water , proteoglycans and collagen. In the knee this hyaline cartilage covers the femoral condyles, the tibial plateau and the posterior surface of the patella and these are collectively known as ‘chondral’ surfaces. The frictional coefficient of articular cartilage has been compared with being five times smoother than rubbing ice on ice. This allows a very smooth gliding surface and reduces the shear force across two bones. A large part of the cartilage is fluid and thus it is also able to resist compressive forces very well as the fluid is able to ‘move’ under the load and absorb this load (19). With this exceptional ability to distribute load, peak stresses imposed on subchondral bone are minimised. Yet despite the durability of articular cartilage under normal joint loading, excessive joint loading can damage it, causing loss of joint motion, instability, deformity and pain(3).

Single event-type injuries usually occur in the younger sports person; for example, a sudden forceful lunge, a patella dislocation, or a major instability episode to the knee that may also injure the anterior or posterior cruciate ligament. It has been postulated that forces greater than 25 newtons per square millimetre are enough to damage the articular cartilage as a one-off event (21). In these events, the shear force across the joint with an added compressive and/or torsional element may shave off a segment of cartilage and create a chondral or osteochondral defect or the joint compression may indent the cartilage to cause significant chondral damage. Even if these acute events do not result in full thickness chondral defects, they may start the cascade of cartilage degeneration that may then lead to a full thickness loss in cartilage over time.

The chronic repetitive-type lesions usually occur in older athletes and the older population. With repetitive loading the cartilage undergoes a number of mechanical and histological changes (3,12):a. Loss of proteoglycans and cartilage swelling;b. Increase in diameter of chondral collagen fibres;c. Altered relationship between collagen and proteoglycans;d. Progressive chondral thinning.

The progressive cascade of events in

chondra l in jury usua l l y inc lude (Outerbridge classification(18):1. Grade 1. Early softening and swelling of the articular cartilage;2. Grade 2. Fissures and cracks in the surface of the cartilage less than 0.5 inch; 3. Grade 3. Severe fissures and cracks greater than 0.5inch;4. Grade 4. Exposure of the subchondral bone.

Table 1 above shows how the Outerbridge classification relates to expected MRI findings in the cartilage(26).

Signs and symptomsTypically injuries to the articular cartilage will present as pain and functional limitation within the knee. Movements that load the knee into flexion such as running, climbing stairs, lunging and

Modified Outerbridge Classification system for cartilage damage

Grade Macroscopy MRI

0 Normal cartilage

Normal cartilage

1 Rough surface; chondral softening

inhomogenous, high signal; surface intact

2 Irregular surface defects; <50% of cartilage thickness

Superficial ulceration, fissuring fibulation; <50% of cartilage thickness

3 Loss of >50% of cartilage thickness

ulceration, fissuring, fibrillation; >50% of the depth of cartilage

4 Cartilage loss Full thickness of chondral wear with exposure of subchondral bone

(From Zilkens et al 2011)


loaded knee flexion such as squatting will be pain-limited. Often a knee joint effusion will be present, and due to gross knee joint effusions full knee extension may be limited.

The athlete may remember a particular knee loading movement that has created the articular cartilage injury such as a loaded twisting movement on a flexed knee; or more commonly the pain may start insidiously after repetitive knee flexion loading movements. The knee may suffer from episodes of catching, giving way and locking in the presence of more significant cartilage injuries.

The sports medicine practitioner will be alerted to a possible chondral lesion in the athlete as the ongoing knee joint effusion, possible locking and catching sensations and the functional limitations such as pain and inhibition in knee flexion positions will encourage the sports medicine practitioner to seek some imaging modalities. MRI has the best ability to visualise the chondral defects without the need to direct arthroscopic assessment(4). For more detailed descriptions on the exact MRI findings to expect in chondral lesions, refer to Chang et al (2011)(4).

ManagementArticular cartilage defects that extend to the subchondral bone vary rarely heal w i t h o u t s u r g i c a l i n t e r v e n t i o n . Occasionally some patients with full thickness cartilage defects may be functionally unaffected in the early stages following this injury; however, over time these can become quite debilitating and will lead to slow and progressive loss of knee function(10).

A number of interventions have been suggested that may aid cartilage healing without the need for major surgery and long-term rehabilitation. Platelet-rich plasma (PRP) injections have been suggested as a means to stimulate cartilage healing(22). PRP works by injecting the athlete’s own plasma onto the cartilage defect to stimulate a proliferation of chondrocytes and the differentiation of mesenchymal cells of the subchondral bone into the chondrogenic line. PRP is also thought to have an anti-inflammatory action on the synovial membrane, promoting early improvement in function of the joint injected. PRP is believed to exert its effect through direct stimulation of chondrocytes and mesenchymal stem cells of the subchondral bone and, especially in the early stages, through a direct anti-inflammatory action in the

synovial membrane. However, research into the long-term benefits of PRP as a stand-alone therapy for chondral defects have not been well conducted and in the interim it appears that PRP may be used as an adjunct to promoting a healing environment for a chondral defect after a surgical intervention.

Surgery for Chondral DefectsThe types of surgery available for full thickness chondral defects include:1. Abrasion;2. Drilling;3. Osteochondral autografts transfer;4. Osteochondral allografts;5. Repair with synthetic resorbable scaffolds;6. Autologous chondrocyte cell implantation (ACI);7. Matrix assisted autologous chondrocyte cell implantation (MACI procedures);8. Microfracture technique for chondral resurfacing;9. Mechanical fixation of osteochondral fractures.

The microfracture procedure was first proposed by Steadman in 1980. The microfracture procedure is a single stage arthroscopic, minimally invasive procedure that is based on the principle that stimulating the bone marrow through micropenetration of the subchondral bone leads to subsequent recruitment of platelets, growth factors and mesenchymal s tem cel ls to s t imulate chondral repair(23,24,25). The resultant ‘bleeding’ into t h e c h o n d r a l d e f e c t l e a d s t o a n accumulation of fibrocartilage that ‘fills’ the defect or hole in the cartilage. This is supported by Rand (1985)(20) who make the point that a source of cells and a matrix, an intact subchondral bone surface and some mechanical stimulation are needed in order for healing of articular cartilage to occur.

In this procedure, all the damaged cartilage is removed in order to obtain stable lesion margins, surrounded by hea l thy ca r t i l age , and per fec t l y perpendicular borders. This is necessary in order to allow the clots to adhere in a stable manner to the bottom of the lesion and to reduce the direct load on the lesion, thereby allowing a better repair. It is important that the subchondral bone is not affected during the debridement of the cartilage margins. Small ‘microfractures’ in the subchondral bone are made using an awl at 45°. The fractures start on the periphery and then move in a centripetal

direction, from the margins to the centre of the lesion typically spaced 3-4 mm apart and drilled to a depth of about 4-5 mm. This ensures penetration of the medullary cavity. Achievement of the correct depth is confirmed by arthroscopic visualization of fat droplets in the joint after drilling (13).

However, not all ‘microfracture’ procedures are fully successful. With a ‘microfracture’ procedure the lesion is repaired with fibrocartilage and this type if cartilage has a reduced ability to absorb mechanical load. As fibrocartilage conta ins more co l lagen and less proteoglycans than normal intra-articular hyaline cartilage, and a much greater concentration of type I compared with type II collagen, it is more prone to future wear and tear damage(8). Furthermore, while hyaline cartilage is normally subjected to load in compression, fibrocartilage is normally subjected to load in tension, which means that the latter is not biomechanically suited to serve as articular cartilage. In fact, repeated mechanical stresses can eventually lead to failure of a fibrocartilage repair.

Overall, microfracture procedures seem to show significant functional improvement in chondral defect effected knees(2,17,23,24,25). The majority of the improvement happens in the first year, however it usually takes two to three years to see maximum improvement in knee function. Ongoing complaints of symptoms will be common in the first year. Research has shown that it is generally quite effective on lesions that are smaller than 400mm(2) and in patients under the age of 40(11,14,15,16).

It is still the surgical treatment of choice in athletic knees for the following reasons:1. Most competitive athletes are under the age of 40 and ‘microfracture’ suits this age group the best;2. It is minimally invasive as the surgery is performed only once;3. The return to competition is faster than the more physiologically time-dependent procedures such as MACI (these need a two-year rehabilitation period);4. Athletes are back in functional rehabilitation around eight weeks post-operative negating the detrimental psychological effects of long-term rehabilitation in athletes.

ConclusionChondral defects are a common injury affecting the athlete and can be quite debilitating if not managed well. The purpose of this paper was to discuss the


Contributors to this issue

Andrew Hamilton BSc Hons, MRSC, ACSM is a member of the Royal Society of Chemistry, the American College of Sports Medicine and a consultant to the fitness industry, specialising in sport and performance nutrition: www.andrewmarkhamilton.co.uk

Alicia Filley PT, MS. lives in Houston, Texas and has 25 years experience working in rehabilitation. She is currently vice president of DISC Spine Center

Chris Mallac has worked as Head of Performance at London Irish Rugby, Head of Sports Med at Bath Rugby and Head Physio at Queensland Reds Super 14. He is currently teaching globally on Rehab Trainer Courses.

Tracy Ward MSc BSc (HONS) MCSP is a member of the Association of Chartered Physiotherapists in Sports Medicine and is a trained pilates instructor with the Australian Physiotherapy and Pilates Institute. Tracy is currently in private practice in Scotland, specialising in sports injuries and rehabilitation

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relevant physiology of articular cartilage, how it can be injured in the athlete and what are the presenting signs and symptoms. A discussion on the possible management strategies were discussed w i t h p a r t i c u l a r e m p h a s i s o n ‘microfracture’ procedures as first described by Steadman in 1980. These procedures are usually the first choice for surgeons on athletes as they are minimally invasive compared with other chondral repair procedures and have generally the quickest recovery times with very good outcomes in younger athletes with smaller lesions. Part two of this piece will describe in detail the post-surgical rehabilitation needed after a microfracture procedure.

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gulf injuries, tendinitis vs tendinosis, gluteus medius, foot pain, & cartilage injuries

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