Biomechanics of knee complex 9 frontal plane patellofemoral jt stability

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DR. DIBYENDUNARAYAN BID [PT]T H E S A R VA J A N I K C O L L E G E O F P H Y S I O T H E R A P Y,

R A M P U R A , S U R AT

Biomechanics of the

Knee Complex : 9


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Frontal Plane PatellofemoralJoint Stability


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The patellofemoral joint is unique in its potential for frontal plane instability near full knee extension, as well as for degenerative changes resulting from increased patellofemoral joint stresses (in flexion).

This multifaceted problem makes understanding the control of the patella’s frontal plane motion particularly important.


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In the extended knee, instability can be a problem be-cause the patella sits on the shallow aspect of the superior femoral sulcus.


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There is less bony stability and less patellofemoral compression from the quadriceps.

Because of the physiologic valgus that normally exists between the tibia and femur, the action lines of the quadriceps and the patellar tendon do not coincide.

This results in the patella’s being pulled slightly laterally by the two forces (Fig. 11-46).


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The presence of a resultant lateral pull on the patella suggests that soft tissue stabilizers must assume more responsibility for medial-lateral stability in the absence of suitable bony stability.


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Once knee flexion is initiated and the patella begins to slide down the femur and into the femoral sulcus (at about 20 of flexion), medial-lateral stability is increased by the addition of the bony stability of the femoral sulcus.

However, the concomitant increased compression of the patella against the femoral condyles can present another problem.


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Whether the patella is at risk for instability or for increased medial-lateral compression, the position, mobility, and control of the patella in the frontal plane are of utmost concern.

These factors are determined by the relative tension in both the transverse and longitudinal stabilizers of the patella.


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The longitudinal stabilizers of the patella consist of the patellar tendon inferiorly and the quadriceps ten-don superiorly.

The patellotibial ligaments that are part of the extensor retinaculum and reinforce the capsule also are longitudinal stabilizers (see Fig. 11-14).


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The longitudinal stabilizers are capable of providing medial-lateral stability of the patella in knee flexion through increased patellofemoral compression (see Fig. 11-45).


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In the extended knee, this compression is minimal, however, leaving the patella relatively unstable in this position.

When extension is exaggerated, as in genu recurvatum, the pull of the quadriceps muscle and patellar tendon may actually distract the patella somewhat from the femoral sulcus, further aggravating the relative patella instability.


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The transverse stabilizers are composed of the superficial portion of the extensor retinaculum.

This retinaculum connects the vastus medialis and vastus lateralis muscles directly to the patella for improved muscular stabilization.


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In addition, passive stabilizers such as the medial and lateral patellofemoral ligaments firmly attach the patella to the adductor tubercle medially, and the IT band laterally.

The role of the medial patellofemoral ligament in assisting normal patellar tracking should not be understated.


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As the thickest portion of the medial retinaculum, the medial patellofemoral ligament alone provides approximately 60% of the passive restraining force against lateral translation (lateral shift) of the patella.


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An additional passive stabilizer that is sometimes overlooked is the large lateral lip of the femoral sulcus (see Fig. 11-2).

The steep lateral facet acts as a buttress to excessive lateral patellar shift.

Therefore, even large lateral forces can be prevented from subluxing or dislocating the patella, provided that the lateral lip of the femoral sulcus is of sufficient height.


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In the case of trochlear dysplasia, however, even relatively small lateral forces imposed on the patella can cause the patella to sublux or fully dislocate.


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Both the transverse and the longitudinal structures will influence the medial-lateral positioning of the patella within the femoral sulcus, as well as influence patellar tracking as the patella slides down the femoral condyles and into the intercondylar groove.


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The passive mobility of the patella and its medial-lateral positioning are largely governed by the passive and dynamic pulls of the structures surrounding it.

This is important because the presence of hypermobility could result in patellar subluxations or dislocations, whereas hypomobility could yield greater patellofemoral stresses.

Passive mobility of the patella is maximal when the knee is fully extended and the musculature is relaxed.


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An imbalance in the passive tension or a change in the line of pull of the dynamic structures will substantially influence the orientation of the patella.

This is predominantly true when the knee joint is in extension and the patella sits on the relatively shallow superior femoral sulcus.

Abnormal forces, however, may influence the excursion of the patella even in its more secure location within the intercondylar groove with the knee in flexion.


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As already noted, tension in the active and/or stretched quadriceps muscle helps create compression between the patella and the femur to increase patellofemoral stability.

The force on the patella is determined by the resultant pull of the four muscles that constitute the quadriceps and by the pull of the patellar tendon.

Each of the segments of the quadriceps can make some contribution to frontal plane mobility and stability.


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As noted earlier, the pull of the vastus lateralis muscle is normally 35° lateral to the long axis of the femur,

whereas the pull of the proximal portion of the vastus medialis muscle (VML) is approximately 15° to 18° medial to the femoral shaft with the distal fibers (VMO) oriented 50° to 55° medially (see Fig. 11-34).


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Because the vastus medialis and vastus lateralis muscles not only pull on the quadriceps tendon but also exert a pull on the patella through their retinacular connections, complementary function is critical.

Relative weakness of the vastus medialis muscle may substantially increase the resultant lateral forces on the patella.

The individual pulls of each respective portion of the quadriceps is impossible to measure in vivo, however.


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Although measurements of muscular force cannot be made, the literature supports the contention that muscle activity of the two portions of the vastus medialis (VMO and VML) and the vastus lateralis muscles are not selectively altered in patients with patellofemoral pain.


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Anatomic variations may contribute to asymmetrical pulls on the patella.

In general, the VMO inserts into the superomedial aspect of the patella about one third to one half of the way down on the medial border.

In instances of patellar malalignment, the VMO insertion site may be located less than a fourth of the way down on the patella’s medial aspect, and as a result, the vastus medialis muscle cannot effectively counteract the lateral motion of the patella.


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Although individual components of the quadriceps may not necessarily be influenced by pain, the quadriceps muscle as a whole does appear to be susceptible to the inhibitory effects of the acute joint effusions caused by injury.

This inhibition can result in hypotonia and atrophy, minimizing the compressive role of the quadriceps and thus altering the resultant pull on the patella.


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Asymmetry of Patellofemoral Stabilization

The orientation of the quadriceps resultant pull with respect to the pull of the patellar tendon provides information about the net force on the patella in the frontal plane.

The net effect of the pull of the quadriceps and the patellar ligament can be assessed clinically using a measurement called the Q-angle (quadriceps angle).

The Q-angle is the angle formed between a line connecting the ASIS to the midpoint of the patella and a line connecting the tibial tuberosity and the midpoint of the patella (Fig. 11-47).


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A Q-angle of 10 ° to 15 ° measured with the knee either in full extension or slightly flexed is considered normal.

Any alteration in alignment that increases the Q-angle is thought to increase the lateral force on the patella.

This can be harmful because an increase in this lateral force may increase the compression of the lateral patella on the lateral lip of the femoral sulcus.


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In the presence of a large enough lateral force, the patella may actually sublux or dislocate over the femoral sulcus when the quadriceps muscle is activated on an extended knee.


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The Q-angle is usually measured with the knee at or near full extension because lateral forces on the patella may be more of a problem in these circumstances.

With the knee flexed, the patella is set within the intercondylar notch, and even a very large lateral force on the patella is unlikely to result in dislocation.

Furthermore, the Q-angle will reduce with knee flexion as the tibia rotates medially in relation to the femur.


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It has been postulated that women have a slightly greater Q-angle than do men because of the presence of a wider pelvis, increased femoral anteversion, and a relative knee valgus angle.

However, other authors have disputed this, and the presence of a gender difference in the Q-angle is still a matter of debate.

Although an excessively large Q-angle of 20° or more is usually an indicator of some structural malalignment, an apparently normal Q-angle will not necessarily ensure the absence of problems.


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Large Q-angles are thought to create excessive lateral forces on the patella that may predispose the patella to pathologic changes.

One problem with using the Q-angle as a measure of the lateral pull on the patella is that the line between the ASIS and the mid-patella is only an estimate of the line of pull of the quadriceps and does not necessarily reflect the actual line of pull in the patient being examined.


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If a substantial imbalance exists between the vastus medialis and vastus lateralis muscles in a patient, the Q-angle may lead to an incorrect estimate of the lateral force on the patella because the actual pull of the quadriceps muscle is no longer along the estimated line.

Furthermore, a patella that sits in an abnormal lateral position in the femoral sulcus because of imbalanced forces will yield a smaller Q-angle because the patella lies more in line with the ASIS and tibial tuberosity.


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There are several abnormalities that can yield increased lateral forces.

There is a potential for imbalance between the vastus lateralis and vastus medialis muscles, although, as identified earlier, this imbalance cannot be measured in vivo.

The presence of a tight IT band could also limit the mobility of the patella and restrict its ability to shift medially during flexion, contributing to increased stress under the lateral facet of the patella.


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When the IT band moves posteriorly with knee flexion, it exerts an even greater lateral pull on the patella, which results in a progressive lateral tilting as knee flexion increases.

The increased lateral tilt could further load the lateral facet, increasing joint stress.


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The frontal plane deviation of genu valgum increases the obliquity of the femur (see Fig. 11-7A) and, concomitantly, the obliquity of the pull of the quadriceps.

In contrast, individuals with genu varum exhibit less obliquity of the femur (see Fig. 11-7B), and therefore should have a diminished lateral quadriceps pull.


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The transverse plane deviation of medial femoral torsion (or femoral aneversion) generally results in the femoral condyles being turned in (medially rotated), carrying the patella medially with the femoral condyles and increasing the Q-angle by increasing the obliquity of the pull of the quadriceps on the patella.

Medial femoral torsion is often associated with lateral tibial torsion in the older child or adult, or it may exist independently.


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In lateral tibial torsion, the tibial tuberosity lies more lateral to the patella, increasing the Q-angle by increasing the obliquity of the patellar tendon.

When medial femoral torsion and lateral tibial torsion coexist, the Q-angle will increase substantially, resulting in a substantial lateral force on the patella (Fig. 11-48).


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As we will see in Chapter 12, the presence of excessive or prolonged pronation in the foot can contribute to excessive or prolonged medial rotation of the lower extremity that moves the patella medially, increasing the Q-angle and promoting a greater lateral force on the patella in a way similar to that of medial femoral torsion.

Each of these conditions can predispose the patella to excessive pressure laterally or to lateral subluxation or dislocation.


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Forces other than the alignment and balance of the quadriceps muscle components may influence patellar positioning.

Either laxity of the medial retinaculum or excessive tension in or adaptive shortening of the lateral retinaculum may contribute to a laterally tilted patella in the femoral sulcus (Fig. 11-49).


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In addition, a tight IT band may exert an excessive lateral pull on the patella through the lateral patellofemoral ligament.

Such deficits in the passive stabilizers, as well as weakness in the medial active stabilizers, result in increased lateral compressive forces.

It is currently unknown whether such changes in the passive structures are primary or are secondary to abnormalities in the dynamic stabilizers.


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Weight-Bearing versus

Non-Weight-Bearing Exercises with

Patellofemoral Pain


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Both weight-bearing and non-weight-bearing exercises are often prescribed for patients with patellofemoral pain.

Each mode of exercise influences the patellofemoral joint differently on the basis of the knee’s position within the ROM.

Effective quadriceps strengthening in a patient with pain must be performed in a pain-free range.


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This necessitates a complete understanding of how both weight-bearing and non–weight-bearing exercises influence the contact area and force across the patellofemoral joint.

We already noted that in non-weight-bearing extension, such as the seated knee extension, the quadriceps must work harder as extension progresses (quadriceps force increases with decreasing knee flexion angle) (see Fig. 11-37).


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The increased work of the quadriceps near extension is necessary to compensate for the increased MA of the resistance.

However, the greater compressive force generated by the increased quadriceps contraction can be detrimental for an individual with patellofemoral pain, especially if the degeneration is located on the inferior aspect of the patella that is in contact with the femur near extension.


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In contrast, a weight-bearing exercise requires greater quadriceps activity with greater knee flexion (e.g., at the bottom of a squat) as the MA of the resistance increases (see Fig. 11-38).


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During weight-bearing exercise, greater knee flexion will therefore increase the compressive force across the patellofemoral joint both because of increased force demands on the quadriceps muscle and because of the increased patellofemoral compression that occurs even with passive knee flexion.

The substantial patellofemoral compression will aggravate patellofemoral pain.


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Exercise recommendations for the person with patellofemoral pain can be based on changing patellofemoral joint stress with weight-bearing and non-weight-bearing exercises and knee flexion angle (Fig. 11-50).

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Figure 11-50 Simulations showed patellofemoral joint stress to be greater during loaded non–weight-bearing exercises than weight-bearing exercises when the knee was closer to knee extension. Patellofemoral joint stress was higher, however, during weight-bearing exercises when knee flexion exceeds approximately 50. [Data from Cohen ZA, Roglic H, Grelsamer RP, et al: Patellofemoral stresses during open and closed kinetic chain exercises. An analysis using computer simulation. Am J Sports Med 29:483–484, 2001.]

Pending….


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It has been recommended that those with patellofemoral pain avoid deep flexion while doing weight-bearing extension exercises and avoid the final 30° of extension during non–weight-bearing knee extension exercises.


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Effects of Injury and Disease

The joints of the knee complex, like other joints in the body, are subject to developmental defects, injury, and disease processes.

A number of factors, however, make the knee joint unique in its development of various pathologies.

The knee, unlike the shoulder, elbow, and wrist, must support the body weight and at the same time provide considerable mobility.


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Although the hip and ankle joints similarly support the body’s weight, the knee is a more complex structure than either the hip or ankle.

The anatomic complexity is necessary to dissipate the enormous forces applied through the joint as two of the longest levers in the body meet at the knee complex.


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Tibiofemoral Joint Injury

The tremendous forces applied through the knee have the potential to contribute to numerous injuries and degenerative damage.

In addition, participation in physical fitness and sports activities that involve jumping, pivoting, cutting, or repetitive cyclic loading among all age groups and both sexes can subject the knee complex to risk of injury.

Injuries to the knee complex may involve the menisci, the ligaments, the bones, or the musculotendinous structures.


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Meniscal injuries are common and usually occur as a result of sudden rotation of the femur on the fixed tibia when the knee is in flexion.

The pivot point during axial rotation in the flexed knee occurs through the medial meniscus.

Therefore, the more rigidly attached medial meniscus may tear under the sudden load.


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Ligamentous injuries may occur as a result of a force that causes the joint to exceed its normal ROM, usually the translational ROM.

Although excessive forces may cause ligamentous tears, lower-level forces may similarly cause disruption in ligaments weakened by aging, disease, immobilization, steroids, or vascular insufficiency.


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Cyclic loading (whether short term and intense or over a prolonged period) may also affect visco-elasticity and stiffness.

A weakened ligament may take 10 months or more to return to normal stiffness once the underlying problem has been resolved.

After a ligament injury or reconstruction, the new or damaged tissue must be protected to minimize excessive stress through the healing tissue.


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Absence of tissue stress, however, is also detrimental, because the new tissue will not adapt and become stronger under unloaded conditions.

Rehabilitation of the repaired or reconstructed ligament, therefore, is a balance between too much applied stress and too little.


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The bony and cartilaginous structures of the tibiofemoral joint may be injured either by the application of a large direct force, such as during a twist or fall, or by forces exerted by abnormal ligamentous and muscular forces.

Knee osteoarthritis is often seen in older adults and is particularly common in women.


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This progressive erosion of articular cartilage may be initiated by a previous traumatic joint injury, obesity, malalignment, instability, or quadriceps muscle weakness, to name just a few of the many suspected contributors to the development of osteoarthritis.

Tibial plateau fractures can occur when large magnitudes of force are applied through the joint.


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Knee joint instability, as frequently seen in the knee after ACL injury, can lead to progressive changes in the articular cartilage, in the menisci, and in the other ligaments attempting to restrain the increased joint mobility.

The presence of ligamentous instability induces abnormal forces through the joint, inasmuch as excessive shearing can often occur.


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In addition, this excessive laxity must be controlled in order to avoid episodes of giving way.

Because the knee has poor bony congruency, the muscles must provide greater control of all fine movements of the tibiofemoral joint in the absence of ligaments.


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Increased muscular co-contraction, however, may generate greater compressive forces through the joint, contributing to articular cartilage degeneration.

An improved method of providing dynamic stability to a lax joint, therefore, is to generate isolated muscle contractions as needed, rather than a massive co-contraction to stiffen the joint.


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The numerous bursae and tendons at the knee are also subject to injury. The cause of injuries to these structures may be either a direct blow or prolonged compressive or tensile stresses.

Bursitis is common after either blunt trauma or repetitive low-level compressions, which can irritate the tissue.


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The pre-patellar bursa, the superficial infra-patellar bursa (known as housemaid’s knee when it is inflamed), and the bursa beneath the pes anserinus are common locations for injury.

Tendinitis results from repetitive low-level stresses to the tissues of the tendon.


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Frequently this is caused by an overworking of the muscle and can occur in response to a previous ligamentous injury.

Another potential source of pain and dysfunction in the knee joint is the irritation of a patellar plica.

Classic symptoms include pain with prolonged sitting, with stair climbing, and during resisted extension exercises.


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In flexion, the medial patellar plica is drawn over the medial femoral condyle and can become pressed beneath the patella.

The resulting tension in the band may cause plica to become inflamed.


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If the inflamed plica becomes fibrotic, it may create a secondary synovitis around the femoral condyle, and deterioration of the condylar cartilage may occur.

A thickened or inflamed superior plica may erode the superior aspect of the medial facet of the patella.


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Patellofemoral Joint Injury

We have presented the mechanics of a number of problems that may predispose the knee to patellofemoral dysfunction.

Any one problem in isolation or various combinations of problems may lead to excessive pressure on the lateral facets of the patella, to lateral subluxation, or to lateral dislocation.


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Both patellar instability and increased patellofemoral compression are commonly associated with: knee pain, poor tolerance of sustained passive knee flexion

(as in sitting for long periods), “giving way” of the knee, and exacerbation of symptoms by repeated use of the

quadriceps on a flexed knee.


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Often this results in diminished use of the quadriceps, leading to atrophy and subsequently a further deterioration of patellar control.

As muscle function declines, patellofemoral dysfunction may progress, necessitating a reversal of muscle function under a series of controlled situations to generate hypertrophy of the quadriceps, while minimizing discomfort.


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Among the causes of increased patellar compression include: a tight IT band, large Q-angle (e.g., as in genu valgum or femoral

anteversion with lateral tibial torsion), relative vastus medialis muscle weakness, or patellar hypomobility.


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With patellar hypermobility, lax medial structures, and a short lateral femoral condyle, the risk of lateral patellar subluxation or dislocation is increased.

After a lateral patellar subluxation or dislocation, the medial retinaculum is stretched as the patella deviates toward or slips over the lateral lip of the femoral sulcus or condyle.


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The return of the patella into the intercondylar notch may affect the medial patella (occasionally causing an osteochondral fracture).

There are a host of other pathologies that can occur around the patellofemoral joint, including: pain from the lateral patellofemoral ligament, inflammation of the medial patellar plica (discussed

previously), and pain from the quadriceps tendon above or the

patellar ligament below.


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Patellofemoral pain is most often observed in adolescents and may resolve spontaneously.

In addition, patellar subluxation is more often seen in younger patients, who may have a less developed patella and lateral condyle to resist an excessive lateral force on the patella.


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Cartilaginous changes seen on the lateral patellar facet were once considered to be diagnostic of patellofemoral dysfunction, and the term chondromalacia patella (softening of the cartilage) was assigned.


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With the knowledge that similar cartilaginous changes can be found in asymptomatic knees and that the medial patellar facet can show greater change without symptoms or progressive cartilage deterioration, more general diagnoses have been used, including patellofemoral arthralgia or patellofemoral pain syndrome.


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The use of this more general terminology suggests that the damage extends beyond the articular cartilage.

Cartilage is aneural and therefore cannot be the cause of pain.

Instead, patients with patellofemoral pain can experience discomfort from damage to subchondral bone, the synovial membrane, and ligamentous or musculotendinous structures.


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Summary

Given the range of possible problems that can occur in the knee joint, an exhaustive discussion is beyond the scope of this text.

A thorough knowledge of normal structure and function, however, can be used to predict or understand the immediate impact of a specific injury and the secondary effects on intact structures.

The variety of forces transmitted through the knee complex arises from gravity (weight-bearing forces), muscles, ligaments, and other passive soft-tissue structures.


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Any alteration of the knees anatomy can substantially influence these forces and can have a dramatic impact on the function of the knee joint.

Damage to the tibiofemoral joint or the patellofemoral joint can result from either a large rapid load or the accumulation of smaller repetitive loads.

An understanding of both the primary and secondary effects of injury is important in order to gain a full appreciation for the pathogenesis of knee disorders.


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Thanks for your attention………………….


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End of Part - 9

Biomechanics of knee complex 9 frontal plane patellofemoral jt stability

Health & Medicine

relative patella

mediallateral stability

mediallateral positioning

femoral sulcus

medial patellofemoral

medial retinaculum

large lateral forces

large lateral lip