Understanding The Biomechanics Of Plantar Plate Injuries

Given the common incidence of plantar plate injuries and the complications that can arise from more severe tears, this author offers a comprehensive guide to the biomechanics inherent to the plantar plate as a foundation for effective treatment of related injuries. 

The plantar plate is a fibrocartilaginous structure that lies directly plantar to the lesser metatarsal heads and acts as a sesamoid-like mechanism for each lesser metatarsophalangeal joint (MPJ) of the foot.^1-3 At its proximal aspect, the plantar plate is attached to the deep slips of the plantar fascia (i.e. central component of the plantar aponeurosis) and functionally, we may consider it to act as a distal extension of the plantar fascia. At its distal aspect, the plantar plate inserts onto the base of the proximal phalanx of the lesser digits via tightly interwoven collagen bundles.⁴ The dorsal surface of the plantar plate, which is slightly concave, is in direct contact and congruous with the plantar articular cartilage of each lesser metatarsal head.⁵

The longitudinal orientation of its fibers suggests that the plantar plate is subject to significant tension loading forces from the plantar fascia. In addition, the plantar plate is subject to significant compression loading forces due to the large magnitudes of ground reaction force (GRF) that act on the plantar metatarsal heads during weightbearing activities.^1,2 Thus, during weightbearing activities, the plantar plate is subject to significant tension and compression loading forces, which may cause an increased risk of plantar plate injury.⁶

The medial and lateral borders of the plantar plate also attach and merge with the collateral ligaments of the MPJ that, in turn, attach to the medial and lateral aspects of the metatarsal heads. The medial collateral ligament of the MPJ helps prevent abduction of the digit and the lateral collateral ligament helps prevent adduction of the digit. Together, the medial and lateral collateral ligaments increase the transverse plane stability of the digit.¹ As a result of the unique anatomical arrangement of the plantar plate and collateral ligaments, a “soft tissue pocket” forms around each metatarsal head. This soft tissue pocket not only allows the metatarsal head to glide smoothly on the plantar plate during MPJ dorsiflexion and plantarflexion, but also keeps the digit in a plantigrade position and well aligned within the transverse plane, parallel to the other digits.^7-10

The deep transverse intermetatarsal ligament also serves to attach the soft tissue pocket of each metatarsal head to its adjacent metatarsal heads, providing a transverse plane mechanical connection between all the adjacent metatarsal heads. Stainsby described this side-to-side tethering of the metatarsal heads by the deep transverse metatarsal ligament as a “transverse tie-bar,” which prevents splaying (i.e., widening) of the forefoot.¹¹ In effect, the anatomical arrangement of the plantar plates, collateral ligaments and deep transverse intermetatarsal ligaments all work in unison to help stabilize the metatarsal heads and the digits relative to each other within the transverse and sagittal planes.

Since the plantar plate is attached to both the plantar fascia proximally and the proximal phalanges of the lesser digits distally, tension forces that occur within the plantar fascia during weightbearing activities directly transfer as tension forces to its insertion at the proximal phalanx base. Using cadaver limbs in a dynamic gait simulator apparatus, researchers showed that the magnitude of force acting through the plantar fascia just before heel-off at its peak is 0.96 times body weight.¹²

In addition, since the plantar plate is located directly plantar to and is in direct contact with the head of the metatarsal, ground reaction force acting on the plantar metatarsal head will directly transfer to the plantar plate as a compression loading force that will tend to increase the compression stress within its fibrocartilaginous structure. Activities such as barefoot walking on hard surfaces, wearing high-heeled shoes and high-impact activities such as running or jumping increase the ground reaction force plantar to the lesser metatarsal heads, and may increase the risk of plantar plate tears.^3,5,13-15   

Partial or complete tears to the plantar plate may result in pain with ambulation, plantar edema and digital deformities within the affected plantar MPJ.^16-18 In the early 1980s, during my own podiatric student and residency years, plantar plate injuries were called metatarsophalangeal joint capsulitis with no mention of the plantar plate being the source of the plantar edema and pain associated with the “capsulitis.” Yu and colleagues coined the term predislocation syndrome and Gerbert used the term MPJ stress syndrome to describe the signs and symptoms associated with plantar plate tears.^19,20

Currently, most authors now use the term plantar plate tear to describe the clinical condition of plantar MPJ pain, edema, sagittal plane MPJ instability and digital deformity caused by structural defects within the plantar plate. Beyond the scope of this discussion are the various surgical techniques (including proximal interphalangeal joint arthrodesis, flexor transfer and direct plantar plate repair) that we have used over the years to correct for the digital deformity that may result from plantar plate tears.^{4,14,17,19,21-28}

A Guide To The Diagnosis And Presentation Of Plantar Plate Tears

Plantar plate tears may produce tenderness within the plantar aspect of the MPJ with the area of maximum tenderness most commonly occurring at the insertion of the plantar plate into the proximal phalanx base.^16-18 The most severe cases of plantar plate tear clinically demonstrate a plantar protuberance at the affected metatarsal head, which is easily visible from across the exam room. In milder cases, the soft tissue edema may not be clinically visible but may be palpable as a slight induration at the plantar aspect of the MPJ.

Umans and colleagues studied periarticular MPJ tissue changes clinically evident in magnetic resonance imaging (MRI) of plantar plate tears.²⁹ The authors found pericapsular fibrosis, bursitis and even a ganglion within the second interspace in a total of 21 second MPJ plantar plate tears without identifying a single second interspace neuroma. It is likely that the pericapsular tissue changes common in second MPJ plantar plate tears cause many of the second intermetatarsal space symptoms of neuritis that physicians commonly confuse as a second intermetatarsal space neuroma.

To further aid the clinical diagnosis of plantar plate tears, Thompson and Hamilton described an excellent clinical test, commonly known as the dorsal drawer test, three decades ago.³⁰ The dorsal drawer test is positive when there is increased dorsal excursion of the proximal phalanx base relative to the metatarsal head with increasing dorsal excursion of the proximal phalanx base occurring with increasing severity of plantar plate tears. Also, during clinical examination, dorsiflexion range of motion of the MPJ is non-painful but plantarflexion of the MPJ will often be very painful in patients with more symptomatic plantar plate tears.  

Research correlating diagnostic ultrasound and MRI scans of cadaver specimens to histologic examination of the plantar plate demonstrates that plantar plate tears are more common than previously suspected, and that many feet with plantar plate tears may be asymptomatic.³ Tears were present in 23 of the 24 MPJs (96 percent) of six embalmed cadaver feet that researchers examined with direct inspection. All plantar plate tears were located at the insertion of the plantar plate onto the plantar base of the proximal phalanx. Partial tears were even present in six of the eight plantar plates examined in the one young (19-year-old) fresh cadaver specimen analyzed.

In another study using diagnostic ultrasound and MRI on 40 asymptomatic feet and 40 symptomatic feet (i.e., live subjects), ultrasound detected plantar plate tears in the asymptomatic feet at a rate of 46.8 percent and MRI detected tears at a 34.3 percent rate.³¹ In the symptomatic patients, plantar plate tears were present at a rate of 86.8 percent as detected by ultrasound and a rate of 88.7 percent detected by MRI. Clearly, the discovery of a plantar plate tear by MRI or diagnostic ultrasound does not necessarily mean that the patient is symptomatic since plantar plate tears seem to be present in many asymptomatic feet. However, it is also likely that more substantial plantar plate tears cause more symptoms and more risk of a digital deformity developing.

Plantar plate tears occur much more commonly at the second MPJ than at any of the other lesser MPJs. In the four studies to date that have compared the frequency of plantar plate tears in live patients, the second MPJ accounted for 63 to 90 percent of all lesser MPJ plantar plate tears.^15,27,29,32 The third MPJ accounted for 10 to 33 percent and the fourth MPJ accounted for 0 to 4 percent of all plantar plate tears. Authors reported no plantar plate tears at the fifth MPJ. The most likely biomechanical etiology of the greatly increased rate of second MPJ plantar plate tears is the increased ground reaction force and the resultant increased compression and tension stresses within the plantar plate of the second MPJ during weightbearing activities.

Why ‘First Ray Hypermobility’ Is A Misnomer

Higher magnitudes of ground reaction force may occur at the plantar second metatarsal head due to an elongated second metatarsal or due to the first metatarsal head not bearing its normal share of plantar loading forces. Over 80 years ago, Morton first described the concept of “hypermobility of the first metatarsal segment” when he stated that the first ray could become “ineffective as a weightbearing structure” if the plantar ligaments of the first ray were “slack” in comparison to the plantar ligaments of the lesser metatarsal rays.³³ Since that time, other authors have continued to use the clinical term “first ray hypermobility” to describe the inability of the first metatarsal head to bear its normal share of the forefoot loading forces with resultant transfer of increased ground reaction force to the second metatarsal head.^34,35

Recently, authors have described the term “first ray hypermobility” as a biomechanically inaccurate term that attempts to characterize the load versus deformation characteristics of the first ray. The term “first ray hypermobility” is mathematically unquantifiable and does not recognize the obvious variable amounts of loading force applied to the plantar metatarsal head that causes first ray dorsiflexion.
The term that better describes the load versus deformation characteristics of the first ray and is consistent with the modern biomechanics literature is decreased first ray dorsiflexion stiffness.^36,37 In other words, we should discard Morton’s 80-plus year-old term of “hypermobility of the first metatarsal segment” or what most podiatrists call “first ray hypermobility” from the podiatric lexicon since it does not accurately describe the load versus deformation characteristics of the first ray relative to the lesser rays.  
 
Key Insights On Plantar Fascia Functions As They Relate To The Plantar Plate

If the first metatarsal is congenitally, traumatically or surgically elevated or shortened, or if there is a decrease in first ray dorsiflexion stiffness, similar to what would occur with a significant hallux abducto valgus deformity, the second metatarsal head will be subject to increased magnitudes of ground reaction force during weightbearing activities.³⁸ When the first metatarsal head is not bearing its normal share of ground reaction force, the plantar plate of the second MPJ will be subject to higher magnitudes of ground reaction force that will, over time, increase not only the compression stress but will also increase the tension stress within the plantar plate. These increased compression and tension stresses within the fibrocartilaginous structure of the plantar plate will, over time, increase the risk of plantar plate injury.^39,40

To understand the biomechanics of the plantar plate and therefore understand the pathomechanics of plantar plate tears, one must first comprehend the multiple functions of the plantar fascia since the plantar plate is the distal tension load-bearing extension of the plantar fascia.⁴¹

The plantar fascia is a band of fascial tissue that is passive, not active (i.e., muscular) in nature. As such, the tension forces that develop within the plantar fascia during weightbearing activities are not directly controlled by efferent neural activity from the central nervous system (CNS) as would be the case with any of the other extrinsic and intrinsic muscles of the foot. In other words, the plantar fascia and plantar plate can only develop tension forces when the forefoot and/or digits are dorsiflexed relative to the rearfoot. This would be the case when the plantar forefoot is loaded by ground reaction force during standing, walking, running and other weightbearing activities.⁴²

When ground reaction force acts on the plantar forefoot, the resultant dorsiflexion motion of the forefoot relative to the rearfoot causes a flattening and lengthening of the longitudinal arch that, in turn, increase the tension force within the plantar fascia and plantar plate.42 The increase in plantar fascia and plantar plate tension causes an MPJ plantarflexion moment, which, in turn, increases the ground reaction force plantar to the digit, and creates a situation of rotational equilibrium and sagittal plane digital stability at the MPJ. The MPJ plantarflexion moment from the passive tension within the plantar fascia and plantar plate will increase during the latter half of midstance, which will tend to plantarflex the proximal phalanx harder into the ground and thus increase the ground reaction force plantar to the digit.¹²

Due to the integral mechanical link between the plantar fascia, plantar plate and the proximal phalanx of the digit, when a partial or complete tear of the plantar plate occurs, the plantar fascia can no longer exert the same amount of MPJ plantarflexion moment. This subsequently results in a reduction in digital purchase force and an increased risk of dorsiflexion deformity of the digit.^43-47 Loss of proper tension within the plantar fascia and plantar plate may also occur due to plantar fascial tear, plantar fasciotomy, or from shortening of the lesser metatarsal from fracture or surgery.  

Shortening of the metatarsal, whether by trauma or surgery, will reduce the passive tension force within the slip of the plantar fascia to the digit, which will subsequently reduce the digital purchase force and increase the risk of sagittal plane digital deformities developing over time.⁴⁸ In support of the idea that metatarsal length mechanically affects plantar fascia tension and digital function, researchers have reported dorsiflexion deformities of the lesser MPJs in response to surgical shortening of the lesser metatarsals.⁴⁹ Therefore, any injury or surgery that reduces the passive plantar fascia tension force to any of the lesser digits will lessen the digital purchase force, which may result in floating toes or other digital deformities occurring over time.³⁹

How The Flexor Digitorum Longus And Flexor Digitorum Brevis Affect Plantar Plate Biomechanics

Further complicating the biomechanics of plantar plate tears is the mechanical interrelationship between the function of the plantar fascia as a passive MPJ flexor and the function of flexor digitorum brevis and flexor digitorum longus muscles as active MPJ flexors. Contractile activity of the flexor digitorum brevis creates a proximal interphalangeal joint plantarflexion moment, which tends to plantarflex the proximal interphalangeal joint. Contractile activity of the flexor digitorum longus creates a plantarflexion moment at both the proximal interphalangeal joint and the distal interphalangeal joint, which tends to plantarflex both the distal interphalangeal joint and proximal interphalangeal joint.³⁵

Since there are no intrinsic or extrinsic foot muscles that insert directly onto the plantar aspect of the proximal phalanx of the lesser digits, there is no pedal muscle that can cause an isolated proximal phalanx plantarflexion moment at the MPJ during weightbearing activities. Only the plantar fascia can exert an isolated proximal phalanx plantarflexion moment and, as I mentioned previously, the increase in proximal phalanx plantarflexion moment that results from increased plantar fascia tension force occurs when greater amounts of ground reaction force act on the plantar forefoot.¹²

Therefore, an intact plantar fascia and plantar plate create an isolated MPJ plantarflexion moment that plantarflexes the proximal phalanx of the digit harder into the ground to aid proper digital purchase and stabilize the digit within the sagittal plane. As Hicks first noted over 60 years ago, the passive increase in plantar fascia tension that plantarflexes the digits during weightbearing activities is an “automatic” mechanism, which he called the “reverse windlass effect,” and is dependent only on weightbearing forces acting on the plantar foot, and not directly dependent on muscular activity or efferent neural activity from the central nervous system.^50-52  

The plantar digital stabilization that is provided by an intact plantar fascia and plantar plate is very important to maintain proper digital purchase, especially when considering the functions of the flexor digitorum brevis and flexor digitorum longus. During weightbearing activities, when the flexor digitorum brevis is active, the proximal interphalangeal joint plantarflexion moment that results will tend to plantarflex the proximal interphalangeal joint, but will also create a retrograde force that will tend to dorsiflex the MPJ. When the flexor digitorum longus is active, the proximal interphalangeal joint and distal interphalangeal joint plantarflexion moment that results will tend to plantarflex both the proximal interphalangeal joint and distal interphalangeal joint but, in doing so, will also create a retrograde force that tends to dorsiflex the MPJ.  

When a significant plantar plate tear occurs, the passively generated MPJ plantarflexion moment from the plantar fascia is reduced, which lessens the ability of the plantar fascia to maintain proper digital purchase and counterbalance the MPJ dorsiflexion effects from flexor digitorum brevis and flexor digitorum longus muscular activity. Therefore, the gradual dorsiflexion deformity of the MPJ that invariably develops due to plantar plate tears is likely due to the other digital flexors (e.g., flexor digitorum brevis and flexor digitorum longus) gradually dorsiflexing the MPJ along with, of course, the MPJ dorsiflexion moments that normally occur from ground reaction force and the digital extensors. It is clear that, upon detailed biomechanical analysis, for proper digital purchase to occur, the plantar fascia and plantar plate must provide passive tension forces to plantarflex the proximal phalanx of the digit against the ground, which counterbalances the MPJ dorsiflexion moments that would tend to, over time, lead to the development of sagittal plane digital deformities.⁵¹
    
In Summary

The plantar plate, as the distal tension load-bearing extension of the plantar fascia, needs to remain intact and uninjured to allow it to maintain a straight, plantigrade and mechanically stable digit. Plantar plate tears are not only common in symptomatic lesser MPJs but may also occur in asymptomatic lesser MPJs. Milder plantar plate tears will cause slight pain, no digital deformity and slight plantar MPJ induration. More severe plantar plate tears will cause moderate to significant localized MPJ plantar edema, progressive digital deformity, painful ambulation and even digital neuritic symptoms. The podiatric physician must develop a complete understanding of the multiple biomechanical functions of the plantar fascia and plantar plate to treat his or her patients with plantar plate tears more effectively, both conservatively and surgically.

Dr. Kirby is an Adjunct Associate Professor within the Department of Applied Biomechanics at the California School of Podiatric Medicine at Samuel Merritt University in Oakland, Calif. He is in private practice in Sacramento, Calif.

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