The challenges associated with recovery from plantar plate injury include understanding the biomechanics, histologic and gross anatomy, the properties of the tissue, and the appreciation of extrinsic factors. Not unlike fibrocartilage found elsewhere including the meniscus of the knee, spring ligament and intervertebral bodies, pathology to the plantar plate is often challenging to address. Not only is there a need for the management of extrinsic factors but the intrinsic nature of the tissue can lead to difficulty in restoring its function. Having a better appreciation of these factors will help the practitioner in instituting appropriate treatment alternatives, particularly within a timeline of care.
The plantar plate is an array of parallel collagen fibers in a composite structure with an interfibrillar substance designed to resist tension. There are tendons throughout the body that wrap themselves around joints in order to receive perpendicular compressive forces. At these areas, an articular pad with a cartilaginous surface is designed to withstand pressure and frictional forces. Histologically, these tissues demonstrate thickened collagen fibers, increased proteoglycans (ground substance) and chondrocytes.
Specifically at the plantar plate, one sees increased chondrocytes toward the metatarsal head with increasing fibroblasts as one moves distally to the phalangeal base. This would suggest an articular component at the metatarsal head and a more ligamentous component toward the phalanx. With our current understanding and appreciation of challenges in treating articular and ligamentous injuries elsewhere, we can immediately appreciate why the plantar plate may pose similar problems as it inherently demonstrates both components.
Fibroblasts serve two principal functions: generating the over 75 percent of type I collagen that makes up this tissue and generating the extracellular matrix of proteoglycans. There is very little elastin content within the plantar plate. Interestingly, the extracellular matrix demonstrates increased glycosaminoglycan, which is present in large proteoglycans associated with the tendon’s ability to withstand compressive forces.1
Within the parallel array of collagen fibers, animal model studies looking at the knee meniscus have found an extra characteristic: evidence of crimping.2 We can best describe crimping as a folding of the collagen sides that allows the collagen fibers to become taut before exerting reinforcement and countering resistance to loading. One can appreciate this mechanism in a fanciful way with the use of finger traps, which produce greater resistance with increased force. Another analogy is the currently available fabric garden hoses that expand to great lengths when water flows but collapse onto themselves when water pressure drops. Apsden and Hukins have described this crimping in a “Hoop Stress” theory that suggests this tissue has the ability to dampen and resist loading and, in fact, provide counter resistance.2 This may be the case until there is disruption of the fibers.
One can picture the expanding breach of a rubber tire or a splitting of two zippered ends to understand how this fissure of connected collagen fibers would limit the ability of the tissue to function normally in fibrocartilage. In other words, an attenuation or local tear within the plantar plate would dampen its resistance to loading and expand over time as the injury process continues. Early appreciation of this process and mitigating the factors of disruption are critical in retarding progression of the plantar plate injury.
A Closer Look At The Structure And Biomechanical Function Of The Plantar Plate
Grossly, the plantar plate is trapezoidal in shape with thickness ranging from 2 to 5 mm, length ranging from 12 to 23 mm and width ranging from 10 to 16 mm. The proper collateral ligament extends from the metatarsal tubercle in an oblique manner to the base of the phalanx. There are accessory ligaments from the metatarsal tubercle inserting into the plantar plate. There is a confluence of the plantar plate with the deep transverse metatarsal ligament. Immediately inferior is the long flexor tendon of the digit. This fine balance of structures imparts the biomechanical function of the plate.
There is little documentation regarding the vascular supply of the plantar plate. It is a relatively avascular structure. If one considers the identified vascular supply of the knee meniscus, we can suggest the vascular supply of the plantar plate would be similar emanating from the periphery developing from the proximal attachment of accessory and suspensory ligaments as these ligaments are intimate with the vascular supply to the metatarsal head and neck.
The biomechanical function of the plantar plate is to provide static stability around the metatarsophalangeal joint. Dynamic stability occurs via both extrinsic and intrinsic muscle tendons. To have dynamic stability, there must be an intact plantar plate. With disruption of the plantar plate, we begin to see luxation of the proximal phalanx dorsally.
There are many studies reviewing the progression of deformity when different components that maintain stability of the metatarsophalangeal joint are sacrificed. Suero and colleagues demonstrated a 19 percent increase in dorsal excursion with isolated plantar plate involvement.3 In the study, once surgeons incised a single collateral ligament, this caused displacement to rise to 63 percent. Barg and colleagues found that sectioning of the accessory ligament was more consequential than simple sectioning of the proper collateral ligament.4 They also found that repair of the accessory ligament resulted in a more robust correction than interosseous tendon transfer.
Deland and Sang identified that the advancement of a pure sagittal plane deformity involves transverse and crossover toe deformity when there is more than 50 percent attenuation of plantar plate, contraction of the medial collateral ligament, rupture of the lateral collateral ligament, and medial subluxation of the flexor tendons.5
Putting this picture together, we have a tissue that must accept and resist significant loading. Once the tissue is breached there is a tendency for progression, which further reduces the tissue’s ability to resist strain load. A tenuous vascular supply compounds the challenge for healing.
What The Literature Reveals
There are few prospective studies demonstrating the advancement of this condition from its prodromal state to end-stage disease and presentation of frank subluxation of the joint. This clearly is understandable based on what I have seen in my clinical experience. Most often, by the time the patient presents for evaluation, the pain may have been present for several weeks or there is already evidence of early onset deformity of the digit or frank dislocation. It is critical that the practitioner appreciates the early findings and advancing signs of plantar plate pathology.
The majority of cases present around the second metatarsophalangeal joint and much of our consideration for this condition has been focused on this area. The most likely culprit for this harkens back to the work of Dudley Morton, MD, in the early 20th century.6 It was his contention that the majority of the maladies afflicting the human foot were secondary to insufficiency of the medial column, specifically the first ray. Whether it was due to hypermobility, a shortened ray or atavism of the cuneiform resulting in metatarsus primus varus, inadequate loading of the medial column or “inner pillar” occurred, resulting in excessive loading under the adjacent second metatarsal.
This repetitive loading produces microtrauma of the plantar plate. When a patient presents with pain in the sub-second metatarsal, it is critical to appreciate the structural presentation of the first ray and its impact to loading of the foot. Focused attention to the area of pain suggests discomfort with axial loading directly under the metatarsal head. One may accentuate this discomfort with dorsiflexion of the digit and direct loading from the toe sulcus into the metatarsal as the plantar plate advances forward in this maneuver.
Current Insights On Diagnosis And Treatment
Clinicians often misdiagnose plantar plate discomfort as a second intermetatarsal neuroma. Subjective complaints of the patient may suggest a neuritic process but we must be cautious as connective tissue type discomfort one may encounter with tendinopathies and fasciopathies can suggest focal burning and altered aesthesia to the area.
Frankly, after 25 years of practice, I have discounted the relative equal incidence of the second intermetatarsal space neuroma to that of the third, as suggested by studies, as a misdiagnosis of early plantar plate disturbance.7 If a patient presents in this state, it is critical to offload the injured area with appropriate padding, an offloading insole or shoe modification. Consider pharmacotherapy, including topical and systemic anti-inflammatories. At no point do I consider intraarticular corticosteroid injections. Even if I consider a judicious use of a singular injection, such as dexamethasone phosphate, I also consider the increasingly understood deleterious effects of this drug to the joint and whether the physical instillation of fluid into a confined joint space may be adequate to mechanically worsen local tears.
Once advancement of an inflammatory response to injury of the plantar plate has proceeded to early attenuation or frank tear, the challenge of resolving this condition intensifies. Clinical findings of early transverse drifting of the digit are apparent. Increased vertical instability of the toe is often visible with the performance of a mini-Lachman exam and increasing pain. As the toe dorsally luxates and there is loss of passive plantarflexion of the digit, the ability to forcibly purchase the ground disappears.
Radiographic imaging can be predictive of plantar plate injury and one should consider it. Klein and colleagues looked at 88 patients and 106 feet with suspected disease.1 They compared their radiographic findings and operative findings, and noted a 91.5 percent confirmation. The significant predictive findings included evidence of medial deviation of the second toe, intermetatarsal angles of greater than 12 degrees correlated with a two- to threefold increase in plantar plate pathology, and those with second metatarsal protrusion of greater than 2 mm had a 90 percent increased risk of disease.
With clinical and radiographic findings supporting diagnosis of plantar plate attenuation or tear, it is critical to preserve anatomic alignment to restore or maintain function of the toe, and limit advancing deformity. One can do this with continued strapping of the digit and offloading of the area. I would suggest attempting this for at least three months prior to investigating alternative treatments.
Unfortunately, given the increasingly notable attention to surgical repair of this tissue over the past few years, it is clear that conservative care may not be adequate in restoring the static stabilizing effect the plate has to the metatarsophalangeal joint. With the continuation of dynamic deforming forces to a tissue that is progressively losing its ability to withstand, resist and even counter-resist loading, frank subluxation of the joint is often inevitable.
The timing of surgical intervention is always a challenge. Clearly no surgeon wishes to invade tissue and create iatrogenic trauma by the nature of the procedure if it is not necessary. However, by not intervening sooner, are we permitting a condition to advance with the deterioration of tissue that makes direct repair of the anatomy impossible and leaves us with less desirable indirect repairs? I suggest this requires both knowledge of the condition and surgeon experience.
Dr. Theodoulou is an Instructor of Surgery at Harvard Medical School. He is an Attending Surgeon at Cambridge Health Alliance in Cambridge, Mass. Dr. Theodoulou is a Fellow of the American College of Foot and Ankle Surgeons.
- Klein E, Weil Jr L, Weil Sr L, Knight J. The underlying osseous deformity in plantar plate tears: a radiographic analysis. Foot Ankle Spec. 2013; 6(2):108-18.
- Apsden RM, Hukins DW. Structure, function, mechanical failure of the meniscus. In: Yettran AL (ed): Mechanical Properties and Stress Analysis in Biomechanics. Manchester University Press, Manchester, 1989, pp. 109-122.
- Suero EM, Myers KN, Bohne WH. Stability of the metatarsophalangeal joint of the lesser toes: a cadaveric study. J Orthop Res. 2012; 30(12):1995-8.
- Barg A, Courville XF, Nikisch F. Role of collateral ligaments in metatarsophalangeal joint stability: a cadaver study. Foot Ankle Int. 2012; 33(10):887-882.
- Deland JT, Sung IH. The medial crossover toe: a cadaver dissection. Foot Ankle Int. 2000; 21(5):375-378.
- Morton DJ. Hypermobility of the first metatarsal bone: the interlinking factor between metatarsalgia and longitudinal arch strains. J Bone Joint Surg Am. 1928; 10(2):187-196.
- Valero J, Gallart J, González D, et al. Multiple interdigital neuromas: a retrospective study of 279 feet with 462 neuromas. J Foot Ankle Surg. 2015;54(3):320-2.
Editor’s note: For further reading, see “Emerging Concepts In Plantar Plate Repair” in the February 2015 issue of Podiatry Today or “Current Concepts In Plantar Plate Repair” in the April 2012 issue.