Why Don’t We Understand Hammertoes?

It is the most common musculoskeletal condition affecting the feet of older individuals yet the underlying cause of digital deformities in the human foot remains poorly understood.^1,2

Digital deformities, including hammertoes, mallet toes, crossover toes and claw toes, rank second (60 percent) behind toenail deformities (75 percent) in terms of the prevalence of all foot and ankle conditions in older adults.¹ While pain and deformity in the toes are relatively nonexistent in young children, the prevalence of this condition increases linearly with age to become the most common musculoskeletal complaint of the feet in people over the age of 70 years.²

When writing my textbook Pathomechanics of Common Foot Disorders, I was struck by the fact that there are no credible studies that validate any of the proposed mechanisms for the development of digital deformities in the human foot.³ Even plantar plate injury, a known cause of digital deformity, is a pathology which does not have widespread understanding or agreement about its underlying cause.^4-6 Most authorities recognize that some type of muscle imbalance leads to contracture of the digits.^7-9 However, this notion of abnormal muscle function in the feet of healthy individuals causing acquired toe deformities has not been validated with any electromyographic studies. There is also a lack of any studies that identify any extrinsic or intrinsic risk factors for developing digital deformities.

It is no wonder that the choice of surgical procedures to correct digital deformities reflects a lack of understanding about the underlying pathomechanics of this common problem. In fact, the surgical solution for hammertoes and claw toes focuses on a single surgical procedure involving proximal interphalangeal joint (PIPJ) arthrodesis, a trend which has not changed for over 40 years.^10-14 While advances do exist with devices that provide intramedullary fixation for arthrodesis of the proximal interphalangeal joint, there is the question as to whether any of these newer technologies are superior to traditional methods of fixation.^15-17   

Recently, Dang and Coughlin published a 40-year retrospective review of the development of surgical procedures to correct forefoot pathologies.¹⁸ They cite a large number of studies assessing the use of newer technologies to fixate surgically corrected hammertoe deformities and concluded that intramedullary devices show no significant advantage over traditional K-wire fixation.¹⁸ 

Concluding their review, Dang and Coughlin state: “As much as today’s surgeon is able to accurately diagnose and treat patients’ forefoot woes, there remains room for improvement—both in knowledge of the disease and development of improved techniques.”¹⁸

In my research into the pathomechanics of digital deformities, it became clear that the best insights exist in the podiatric literature, most notably by Green and coworkers.^19-20 They propose three different mechanisms that create muscle imbalance leading to digital deformity. Flexor stabilization, flexor substitution and extensor substitution can all create a state of chronic hyperextension of the lesser digits at the metatarsophalangeal joint (MPJ).²⁰ Chronic hyperextension of the lesser digits at their respective MPJs will theoretically weaken the plantarflexion moment arm normally provided by the lumbricals and the interossei muscles acting at the lesser MPJ and extension of the PIPJ via the extensor expansion.^19-20

Flexor stabilization and flexor substitution are compensatory mechanisms whereby the flexor digitorum longus (FDL) muscle is overactive during the stance phase of gait. Clinicians can find this compensation in individuals with weakness or loss of the tibialis posterior muscle as one may see in cases of acquired flatfoot deformity. If the plantar plate, the interossei or the lumbricales fail to stabilize the digit while the flexor digitorum longus is overactive, a process called reverse buckling will cause dorsal contracture of the MPJ along with plantarflexion of the proximal interphalangeal joint.²⁰

One most commonly sees extensor substitution in cavus deformity and it occurs during the swing phase of gait. Forefoot equinus or ankle joint equnius, both of which are common in cases of cavus deformity, will require increased activity of the extensor digitorum longus (EDL) to increase dorsiflexion for toe clearance during the swing phase of gait. Without any active muscle activity during swing phase to oppose the extensor digitorum longus, chronic extension of the MPJs will compromise the plantarflexion moment arm of the interossei and lumbricales.²⁰

In a cadaver study, Sarrafian and Kelikian showed that activation or pull on both the flexor digitorum brevis and flexor digitorum longus muscles on the plantar side of the toe combined with simultaneous pull of the extensor digitorum brevis and extensor digitorum longus on the dorsal side will result in a claw toe.²¹ The claw toe characteristically exhibits hyperextension of the MPJ and marked flexion of the proximal interphalangeal joint and the distal interphalangeal joint.⁸ In the healthy foot, the combined action of these four muscles are counteracted by the interossei and lumbricals, providing flexion stability of the MPJ and extension of the proximal interphalangeal and distal interphalangeal joints.²⁰ Even more important is the static and dynamic contribution from the plantar aponeurosis, via the plantar plate, to prevent hyperextension of the MPJ, facilitating the extensors to act distally on the toes to extend the proximal interphalangeal and distal interphalangeal joints.⁴ 

Plantar plate injuries can be a primary cause of digital deformity or they can be a result of chronic long-term hyperextension of the MPJ.^22-25 In a 2007 study of crossover second toe deformities, Kaz and Coughlin assessed 169 patients with 86 percent of the patients being women.²⁶ They found an increased incidence of hallux valgus and first MPJ degenerative arthritis in the study patients as well as a peak incidence among women over 50 years of age. This suggests that, at least for plantar plate injuries, footwear may play a role in the underlying etiology.

Therefore, there are multiple proposed mechanisms that may cause a muscle imbalance leading to acquired digital deformity. Unfortunately, none of these mechanisms have been studied in any detail to validate their role in digital deformities. Much of the theory of muscle imbalance and digital deformities hinges upon theory as well as anecdotal evidence.

Notwithstanding, it is baffling that surgeons approach digital surgery targeting the resulting deformity alone without regard for evaluating any contributory underlying mechanism. Indeed, two of the three mechanisms proposed to cause toe deformities occur at opposite times during the walking gait cycle with extensor substitution occurring during the swing phase of gait while flexor substitution occurs during stance phase. One proposed mechanism, flexor stabilization, occurs most frequently in cases involving flatfoot while another possible mechanism, extensor substitution occurs in those with cavus feet. In all three mechanisms, the digital deformity occurs from compromise in the function of two key intrinsic foot muscles: the intereossei and the lumbricales. Currently, there are no reliable surgical procedures that restore any of the muscle imbalances that cause digital deformities. Instead, the surgeon fuses a joint to try to negate the effects of the muscle imbalance.

More importantly, we need to recognize that digital deformities are an acquired disorder with significant public health implications. We are not born with hammertoes. Digital deformities begin to increase in frequency by age 25 and there is increased incidence linearly with age.² Digital deformities are a significant risk factor for catastrophic falls in older adults.^27,28 Therefore, one has to ask: Why are we not able to prevent this inevitable malady of the human foot, which will affect over half the population in later life? Are there exercises or foot orthotic devices that might be effective in preventing digital deformities if they are implemented at a younger age?

I pose this final question to my colleagues: Why is there so little research conducted studying the contributory factors causing digital deformities yet new technologies for fixating proximal interphalangeal joint arthrodesis continue to be introduced into the marketplace every year? 

Maybe we do not need fancy implants to fuse a joint if we can develop new surgical procedures that focus directly on the muscle imbalance, which leads to one of the most common musculoskeletal conditions affecting the foot.  

Dr. Richie 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 a Fellow and Past President of the American Academy of Podiatric Sports Medicine. Dr. Richie is a Fellow of the American College of Foot and Ankle Surgeons, and the American Academy of Podiatric Sports Medicine. Dr. Richie is the author of a new book titled "Pathomechanics of Common Foot Disorders," which is available from Springer at https://www.springer.com/us/book/9783030542009 .

References

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