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Rethinking The Treatment Algorithm For Plantar Fasciitis

Current etiologies of plantar fascia pathology have been generally accepted in the profession despite a lack of clear evidence for their role. Accordingly, the author examines the current literature and proposes a revised model of understanding surrounding plantar heel pain.

Chronic plantar heel pain is most likely one of the most common, disabling foot conditions to come through your practice door. While many conditions may result in chronic plantar heel pain, plantar fasciitis remains the most common diagnosis.1 Clinically, plantar fasciitis is characterized by pain localized to the attachment of the plantar fascia, which is of insidious onset and worse with weightbearing after rest. Although there is evidence that symptoms associated with plantar fasciitis typically resolve within six to 18 months in the majority of cases, the prognosis of conservative treatment is difficult to predict.2,3 

To make matters worse, there is not a large body of evidence supporting one treatment over another. This may be, in part, because many of the studies evaluating treatments in plantar fasciitis often lack an underlying theory or model that explains the development and progression of the condition. In considering the treatment algorithm for plantar fasciitis, we first need to address fundamental questions concerning our understanding of the mechanisms that drive the development of plantar fasciitis and chronic heel pain.

What The Research Reveals About The Commonly Accepted Causes Of Plantar Fasciitis 

Traditionally, clinicians have thought that mechanical overload plays a major role in plantar fasciitis but the mechanism itself is poorly understood.2  Animal studies have demonstrated an association between mechanical overload and tendon degeneration, but repeated mechanical loading on its own is not sufficient to induce degenerative changes.4 Some other intrinsic or extrinsic factor is necessary before overt degeneration is evident.5,6 

Intrinsic factors for the development of plantar fasciitis have been well considered by clinicians and researchers. Internal factors including age, body mass index (BMI), foot type, heel pad properties, arch deformation, ankle and rearfoot motion have been clinically implicated in plantar fasciitis.7,8 According to the mechanistic model proposed by Rome over 20 years ago (see “A Quick Overview Of Intrinsic Risk Factors With Plantar Fasciitis” on page 34), these intrinsic factors are risk factors that predispose an individual to developing plantar fasciitis.7 With exposure to an external risk factor such as unaccustomed exercise, prolonged standing or inappropriate footwear, plantar fasciitis ensues. Intrinsic risk factors are widely believed to increase the likelihood of developing plantar fasciitis by increasing tensile strain at the attachment of the plantar fascia, primarily by elongating the medial longitudinal arch via foot pronation or by increasing direct compressive stress at the enthesis.9,10 

However, there is little scientific data to support the argument that these factors increase the risk of developing heel pain.8 Rather, studies in unilateral plantar fasciitis arguably suggest that many parameters traditionally considered risk factors for plantar fasciitis are not actually so. They are instead likely to be aggravating factors that do not influence the risk of developing the condition but merely modulate the level of heel pain once it is present.11-13 This has resulted in our team developing a simple but testable model of plantar fasciitis evaluation (“Reassessing Potential Deficits As Etiologies For Plantar Fasciitis” to the right).14 

A Closer Look At A Revised Model Of Plantar Fasciitis

The revised model is supported by observations that thickening of the plantar fascia enthesis, which is characteristic of plantar fasciitis, may also occur in the asymptomatic limb (although to a lesser extent) and in the absence of a history of pain.12,15-17 Such bilateral thickening of the plantar fascia enthesis suggests that plantar fasciitis may represent a systemic process.12 

The development of plantar fasciitis, therefore, may possibly proceed via two mechanisms. First, a mechanically sound plantar fascia is exposed to abnormal levels of stress bilaterally. Alternatively, there is an inherent deficiency of the plantar fascia, which renders it incapable of tolerating the normal levels of stress to which it is exposed. When this is combined with an extrinsic factor, such as unaccustomed activity, prolonged standing or inappropriate footwear, the upper strain threshold for healthy remodelling of the plantar fascia is exceeded. Microdamage to the plantar fascia accumulates and if this continues, degenerative change ensues.14,18 

While the revised model has simplified the approach to heel pain, there are still a number of areas that need further research to improve our understanding and guide therapeutic approaches. For instance, how degenerative change within the fascia leads to pain is still unclear. Similarly, it is still unknown if the structural and functional properties of the fascia recover after plantar fasciitis.

Where Does Pain Fit In This Model?

The source and mechanism underlying the development of pain associated with plantar fasciitis require more research. Traditionally, the pain linked with plantar fasciitis was thought to originate from either inflammation or disruption of collagen fibers. However, inflammatory cell infiltrate is not common on histopathological examination of chronic plantar fasciitis and collagen disruption (as depicted with medical imaging) is poorly correlated with clinical symptoms.16,19 Although researchers have demonstrated pain levels in plantar fasciitis to be positively correlated with neovascular ingrowth, as determined by power Doppler ultrasonography, positive color flow and hypoechogenicity are neither specific to nor are they consistent findings in plantar fasciitis, and are often reported in the fascia of asymptomatic limbs.20,21

Neovascularization is, therefore, not likely the primary cause of pain in plantar fasciitis. Researchers have suggested alternative biochemical hypotheses involving neurotransmitters, such as glutamate and substance P, for tendon pain but the significance of these factors in plantar fasciitis has not been established.22

Research undertaken more than two decades ago demonstrated that peripheral nerves can directly modulate local inflammatory and immune responses in animal models, and highlighted the potential modulatory role of the central nervous system in musculoskeletal pain.23, 24 However, such research topics are only now being explored in foot pain and plantar fasciitis. For instance, researchers have observed widespread pressure hypersensitivity bilaterally in unilateral cases of plantar fasciitis, suggesting that central nociceptive pain processing is altered in chronic heel pain.25,26 Similarly, emerging evidence suggests pain-sensitizing neuroendocrine and neuroimmune pathways may underlie the observed link between obesity and chronic heel pain, which, if verified, will likely present new therapeutic approaches in plantar fasciitis.27 While linked to plantar fasciitis, the potential roles of obesity and aging are still yet to be elucidated.

Evaluating The Role Of Intrinsic Risk Factors In Plantar Fasciitis

What research has shown to date is that intrinsic factors, such as the shape of the medial longitudinal arch, rearfoot and midfoot loading, and the energy dissipating properties of the heel pad, are likely to be moderating (or pain aggravating) rather than risk factors in heel pain.11-13,28,29 Cineradiographic studies of walking gait have found no significant difference in the structure and movement of the medial longitudinal arch in individuals with and without plantar fasciitis.12 However, researchers have associated lower arch structures with greater levels of pain and fascial thickening.30 

Similarly, altered loading of the rearfoot and midfoot during walking is associated with greater self-reported levels of heel pain, suggesting that both tensile and compressional force may aggravate pain.29,31 A 2009 study revealed that altered energy-dissipating properties of the heel pad may also be involved in plantar fasciitis.13 The energy-dissipation ratio is a measure of the energy lost by viscous friction within tissue and is thought to be important in damping high frequency vibration. Reduced energy dissipation of the heel pad during walking, therefore, may increase the vibrational loading at the calcaneal attachment of the plantar fascia and lead to adaptational thickening of the stress–dissipating fibrocartilaginous enthesis.13 In support of such a concept, Rubin and colleagues have demonstrated that small amplitude, high–frequency vibrations induce an anabolic adaptive response in trabecular bone.32 

Examining The Evidence For Inherent Material Deficit And Neuromuscular Deficit As Potential Causes Of Plantar Fasciitis

Researchers have hypothesized about two types of deficit resulting in plantar fasciitis. One theory involves a material deficit of the plantar fascia leading to a reduced capacity of the plantar fascia to cope with loading. Another hypothesis centers on a neuromuscular deficit leading to reduced muscular activity in the foot.

Direct evidence for an intrinsic material deficit of the plantar fascia as a cause  in fasciitis is scant. Degenerative tendon thickening, similar to what one might find with plantar fasciitis, is thought to proceed asymptomatically and is known to reduce the ultimate tensile strength of tendon in animal models.4 Recent studies employing axial strain elastography and shear wave elastography also tend to suggest that thickened symptomatic fasciae are also softer and more compliant than asymptomatic fasciae.33-35                         

Researchers have reported comparable degenerative change in what was previously considered to be overuse injuries of the intervertebral disc, the cruciate ligaments of the knee and the Achilles and rotator cuff tendons.36,37 

Emerging evidence also suggests there may be a genetic component to the degenerative changes one sees in these structures. For instance, polymorphs of COL5, an important regulator of fibrillogenesis and fibril growth, have been associated with Achilles tendinopathy and human cruciate ligament ruptures.38,39 Similarly, COL9A2 polymorphs (involved in bridging collagens to non-collagenous proteins) are thought to play a role in degenerative disc disease but the role of these polymorphs and others in the development of degenerative changes is as yet uncertain.40,41

Similarly, potential gene–gene and gene–environment interactions are poorly understood although there is evidence that COL9A3 gene polymorphisms and persistent obesity may act synergistically to increase the risk of degenerative disease albeit in the lumbar disc.42 The potential for genetic components to predispose development of plantar fasciitis in individuals is fundamental to the revised model and, if supported by research, represents an exciting new area for personalized medicine.

Both active (muscle) and passive (plantar fascia and ligament) elements are important in the maintenance of the medial longitudinal arch. Researchers have documented reduced strength of the ankle and digital plantarflexors in plantar fasciitis, thereby leaving passive structures such as the plantar fascia to bear a relatively greater proportion of load.43,44 

Although such an observation does not preclude the potential role of reflex inhibition of muscles secondary to heel pain, Chundru and colleagues have shown that plantar fasciitis is significantly more common in people with atrophy of the abductor digiti minimi, suggesting that muscular changes lead clinical symptoms.45 Such a mechanism may also account for the fascial thickening noted in people with diabetic neuropathy, in whom intrinsic foot muscle atrophy is common.46 

Is It Time To Rethink The Treatment Algorithm For Plantar Fasciitis?

From the perspective of the revised model, treatments aiming to maintain arch shape, modify foot loading and/or improve shock absorbency of the heel may assist in reducing pain associated with plantar fasciitis. However, these treatments are unlikely to address the true cause of the condition, which remains unknown. There is now an abundance of randomized clinical trials of variable quality evaluating interventions for plantar fasciitis. Of the treatment modalities that have been evaluated with robust research designs, extracorporeal shockwave therapy (ESWT) has arguably the best evidence to date. Although inferior to stretching for acute symptoms, ESWT has consistently shown positive efficacy in the medium- to long-term for most patient-reported outcomes.47-50 

Although systematic reviews and meta-analyses have questioned the role of many therapeutic approaches (including foot orthoses) for chronic plantar fasciitis, this is not to say such treatments are ineffective. Arguably, it more likely reflects a limitation of research, which to date has largely compared various treatments without considering the mechanisms that underpin the development of plantar fasciitis, factors that moderate its progression or how these interact with pain and its persistence. 

In Conclusion

Given that recurrence of plantar fasciitis may be as high as 50 percent, it would seem reasonable to argue that self-reported pain and function may not be the best outcomes for deciding to cease treatment or for monitoring therapeutic approaches in chronic heel pain.51,52 Once we have a well-informed model explaining the mechanisms underpinning chronic plantar fasciitis, we will be better able to develop and compare treatments in a meaningful way. 

Dr. Wearing is a Professor in the School of Clinical Sciences and Institute of Health and Biomedical Innovation at Queensland University of Technology in Australia. He is also a Visiting Professor, Faculty of Sports and Health Sciences at the Technical University of Munich in Germany.

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References

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