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This work has been submitted to NECTAR, the Northampton Electronic Collection of Theses and Research. Article
R A T C E N
Title: Plantar fasciopathy: revisiting the risk factors Creator: Beeson, P.
Example citation: Beeson, P. (2014) Plantar fasciopathy: revisiting the risk factors. Foot and Ankle Surgery. 20(3), pp. 160-165. 1268-7731. Version: Accepted version
Official URL: http://dx.doi.org/10.1016/j.fas.2014.03.003
Note: This is the author’s version of a work that was accepted for publication in Foot and Ankle Surgery. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Foot and Ankle Surgery volume 20, issue 3 (2014), DOI: 10.1016/j.fas.2014.03.003. http://nectar.northampton.ac.uk/6575/
Accepted Manuscript Title: Plantar fasciopathy: revisiting the risk factors Author: P. Beeson PII: DOI: Reference:
Please cite this article as: Beeson P, Plantar fasciopathy: revisiting the risk factors, Foot and Ankle Surgery (2014), http://dx.doi.org/10.1016/j.fas.2014.03.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Dr P. Beeson BSc, MSc, PhD, FFPM RCSP(Glasg) Senior Lecturer School of Health, The University of Northampton
Plantar fasciopathy: revisiting the risk factors
Dr Paul Beeson Senior Lecturer School of Health The University of Northampton Park Campus, Boughton Green Road Northampton NN2 7AL England Tel: 01604 892304 Email: [email protected]
Similar to other conditions where pathological origin is unclear, chronic
plantar heel pain has become a generalized term that includes several
pathological conditions that affect the heel. Heel pain may be the result
of arthritic, neurological, traumatic, or other systemic conditions, although
the overwhelming cause is mechanical in origin.[2, 3]
Plantar fasciitis is a commonly reported cause of plantar heel pain.[4-7]
Terminology for this condition is confusing, as a degenerative process of
micro tears (fasciosis) similar to tendinosis, a degeneration of collagen in
tendons, and fascial thickening predominates over inflammatory
changes. Similar histopathological changes have been reported in tendon
and ligament disorders elsewhere hence redefinition of the condition
from plantar fasciitis to plantar fasciopathy (PF) may better reflect the
underlying pathology within the fascia, which rarely includes inflammatory
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of risk factors.
There is no widely accepted test or ‘gold standard’ for diagnosing PF.
Ultrasound can be used to confirm clinical diagnosis and classify the
The purpose of this paper is to critically reevaluate risk factors for PF.
Relevant clinical aspects of PF are included to help support the discussion
Page 3 of 28
disease pattern. Ultrasound diagnosis of PF includes reduced
echogenicity and plantar fascia thickening (>4-4.5mm) at its calcaneal
insertion[10-12]. Jeong et al also found discrete fibromata and thickening
in those with pure distal (non-insertional disease). More importantly there
is disorganization of the normal reflective structure and loss of normal
organized ligament architecture.
Jeong et al examined 125 consecutive feet with symptoms of
recalcitrant PF. All had failed to respond to a stepwise conservative
management protocol. Disease characteristics were evaluated using
diagnostic ultrasound. A high proportion of atypical non-insertional PF was
reported. This would not be detected without imaging studies. The use
of ultrasound in cases of recalcitrant plantar heel pain that have failed
proper first-line management is recommended.[12, 13] It was concluded
92 93 94 95
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that ultrasound confirmed clinical diagnosis and classification characteristics as either insertional (proximal), non-insertional (distal) or mixed disease PF.
Plantar fasciopathy is a clinical diagnosis, characterized by the insidious
onset of plantar heel pain after prolonged periods of rest.[2, 6] It is usually
worse in the morning after the first few steps or starting to walk after a
period of inactivity. Although walking helps initially, the pain can recur
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with further exertion. Some patients complain of pain on toe extension
due to invocation of the windlass mechanism. Pain may worsen towards
the end of the day and with increased weight-bearing activity.
Although patients exhibit similar patterns of symptoms, the clinical
presentation can vary in location, level of pain and duration. Up to one
third of patients with PF will present with bilateral symptoms.[16, 17] The
condition affects both sedentary[18-20] and athletic individuals[21, 22],
including military personnel[23, 24]; as such a diverse patient population is
observed. The condition has been reported to peak between 40 to 60
The prevalence of heel pain in the general population is estimated to
range from 3.6% to 7%[20-22], and the disorder has been reported to
account for about 8% of all running related injuries.[25, 26] A retrospective
review of 1407 patients from an outpatient sports medicine clinic, found
116 117 118 119 120
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that younger athletes had a lower prevalence of PF (2.5%) than older athletes (6.6%). The literature is inconsistent regarding the association
between gender and PF. Some studies show an increased prevalence in men; while others show greater prevalence in women.[18, 22]
Plantar fasciopathy is commonly described as a self-limiting condition.[5,6]
Crawford & Thomson undertook a systematic review supporting this
observation. However, PF can be a painful and disabling condition with
detrimental effects on health-related quality of life and subsequently be
frustrating for patients. There is a higher risk of prolonged symptoms in
overweight patients, those with bilateral involvement and when there
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is a long delay before seeking medical attention.[30, 31]
Impact on health
Patients are unlikely to be satisfied with evidence of the self-limiting
nature of the condition and most are likely to demand treatment for their
symptoms. Irving et al demonstrated that chronic heel pain has a
significant negative impact on foot-specific and general health-related
quality of life. The degree of negative impact does not seem to be
associated with age, sex, or BMI. Physical inactivity is recognized as
one of the greatest public health challenges in Western countries. The
morbidity of PF can result in immobility and reduced activity levels.
Furthermore, patients who develop PF are often overweight and therefore
subsequent loss of weight becomes increasingly difficulty due to the pain
of everyday weight bearing. The duration of obesity in obese patients
may be important to the development of heel pain in such patients.
Inactivity and an increased body weight are major risk factors for many
142 143 144 145 146
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diseases such as obesity, cardiovascular disease, diabetes and
osteoarthritis making it imperative that treatment for PF is instituted rather than waiting for spontaneous resolution.
Plantar fasciopathy is an important public health disorder due to its
frequent occurrence. Researchers have estimated that 10% of people in
the USA may present with heel pain over the course of their lives, with
83% of these patients being active working adults.[36, 37] With people
working and living longer the age range for this condition may be 6
Page 6 of 28
potentially extending. An estimated one million visits per year were made
to physicians and hospital outpatients in the USA for treatment of PF,
representing an important economic burden to health services.
Frequently, patients do not seek treatment until symptoms are considered
chronic. At this point treatment regimens can become costly, as
symptoms are recurring, recovery is lengthy and the response to
treatment is unpredictable. Furthermore the potential for longer-term
health consequences related to immobility such as weight-gain,
hypertension, coronary artery disease and non-insulin dependent diabetes
in chronic PF exist.
The following criteria were used to search the literature:
1. English language human studies.
2. Published after 1988.
168 169 170
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3. Electronic databases: Cochrane library, BioMed Central, EMBASE, CINAHL, AMED, Ovid, Swetswise, PubMed, Highwire, SportDiscus, ISI web of knowledge, Science direct, Science citation index, The Lancet.com, BMJ clinical evidence, MEDLINE, Scirus.com, Index to
thesis, Controlledtrials.com UK national research register for on-going/
recently completed trials.
4. MeSH terms used alone or in combination: plantar fasciitis, fasciopathy, sub-calcaneal, heel pain, aetiology, risk factors.
Page 7 of 28
5. Search limited to: peer-reviewed journals, systematic reviews/ meta-
analyses, cohort studies, case control studies and surveys. Case reports
and letter to editors were excluded. 6. Research papers were chosen based upon evaluation of PF risk factors.
7. Series with n > 10.
8. Results for each risk factor were separable if > 1 discussed.
Although PF is the most common soft-tissue cause of heel pain[5, 19] its
aetiology is not fully understood.[22, 38, 39, 40, 41] The condition is considered
to be multifactorial[6, 17, 20] and numerous risk factors are implicated in its
development (Table 1). The evidence supporting these factors is limited
and their relative importance is unclear. Several causes have been
190 191 192 193
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hypothesized, with the most common being overuse due to prolonged weight-bearing, obesity, unaccustomed walking or running, limited ankle joint dorsiflexion, posterior muscle group tightness and standing on hard surfaces.[2, 5, 19, 20, 32, 40, 41, 51]
The presence of co-existing calcaneal spurs has often been reported[9, 11,
association. Some suggest that calcaneal spurs may be an adaptive
response to vertical compression of the heel rather than longitudinal
traction at the calcaneal enthesis. A study examining prehistoric
but confusion exists as to whether it is a causal or significant
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skeletal remains concludes that plantar calcaneal spurs are a modern
phenomenon resulting from long periods of standing, excess weight and
associated with lower limb osteoarthritis. Wainwright et al reported a
strong correlation with calcaneal spurs over 1mm long and PF and Johal &
Milner found a higher prevalence of calcaneal spurs in patients with PF.
Further research is warranted to assess whether the association is
Typically PF affects middle-aged or older people, often women more than
men. The association of PF with increasing age is consistent with the
histopathological findings of degenerative changes within the plantar
fascia. These degenerative findings support the hypothesis that PF is
secondary to repetitive micro trauma caused by prolonged weight-bearing
activities. The constant overload inhibits the normal repair process,
resulting in collagen degeneration, which causes both structural changes
and perifascial oedema. These changes in turn lead to a thicker heel
pad, which has been shown to be associated with pain in individuals with
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The current literature is inconsistent regarding the association between
gender and PF (Table 1). No theories exist hypothesizing the reason for a
difference in prevalence between the sexes. This may relate to hormonal
214 215 216 217
PF. Increasing heel pad thickness leads to a loss of heel pad elasticity; both of these factors are associated with increasing age and increasing BMI.[53, 54] The decrease in elasticity of the fascia seen with increasing age
is associated with a decrease in shock absorbing capabilities, which may be a result of the degenerative fascia’s inability to resist normal
Page 9 of 28
differences or structural changes like those seen in tendinopathy or
differences caused by genetic variations.
Increased body weight  and increased body mass index (BMI)[19, 29]
have been shown to be significant risk factors for PF (Table 1). A BMI of
more than 30 kg/m2 having an odds ratio of 5.6 (95% confidence interval,
1.9 to 16.6; p < 0.01) compared with a BMI of less than 25 kg/m2
cardiovascular risk) represents a reasonable goal for weight loss that may
reduce heel pain. Frey and Zamora  demonstrated a 1.4-fold increased
probability of PF being diagnosed in an overweight or obese patient.
Rome et al suggested that BMI is not related to plantar fasciitis pain in
the athletic population, but other factors such as a low oestrogen levels in
female athletes which leads to reduced collagen elasticity.
Previous research has suggested that limited ankle dorsiflexion,
obesity and prolonged weight bearing may increase the risk of PF.
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239 240 241 242
. Rano et al also concluded that a BMI of 25 (the target for
Those studies, however, involved the use of univariate analytical
approaches and, in some cases, did not include a control group. Riddle et al hypothesized that reduced ankle dorsiflexion is the most important
risk factor for development of PF and reported that individuals with <0o of dorsiflexion have an odds ratio of 23.3 (95% CI 4.3-124.4). Riddle et
al hypothesized that increased ankle equinus can result in more
compensatory foot pronation and subsequently greater tensile loading on
the plantar fascia. Limited ankle dorsiflexion appears to have a biologically
plausible explanation for causality. Individuals who spend the majority of
the workday weight-bearing and those who are obese also theoretically
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have increased tensile loads on the plantar fascia compared with those
who spend less time weight-bearing and those who have a normal body
It is unclear whether limited ankle dorsiflexion is a cause or a
consequence of PF. It is possible that limited dorsiflexion may develop
after the onset of the disorder. Theoretically, if PF had caused the loss of
dorsiflexion, then the motion on the involved side would have been
reduced and the motion on the uninvolved side would not have been
reduced. Riddle et al undertook a case-control study where only cases
of unilateral PF were used. The uninvolved side was used as the control
for ankle joint dorsiflexion. It was found that dorsiflexion on the
uninvolved side was also reduced relative to that in the control group.
A “dose-response” relationship was found for the risk factor of limited
dorsiflexion on the uninvolved side. Thus it was hypothesized that
ankle dorsiflexion may have been limited before the onset of the
265 266 267 268
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More recently Bolivar et al found an association between posterior leg muscle tightness (hamstring as well as triceps surae) and PF in a controlled trial of 100 participants. Labovitz et al and Harty et al also found an association with hamstring tightness and PF. Harty et al concluded that this was found to prolong forefoot loading and through the
windlass mechanism might be a factor that increases repetitive injury to
the plantar fascia.
The most common cause cited for plantar heel pain is biomechanical
stress of the plantar fascia at its enthesis of the calcaneal tuberosity.
Page 11 of 28
Mechanical overload, whether the result of biomechanical faults, obesity,
or occupation, may contribute to the symptoms of heel pain. Foot
pronation alone, as measured by the Foot Posture Index has also been
shown to be significantly greater in patients with chronic plantar heel
pain. This is supported by Lee et al who demonstrated a high
correlation between arch height (r = 0.642), plantar fascia tension (r = -
0.797) maximum rearfoot eversion (r = -0.518). It is hypothesized that a
lack of cushioning in a rigid high arched foot may also result in PF but this
has not been proven.
Stress shielding (failure of a stress deprived deep structure to heal
because of the superficial element bearing most of the load) has been
implicated in enthesopathy. It has been suggested that that proximal
tendinopathy of the flexor digitorum brevis muscle (which is deep to the
plantar fascial ligament) is implicated in the pathology of PF.
Localized nerve entrapment of the medial calcaneal or muscular (first)
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associated with PF.[19, 23, 35, 40]. Riddle et al found a significant
association (OR 3.6, 95% CI 1.3-10.0) of the reported cases of PF with
time spent working on feet (>80% of work day). There was however,
no data presented on the extent and duration of exposure; nor the
particular occupations and work histories of the cases and controls.
289 290 291
branch of the lateral plantar (Baxter’s) nerve may be a contributory factor to plantar heel pain. The presence of sensory disturbances including
radiation of pain is indicative of neurological pathology thereby differentiating it from PF.
Work-related prolonged weight bearing has been reported to be
Page 12 of 28
Inappropriate footwear[5, 19, 48] and rapid increases in activity levels[5, 19]
have also been reported as risk factors associated with PF.
In athletes PF is primarily believed to be an overuse injury combined with
training errors, training surfaces, biomechanical alignment and muscle
dysfunction and inflexibility.[5, 22, 25, 26] Additionally, PF has been
associated with individuals engaging in sports involving jumping.
Excessive foot pronation can lead to increased plantar fascial tension
during the stance phase of running.[25, 26] Furthermore, heel strike during
running causes compression of the heel pad up to twice body weight.
For athletes with inadequate muscle strength or flexibility and decreased
shock-absorbing capabilities, the initiation of a new training program may
exacerbate overloading of the plantar fascia. Increases in tensile
loading, seen with new increases in running intensity or frequency and
changes in general footwear have been associated with overloads of the
plantar fascia leading to micro tears. In particular, firm footwear may
exacerbate the developing PF in such patients.
315 316 317
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These risk factors combine to create a pathological overload of the plantar fascia at its origin, causing micro tears in the fascia that subsequently
lead to perifascial odema and increasing heel pad thickness.[20, 38, 52] As these micro tears increase in size, they may coalesce to form a large
symptomatic mass causing an increase in heel pad thickness. These
changes in fascial thickening (particularly proximal portion), and
oedema of the adjacent fat pad and underlying soft tissues can typically
be seen on ultrasound or MRI.
To-date no research has considered a possible genetic basis to PF. 13
Page 13 of 28
Candidate gene variants for tendinopathy (a degenerative process not
dissimilar to PF) have been examined and various associations
revealed.[58-64]. Some of the candidate gene variants based on tendon
studies may also be relevant to ligaments such as the plantar fascia
(Table 1). As in tendinopathy a range of candidate gene variants may
also contribute to the development of PF. Individuals may possess certain
genetic risk factors that predispose them to PF. These genetic factors may
interact with other factors (intrinsic and extrinsic) to increase their overall
risk profile for developing PF. Research to examine a possible genetic
basis for PF may add to our understanding of the intrinsic risk profile for
this condition. Furthermore, it may help to predict the patients at risk
from developing chronic PF.
Inflammatory disease[65-67] or drug therapy may also be implicated in the
development of PF in a few cases that is unresponsive to common
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339 340 341 342 343
Plantar fasciopathy is a common cause of sub calcaneal heel pain. The condition represents an important economic burden to health services due its potential to become chronic in nature. Studies supporting both intrinsic and extrinsic risk factors suggest complex multifactorial soft tissue
pathology. Research to examine a possible genetic basis for developing
this condition may advance our knowledge of the intrinsic risk profile,
provide a novel and alternative approach to understanding this
challenging condition and help rank the significance of risk factors.
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