Journal of Anatomy

J. Anat. (2017) 230, pp743--751 doi: 10.1111/joa.12607

REVIEW ARTICLE

The plantar calcaneal spur: a review of anatomy,

histology, etiology and key associations
Joshua Kirkpatrick,1 Omid Yassaie2 and Seyed Ali Mirjalili1
1
Department of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand
2
Department of Orthopedic Surgery, Wellington Hospital, Wellington, New Zealand

Abstract
The plantar calcaneal spur (PCS) is a bony outgrowth from the calcaneal tuberosity and has been studied using
various methods including cadavers, radiography, histology and surgery. However, there are currently a number
of discrepancies in the literature regarding the anatomical relations, histological descriptions and clinical
associations of PCS. Historically, authors have described the intrinsic muscles of the foot and/or the plantar
fascia as attaching to the PCS. In this article we review the relationship between the PCS and surrounding soft
tissues as well as examining the histology of the PCS. We identify a number of key associations with PCS,
including age, weight, gender, arthritides, plantar fasciitis and foot position; these factors may function as risk
factors in PCS formation. The etiology of these spurs is a contentious issue and it has been explained through a
number of theories including the degenerative, inflammatory, traction, repetitive trauma, bone-formers and
vertical compression theories. We review these and finish by looking clinically at the evidence that PCS causes
heel pain.
Key words: bony outgrowth; calcaneal tuberosity; plantar calcaneal spur.

Subhadrabandhu, 1994; Barrett et al. 1995; Riepert et al.

Introduction
The plantar calcaneal spurs (PCS) are a bony outgrowth
from the calcaneal tuberosity and has been studied via
numerous methods including cadavers, radiography, histol-
ogy and during surgery (Abreu et al. 2003) (Fig. 1). PCS are
typically described as bony outgrowths arising just anterior
to the medial process of the calcaneal tuberosity, but there
is no consistent definition in the literature (Chang & Milt-
ner, 1934; Gerster et al. 1977; Tountas & Fornasier, 1996;
Abreu et al. 2003; Franson, 2008). Some authors define
them as projections of larger than 1 or 2 mm, while others
use microscopy or subjective assessment (Resnick et al.
1977; Prichasuk & Subhadrabandhu, 1994; Kumai & Ben-
jamin, 2002; Abreu et al. 2003). In the young to middle-
aged population PCS prevalence is 11–21%. This is constant
across various ethnicities with rates of 11% in India, 13% in
Ireland, 15% in Zimbabwe, 16% in Thailand, 17% in Europe
and 21% in America (Banadda et al. 1992; Prichasuk &
Correspondence
Seyed Ali Mirjalili, Department of Anatomy and Medical Imaging,
University of Auckland, Auckland, New Zealand.
E: a.mirjalili@auckland.ac.nz
Accepted for publication 14 February 2017
Article published online 29 March 2017
1995; Kullar et al. 2014; Moroney et al. 2014). This rate
increases with age to 55% in those over 62, to 59–78% in
those with current or previous heel pain, and up to 81% in
those with osteoarthritis (Table 1; Tanz, 1963; Bassiouni,
1965; Gerster et al. 1977; Prichasuk & Subhadrabandhu,
1994; Barrett et al. 1995; Riepert et al. 1995; Wainwright
et al. 1995; Li & Muehleman, 2007; Menz et al. 2008). In the
past, gonorrhea, syphilis, hereditary factors, metabolic dis-
turbances and gout were all proposed to be related to the
development of PCS; these have subsequently been discred-
ited (Winthrop, 1909; Griffith, 1910; Roland, 1912; Waech-
ter & Sonnenschein, 1915; Paul & Henry, 1916; Von Lackum
& Palomeque, 1930; Chang & Miltner, 1934; Steindler &
Smith, 1938; Gould, 1942). A number of robust associations
do exist, however; these are potential risk factors for spur
development and will be dealt with in this review along
with how they may relate to PCS etiology.
Anatomy of PCS
PCS originate from the calcaneal tuberosity, located on the
posterior plantar surface of the calcaneus. The majority of
PCS arise from the medial process of the tuberosity, but
they can also originate from the lateral processes and the
sulcus (Roland, 1912; Duvries, 1957; Rubin & Witten, 1963;
Tanz, 1963). The anatomical appearance of PCS is highly

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744 A review of the plantar calcaneal spur, J. Kirkpatrick et al.
A B
C D
E F
variable but can be broadly categorized as simple or irregu-
lar (Mason et al. 1959; Rubin & Witten, 1963; McCarthy &
Gorecki, 1979). Simple PCS are triangular structures that
taper to a sharp point from a broad base (Duvries, 1957;
Brody, 1962; McCarthy & Gorecki, 1979). They have defined
smooth sclerotic cortical borders and well developed trabec-
ulae (Rubin & Witten, 1963; Resnick et al. 1977). In contrast,
irregular spurs have poorly defined borders and no clear
trabeculae (Rubin & Witten, 1963).
It is important to understand the anatomy of the foot to
understand PCS. The plantar fascia (PF) is a critical structure
in this regard; it consists of a dense connective tissue arising
from the medial process of the calcaneal tuberosity and
inserting into the digits of the foot (Barrett et al. 1995;
Wearing et al. 2006). The PF functions to maintain the med-
ial longitudinal arch of the foot as well as absorbing forces
placed on the foot across the mid-tarsal joints (Schepsis
et al. 1991). The PF contains fibrocytes and is known not
only to transmit energy passively but also to respond to the
requirements placed on it by changing the extracellular
matrix composition (Wearing et al. 2006). The PF is signifi-
cantly thicker in patients with PCS than in those without,
4.95–6.1 mm vs. 3.22–4.0 mm (Berkowitz et al. 1991; Kumai
& Benjamin, 2002; Abreu et al. 2003). The relationship
Fig. 1 The black and white arrowheads
indicate the PCS spur, (A) skeleton lateral
view, (B) skeleton inferior view, (C) sagittal
plastinated medial cadaver transection (E12
technique), (D) sagittal medial MRI, (E)
lateral foot X-ray of simple spur, (F) lateral
foot X-ray of irregular spur.
between the PCS and the PF is highly variable and the PF
may be associate with none, part or all of the spur (Barrett
et al. 1995; Li & Muehleman, 2007). Some authors describe
the PCS as embedded within the PF, whereas other authors
maintain the PF does not attach to the PCS, but rather
remains plantar to it (Duvries, 1957; McCarthy & Gorecki,
1979; Forman & Green, 1990; Kumai & Benjamin, 2002;
Smith et al. 2007). One large study showed histologically
that the PF inserted into the periosteum of the spur in 46%
of cases and that this could occur anywhere along the
length of the spur (Li & Muehleman, 2007).
The first layer of the intrinsic muscles of the foot consists
of the abductor hallucis (AH), flexor digitorum brevis (FDB)
and abductor digiti minimi (ADM); the PCS may be closely
associated with each of these (Forman & Green, 1990; Li &
Muehleman, 2007). The second layer consists of quadratus
plantae and it attaches deep to the PCS (Forman & Green,
1990). Tanz (1963) was one of the earliest authors to show
that PCS can arise from muscle rather than from the PF
itself. The FDB attaches to the medial process of the cal-
caneal tuberosity or the apex of the PCS if present, anterior
and superior to the attachment of the PF (Forman & Green,
1990). The FDB inserts into the periosteum of the PCS along
with the PF in 22% of cases, most commonly at the spurs
© 2017 Anatomical Society
 A review of the plantar calcaneal spur, J. Kirkpatrick et al. 745

Table 1 Prevalence of PCS in various populations.

Prevalence of PCS

Normal Population 16% (n = 400; Prichasuk & Subhadrabandhu, 1994), 16% (n = 1027; Riepert et al. 1995), 21% (n = 200;
Barrett et al. 1995), 27% (n = 461; Rubin & Witten, 1963)
Heel pain 59% (n = 148; Lapidus & Guidotti, 1965), 66% (n = 82; Prichasuk & Subhadrabandhu, 1994)
Age 55% (> 62, n = 216; Menz et al. 2008), 98% with PCS > 40 (n = 425; Rubin & Witten, 1963), 89.5% aged
41–50 vs. 60% aged 21–40 (OA, n = 168; Bassiouni, 1965)
Weight 46% with PCS overweight (n = 425; Rubin & Witten, 1963), 70% XY, most XX with PCS overweight
(n = 37; Duvries, 1957)
Foot pronation 62% with PCS and 81% with symptomatic PCS (n = 1000; Shama et al. 1983)
Arthritides 92% with PCS had osteophytes vs. 23% without PCS (n = 425; Rubin & Witten, 1963)
Ankylosing spondylitis 20% (n = 80; Resnick et al. 1977), 28% (n = 35; Gerster et al. 1977), 29% (n = 38; Mason et al. 1959)
Osteoarthritis 56% (n = 70; Gerster et al. 1977), 80% (n = n = 119; Menz et al. 2008), 81% (n = 168; Bassiouni, 1965)
Psoriatic arthritis 25% (n = 52; Resnick et al. 1977)
Rheumatoid arthritis 22% (n = 282; Bassiouni, 1965), 23% (n = 128; Resnick et al. 1977), 28% (n = 100; Gerster et al. 1977),
43% (n = 81; Mason et al. 1959)
Plantar fasciitis 67% with PCS vs. 2.5% in controls (n = 77; Wainwright et al. 1995), 89% with PCS vs. 32% in controls
(n = 19; Johal & Milner, 2012)

distal tip and inferior aspects (14%), but also at the superior
aspect (8%; Li & Muehleman, 2007). The PCS is oriented
along the axis of the PF and FDB approximately half of the
time (Abreu et al. 2003). The ADM also attaches directly to
the PCS, although not as extensively as the FDB does; the
PCS is aligned with the ADM 20–50% of the time (Bassiouni,
1965; Abreu et al. 2003; Smith et al. 2007). The AH arises
just medial to the FDB origin and has been hypothesized to
contribute to PCS formation (Forman & Green, 1990). PCS
have also been shown to arise from around the calcaneal
insertion point of the long plantar ligament (Bassiouni,
1965; Sebes, 1989).
Histology of PCS
Histological analysis shows that the PCS consists of a core of
mature lamellar bone and demonstrates evidence of degen-
eration and fibro-cartilaginous proliferation, along with
one or more of intramembranous, chondroidal and endo-
chondral ossification occurring at the surface (Tountas &
Fornasier, 1996; Kumai & Benjamin, 2002; Smith et al.
2007). The histological specimens are extremely heteroge-
neous, however, and there is no robust correlation between
histology and clinical outcomes (Tountas & Fornasier, 1996).
The irregular surface of PCS and the presence of osteoclasts
suggest continuous active bone turnover; however, there is
disagreement in studies regarding the type of bone-form-
ing activity occurring, as well as its location (Tountas & For-
nasier, 1996; Kumai & Benjamin, 2002; Smith et al. 2007).
There is some evidence that larger spurs show a greater
level of cortical thickening compared with smaller spurs;
however, this is disputed (Kumai & Benjamin, 2002; Smith
et al. 2007). Variable parts of the spur are covered with a
fibrous connective tissue layer which is richly innervated
and vascularized (Kumai & Benjamin, 2002; Abreu et al.
2003; Li & Muehleman, 2007; Smith et al. 2007). One large
study found this fibrocartilage was present on all spurs, at
the inferior aspect in 38%, the inferior aspect and distal tip
in 30%, and at the inferior aspect, distal tip and superior
aspect in 32% (Li & Muehleman, 2007).
Associations with PCS
PCS and age
The prevalence of PCS increases in older age groups (Rubin
& Witten, 1963; Bassiouni, 1965; Gerster et al. 1977;
Banadda et al. 1992; Prichasuk & Subhadrabandhu, 1994;
Riepert et al. 1995). One study estimated the prevalence of
PCS in individuals over 62 at 55%, whereas in another study,
98.4% of those with a PCS were over 40 (Rubin & Witten,
1963; Menz et al. 2008). Older people also have changes to
their gait pattern which may play a role in PCS develop-
ment. These include a greater relative contact time of both
the heel and mid foot, along with a reduced step length
(Scott et al. 2007).
PCS and weight
The prevalence of PCS increases with weight (Duvries, 1957;
Rubin & Witten, 1963; Smith et al. 2007; Menz et al. 2008).
Rubin & Witten (1963) found that 46% of those with PCS were
overweight compared with 27% in the control group, and
Moroney et al. (2014) found 82% of those with PCS were over-
weight or obese. Furthermore, after adjusting for age and
gender, those with PCS were 6.9 times more likely to be obese
compared with those without PCS (Menz et al. 2008). One
study found that those with PCS were four times as likely to
have diabetes than those without PCS; however, it is unclear if
this is an independent risk factor (Moroney et al. 2014).

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746 A review of the plantar calcaneal spur, J. Kirkpatrick et al.
PCS and foot position
There is a statistically significant correlation between foot
pronation and the development of PCS, with 62% of
patients with a spur and 81% with a painful spur having a
pronated foot radiographically (Shama et al. 1983). One
study showed that individuals with plantar heel pain had a
higher incidence of PCS compared with controls (65.9 vs.
15.5%) and that they also had a lower calcaneal pitch, 15.9°
vs. 20.5° (Prichasuk & Subhadrabandhu, 1994). This is consis-
tent with observational data that patients with PCS gener-
ally have flat feet (Duvries, 1957). Other studies, however,
have found no association between foot posture and PCS
(Lapidus & Guidotti, 1965; Menz et al. 2008).
PCS and gender
There is discrepancy in the literature about whether females
have a higher incidence of PCS. Papers which focus on older
populations generally find no significant difference in inci-
dence (Bassiouni, 1965; Menz et al. 2008). However, papers
with a younger population demonstrate that females have
higher incidence than men. Moroney et al. (2014) found, at
an average age of 37.9, incidences of 17 vs. 9%. Similarly,
Riepert et al. (1995) reported incidences of 16.3 vs. 6.5%
and Banada et al. (1992) incidences of 18 vs. 13%. In one
study that broke the population down into nine age
cohorts, PCS was reported to occur more commonly in
women under 49 years of age than in men. They proposed
that this age-dependent difference may be due to the
altered foot biomechanics of wearing high-heeled shoes
(Toumi et al. 2014; Yung-Hui & Wie-Hsien, 2005).
PCS and arthritides
Spurs occur commonly in all arthritides, with estimates as
high as 80% in osteoarthritis and 72% in rheumatology
patients over 61 years (Davis & Blair, 1950; Mason et al.
1959; Bassiouni, 1965; Gerster et al. 1977; Resnick et al.
1977; Menz et al. 2008; Weiss, 2012). Individuals with a PCS
are 3–10 times more likely to have at least one area of
osteoarthritis compared with the normal population and
92% of those with PCS have osteophytes at other points in
their body vs. 23% in those without PCS (Rubin & Witten,
1963; Moroney et al. 2014). It has been hypothesized that
the gross appearance of PCS may represent the underlying
pathological condition, but these relationships are not
exclusive or diagnostic (Roland, 1912; Rubin & Witten, 1963;
Sebes, 1989).
PCS and plantar fasciitis
PCS are present in 45–85% of those with plantar fasciitis;
they also share a number of risk factors such as obesity and
advancing age, suggesting that the two may be linked
etiologically (Sadat-Ali, 1998; Gibbon & Long, 1999; Ozde-
mir et al. 2005; Irving et al. 2006; Levy et al. 2006; Osborne
et al. 2006;Menz et al. 2008). Plantar fasciitis is hypothe-
sized to be due to mechanical overload of the PF resulting
in microtears; the repeated trauma from heel strike inhibits
the reparative response and results in a chronic fascial
inflammatory condition characterized by remodeling, fibro-
sis and even ossification at the fascial insertion point on the
calcaneus (Kosmahl & Kosmahl, 1987; Schepsis et al. 1991;
Wearing et al. 2006). However, histologically there is little
evidence of an active inflammatory infiltrate being present,
but studies have found an increase in mucoid ground sub-
stance, collagen degeneration, fibrogenic hyperplasia and
calcification, suggesting that this condition is more of a
degenerative fasciosis rather than an inflammatory fasciitis
(Schepsis et al. 1991; Delmi et al. 1995; Mosier et al. 1999;
Lemont et al. 2003).
Etiology of PCS
A growing number of cases report both symptomatic and
asymptomatic posteriorly directed pediatric calcaneal spurs,
suggesting that at least in a minority of cases PCS may rep-
resent variations in the normal development of the calca-
neus (Robinson, 1976; Wiechen, 1987; Carlı et al. 2013). The
etiology of the remaining acquired PCS is still not com-
pletely clear; however, several theories have been pro-
posed. Traditionally it was hypothesized that PCS occur via
repetitive stress/traction of the PF or the intrinsic muscula-
ture at their insertion into the calcaneus. This then results in
subsequent inflammation and spur development (Roland,
1912; Duvries, 1957; McCarthy & Gorecki, 1979; Forman &
Green, 1990; Prichasuk & Subhadrabandhu, 1994; Abreu
et al. 2003). The PF tension is increased when the medial
longitudinal arch is lowered; furthermore, an increase in
bodyweight correlates with greater pressures during walk-
ing (determination coefficient 0.66) with the largest
changes seen in the longitudinal arch pressure (Kogler et al.
1996; Onwuanyi, 2000; Hills et al. 2001). This is consistent
with PCS being associated with obesity. Electron microscopy
of two PCS revealed that PCS fibers, which form as a result
of stress, loosely align along the line of traction that the PF
and intrinsic foot musculature exert (McCarthy & Gorecki,
1979). PCS have also been proposed to be part of the nor-
mal process of aging, with a general tendency toward ossi-
fication of ligaments, such as the long plantar ligament,
and tendons where they insert into bone (Mason et al.
1959; Lapidus & Guidotti, 1965; McCarthy & Gorecki, 1979).
In opposition to this theory, Achilles spurs, which are
known to occur as the result of traction, are positioned
within the Achilles tendon; however, over half of PCS are
not within the PF or the intrinsic muscles of the foot but
rather are surrounded by loose connective tissue (Kumai &
Benjamin, 2002; Li & Muehleman, 2007). Also, despite PF
release and spur excision, recurrence rates of 31–50% were
© 2017 Anatomical Society

found within 9 months, suggesting a different etiology
(Chang & Miltner, 1934; Tountas & Fornasier, 1996).
A number of authors believe inflammation is important
in PCS formation, either occurring secondary to a stress
injury or as the natural progression of plantar fasciitis
(Mason et al. 1959; Gerster et al. 1977; Sebes, 1989; Abreu
et al. 2003). It has been suggested that the inflammation
process results in a localized proliferation around the PF ori-
gin and irregular spur formation (Duvries, 1957; Mason
et al. 1959). Irregular spurs also occur more commonly on
the plantar calcaneal aspect than on the posterior aspect,
consistent with a natural evolution of fasciitis (Gerster et al.
1977). PCS occurred in 89% of patients with plantar fasciitis
compared with 32% in age- and gender-matched controls
(Johal & Milner, 2012). There is also histological evidence of
degenerative changes in the plantar fascia enthesis which
may contribute to PCS formation (Kumai & Benjamin, 2002;
Abreu et al. 2003). MRI analysis, however, showed inflam-
matory changes in only 8% of cases and histological analysis
of both cadaveric and surgical specimens revealed no evi-
dence of concurrent inflammation (Tountas & Fornasier,
1996; Abreu et al. 2003).
More recently, several authors have suggested that PCS
may be an adaptive response to repetitive, vertically orien-
tated forces (Kumai & Benjamin, 2002; Li & Muehleman,
2007; Menz et al. 2008). Larger studies analyzing the trabec-
ular pattern present in PCS show it to be predominantly
perpendicular to the long axis of the spur and the weight-
bearing surface (Kumai & Benjamin, 2002; Li & Muehleman,
2007). The calcaneus transmits the majority of the body-
weight from the talus to the ground. Wolf’s law states that
bone growth is dynamic and adapts to loads placed on it
and this trabecular pattern of growth in spurs is consistent
with a vertically oriented force vector (Li & Muehleman,
2007). The previously mentioned fibrocartilage associated
with the spur is thought to serve the same function as artic-
ular or fibrocartilage in a weight-bearing joint, buffering
the forces transmitted to the surrounding tissue and muscle
(Kumai & Benjamin, 2002; Li & Muehleman, 2007). In the
same way that osteophytes develop to alter the load placed
on synovial joints when they have been compromised by
disease or injury, PCS may represent a comparable adapta-
tion to mechanical stressors to reduce the risk of failure at
the PF calcaneal insertion site or to protect the calcaneus
against microfractures (Kumai & Benjamin, 2002; Benjamin
et al. 2006). The association of PCS with arthritides and obe-
sity further supports this theory (Rubin & Witten, 1963;
Rogers et al. 1997). An increase in bodyweight may also
accelerate the natural degenerative processes of age-
related stiffening on the heel pad, inhibiting its ability to
effectively dampen the force of impacts (Hsu et al. 1998;
Onwuanyi, 2000; Menz et al. 2008). Patients with less soft
tissue under the heel develop greater plantar pressures
while walking (Morag & Cavanagh, 1999). The increased
rate of PCS with age also supports this theory, as there is a
© 2017 Anatomical Society
A review of the plantar calcaneal spur, J. Kirkpatrick et al. 747
relationship between age and increased heel pressure, inde-
pendent of structural and functional variables (Morag &
Cavanagh, 1999). PCS development may be due to repeti-
tive ground reactive forces generating stress and micro-
trauma, resulting ultimately in pathophysiological bone
development (Moretti et al. 2006; Li & Muehleman, 2007).
Historically, Roland hypothesized that the epiphysis of the
calcaneus extends down to the plantar aspect and that
repetitive trauma results in PCS formation (Roland, 1912).
Studies have shown that a single traumatic injury is insuffi-
cient to initiate PCS formation, but repetitive trauma with
low forces can cause histological changes and as the impact
force is increased, fewer repetitions are required (Tanz,
1963; Brand, 2006). A number of both structural and func-
tional factors determine the load exerted on the calcaneal
process during walking and may serve as risk factors in
developing PCS. These factors include gait abnormalities
such as excessive medial loading of the calcaneus during
foot pronation, the area, thickness and elasticity of the
plantar heel fat pad, the longitudinal arch structure, linear
kinematics, the individual’s weight and age, as well as the
shoes worn (Perry, 1983; Hsu et al. 1998; Morag and Cava-
nagh, 1999; Ozdemir et al. 2004; Brand, 2006; Li & Muehle-
man, 2007). Finally, the bone-formers theory suggests that
certain people have a genetic predisposition to form new
bone in response to mechanical stressors (Rogers et al.
1997). This explains why some individuals will develop spurs
whereas others, when subjected to the same or even
greater stress, will not (Li & Muehleman, 2007). Thus
whether a spur is formed may be a result of both the stress
experienced, based on a number of functional and struc-
tural factors, and the individual’s genetic predisposition to
forming bone.
PCS and heel pain
Historically, a causative relationship was assumed between
PCS and heel pain (Waechter & Sonnenschein, 1915;
Chang & Miltner, 1934; Duvries, 1957; Lapidus & Guidotti,
1965; McCarthy & Gorecki, 1979). Observational studies
showed that the point of maximal tenderness was directly
underneath the spur and that those with PCS were 4.6
times more likely to have a current or previous history of
heel pain (Brody, 1962; Menz et al. 2008). The relation-
ship is not this simple, however, as PCS are present in 10–
63% of asymptomatic controls (Tanz, 1963; Lapidus &
Guidotti, 1965; Barrett et al. 1995; Ozdemir et al. 2004;
Osborne et al. 2006). One study showed that 45% of the
heels analyzed were either painful with no PCS or had a
PCS but were not painful (Lapidus & Guidotti, 1965). Fur-
thermore, the outcome of PF release and spur excision is
not based solely on PCS recurrence and some patients
have ongoing pain, suggesting that PCS are not always
the primary cause of pain (Hertzler, 1926; Tountas & For-
nasier, 1996).
748 A review of the plantar calcaneal spur, J. Kirkpatrick et al.
There is, however, a correlation between heel pain and
PCS, and although PCS do occur in asymptomatic people,
they occur at higher rates in those who are symptomatic
(Vyce et al. 2010; Moroney et al. 2014). In those who do
experience pain with PCS, this has been hypothesized to be
due to a wide range of factors, including the size, shape,
nerve compression and associated inflammation, as well as
whether the PCS is weight-bearing or there is a micro frac-
ture present (Duvries, 1957; Tanz, 1963; Wainwright et al.
1995; Sadat-Ali, 1998; Smith et al. 2007). Two meta-analyses
have revealed body mass indext (BMI) and PCS are two fac-
tors associated with chronic plantar heel pain. There is also
some evidence of an association with age, decreased dorsi-
flexion at the ankle and prolonged periods of standing (Irv-
ing et al. 2006; McMillan et al. 2009). PCS has also been
hypothesized to decrease the elasticity of the heel fat pad,
an important factor in the etiology of heel pain (Baxter &
Zingas, 1995; Ozdemir et al. 2004). The inferior calcaneal
nerve, a branch of the lateral plantar nerve, is susceptible to
compression from PCS, as it passes between the intrinsic
muscles of the foot and the calcaneal tuberosity to inner-
vate the ADM muscle (Tanz, 1963; Forman & Green, 1990;
Delfaut et al. 2003; Chundru et al. 2008). Nerve entrapment
(Baxter’s neuropathy) results in ADM atrophy and heel pain
(Tanz, 1963; Louisia & Masquelet, 1999). There is a signifi-
cant association between ADM atrophy and calcaneal spurs,
with an odds ratio of 3.6 after multivariate logistic regres-
sion (Chundru et al. 2008). Branchinng off from the inferior
calcaneal nerve there is also a calcaneal branch which sup-
plies the calcaneal tuberosity and this has also been shown
to be susceptible to PCS compression and may result in heel
pain (Rondhuis & Huson, 1986; Louisia & Masquelet, 1999).
Inflammation in the soft tissue surrounding the spur may
be important in determining whether the spur is painful or
not (Li & Muehleman, 2007). In one study, individuals with
a painful heel who had both a PCS and plantar fasciitis
underwent shock wave therapy (Moretti et al. 2006). Dur-
ing the study there were no significant changes in spur size;
however, in 61% inflammation disappeared, and this was
strongly correlated with a decrease in pain (Moretti et al.
2006). Low dose tissue irradiation, which is well known for
its anti-inflammatory effects, has also proven to be an effec-
tive method of decreasing heel pain associated with PCS,
with marked improvement seen in 61–97% of patients and
benefits lasting up to several years (Micke & Seegen-
schmiedt, 2004; Muecke et al. 2007; Hermann et al. 2013;
Uysal et al. 2015). Randomized control trials comparing
individual doses of 0.1–1.0 Gy and total doses of 0.6–6.0 Gy
have shown the long-term effectiveness of a single dose at
0.5 Gy, given twice a week up to a total dose of 3.0 Gy
(Heyd et al. 2007; Niewald et al. 2008, 2015; Ott et al. 2013,
2014). The current hypothesized mechanism is via altered
cytokine and chemokine release, as well as changes to
adhesion molecules and decreased oxidative burst forma-
tion (Voll et al. 1997; Kern et al. 2000; Schaue et al. 2002;
Ro€ del et al. 2008). An MRI study found edema at the plan-
tar fascia enthesis (suggestive of plantar fasciitis) in approxi-
mately 50% of PCS cases (Ali et al. 2006). Furthermore, the
pain associated with PCS in those with plantar fasciitis is
more likely to be moderate (60%), compared with controls
(2.5%) matched for length of spur, age and sex (Wain-
wright et al. 1995). Duvries (1957) postulated that both
inflammatory changes and whether the spur was weight-
bearing are important in determining whether PCS cause
pain. PCS may become weight-bearing due to altered foot
anatomy such as a depression in the longitudinal arch. PCS
shape may also be important, with sharp spurs being associ-
ated with symptoms lasting less than 6 months and blunt
spurs with symptoms lasting more than 6 months (Sadat-
Ali, 1998).
Although PCS are associated with heel pain in over 50%
of cases, there are also many other causes of heel pain, such
as tears in the plantar fascia, plantar fasciitis, calcaneal frac-
tures and fat pad atrophy (Furey, 1975; Burks & Buk, 2003;
Li & Muehleman, 2007; Smith et al. 2007; Alshami et al.
2008; Johal & Milner, 2012). These factors have all been
found in both the presence and absence of PCS, suggesting
that the spur is only one of a number of factors which con-
tributes to heel pain.
Conclusion
The PCS is bony outgrowth of the calcaneal tuberosity and
occurs in the general population in around 15% of people
and in higher proportions in the elderly, the overweight,
those with heel pain, plantar fasciitis, arthritides and abnor-
mal foot biomechanics. It was initially thought that PCS
were the result of traction from the plantar fascia or intrin-
sic muscles of the foot; however, it is now known that the
majority are found deep to the PF, surrounded by fibrocar-
tilage. They are hypothesized to function as an adaptive
skeletal response to redistribute the impact forces away
from the calcaneal insertion site to the surrounding tissues
via a buttressing effect. The PCS trabecular pattern is consis-
tent with a vertically oriented ground force vector and is in
agreement with key associations listed above, namely,
increasing weight, age, and alterations in foot structure, all
factors that determine the heel pressure generated. There is
also evidence that certain individuals have a genetic predis-
position to generate new bone and undergo osteogenesis
at levels of mechanical stress which are not sufficient to ini-
tiate bone growth in others. This is further supported by
the association of PCS and osteoarthritis.
The relationship between PCS and painful heels has been
confirmed via multiple meta-analyses. However, a subpopu-
lation of those with PCS are completely asymptomatic. Fac-
tors which may be important in determining whether a
given PCS will cause an individual heel pain include the size
of the spur, whether there is compression of the inferior cal-
caneal nerve, spur factures, concurrent inflammation, fat
© 2017 Anatomical Society

pad abnormalities or degeneration, and the individual’s
occupational environment. A number of other potential
causes of heel pain appear prominently in the etiology of
PCS, including tears in the plantar fascia, plantar fasciitis,
calcaneal fractures and fat pad atrophy.
A consistent definition of what constitutes a calcaneal
spur would benefit future research in this area. According
to this literature review, a bony growth larger than 2 mm
should constitute a spur, clearly distinguishing them from
simple cortical irregularities. Further research on the normal
anatomy and histology of the calcaneal tuberosity along
with the variation present within the population would
provide a valuable comparison for those with symptomatic
heels both with and without PCS. A number of papers on
shock wave therapy and low dose tissue irradiation are
demonstrating effective interventions for those experienc-
ing heel pain associated with PCS. However, current
research regarding PCS would predict that it is going to
become a worsening problem in the future with an aging
population, a corresponding increase in degenerative bone
conditions, and a global rise in obesity.
Author contributions
Conceived study: SAM. Literature search: OY. Data analysis:
JK. Drafted manuscript: JK. Critically revised manuscript and
approved the final draft: SAM.
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