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Research, heel
pain, 3
234 May/June 2003 Vol 93 No 3
Journal of the American Podiatric Medical
Association
Plantar fasciitis is presumed to be
synonymous with inflammation of the plantar fascia.
In fact, the suffix -itis inherently implies an
inflammatory disease.
However, is plantar fasciitis really
an inflammatory disorder?
Plantar fasciitis is widely
described in the literature
as having a multifactorial and
widely disputed etiology. Interestingly, in 1965,
Lapidus and Guidotti,1
in their article entitled Painful
Heel, stated that the name of painful heel is used
deliberately in preference to any other more precise
etiological diagnosis, since the cause of this definite
clinical entity still remains unknown.
Now, nearly 40 years
later, this
statement can still be considered
accurate. Although the exact definition of plantar
fasciitis varies in the literature, this term is frequently
used interchangeably with heel spur
syndrome2
and
painful heel
syndrome.3
Plantar fasciitis is
almost always used
to describe a painful heel with
inflammation of the plantar fascia at its origin, as
opposed to pain originating along the course of the fascia. For
example, Hicks4 noted that the repetitive excessive loads
that occur with long-distance running may
induce an inflammatory process, leading to fibrosis or
degeneration, and Sewell5 stated that the pain of
plantar inflammation may sometimes be secondary to
periostealinflammation of the os calcis.
Although authors writing
on the subject describe inflammation
as being present in plantar fasciitis, they
provide no objective clinical or histologic evidence to
support their claims.
In addition, when photomicrographs
are provided, they are often mislabeled as showing
inflammation.Lemelle et al,6 for example, suggested
that inflammationis found in plantar fasciitis, but
they provided only photomicrographs of dense
fibrous tissue. In allof these cases, the term
inflammation seems only to be suggested, without any
evidence being provided.
So, what evidence should be present
to establish plantar fasciitis as an inflammatory
disorder? By definition, inflammation is
characterized in its acute stage by the classic clinical
signs of pain, heat, redness, swelling, and loss of
function, and histologically by leukocyte accumulation. In its
chronic stage, inflammation is characterized
histologically by infiltration with macrophages, lymphocytes, and
plasma cells; tissue destruction; and
repair involving new vessel proliferation and
fibrosis.7
Therefore,
not only must the cardinal signs of
inflammation be observed.
Plantar Fasciitis
A Degenerative Process (Fasciosis)
Without Inflammation
Harvey Lemont, DPM*
Krista M. Ammirati, BS*
Nsima Usen, MPH*
*Temple University School of
Podiatric Medicine, Philadelphia,
PA.
Corresponding author:
Harvey
Lemont, DPM, Temple
University School of Podiatric
Medicine, Eighth at Race St,
Philadelphia, PA
19107.
CLINICAL
PATHOLOGY
The authors review histologic
findings from 50 cases of heel spur surgeryfor chronic plantar fasciitis.
Findings include myxoid degeneration with fragmentation and degeneration of
the plantar fascia and bone marrow vascular ectasia. Histologic
findings are presented to support the thesis that plantar fasciitis is a
degenerative fasciosis without inflammation, not a fasciitis. These findings
suggest that treatment regimens such asserial corticosteroid injections
into the plantar fascia should be reevaluated in the absence of inflammation and
in light of their potential to induce plantar fascial rupture. (J Am
Podiatr Med Assoc 93(3): 234-237,
2003) Journal of the American Podiatric
Medical Association Vol 93 No 3 May/June
2003 235
clinically, but the classic
histologic signs of inflammation should also be present.
Typically, however, a
diagnosis of plantar fasciitis is
established solely by
history and elicitation of pain on
the plantar aspect of the heel. Radiographic evidence
may be included but does not in itself provide
evidence of inflammation.
Clinical and histologic evidence of
inflammation is usually lacking. In contrast,
objective evidence is available in the literature to
support the presence of degenerative noninflammatory
pathologic changes in plantar fasciitis. Schepsis et
al 8
evaluated
specimens obtained during plantar heel spur
surgery and observed marked thickening and
fibrosis of the plantar fascia at its origin on the
medial tubercle.
Tountas and Fornasier 9 also obtained specimens
for histologic evaluation from operative
resections of the proximal attachment of the
plantar fascia and the heel spur, if present, in patients
with subcalcaneal pain refractory to conservative
treatment. Similarly, examination revealed degeneration of
the plantar fascia with no evidence of
inflammation.
Histologic examination of surgical biopsy
specimens in a study
by Snider et al 10 showed collagen necrosis,
angiofibroblastic hyperplasia, chondroid metaplasia,
and matrix calcification. Again, no
cellular proof of an inflammatory response was cited.
Also in support of the argument that
the changes in plantar fasciitis are
noninflammatory, Grasel et al 11
examined magnetic resonance images
of the plantar fascia in patients clinically
diagnosed as having plantar fasciitis. These authors ruled out
inflammation as a cause because of the linearity and
low prevalence of signal intensity within the
fascia. They concluded that the changes noted are best
interpreted as perifascial edema due to microtears in the
plantar fascia in the area of its insertion into
the calcaneus.
Of 50 heel spur samples submitted
for pathologic analysis to the Laboratory of
Podiatric Pathology at Temple University School of
Podiatric Medicine, Philadelphia, Pennsylvania, 10 exhibited normal
plantar fascial enthesis characterized by a
regular transition of bone to fibrocartilage to fascia
(Fig. 1), with fibrocartilaginous fibers running parallel to each
other(Fig. 2). In addition, 16 samples
demonstrated fiber fragmentation in association with
myxoid degeneration characterized by basophilic zones of
mucopolysaccharide stained positive with alcian blue
(pH 2.5) (Fig. 3).
In two samples, fascial
artifacts and fragmentation
in association with crystalline
material noted in the area before processing
was suggestive of previous corticosteroid
injections (Fig. 4). Approximately 12 of the 16 samples
also demonstrated vascularization of the attached bone
marrow (Figs. 5 and 6). Low-power
cross-sections of bone re- Figure 1. Normal fascial enthesis
exhibiting metaplasia of bone to fibrocartilage to fascia
(H&E, ×
40).
Figure 2. Fibrocartilage interface
between bone and fascia (H&E, ×40).
moved from the attachment site
demonstrated multiple dilated vessels. Hyperemia may be
responsible for the reports of bone
contusion in patients with heel spurs on T2-weighted
images. 11
The
remaining samples were submitted in sections,
preventing adequate pathologic analysis.
In all of the samples reviewed,
there was no evidenceof inflammation histologically. A
review of the literature and the experience of the
authors indicate that credible evidence for the
assumption that plantar fasciitis is associated with
inflammation is lacking.
On the other hand, there seems to be
substantial evidence that this disorder is
associated with degenerative changes in the fascia, which may
best be classified as a fasciosis rather
than fasciitis. This redefinition of plantar fasciitis as
plantar fasciosis is warranted from an academic
perspective in the same way that posterior tibial
tenosynovitis has been reclassified as tendinosis and osteoarthritis has
been
236 May/June 2003 Vol 93 No 3
Journal of the American Podiatric Medical
Association
reclassified as osteoarthrosis.
Because principles of management are based on a sound
understanding of pathology and physiology, common
treatment approaches for heel spur syndrome or
plantar fasciitis should be reexamined. For example,
the use of serial corticosteroid injections to
control inflammation in plantar fasciitis should be
questioned and reviewed in the absence of documented
evidence of inflammation.
Corticosteroid injections into the
region of pain are one of the most common
conservative treatments for plantar fasciitis. However, such
injections have been associated with serious
side effects. Recently, Acevedo and Beskin12 reported that in a
group of 765 patients with a clinical
diagnosis of plantar
Figure 3. A, Zones of dark-staining
areas representing mucopolysaccharide (curved
arrows), with degeneration of collagen (straight arrow); B,
close-up view of degenerated collagen (fascia)
(alcian blue [pH 2.5], ×40).
Figure 4. Artifacts within fascia
representing areas of probable previous corticosteroid
deposits (H&E, ×40).
Figure 5. Low-power view of calcaneal
marrow demonstrating
vascular engorgement (H&E,×20).
Figure 6. High-power view of calcaneal
marrow demonstrating dilated vasculature (H&E, ×40).
A B
Journal of the American Podiatric
Medical Association Vol 93 No 3 May/June
2003 237 fasciitis, 51 were diagnosed as
having a plantar fascia rupture. Of these 51 ruptures, 44
(86%) were associated with corticosteroid injection. In
another study, Leach et al 13 reported plantar fascial
rupture in five of six athletes previously treated
with repeated local injections of a corticosteroid.
Moreover, Sellman14
observed a series of 37 patients
with a presumptive diagnosis of plantar fascial rupture
and previous heel pain diagnosed as plantar fasciitis
and treated with corticosteroid injection into the
calcaneal origin of the fascia. One-third of these
patients were reported to have rupture of the plantar
fascia, described as a sudden tearing episode in the heel,
and the remainder described mild-to-moderate
pain.
Conclusion
Although corticosteroid injections
may be helpful in the treatment of plantar
fasciitis, they may predispose to plantar fascial rupture, and
their routine use should be reevaluated, especially in
the absence of proof that inflammation
exists.
References
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