Osteonecrosis in the Foot

Christopher W. DiGiovanni, MD
Amar Patel, MD
Ryan Calfee, MD
Florian Nickisch, MD

Dr. DiGiovanni is Associate Professor

and Chief, Division of Foot & Ankle
Surgery, Department of Orthopaedic
Surgery, Rhode Island Hospital, Brown
Medical School, Providence, RI.
Dr. Patel is Resident, Department of
Orthopaedic Surgery, Rhode Island
Hospital, Brown University. Dr. Calfee is
Fellow, Department of Orthopaedic
Surgery, Rhode Island Hospital, Brown
University. Dr. Nickisch is Assistant
Professor, Department of Orthopaedics,
University of Utah School of Medicine,
Salt Lake City, UT.
None of the following authors or the
departments with which they are
affiliated has received anything of value
from or owns stock in a commercial
company or institution related directly or
indirectly to the subject of this article:
Dr. DiGiovanni, Dr. Patel, Dr. Calfee, and
Dr. Nickisch.
Reprint requests: Dr. DiGiovanni,
Department of Orthopaedic Surgery,
Rhode Island Hospital, Brown Medical
School, 593 Eddy Street, Providence,
RI 02903.
J Am Acad Orthop Surg 2007;15:208217
Copyright 2007 by the American
Academy of Orthopaedic Surgeons.

208

Abstract
Osteonecrosis, also referred to as avascular necrosis, refers to the
death of cells within bone caused by a lack of circulation. It has
been documented in bones throughout the body. In the foot,
osteonecrosis is most commonly seen in the talus, the first and
second metatarsals, and the navicular. Although uncommon,
osteonecrosis has been documented in almost every bone of the
foot and therefore should be considered in the differential diagnosis
when evaluating both adult and pediatric foot pain. Osteonecrosis
is associated with many foot problems, including fractures of the
talar neck and navicular as well as Kohlers disease and Freibergs
disease. Orthopaedists who manage foot disorders will at some
point likely be faced with the challenges associated with patients
with osteonecrosis of the foot. Because this disease can masquerade
as many other pathologies, physicians should be aware of the
etiology, presentation, and treatment options for osteonecrosis in
the foot.

steonecrosis, also called avascular necrosis, refers to cellular

death within bone caused by a lack
of circulation. This circulatory compromise may arise from a mechanical disruption of the vessels or from
occlusion of either arterial inflow or
venous outflow. Potential sources of
occlusion include thrombosis, embolism, circulating fat, and abnormally shaped cells (eg, sickle cells).1
Corticosteroid use, alcohol intake,
and Gauchers disease produce osteonecrosis by increasing intramedullary pressure, thereby decreasing
perfusion.2-6 Trauma remains the
most common mechanical cause of
osteonecrosis throughout the body,
particularly in the foot.7
Following circulatory compromise, few histologic changes are
seen within the first week. In the
second week, the death of hematopoietic cells, capillary endothelial
cells, and lipocytes can be confirmed

microscopically. The lipocytes release lysosomes that acidify the tissue, the osteocytes begin to shrink,
and the water content in the bone
increases. These changes represent
the first abnormalities detectable on
magnetic resonance imaging (MRI).
Regardless of the cause of osteonecrosis, the final radiographic finding
remains the same: a resultant relative increase in the radiodensity of
the bone. This change is caused by
bony collapse, saponification of fat,
creeping substitution, and a relative
density difference between the avascular and surrounding vascularized
bone. Without the ability to repair
itself, such dysvascular bone eventually collapses, appearing fragmented
and sclerotic. This process increases
with additive microtrauma.1
The radiographic modalities used
to diagnose osteonecrosis continue
to advance. Conventional radiographs are useful for diagnosis only

Journal of the American Academy of Orthopaedic Surgeons

Christopher W. DiGiovanni, MD, et al

after the development of sclerosis,

articular collapse, or a crescent sign.
The relative usefulness of bone scintigraphy is dependent on the stage of
osteonecrosis. During the acute ischemic phase, the entire affected
area may demonstrate high uptake
from increased osteoblastic activity.
In later stages, however, a demarcated rim of increased activity surrounding the hypoperfused necrotic
core will become apparent. Singlephoton emission computed tomography (SPECT) can aid in maximizing
resolution. Current MRI techniques
are sensitive to changes in bone marrow composition. Diffuse marrow
edema is seen in early osteonecrosis
and produces a low signal intensity
on T1-weighted images and a high
signal intensity on T2-weighted images. In advanced stages of the disease, both T1- and T2-weighted
images demonstrate low signal intensity.7 Although positron emission
tomography scanning has been used
to determine blood flow to the femoral head with suspected osteonecrosis, its use for detecting this disease
is still not well-defined.8
Although a relatively uncommon
diagnosis, osteonecrosis has been
identified in almost every bone in
the foot and has been extensively
studied in the talus, the first and second metatarsals, and the navicular.7
Because this disease can masquerade
as many other pathologies, it is mandatory that the orthopaedist understand the etiology and management
of osteonecrosis. Appropriate recognition and treatment can affect outcome; thus, osteonecrosis must be
considered when evaluating foot
pain in any population.

Osteonecrosis in the
Hindfoot: The Talus
The talus is commonly affected by
osteonecrosis. Although atraumatic
causes have been estimated to account for up to 25% of talar osteonecrosis, the etiology usually can be
traced back to an injury.9
Volume 15, Number 4, April 2007

Figure 1

Extraosseous vascular supply to the talus. (Reproduced from Fortin P, Balaszy J:

Talus fractures: Evaluation and treatment. J Am Acad Orthop Surg
2001;9:114-127.)

Vascular Supply
The talus has no tendinous attachments or muscular origins; thus,
it relies on direct vasculature for its
blood supply. Furthermore, its lack
of vascular redundancy (more than
half of this bone is covered with articular cartilage) makes each vascular contribution vitally important.
All three primary arteries of the
foot support the extraosseous supply10-12 (Figure 1). The posterior tibial
artery is the principal blood supply
for the talar body via the artery of the
tarsal canal and the deltoid artery.
The artery of the tarsal canal passes
between the sheaths of the flexor
digitorum longus and the flexor hallucis longus to enter the tarsal canal
and supply most of the talar body.
The deltoid artery arises near the origin of the artery of the tarsal canal
and enters the talar body medially.
The artery of the tarsal sinus is
formed from branches of the dorsalis
pedis and perforating peroneal arteries and merges with the artery of the
tarsal canal. Together they feed most
of the talar neck and head.11
Two smaller contributors are the
peroneal artery, which supplies the

posterior process via direct branches,

and the superomedial branches of
the dorsalis pedis, which supply the
talar head.
Incidence and Etiology
Osteonecrosis of the talus commonly follows talar neck fractures,
which typically are the result of
forced dorsiflexion caused by highenergy trauma.10 Hawkins13 developed a commonly used classification
system that stratifies the future risk
of osteonecrosis based on fracture
displacement and joint congruency.
Type I talar neck fractures are nondisplaced and have an approximately 10% chance of developing osteonecrosis. Type II fractures are
displaced and have an associated disruption of the subtalar articulation,
carrying an approximate 40% risk of
osteonecrosis. Type III fractures are
also displaced, with incongruity of
both the ankle and subtalar joints.
Type III fractures have an approximate 90% incidence of osteonecrosis.
Canale and Kelly14 further refined
the classification, adding a fourth
type, which signifies extrusion of
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Osteonecrosis in the Foot

Table 1
Ficat and Arlet Radiographic Appearance of Osteonecrosis of the Talus
Stage
I
II
III
IV

Radiographic Appearance
Normal
Cystic and sclerotic lesions, normal contour of the talus
Crescent sign, subchondral collapse
Narrowing of the joint space, secondary changes in the tibia

Reproduced with permission from Delanois RE, Mont MA, Yoon TR, Mizell M,
Hungerford DS: Atraumatic osteonecrosis of the talus. J Bone Joint Surg Am
1998;80:529-536.

Figure 2

Anteroposterior (A) and lateral (B) radiographs of a displaced talar neck fracture
treated with surgical fixation. These radiographs, taken 12 weeks after injury,
demonstrate bony sclerosis of the lateral aspect of the talar body, which is indicative
of osteonecrosis. (Courtesy of C.W. DiGiovanni, MD, Providence, RI.)

the talar body and subluxation of the

talonavicular joint. Such injury virtually guarantees osteonecrosis. Because the blood supply to the talus
has a significant retrograde component from head to body, most patients with talar neck fracture exhibit osteonecrosis in the talar body.
The risk of osteonecrosis increases as fractures of the talar body become more displaced and comminuted.15 In general, talar body
fractures do not differ significantly
210

from talar neck fractures in terms of

the development of osteonecrosis.16
Talar head fractures signify highenergy talar injury. These fractures
are associated with osteonecrosis as
a result of concomitant fractures of
the neck and body.
Less common atraumatic etiologies of talar osteonecrosis include
alcoholism,17 sickle cell disease,18
corticosteroid use, dialysis,19 hemophilia,20 hyperuricemia,21 and lymphoma.22 Delanois et al23 document-

ed a series of cases of atraumatic

osteonecrosis that primarily affected
the posterolateral talar dome. Most
of these patients, however, had a history of corticosteroid use.
Diagnosis and Treatment
The clinical presentation of talar
osteonecrosis is primarily determined by the integrity of the articular surface. Before articular collapse,
the patient may be asymptomatic.
The pain and mechanical symptoms
associated with increasing articular
incongruity typically represent the
primary complaints. Imaging should
begin with plain radiography, which
is notable for early findings of sclerosis, cystic changes, and advanced
changes of collapse. An adaptation of
the Ficat and Arlet classification
characterizes the extent of talar disease23 (Table 1). MRI further illustrates the extent of disease and can
be used to further stage osteonecrosis of the talus.24
The traditional approach for managing displaced talus fracture has
been timely, rigid anatomic reduction and internal fixation, with the
intent of minimizing vascular insult,
stiffness, posttraumatic arthritis, and
osteonecrosis. The optimal timing of
fracture management, however, remains poorly defined. Recent data
suggest that treatment can be safely
delayed in the absence of frank joint
dislocation, open wounds, or neurovascular compromise.25
Most cases of posttraumatic osteonecrosis manifest within the first
10 months after injury, although the
disease can take longer than 2 years
to see on imaging studies.25 Subchondral lucency (ie, Hawkins sign)
seen at 6 weeks after injury is reliable evidence of revascularization.14
In contradistinction, a sclerotic, radiodense talar body suggests osteonecrosis23 (Figure 2; Table 1).
The treatment algorithm is dictated by clinical symptoms. Most
protocols incorporate limited weight
bearing and activity modification.9
However, there is no consensus on

Journal of the American Academy of Orthopaedic Surgeons

Christopher W. DiGiovanni, MD, et al

either the duration or degree of restricted weight bearing, or on the

utility of bracing or immobilization,
in minimizing the sequelae of osteonecrosis. Nonsurgical therapy often is sufficient to meet patient
functional expectations. When nonsurgical management fails, however,
the patient can be treated with a variety of surgical interventions.
Arthroscopy is useful in evaluating joint surfaces and removing
loose bodies. More aggressive surgical intervention depends on the
stage and extent of disease. Procedures range from open and arthroscopic methods of core decompression to ankle, subtalar, and pantalar
arthrodesis with vascularized bone
grafting.26-28 Fusion must be approached cautiously in the patient
with osteonecrosis because of the
possibility of serious sequelae. Ankle arthroplasty, although controversial in the setting of osteonecrosis,
may offer an alternative to fusion.
Currently, however, there are no
long-term results available for ankle
arthroplasty in these often young patients. There are anecdotal reports of
satisfactory functional results with
salvage using a stainless steel talar
body prosthesis.29
Delanois et al23 presented their
experience with 37 ankles with
atraumatic talar osteonecrosis. Most
ankles presented in Ficat stage II and
were initially treated nonsurgically
with an ankle-foot orthosis, nonsteroidal anti-inflammatory drugs, and
partial weight bearing. Thirty-two of
the ankles proceeded to core decompression, and three were treated with
fusion. There was a correlation between disease severity at presentation with disease progression and the
rate of ultimate surgical fusion.23
Prognosis
There are few outcome studies regarding traumatic talar osteonecrosis. In two small series, nonsurgical
management yielded satisfactory results in 38% to 46% of patients.30
Canale and Kelly14 reported satisfacVolume 15, Number 4, April 2007

tory results in all patients who were

kept nonweight bearing for an average of 8 months. Interestingly, there
was no clear correlation between the
amount of talar dome involvement
and symptom severity. Published results indicate that tibiotalar and tibiotalocalcaneal fusion can be reliably
performed in the presence of osteonecrosis.9,31
Outcome data of atraumatic talar
osteonecrosis is even more limited.
In the series of Delanois et al,23 29 of
32 ankles treated with decompression had fair to excellent outcomes
at a mean 7-year follow-up. Followup on the arthrodeses was limited,
but promising. At mean 7 months
postoperatively, all six ankles managed with arthrodesis had fused.

Osteonecrosis in the
Midfoot: The Navicular
Navicular osteonecrosis can be either idiopathic or traumatic. Fractures of the navicular, which are often high-energy injuries, represent
the most common etiology of osteonecrosis.32 Kohlers disease and
Mller-Weiss disease are manifestations of idiopathic osteonecrosis in
the pediatric and adult populations,
respectively.
Vascular Supply
The navicular vascular supply is
precarious. The dorsalis pedis or one
of its tributaries provides several perforating branches. The plantar surface is fed primarily through branches from the medial plantar artery.
The intraosseous blood flow is centripetal and has a central watershed
area, which places the navicular at
significant risk of osteonecrosis in
the presence of obstructed peripheral blood flow.32
Kohlers Disease
Kohler first described childhood
navicular osteonecrosis at the turn
of the 20th century; Williams and
Cowell33 subsequently described its
natural history. Patients typically

present between ages 2 and 9 years

with the primary complaint of midfoot pain. Navicular sclerosis, fragmentation, and flattening are noted
radiographically. However, these
changes may represent a normal
variant in asymptomatic patients;
thus, the diagnosis of osteonecrosis
must be corroborated by clinical suspicion and supportive radiographs.
Treatment and Prognosis
In the Williams and Cowell series,33 all patients were asymptomatic and, with nonsurgical management, had a radiographically normal
navicular at 9-year follow-up. Casting provided earlier resolution of
symptoms. Weight-bearing status
did not affect outcome. These results agree with those of the study
by Ippolito et al,34 which followed
patients for more than 30 years.
Mller-Weiss Disease
Adult-onset navicular osteonecrosis, or Mller-Weiss disease (also
known as Brailsfords disease35), was
first described in the 1920s. The proposed etiology of this condition includes trauma as well as a delay in
navicular ossification that results in
an abnormal osseous product.36 Pain
that begins insidiously in the fifth
decade is the most consistent clinical finding of Mller-Weiss disease.
Heel varus is a hallmark of the disease that, when associated with pes
planus, results in a paradoxical pes
planovarus. Navicular sclerosis and
fragmentation are noted radiographically. The talar head often points
laterally, and changes in the orientation of the remainder of the forefoot
bones are observed36 (Figure 3; Table
2).
The anteroposterior view of the
foot gives the clearest view of navicular pathology. In severe cases, the
talus appears to contact the cuneiforms directly. These findings may
mimic the appearance of tarsal coalition, Charcot neuropathy, or an accessory navicular. Surgical options
include internal fixation of the na211

Osteonecrosis in the Foot

Figure 3

Graphic representation demonstrating the increasing grades of navicular deformity in Mller-Weiss disease. The lateral aspect
of the navicular collapses, causing the talar head to move laterally and appear to contact the cuneiforms themselves. (Adapted
with permission from Maceira E, Rochera R: Mller-Weiss disease: Clinical and biomechanical features. Foot Ankle Clin
2004;9:105-125.)

Table 2
Radiographic Appearance of Osteonecrosis of the Navicular36
Stage
I

II
III
IV
V

Description
Normal radiographs
Positive technetium Tc-99m scan, computed tomography, and
magnetic resonance imaging
Subtalar varus
Navicular compression
Hindfoot equinus
Complete extrusion of the navicular

vicular, triple arthrodesis, talonavicular arthrodesis, and talonavicular

cuneiform bone block arthrodesis.
Outcomes with talonavicularcuneiform bone block arthrodesis have
been promising at limited followup.37
Traumatic Osteonecrosis
of the Navicular
The increased incidence of navicular fractures may be the result of
advances in automobile safety that
protect occupants vital structures
but leave their feet unprotected.38
Navicular injuries range in severity
from small avulsions to highly comminuted fractures. Sangeorzan classified navicular body fractures into
three main types.32 Type 1 fractures
divide the bone into an anterior and
a posterior fragment. Type 2 fractures, the most common, propagate
212

in a direction from dorsolateral to

plantarmedial. Type 3 fractures produce comminution in the middle
and lateral navicular, with disruption of the naviculocuneiform joint.
Type 1 and 3 fractures are most
commonly associated with navicular necrosis, which presumably is
caused either by soft-tissue stripping
resulting from displacement or by
surgical exposure. Anatomic reduction and fixation is recommended
for displaced and comminuted fractures.39 In the series of Sangeorzan et
al,32 67% of the 21 patients with
navicular fractures who were surgically treated had good results. Of the
patients with a good result, osteonecrosis developed in six. Most of the
patients with partial necrosis of the
navicular still had good results. Anatomic fracture reduction and stabilization done while taking care to

minimize iatrogenic vascular insult

is the most effective means of preventing navicular osteonecrosis.
Late treatment of symptomatic collapse to eliminate painful motion
and maintain medial column length
is done with either bone-block midfoot fusion or triple arthrodesis.

Common Locations for

Osteonecrosis in the
Forefoot
First Metatarsal
First metatarsal osteonecrosis,
which primarily affects the head, occurs most commonly after hallux
valgus correction. The etiology of
this iatrogenic first metatarsal osteonecrosis is thought to be related
to the amount of soft-tissue dissection and location of the osteotomy.
Meanwhile, idiopathic osteonecrosis
of the first metatarsal is rare.40-42
Vascular Supply

Injection studies have demonstrated that the first metatarsal head

is enveloped by an extensive vascular network formed by branches of
the dorsalis pedis and posterior tibial arteries.43 The dorsalis pedis artery
provides the first dorsal metatarsal
artery and the first plantar metatarsal artery. The first dorsal metatarsal
artery gives rise to two to three additional branches. The most superfi-

Journal of the American Academy of Orthopaedic Surgeons

Christopher W. DiGiovanni, MD, et al

Figure 4

Figure 5

Lateral view of the vascular supply to the first metatarsal head with the associated
Chevron osteotomy cut lines (dashed lines). The shaded area represents the area of
the lateral release. (Adapted with permission from Easley ME, Kelly IP: Avascular
necrosis of the hallux metatarsal head. Foot Ankle Clin 2000;5:591-608.)

cial of these branches, the dorsomedial hallucal artery, provides a

pericapsular network of perforators
to the metatarsal head.
A deeper branch of the dorsal
metatarsal artery courses plantarly
and obliquely under the metatarsal
shaft and joins with a branch from
the posterior tibial artery. From this
anastomosis, branches arise that feed
the head. The nutrient artery enters
the junction of the proximal and
middle third of the bone. The posterior tibial artery contributes the superficial branch of the medial plantar
artery that joins with the first plantar metatarsal artery. As shown in
Figure 4, the dorsal metaphyseal vessels supply the dorsal two thirds of
the head, while the plantar vessels
supply the lower one third.44 The
capital arteries supply the medial and
lateral fourths of the head.45
Incidence and Etiology

Because idiopathic osteonecrosis

of the first metatarsal is rare, evidence is limited to case reports. OsVolume 15, Number 4, April 2007

teonecrosis following hallux valgus

correction is more common, with
most reports focusing on distal osteotomies as the cause of the osteonecrosis. The incidence of postosteotomy osteonecrosis is reported
to be as high as 20%.46 Radiographic
signs of osteonecrosis may not be
predictive of clinical symptoms.47
Debate regarding the causal relationship between distal soft-tissue
release and osteonecrosis has centered on the vascular implications of
this procedure. Retrospective reviews have not definitively linked
osteonecrosis to osteotomy performed in conjunction with lateral
release.48,49 Cadaveric studies have
demonstrated that perfusion to the
metatarsal head is not adversely affected when the lateral release is performed in conjunction with a distal
osteotomy. It is evident, however,
that careless saw placement could
sever the first dorsal metatarsal artery.49
Resch et al50 prospectively followed 36 chevron osteotomies with

Anteroposterior radiograph
demonstrating cyst formation and
collapse after osteotomy of the distal
first metatarsal in a patient with
osteonecrosis. (Courtesy of C.W.
DiGiovanni, MD, Providence, RI.)

technetium Tc-99m scintigraphy

and reported that an initial filling defect was present in the 19 patients
who had undergone concurrent lateral release. All final scans were normal, however. Although the debate
over lateral release continues, it remains important to follow basic surgical concepts. Soft-tissue stripping
should be performed only to the extent necessary, and power saw entry
and exit should be well controlled.
Diagnosis

The diagnosis of first metatarsal

osteonecrosis is based on radiographic evidence of bony sclerosis, fragmentation, and collapse (Figure 5).
The finding could be incidental, either noted on a postoperative radiograph or identified during evaluation
of a patient with medial forefoot
pain. MRI allows earlier diagnosis,
but it is generally not a cost-effective
screening tool.
213

Osteonecrosis in the Foot

Figure 6

primarily focused on osteonecrosis

of the metatarsal heads, especially in
the second ray.
Vascular Supply

Anteroposterior radiograph of a patient

with Smillie stage III Freibergs disease.
(Courtesy of K. Klaue, MD, Lugano,
Switzerland.)
Treatment

Treatment of mildly symptomatic

patients includes activity modification and full-length orthotic wear to
reduce stress on the first metatarsal.
Moderate symptoms warrant simple
surgical intervention, such as synovectomy and dbridement, or subchondral drilling.51 Salvage procedures for severe symptoms include
first metatarsophalangeal arthrodesis,
performed in situ or via interpositional bone graft to preserve length.52
Prognosis

The early radiographic changes

of postosteotomy osteonecrosis, including subchondral cysts, fragmentation, and sclerosis, may resolve
with time. Typically, such patients
progress well clinically and go on to
radiographic union, even in the
event of osteonecrosis. When first
metatarsophalangeal arthrodesis is
required for salvage, Myerson et al52
reported healing within an average
of 14 weeks.
Lesser Metatarsals
Osteonecrosis of the lesser metatarsals is another relatively common
cause of forefoot pain. Attention has
214

The second through fourth metatarsals have similar arterial supply

patterns, originating from the dorsal and plantar metatarsal arteries.
Branches pierce the diaphysis along
the dorsal, medial, and lateral surfaces. The nutrient artery pierces the
lateral base of these bones and bifurcates into both proximal and distal
branches.53 In contrast, the fifth
metatarsal has a nutrient vessel that
pierces the bone on its medial aspect. The proximal portion is supplied by metaphyseal branches. A
watershed area is thereby formed between these two systems, which potentially could prevent fracture healing. There have been no case reports
of osteonecrosis in this area.
Freibergs Disease

Incidence and Etiology In 1914,

Freiberg published a description of
the disease that eventually bore his
name.54 Dubbed an infraction at
that time, Freiberg suspected a traumatic etiology. In addition, he postulated that altered joint mechanics contributed to this condition.
Freibergs disease preferentially affects the second metatarsal, the
longest metatarsal in the weightbearing foot.
The mechanics behind resultant
dorsal subchondral collapse of the
metatarsal head have been evaluated
in several studies. McMaster55 originally described an osteochondral lesion produced by the proximal phalangeal base contacting the second
metatarsal head with forced dorsiflexion. Gauthier and Elbaz56 found
that these lesions occur on the dorsal and anterior aspect of the metatarsal head. These authors postulated that collapse was caused by
microfracture and necrosis of the
subchondral bone. Helal and Gibb57
linked this dorsal lesion with traumatic effusions.

Diagnosis Typically, Freibergs

disease presents in girls during the
adolescent growth spurt. Classically,
there is pain on weight bearing and
tenderness over the affected metatarsal head. There may be fullness at
the joint because of an effusion.
Smillie58 proposed a staging system
for this condition, based on the radiographic appearance of the metatarsal head, which can demonstrate
various stages of collapse: stage I,
fracture of the epiphysis; stage II,
subsidence of the central portion;
stage III, central reabsorption; stage
IV, loose body separation; and stage
V, flattening, deformity, arthritis
(Figure 6).
Treatment Nonsurgical management includes activity modification,
limited weight bearing with crutches, orthosis use, and shoe modifications that off-load the affected
metatarsal head and limit affected
metatarsophalangeal joint motion.
These modalities are effective in the
early stages of the disease.
Several surgical options have
been advocated. Simple dbridement and loose body removal was
first described by Freiberg. Other
procedures have been used, including osteotomy, elevation of the depressed metatarsal head with bone
grafting, core decompression, metatarsal head excision, metatarsal
shortening, proximal phalanx hemiphalangectomy, and joint arthroplasty. There is little consensus as to
which is the most appropriate or
efficacious.59,60
Prognosis Many patients with
Freibergs disease respond to nonsurgical therapy and do not experience
long-term sequelae. Sproul et al60 examined patients in whom nonsurgical treatment failed. In most of these
patients, partial resection of the dorsal metatarsal head with synovectomy provided long-term relief. Loosening of the dorsal metatarsal
articular surface was a consistent
surgical finding.

Journal of the American Academy of Orthopaedic Surgeons

Christopher W. DiGiovanni, MD, et al

Sesamoids
Osteonecrosis of the sesamoids
has been noted in a limited number
of case reports.

fied weight bearing, and nonsteroidal anti-inflammatory drugs to

control symptoms. When these measures fail, surgical removal of the affected bone is indicated.62,63

Vascular Supply

Each sesamoid has both a proximal and a plantar major arterial perforator that arises from the first
metatarsal artery. The proximal
branch enters the sesamoid at the insertion of the flexor hallucis brevis;
the plantar vessel penetrates the
bone near its midline. These branches eventually meet in the center of
each bone.53
Diagnosis

Sesamoid pathology comprises

12% of great toe complex injuries; osteonecrosis of these bones accounts
for approximately 10% of this subset.61 Several names have been given
to this condition, including Trevors
disease, Schlatters disease, and Ilfelds disease. Pain is the most consistent presenting symptom of this
extremely disabling condition. Plain
radiographs aid in the diagnosis, but
they may not be definitive because
sesamoid fracture, congenital bipartism, and osteonecrosis may appear
similar on such images. A bone scan
may differentiate the high turnover
state in fractures from the low turnover state in late-stage osteonecrosis.
MRI also may aid in differentiating
an acute fracture from osteonecrosis.
On a computed tomography scan, the
osteonecrotic sesamoid may appear
as enlarged and deformed, with irregular densities and fragmentation. The
radiographic appearance of the symptomatic foot should be compared
with the contralateral side.62 The
speculated mechanism of sesamoid
osteonecrosis is secondary to repetitive trauma, which may interrupt
the vascular supply to the sesamoids, thus diminishing their ability to remodel.
Treatment

Nonsurgical management includes activity modification, modiVolume 15, Number 4, April 2007

Rare Locations for

Osteonecrosis in the
Foot
Calcaneus
Unlike the talus, the calcaneus
enjoys a rich vascular supply, which
may explain the absence of posttraumatic calcaneal osteonecrosis. In the
calcaneus, osteonecrosis has been reported in association with sickle cell
disease and heart transplant. In addition, Severs disease, once regarded
as a form of osteonecrosis but now
considered a childhood apophysitis,
can lead to significant pain in the pediatric population.
Vascular Supply

Multiple arterial branches perforate the calcaneus. The artery of the

tarsal sinus, with contributions from
the lateral tarsal artery and the peroneal artery, supplies the anterior aspect of the superior surface. An anastomotic arcade between the anterior
tibial and peroneal arteries feeds the
posterior aspect of the calcaneus.
The lateral surface receives
branches from the proximal lateral
tarsal artery and the peroneal artery.
The medial plantar artery and the
medial calcaneal branches supply
the medial surface.53
Etiology and Diagnosis

Rothschild et al64 radiographically examined patients with sickle cell

disease for bone abnormalities. Fourteen percent had erosive cortical
changes in a dot-dash pattern between the insertion of the Achilles
tendon and the subtalar articular
surface,64 with nearly half reporting
hindfoot pain. All of the sickle cell
patients were treated nonsurgically,
and only one patient reported persistent pain at last follow-up.64
A second instance of calcaneal os-

teonecrosis was reported in a 38year-old heart transplant patient

who received two postoperative
courses of corticosteroid.65 The patient was successfully managed nonsurgically.65
Severs Disease

Historically, Severs disease was

regarded as a form of calcaneal osteonecrosis. Today, however, it is
considered to be a calcaneal apophysitis, and it represents one of the
most common causes of foot pain in
the immature athlete. Radiographically, the sclerotic apophysis seen
in Severs disease mimics the appearance of osteonecrosis in other
bones. Although of unknown etiology, some have implicated an apophyseal traction injury from the Achilles tendon and the plantar fascia.66
This mechanical disruption may impede the endochondral mechanism
of microfracture healing, leading to a
cycle of nonrepairing injury. Thus,
although there may be an intrinsic
dysvascularity as a result of these
factors, current available evidence
suggests that Severs disease is not a
form of osteonecrosis but rather is a
self-limiting apophysitis devoid of
long-term sequela.66
Cuneiforms
There are several case reports of
cuneiform osteonecrosis.67-69
Diagnosis

Patients with cuneiform osteonecrosis present with insidious midfoot pain that is activity-related and
occurs at night. The diagnosis is
based on radiologic findings of cuneiform collapse and sclerosis in patients with clinical symptoms.
Treatment and Prognosis

In general, nonsurgical management consisting of modified activity

and immobilization results in nearly universal symptom improvement
or elimination. In one patient, medial cuneiform drilling resulted in
symptom resolution.69
215

Osteonecrosis in the Foot

Cuboid
There is only one English-language case report of cuboid osteonecrosis, in a 63-year-old kidney recipient treated with prednisone.70
Within 3 months, midfoot pain and
swelling developed. Biopsy demonstrated necrosis from blood vessel
infiltration with fungal elements.
Definitive management consisted of
cuboid excision.

2.

3.

4.

Summary
Osteonecrosis must always be considered in the differential diagnosis
of both the pediatric and adult patient with chronic foot pain. The disease most commonly affects the talus, navicular, second metatarsal,
and first metatarsal. Its etiology is
usually posttraumatic; however, systemic disease (eg, Gauchers, sickle
cell) also can produce osteonecrosis.
Nonsurgical management remains
the mainstay of initial treatment
and can be effective in ameliorating
symptoms. Surgery is recommended
only when nonsurgical management
is unsuccessful. Because of its varying incidence, presentation, and sequelae in these bones, there is currently no standard algorithm for
managing osteonecrosis in the foot.
Therapy is determined on an individual basis. Because of the disability that occa-sionally occurs in even
optimally managed patients affected
with this disease, more research is
paramount to understanding the
most effective means of treating and,
more importantly, preventing osteonecrosis in the foot.

5.

6.

7.

8.

9.

10.

11.

12.

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