A classification method for neurogenic heterotopic ossification of the hip.

Abstract

Existing classifications for heterotopic ossification (HO) do not include all HO types; nor do they consider the anatomy of the involved joint or the neurological injury. Therefore, we performed this study to propose and evaluate a classification according to the location of neurogenic HO and the neurological injury.
We studied the files of 24 patients/33 hips with brain or spinal cord injury and neurogenic HO of the hip treated with excision, indomethacin, and radiation therapy. We classified patients according to the Brooker classification scheme as well as ours. Four types of neurogenic HO were distinguished according to the anatomical location of HO: type 1, anterior; type 2, posterior; type 3, anteromedial; type 4, circumferential. Subtypes of each type were added based on the neurological injury: a, spinal cord; b, brain injury. Mean follow-up was 2.5 years (1-8 years).
The Brooker classification scheme was misleading-all hips were class III or IV, corresponding to ankylosis, even though only 14 hips had ankylosis. On the other hand, our classification was straightforward and easy to assign in all cases. It corresponded better to the location of the heterotopic bone, and allowed for preoperative planning of the appropriate surgical approach and evaluation of the prognosis; recurrence of neurogenic HO was significantly higher in patients with brain injury (subtype b), while blood loss was higher for patients with anteromedial (type 3) and circumferential (type 4) neurogenic HO.
Our proposed classification may improve the management and evaluation of the prognosis for patients with neurogenic HO.

Full text

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ORIGINAL ARTICLE
A classification method for neurogenic heterotopic ossification
of the hip
Andreas F. Mavrogenis•Giovanni Guerra•
Eric Lodwijk Staals•Giuseppe Bianchi•
Pietro Ruggieri
Received: 15 June 2011/Accepted: 15 March 2012/Published online: 4 April 2012
? The Author(s) 2012. This article is published with open access at Springerlink.com
Abstract
Background
fication (HO) do not include all HO types; nor do they
consider the anatomy of the involved joint or the neuro-
logical injury. Therefore, we performed this study to pro-
pose and evaluate a classification according to the location
of neurogenic HO and the neurological injury.
Materials and methods
We studied the files of 24
patients/33 hips with brain or spinal cord injury and neu-
rogenic HO of the hip treated with excision, indomethacin,
and radiation therapy. We classified patients according to
the Brooker classification scheme as well as ours. Four
types of neurogenic HO were distinguished according to
the anatomical location of HO: type 1, anterior; type 2,
posterior; type 3, anteromedial; type 4, circumferential.
Subtypes of each type were added based on the neurolog-
ical injury: a, spinal cord; b, brain injury. Mean follow-up
was 2.5 years (1–8 years).
Results
The Brooker classification scheme was mislead-
ing—all hips were class III or IV, corresponding to anky-
losis, even though only 14 hips had ankylosis. On the other
hand, our classification was straightforward and easy to
assign in all cases. It corresponded better to the location of
the heterotopic bone, and allowed for preoperative plan-
ning of the appropriate surgical approach and evaluation of
theprognosis;recurrence
Existing classifications for heterotopic ossi-
of neurogenic HOwas
significantly higher in patients with brain injury (subtype
b), while blood loss was higher for patients with antero-
medial (type 3) and circumferential (type 4) neurogenic
HO.
Conclusions
Our proposed classification may improve
the management and evaluation of the prognosis for
patients with neurogenic HO.
Keywords
Brain injury ? Spinal cord injury
Neurogenic heterotopic ossification ? Hip ?
Introduction
Heterotopic ossification (HO) is true osteoblastic activity
and abnormal formation of mature lamellar bone within
extraskeletal soft tissues where bone does not normally
exist [1–5]. HO has been classified according to the
clinical setting, location of HO, and progressive or iso-
lated occurrence [1–5] into post-traumatic, nontraumatic
or neurogenic, and myositis or fibrodysplasia ossificans
progressiva [2–11]. Nontraumatic or neurogenic HO or
myositis ossificans circumscripta without trauma is fre-
quent in patients with neurological injury; it occurs in
3.4–47 % of patients after spinal cord injury, 10–20 % of
patients after closed head injury, and less often after
burns, stroke, brain tumors, sickle cell anemia, hemo-
philia, tetanus, poliomyelitis, multiple sclerosis, and toxic
epidermal necrolysis [2, 7, 11]. The incidence is higher in
a spastic extremity, patients with complete spinal cord
injuries, prolonged immobilization, a high Glasgow coma
score, patients in a long coma, and in those with severe
spasticity, deep venous thrombosis, hypercalcemia, and
hematomas [2, 8, 10, 12, 13]. The most frequent site of
neurogenic HO is the hip joint, where it most commonly
Investigation performed at the Istituto Ortopedico Rizzoli, Bologna,
Italy.
A. F. Mavrogenis ? G. Guerra ? E. L. Staals ? G. Bianchi ?
P. Ruggieri (&)
Department of Orthopaedics, Orthopaedic Oncology Service,
Istituto Ortopedico Rizzoli, University of Bologna,
Via Di Barbiano 1/10, 40136 Bologna, Italy
e-mail: pietro.ruggieri@ior.it
123
J Orthopaed Traumatol (2012) 13:69–78
DOI 10.1007/s10195-012-0193-z

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occurs in the flexor (anterior) or adductor (medial) com-
partments [2, 8, 10, 11].
There are limited data on the evaluation and manage-
ment of patients with neurogenic HO [2, 11–14]. Several
treatments have been proposed, including surgical excision
of the heterotopic bone, radiation therapy, physical therapy,
and drugs such as nonsteroidal anti-inflammatory drugs and
bisphosphonates [15, 16]. However, most of the data derive
from studies on post-traumatic HO, most commonly after
total hip arthroplasty [17–19], and most treatments have
been based on empirical findings [2, 13]. Additionally,
classifications of neurogenic HO are lacking; the classifi-
cations that are currently available are related to post-
traumatic HO [20–22], and do not address the mechanism
of neurological injury or the anatomical compartment
involved with the heterotopic bone in order to guide the
surgical approach [2–5, 7, 8, 10, 11]. To address these
issues, we performed a clinical study of patients with brain
and spinal cord injury and neurogenic HO of the hip joint,
aiming (1) to propose a classification according to the
location of HO at the hip joint and the neurological injury
of the patient, and (2) to estimate the prognosis of neuro-
genic HO based on this classification with respect to range
of motion and clinical ankylosis of the hip joint, blood loss
and transfusion requirements, and recurrence of the neu-
rogenic HO after combined treatment.
Materials and methods
We retrospectively studied the medical files of 24 patients
with neurogenic HO of the hip joint after central nervous
system injury who were diagnosed and treated at the
authors’ institution from June 2002 to September 2008.
There were 17 male and 7 female patients, with a mean age
of 38 years (range, 18–63 years). Sixteen patients had
neurogenic HO after brain injury and 8 patients after spinal
cord injury; 13 patients were paraplegic, 7 tetraplegic, and
4 hemiplegic. Eighteen of the 24 patients had variable
neurogenic HO of the contralateral hip joint; 9 of the 18
patients (patients 4, 9, 10, 12, 15, 18, 19, 21, and 23) also
had treatment for neurogenic HO of the contralateral hip at
an interval of 6–12 months. Overall, 24 patients/33 hips
were included in this study (Table 1). The mean follow-up
was 2.5 years (range, 1–8 years); no patient was lost to
follow-up. All patients gave written informed consent to be
included in this study. This study was approved by the
institutional review board/ethics committee of the authors’
institution, and conforms to the latest revision of the
Declaration of Helsinki.
Neurogenic HO was classified according to the Brooker
classification [1] for post-traumatic HO after total hip
arthroplasty (Table 2) as well as the classification proposed
herein (Table 3). Our classification is based on the (1)
anatomical location of the heterotopic bone as shown in
axial computed tomography (CT) scans of the hip and
proximal femur, (2) clinical ankylosis of the hip joint, and
(3) the etiology of the neurological injury (brain or spinal
cord injury). All imaging studies were reviewed by the
authors and two radiologists who were asked to classify
neurogenic HO according to these two classifications on a
consensus basis.
In all patients, the pre-treatment evaluation included
clinical evaluation of the range of motion (flexion, exten-
sion, rotation, abduction, and adduction) and ankylosis of
the respective hip joint, serial serum alkaline phosphatase
measurements and a preoperative measurement of serum
hemoglobin, standard radiographs, and at least two three-
phase technetium-99 m (99mTc) methylene diphosphonate
bone scans to evaluate the maturation of HO. Treatment
was applied at a mean of 1 year (range, 0.5–7 years) after
the initial imaging evidence of HO to allow for the matu-
ration of HO and facilitate resection with minimum trauma
to the surrounding tissue [2]. In all 24 patients/33 hips,
treatment included surgical excision of the heterotopic
bone followed by radiation therapy in a single fraction of
600 cGy administered within 72 h postoperatively (range,
48–72 h), and indomethacin administration in daily doses
of 50–100 mg starting from the first postoperative day for
6 weeks. Postoperatively, blood transfusion requirements
were recorded and serum hemoglobin was measured. Post-
treatment evaluation, including clinical examination of
range of motion and imaging evaluation of the respective
hip joint using radiographs and CT scans, was performed at
6-month intervals to evaluate the effect of treatment and
the evidence for recurrence of HO. Recurrent neurogenic
HO was defined as a reduction in the range of motion
obtained after surgery and imaging evidence of HO.
Statistical analysis was performed using Student’s t test
and the chi-square test. The data were recorded in a
Microsoft?Excel?2003 spreadsheet (Microsoft Corpora-
tion, Redmond, WA, USA) and analyzed using MedCalc?
software, version 11.1 (MedCalc Software, Mariakerke,
Belgium).
Results
We distinguished four types of neurogenic HO (Fig. 1):
type 1 is characterized by anterior (Fig. 2), type 2 by
posterior (Fig. 3), type 3 by anteromedial (Fig. 4), and type
4 by circumferential heterotopic bone formation (Fig. 5). A
subtype was added to each type according to the etiology of
the neurological injury: a, spinal cord injury; b, brain injury
(Tables 1, 3). In all patients/hips, the classification pro-
posed herein was straightforward and easy to assign.
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Table 1 Details of the 24 patients/33 hips included in this study
Patient
no.
Gender, age,
plegia, treated hip
Brooker
classification
[1]
Authors’
classification
Follow-
up
(years)
ROM pre-treatment (?)
ROM post-treatment (?)
Hb pre-
treatment
(g/dl)
Hb post-
treatment
(g/dl)
Transfusion
(blood
units)
1
M, 50,
tetraplegia,left hip
Class IV
Type 1a
2
Flexion 10, extension 0;
rotation: internal 5, external 5;
abduction 0, adduction 0
Flexion 70, extension 20;
rotation: internal 30, external 25;
abduction 25, adduction 15
15.1
8.9
2
2
M, 45,
paraplegia,
right hip
Class IV
Type 1a
8
Ankylosis
Flexion 50, extension 10;
rotation: internal 15, external 15;
abduction 20, adduction 15
12.7
12
–
3
M, 27,
tetraplegia,
right hip
Class IV
Type 1a
6
Flexion 20, extension 0;
rotation: internal 5, external 5;
abduction 10, adduction 0
Flexion 80, extension 10;
rotation: internal 30, external 25;
abduction 25, adduction 20
12.8
10.4
2
4
M, 63,
tetraplegia,
right hip
Class III
Type 1b
5
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 10, adduction 5
Flexion 90, extension 10;
rotation: internal 30, external 30;
abduction 30, adduction 25
13.9
10.6
–
Left hip
Class III
Type 1b
4.5
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 10, adduction 5
Flexion 90, extension 10;
rotation: internal 25, external 25;
abduction 30, adduction 25
13.9
10.8
–
5
M, 42,
paraplegia,
right hip
Class III
Type 2a
2
Flexion 40, extension 0;
rotation: internal 5, external 10;
abduction 0, adduction 0
Flexion 90, extension 20;
rotation: internal 15, external 25;
abduction 20, adduction 10
12
9.8
–
6
F, 46,
paraplegia,
left hip
Class IV
Type 2a
1
Ankylosis
Flexion 60, extension 20;
rotation: internal 10, external 15;
abduction 15, adduction 5
12
9.4
1
7
F, 44,
tetraplegia,
right hip
Class IV
Type 2b
1
Ankylosis
Flexion 80, extension 15;
rotation: internal 10, external 10;
abduction 10, adduction 5
13
11
–
8
M, 52,
paraplegia,
left hip
Class III
Type 2b
1.5
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 0, adduction 0
Flexion 75, extension 15;
rotation: internal 15, external 25;
abduction 20, adduction 10
11
9.6
–
9
M, 45,
tetraplegia, left hip
Class IV
Type 3a
5
Ankylosis
Flexion 80, extension 10
rotation: internal 30, external 30
abduction 30 adduction 20
13.9
9.4
4
Right hip
Class IV
Type 3a
4
Flexion 30, extension 0
rotation: internal 15, external 20
abduction 20 adduction 10
Flexion 80, extension 10
rotation: internal 30, external 30
abduction 30 adduction 25
14
9
3
10
F, 49,
paraplegia,
left hip
Class III
Type 3a
2.5
Flexion 30, extension 0
rotation: internal 5, external 5
abduction 10, adduction 0
Flexion 90, extension 20
rotation: internal 30, external 20
abduction 20, adduction 15
11.1
9.5
3
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Table 1 continued
Patient
no.
Gender, age,
plegia, treatedhip
Brooker
classification
[1]
Authors’
classification
Follow-
up
(years)
ROM pre-treatment (?)
ROM post-treatment (?)
Hb pre-
treatment
(g/dl)
Hb post-
treatment
(g/dl)
Transfusion
(blood
units)
Right hip
Class III
Type 3a
2
Flexion 10, extension 0
rotation: internal 5, external 5
abduction 5, adduction 0
Flexion 80, extension 20
rotation: internal 25, external 20
abduction 20, adduction 15
15
9.8
3
11
M, 29,
paraplegia,
right hip
Class IV
Type 3a
1.5
Ankylosis
Flexion 90, extension 20
rotation: internal 30, external 30
abduction 30, adduction 20
13.5
7.5
2
12
M, 35,
paraplegia,
right hip
Class III
Type 3a
3.5
Flexion 40, extension 5
rotation: internal 10, external 10
abduction 5, adduction 0
Flexion 80, extension 15
rotation: internal 35, external 25
abduction 25, adduction 20
11.5
10.5
–
Left hip
Class III
Type 3a
3
Flexion 20, extension 5;
rotation: internal 10, external 10;
abduction 5, adduction 5
Flexion 90, extension 20;
rotation: internal 35, external 25;
abduction 30, adduction 25
11.6
10.2
–
13
F, 52,
tetraplegia,
right hip
Class III
Type 3b
4
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 0, adduction 5
Flexion 100, extension 20;
rotation: internal 30, external 30;
abduction 30, adduction 25
14
12.5
–
14
M, 19,
hemiplegia,
right hip
Class III
Type 3b
2.5
Flexion 30, extension 30;
rotation: internal 5, external 5;
abduction 10, adduction 0
Flexion 55, extension 30;
rotation: internal 20, external 15;
abduction 15, adduction 10
15.2
11.8
2
15
M, 37,
paraplegia,
right hip
Class IV
Type 3b
1
Flexion 30, extension 30;
rotation: internal 0, external 0;
abduction 0, adduction 0
Flexion 30, extension 30;
rotation: internal 5, external 5;
abduction 5, adduction 5
14.3
8.4
4
Left hip
Class IV
Type 3b
1
Flexion 30, extension 30;
rotation: internal 0, external 0;
abduction 0, adduction 0
Flexion 30, extension 30;
rotation: internal 5, external 5;
abduction 5, adduction 5
14.6
9.2
3
16
F, 52,
hemiplegia,
left hip
Class III
Type 3b
1.5
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 10, adduction 5
Flexion 80, extension 15;
rotation: internal 20, external 20;
abduction 20, adduction 10
10.9
10
–
17
F, 21,
hemiplegia,
left hip
Class III
Type 3b
1.5
Flexion 30, extension 0;
rotation: internal 10, external 15;
abduction 10, adduction 5
Flexion 90, extension 20;
rotation: internal 30, external 30;
abduction 30, adduction 20
11.5
10.5
–
18
M, 46,
paraplegia,
right hip
Class IV
Type 3b
4
Ankylosis
Flexion 50, extension 10;
rotation: internal 20, external 15;
abduction 15 adduction 5
12.4
11
1
Left hip
Class IV
Type 3b
3
Flexion 50, extension 0;
rotation: internal 10, external 5;
abduction 5 adduction 5
Flexion 70, extension 10;
rotation: internal 20, external 10;
abduction 15 adduction 10
12
9
1
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Table 1 continued
Patient
no.
Gender, age,
plegia, treatedhip
Brooker
classification
[1]
Authors’
classification
Follow-
up
(years)
ROM pre-treatment (?)
ROM post-treatment (?)
Hb pre-
treatment
(g/dl)
Hb post-
treatment
(g/dl)
Transfusion
(blood
units)
19
F, 38,
hemiplegia,
left hip
Class III
Type 3b
2.5
Flexion 45, extension 0;
rotation: internal 10, external 15;
abduction 15, adduction 5
Flexion 90, extension 10;
rotation: internal 35, external 30;
abduction 30, adduction 20
12
7.6
2
Right hip
Class III
Type 3b
2.5
Flexion 80, extension 0;
rotation: internal 15, external 15;
abduction 15, adduction 15
Flexion 100, extension 10;
rotation: internal 35, external 30;
abduction 30, adduction 20
10.7
9.3
1
20
M, 42,
paraplegia,
right hip
Class IV
Type 3b
3.5
Flexion 20, extension 0;
rotation: internal 5, external 5;
abduction 10, adduction 10
Flexion 90, extension 20;
rotation: internal 30, external 25;
abduction 25, adduction 20
14.6
9.2
3
21
M, 30,
paraplegia,
right hip
Class IV
Type 4a
3.5
Ankylosis
Flexion 90, extension 20;
rotation: internal 35, external 30;
abduction 35, adduction 25
15.2
11.3
3
Left hip
Class IV
Type 4a
3
Flexion 40, extension 5;
rotation: internal 15, external 10;
abduction 20, adduction 15
Flexion 80, extension 20;
rotation: internal 30, external 30;
abduction 30, adduction 25
12.5
9.5
3
22
M, 30,
paraplegia,
right hip
Class III
Type 4a
3
Flexion 80, extension 0;
rotation: internal 10, external 15;
abduction 20, adduction 15
Flexion 100, extension 20;
rotation: internal 35, external 30;
abduction 40, adduction 25
14.1
9.9
2
23
M, 43,
paraplegia,
left hip
Class III
Type 4a
3
Flexion 30, extension 0;
rotation: internal 5, external 5;
abduction 5, adduction 0
Flexion 90, extension 20;
rotation: internal 25, external 25;
abduction 30, adduction 25
11.3
9.4
3
Right hip
Class III
Type 4a
2.5
Flexion 10, extension 0;
rotation: internal 5, external 5;
abduction 5, adduction 0
Flexion 90, extension 20;
rotation: internal 20, external 20;
abduction 20, adduction 20
13.5
7.5
3
24
M, 24,
tetraplegia,left hip
Class IV
Type 4b
6
Flexion 10, extension 0;
rotation: internal 0, external 0;
abduction 0, adduction 0
Flexion 60, extension 10;
rotation: internal 20, external 15;
abduction 30, adduction 15
14.1
12.6
–
Summary (mean value, range)
Flexion 25 (0–80), extension 2.5 (0–30);
rotation: internal 5.5 (0–15), external 6 (0–20); abduction 6 (0–20), adduction 3(0–15)
Flexion 79 (30–100), extension 17 (10–30);
rotation: internal 25 (5–35), external 23 (5–30); abduction 25 (5–40), adduction
17 (5–25)
13
(10.7–15.2)
9.9
(7.5–12.6)
1.5 (0–4)
Pts patients, ROM range of motion, Hb hemoglobin
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Preoperative planning facilitated the surgical excision of
the heterotopic bone by choosing the appropriate surgical
approach according to the anatomical location (type) of
neurogenic HO; the anterior approach to the hip was used
for anterior and anteromedial neurogenic HO (types 1 and
3), the posterior approach for posterior neurogenic HO
(type 2), and a single-stage combined anterior and posterior
approach for circumferential neurogenic HO (type 4).
Pre-treatment clinical examination showed a reduction
in the range of motion and an inability to achieve a
standing position in all patients, an inability to achieve a
sitting position in 22 patients, hip ankylosis in 7 patients/14
hips, and hip pain in 1 patient (patient 1). According to the
Brooker classification [1], all patients/hips were classified
as class III or IV, which corresponds to hip ankylosis;
however, only 7 patients/14 hips presented clinical or
imaging evidence of ankylosis (Table 1). The mean hip
flexion before treatment was 25? (range, 0–80?), extension
2.5? (range, 0–30?), internal rotation 5.5? (range, 0–10?),
external rotation 6? (range, 0–20?), abduction 6? (range,
0–20?), and adduction 3? (range, 0–15?). After treatment,
no patient had ankylosis of the hip joint, all patients were
able to sit, and the mean range of hip motion significantly
improved (p = 0.001); the mean hip flexion after treatment
was 79? (range, 30–100?), extension 17? (range, 10–30?),
internal rotation 25? (range, 5–35?), external rotation 23?
(range, 5–30?), abduction 25? (range, 5–40?), and adduc-
tion 17? (range, 5–25?). Improvement was statistically
significant for all motions (flexion, p = 0.035; extension,
p = 0.030; internal rotation, p = 0.020; external rotation,
p = 0.030; abduction, p = 0.030; adduction, p = 0.020),
regardless of the type of neurogenic HO (p = 0.460).
Our classification also allowed for the estimation of
blood loss,transfusion requirements, and recurrence of
neurogenic HO. Overall, blood transfusion was necessary
in 14 patients/20 hip operations. Although blood loss can
be related to many factors, blood loss and transfusion
requirements were statistically significantly higher in
patients with type 3 and 4 compared to patients with type 1
and 2 neurogenic HO (chi-square test, p = 0.040). Overall,
clinical and imaging recurrence of neurogenic HO was
Fig. 1 A classification method for neurogenic HO of the hip
according to the anatomical location of HO (types 1–4) and the
neurological injury (subtypes a and b)
Table 2 Brooker classification of HO of the hip
ClassPatients
(n = 24)/hips
(n = 33)
Description
I– Bone islands within soft tissues
about the hip
II– Bone spurs in pelvis or proximal end of
femur, leaving at least 1 cm between the
opposing bone surfaces
III12/17Bone spurs that extend from the pelvis or
the proximal end of the femur, which
reduce the space between the opposing
bone surfaces to less than 1 cm
IV12/16 Radiographic ankylosis of the hip
Table 3 Authors’ classification of neurogenic HO of the hip
TypePatients
(n = 24)/hips
(n = 33)
Description
Type 1
a: Spinal cord injury3/3 Neurogenic HO at the
anterior hip or the
proximal end of the
femur, with or without
ankylosis
b: Brain injury1/2
Type 2
a: Spinal cord injury2/2Neurogenic HO at the
posterior hip or the
proximal end of the
femur, with or without
ankylosis
b: Brain injury2/2
Type 3
a: Spinal cord injury 4/7 Neurogenic HO at the
anterior and medial hip or
the proximal end of the
femur, with or without
ankylosis
b: Brain injury 8/11
Type 4
a: Spinal cord injury 3/5 Neurogenic HO around the
hip (circumferential),
with or without ankylosis
b: Brain injury1/1
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observed at 2 years in 5 patients/7 hips [21 %; patients 4,
6, 7 (bilateral), 10 (bilateral), and 17]; there were 4
patients/6 hips with neurogenic HO after brain injury
(subtype b), and 1 patient/hip after spinal cord injury
(subtype a). Recurrence of neurogenic HO was statistically
significantly higher in patients with brain injury (Student’s
t test, p = 0.040). Although recurrence was higher in
patients with type 3 neurogenic HO, a statistically signifi-
cant difference between the anatomical location of
neurogenic HO and recurrence was not observed (Student’s
t test, p = 0.198).
Discussion
Neurogenic HO is a frequent complication in patients with
central nervous system injury, and a potential cause of
increased morbidity from complications resulting from
Fig. 3 a Axial computed tomography scan and b anteroposterior radiograph of the left hip of a 52-year-old man with posterior neurogenic HO of
the hip after closed brain injury (patient 8; type 2b)
Fig. 2 a Axial computed tomography scan and b anteroposterior radiograph of the right hip of a 63-year-old man with anterior neurogenic HO
of the hip after closed brain injury (patient 4; type 1b)
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immobilization [2, 11–14, 16, 23]. However, neurogenic
HO is less well studied than the other HO types, and
classifications for neurogenic HO are lacking [2, 11–14];
most of the data reported relate to patients with post-trau-
matic HO after total hip arthroplasty [17–19]. Therefore,
we performed this study to propose a classification for
neurogenic HO, to compare that classification with the
Brooker classification [1], and to validate this classification
in a clinical series of patients treated with combined
surgical excision, indomethacin, and postoperative radia-
tion therapy. The classification proposed herein distin-
guishes 4 types of neurogenic HO (types 1–4) according to
the location of heterotopic bone formation around the hip
joint, and 2 subtypes (a and b) according to the etiology of
the neurological injury. Our results showed that the present
classification can be useful for the management of neuro-
genic HO patients. It provides for preoperative planning of
the surgical approach according to the anatomical location
Fig. 5 a Axial computed tomography scan and b anteroposterior radiograph of the left hip of a 43-year-old man with circumferential neurogenic
HO around the hip after spinal cord injury (patient 23; type 4a)
Fig. 4 a Axial computed tomography scan and b anteroposterior radiograph of the left hip of a 49-year-old woman with anteromedial
neurogenic HO of the hip after spinal cord injury (patient 10; type 3a)
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of the neurogenic HO, and permits an estimation of the
prognosis regarding blood loss, transfusion requirements,
and recurrence of the neurogenic HO.
We see four limitations in this study. First, the sample
size is small; however, the lack of a classification for the
specific HO type supports this study. Second, we did not
use three-dimensional CT scan for the preoperative eval-
uation of HO. In this series and our practice, we use CT
scan for the preoperative evaluation of HO patients, and
axial CT scan views to classify HO and to indicate areas
that should be avoided or carefully removed at surgery.
Computed tomography scans may identify a low-density
material in the soft tissue adjacent to areas of ectopic
ossification that are postulated to be immature unossified
connective tissue, the violation of which may be respon-
sible for the serious intraoperative bleeding frequently
experienced during the resection of HO [11]. Compared to
three-dimensional CT reconstruction, axial CT scan is
widely available and more easily read in clinical practice
by most surgeons; also, in our opinion, it provides all of the
information needed for preoperative planning. Third, we
did not perform a volumetric quantification of the hetero-
topic bone, and did not include this volume in our classi-
fication criteria. We based our classification on the
anatomical compartment involved by the neurogenic HO
and not on its volume because we believe that the volume
of HO is only related to the reduction in the range of
motion or ankylosis and ease of surgical excision, not to
the choice of surgical approach or the outcome of neuro-
genic HO. Moreover, including the volume of HO as a
criterion would have made the classification more complex.
Fourth, blood loss from surgical excision of the heterotopic
bone can be related to many factors, and is not validated for
this study’s purpose. However, we measured blood loss and
transfusion requirements in order to provide a prognostic
factor for the surgical treatment of each type of neurogenic
HO.
A classification should meet certain criteria to be valu-
able and widely accepted. These should include ease of
understanding, an ability to be easily recalled, consider-
ation of the anatomy, an understanding of the mechanism
of injury, the proposal of therapeutic guidelines according
to the specific types, and the provision of useful informa-
tion regarding the prognosis of the various types. We
believe that the classification proposed herein addresses all
of the above. The advantages of the Brooker classification
are that it is based solely upon anteroposterior radiographs
of the hip, and so it is a relatively simple and valid mea-
surement that appears to correlate well with the clinical
picture of overall hip function [24]. However, it does not
address the anatomical compartment involved by HO, and
does not correlate with the extent of HO into anatomical
compartments, it cannot guide the surgical treatment or
estimate prognosis, and it does not consider the etiology of
the neurological injury that led to HO. Other methods have
also been reported for the classification of HO in patients
with post-traumatic HO and HO following hip arthroplasty
[20–22]. These methods were based on the anteroposterior
radiographic view of the hip, and classified HO according
to the location around the femoral neck, without detailed
anatomical localization. Some authors attempted to classify
a central and lateral HO with respect to an imaginary
borderline from the greater trochanter to the lateral edge of
the acetabulum [25], or to divide the space around the
femoral neck into thirds (central, lateral and medial) [26];
these classifications have not been widely accepted because
of the complexity and difficulty involved in classifying HO
into nonanatomical (imaginary) areas around the hip joint.
In the present classification, we distinguished 4 types
(types 1–4) of neurogenic HO based on the anatomical
compartments involved by the heterotopic bone. Since the
etiology of neurogenic HO was found to be a statistically
significant predictor for recurrence of HO, we added 2
subtypes (subtypes a and b) based on the etiology of neu-
rological injury. The use of this classification made pre-
operative planning of the appropriate surgical approach
rather straightforward. In the most common cases with
anterior and/or medial HO (types 1 and 3), the anterior
approach to the hip should be used; in cases of posterior
HO (type 2), the posterior approach to the hip should be
used; and in cases of circumferential HO (type 4), a
combined anterior and lateral approach is recommended.
Post-treatment improvement in the range of motion of the
hip was significant in all cases, regardless of the type of
neurogenic HO; therefore, the presence of ankylosis was
not included in the criteria of our classification—it was
only recorded to evaluate the effect of treatment. Addi-
tionally, HO that appears to be bridging according to the
Brooker classification may actually be located either
anterior or posterior to the hip, and thus may not cause
significant loss of range of motion [21, 22]. This was also
observed in the present clinical series; although according
to the Brooker classification all of the patients/hips were
classified as class III or IV, meaning hip ankylosis, clinical
and imaging evidence of ankylosis was observed in only 7
patients/14 hips. The location (type) of neurogenic HO may
also provide an estimate of blood loss and transfusion
requirements. In the present study, blood loss and trans-
fusion requirements were higher for patients with antero-
medial (type 3) and circumferential (type 4) neurogenic
HO. This may be explained by the fact that anteromedial or
circumferential lesions and lesions in proximity to major
vessels are more difficult to excise. A classification should
also address the prognosis of a disease. Recurrence rates of
neurogenic HO ranging from 17 to 58 % have been
reported [10, 11, 13, 27]. In the present study, the
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recurrence rate of neurogenic HO was 21 % (5 patients/7
hips) at 2 years. The etiology of the neurological injury
was found to be a significant prognostic factor for recur-
rence; recurrence was 6 times more common after brain
injury (subtype b) compared to spinal cord injury (subtype
a). We explain this by the fact that spinal cord injury
patients may have a better performance status and selective
motor control in the extremity, and can more easily achieve
a better functional outcome [27–29]. The anatomical
location of neurogenic HO was not found to be a significant
prognostic factor for recurrence.
In conclusion, the management of neurogenic HO
patients is challenging. A new classification specifically
designed for this disorder is necessary. Since the trauma of
surgery may actually aggravate the condition, adequate
classification, preoperative planning, and combined treat-
ment are beneficial.
Conflict of interest
a commercial party related directed or indirectly to the subject matter
of this article.
No benefits have been or will be received from
Open Access
Creative Commons Attribution License which permits any use, dis-
tribution, and reproduction in any medium, provided the original
author(s) and the source are credited.
This article is distributed under the terms of the
References
1. Brooker AF, Bowerman JW, Robinson RA, Riley LH Jr (1973)
Ectopic ossification following total hip replacement: incidence
and a method of classification. J Bone Joint Surg Am
55:1629–1632
2. Garland DE (1991) A clinical perspective on common forms of
acquired heterotopicossification.
263:13–29
3. Naraghi FF, DeCoster TA, Moneim MS, Miller RA, Rivero D
(1996) Heterotopic ossification. Orthopedics 19:145–151
4. Reardon MJ, Tillou A, Mody DR, Reardon PR (1997) Hetero-
topic calcification in abdominal wounds. Am J Surg 173:145–147
5. Thomas BJ (1992) Heterotopic bone formation after total hip
arthroplasty. Orthop Clin North Am 23:347–358
6. Benetos IS, Mavrogenis AF, Themistocleous GS, Kanellopoulos
AD, Papagelopoulos PJ, Soucacos PN (2006) Optimal treatment
of fibrodysplasia ossificans progressiva with surgical excision of
heterotopic bone, indomethacin, and irradiation. J Surg Orthop
Adv 15(2):99–104
7. Gibson CJ, Poduri KR (1997) Heterotopic ossification as a
complication of toxic epidermal necrolysis. Arch Phys Med
Rehabil 78:774–776
8. Inan M, Chan G, Dabney K, Miller F (2006) Heterotopic ossifi-
cation following hip osteotomies in cerebral palsy: incidence and
risk factors. J Pediatr Orthop 26:551–556
9. Randelli F, Pierannunzii L, Banci L, Ragone V, Aliprandi A,
Buly R (2010) Heterotopic ossifications after arthroscopic man-
agement of femoroacetabular impingement: the role of NSAID
prophylaxis. J Orthop Traumatol 11(4):245–250
10. Stover SL, Niemann KM, Tulloss JR (1991) Experience with
surgical resection of heterotopic bone in spinal cord injury
patients. Clin Orthop Relat Res 263:71–77
Clin OrthopRelat Res
11. Subbarao JV, Garrison SJ (1999) Heterotopic ossification: diag-
nosis and management, current concepts and controversies.
J Spinal Cord Med 22(4):273–283
12. McCarthy EF, Sundaram M (2005) Heterotopic ossification: a
review. Skeletal Radiol 34:609–619
13. Simonsen LL, Sonne-Holm S, Krasheninnikoff M, Engberg AW
(2007) Symptomatic heterotopic ossification after very severe
traumatic brain injury in 114 patients: incidence and risk factors.
Injury 38:1146–1150
14. Balboni TA, Gobezie R, Mamon HJ (2006) Heterotopic ossifi-
cation: pathophysiology, clinical features and the role of radio-
therapyforprophylaxis. Int
65(5):1289–1299
15. Garland DE, Alday B, Venos KG, Vogt JC (1983) Diphosphonate
treatment for heterotopic ossifications in spinal cord injury
patients. Clin Orthop Relat Res 176:197–200
16. Ippolito E, Formisano R, Caterini R, Farsetti P, Penta F (1999)
Operative treatment of heterotopic ossification in patients with
coma after brain injury. Clin Orthop Relat Res 365:130–138
17. Banovac K, Williams JM, Patrick LD, Haniff YM (2001) Pre-
vention of heterotopic ossification after spinal cord injury with
indomethacin. Spinal Cord 39:370–374
18. Gregoritch SJ, Chadha M, Pelligrini VD, Rubin P, Kantorowitz
DA (1994) Randomized trial comparing preoperative versus
postoperative irradiation for prevention of heterotopic ossification
following prosthetic total hip replacement: preliminary results.
Int J Radiat Oncol Biol Phys 30:55–62
19. Seegenschmiedt MH, Keilholz L, Martus P (1997) Prevention of
heterotopic ossification about the hip: final results of two ran-
domized trials in 410 patients using either preoperative or post-
operative radiation therapy. Int J Radiat Oncol Biol Phys
39:161–171
20. Arcq M (1988) Zur Problematik der periartikuliren Verkncher-
ungen nach Htiftendoprothese. In: Maaz B, Gierse H (eds) Ak-
tuellerStand derzementfreien
Kaiserwerther Symposium. Thieme, Stuttgart, pp 71–84
21. Schmidt J, Hackenbroch MH (1996) A new classification for
heterotopic ossifications in total hip arthroplasty considering the
surgical approach. Arch Orthop Trauma Surg 115(6):339–343
22. Schuh A, Zeiler G (2005) The modified Brooker classification for
evaluation of heterotopic ossifications in total hip replacement.
Zentralbl Chir 130(4):293–296
23. Van Kuijk AA, Geurts AC, van Kuppevelt HJ (2002) Neurogenic
heterotopic ossification in spinal cord injury. Spinal Cord
40:313–326
24. WrightJG,MoranE,BogochE(1994)Reliabilityandvalidityofthe
grading of heterotopic ossification. J Arthroplasty 9(5):549–553
25. Kjaersgaard-Andersen P, Sletga ˚rd J, Gjerløff C, Lund F (1990)
Heterotopic bone formation after noncemented total hip arthro-
plasty. Location of ectopic bone and the influence of postoperative
antiinflammatory treatment. Clin Orthop Relat Res 252:156–162
26. Orzel JA, Rudd TG (1985) Heterotopic bone formation: clinical,
laboratory and imaging correlation. J Nucl Med 26:125–132
27. Kaplan FS, Glaser DL, Hebela N, Shore EM (2004) Heterotopic
ossification. J Am Acad Orthop Surg 12:116–125
28. Hastings H 2nd, Graham TJ (1994) The classification and treat-
ment of heterotopic ossification about the elbow and forearm.
Hand Clin 10(3):417–437
29. Ring D, Jupiter JB (2003) Operative release of complete anky-
losis of the elbow due to heterotopic bone in patients without
severe injury of the central nervous system. J Bone Joint Surg Am
85A(5):849–857
J RadOncolBiolPhys
Hiftendoprothetik.2.
78 J Orthopaed Traumatol (2012) 13:69–78
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