what-when-how
In Depth Tutorials and Information
FIGURE 39.1
MRI bone edema in transient osteoporosis: this 60-year-old woman with type I OI complained of knee pain for 1 month. There
was no history of trauma.
exhibit a minimal restriction to range of motion.
3,7
The
occurrence of this pain usually leads to a series of diag-
nostic radiologic studies searching for a fracture which
is not found. However, femur neck fracture has been
reported during the course of TMO including during
pregnancy.
8,9
Illustrative is the report of a 36-year-old
woman who had bilateral subcapital femoral neck frac-
tures during the sixth month of pregnancy. Diagnosis
was delayed until postpartum when computed tomog-
raphy and magnetic resonance imaging (MRI) showed
lower bone density in the femoral heads than in the
proximal femurs as well as bone resorption indicating
old fractures. Whole body bone scan showed increased
uptake in both femoral necks. As reported in other
cases of TMO, bone densitometry indicated osteoporo-
sis in the hips and spine.
10
The clinical course of TMO usually involves three
stages: the first stage results in a rapid increase in pain
over the first several weeks with accompanying func-
tional disability occurring in 1 to 2 months. The second
stage occurs over the next 2 to 3 months with symp-
toms reaching a plateau. Radiographs may be normal
in the early stages, but by 2 to 3 weeks show evidence
of patchy or diffuse osteoporosis in the involved
bone.
11
TMO is self-limited and the time requirement
for improvement both of symptoms and resolution of
changes on MRI can vary between 6 and 12 months or
longer.
12
mechanisms that are not yet investigated. The genetic
etiology of OI is discussed in Chapters 1 and 2.
Published accounts of TMO in OI do not report type
I collagen mutations in this disorder. However, this
remains to be investigated.
In their initial report of transient osteoporosis in
pregnancy, Curtiss and Kincaid
1
proposed that preg-
nancy-related pelvic nerve compression caused bone
demineralization in the proximal femur. Recognition
of the migratory pattern or its occurrence postpartum
or unrelated to pregnancy makes this an unlikely cause
for TMO. In patients with involvement of the ankle and
foot the diagnosis of reflex sympathetic dystrophy is
often considered. Several authors including Levesque
have suggested that it is a form of Sudek atrophy or
reflex sympathetic dystrophy (RSD).
2
Sudek atrophy
and RSD are currently grouped under the umbrella
term CRPS: complex regional pain syndrome.
13
However, this association to TMO is not apparent. The
diagnosis of CRPS requires the presence of regional
pain and sensory changes following a traumatic event.
The pain syndrome in CRPS is associated with localized
changes such as abnormal skin color, skin temperature
change, abnormal sweating patterns or skin edema.
As noted by Banas et al., there are distinct differences
between RSD and TMO.
14
RSD usually is proceeded by
trauma, infrequently migrates, commonly involves the
upper or distal extremities (rarely involves the hip and
knee), and often has a chronic course and poor prog-
nosis leading to contractures and chronic circulatory
changes. However, transitory migratory osteoporosis is
a self-limiting condition without long-term sequelae.
Conversion of hemopoetic marrow to fatty mar-
row as a contributing factor to transient osteoporosis
THE ETIOLOGY OF TMO
The etiology of TMO remains undefined. However,
its occurrence in individuals with OI may suggest
