H. Plenk et al., HISTOMORPHOLOGY AND BONE MORPHOMETRY OF THE BONE-MARROW EDEMA SYNDROME OF THE HIP, Clinical orthopaedics and related research, (334), 1997, pp. 73-84
From a prospective study of patients with MR imaging proven bone marro
w edema syndrome of the hip, bone biopsies that were retrieved at core
decompression treatment of 32 femoral heads (from 28 men and 3 women;
age range, 25-63 years) were evaluated microscopically. The undecalci
fied microtome sections showed diffuse or spotty areas of interstitial
and intrasinusoidal fluid in the marrow cavities, together with fat c
ell destruction or fibrovascular regeneration or both in exactly the r
egions exhibiting the magnetic resonance signals for bone marrow edema
, The vital bone trabeculae in these edematous regions showed more or
less continuous, partly osteoblast covered osteoid seams, and often, f
ormation of irregular woven bone (microcallus), pointing to increased
bone formation activity, Preceding or active osteoclastic resorption w
as rarely seen, Computer assisted bone morphometry revealed age relate
d normal to elevated bone volume densities (above 20% bone volume of t
issue volume); thus, no evidence for osteoporosis was present, In addi
tion to increased osteoid volumes, a decreased maximal hydroxyapatite
content and a shift to undermineralized bone was found by mineral dens
itometry of corresponding microradiographs, when compared with age mat
ched femoral heads without bone pathology, These bone mineral changes,
but not transient bone loss, could be the explanation for the more or
less subtle and transient radiolucency in hips affected by bone marro
w edema syndrome, Live trabeculae and active bone formation, however,
paint to increased repair capacity, which seems the key for the sponta
neously reversible course of this syndrome, There is still controversy
whether the bone marrow edema syndrome represents al distinct transie
nt disease or an early reversible phase of avascular necrosis, but bec
ause of the similarities in histopathology reported for early classic
avascular necrosis and bone marrow edema in the literature and in the
authors' own material, a common pathophysiology is discussed for these
seemingly different diseases.