Kl. Bell et al., Intracapsular hip fracture: Increased cortical remodeling in the thinned and porous anterior region of the femoral neck, OSTEOPOR IN, 10(3), 1999, pp. 248-257
It has been shown previously that the anteroinferior cortex is subjected to
maximal tensile stress during a fall onto the greater trochanter. We have
recently shown that in cases of femoral neck fracture, cortical thinning an
d porosity is greatest in the anterior and antero-inferior region of the fe
moral neck. To investigate whether this is due to increased remodeling, we
have quantified surface-based parameters associated with Haversian remodeli
ng in femoral neck biopsies from women with intracapsular hip fracture and
postmortem controls. Cryostat sections of chilled biopsies were reacted for
either tartrate-resistant acid phosphatase (TRAP) or alkaline phosphatase
(ALP) activity. Proportions of active canals were determined in each quadra
nt (inferior, anterior, superior, posterior) of the femoral neck. The biops
ies were then embedded in methacrylate to permit histomorphometry using Gol
dner's and Solochrome sections. In the cases there was no significant incre
ase in the proportion of canals undergoing remodeling in the cortex as a wh
ole (p = 0.846), but the regional distribution of remodeling was markedly d
ifferent from that in the controls. In the anterior cortex, the proportion
of canals undergoing remodeling was increased by 56% (p = 0.0087); in contr
ast there was a relative decrease of 35% in the superior region (p=0.0047).
In the anterior cortex of cases there were 76% and 42% increases in the pr
oportions of eroded (p=0.019) and osteoid-bearing (p = 0.041) canals, respe
ctively. In the superior region, the decrease in the proportion of remodeli
ng sites was due to a marked decrease in canals with an osteoid surface (51
%; p=0.0031). Covariance analysis with cortical porosity as the dependent v
ariable showed that porosity was significantly dependent on the regional di
stribution of eroded (p = 0.033) but not on the distribution of forming (p
=0.153) canals (R(2)adj = 0.51). Cellular levels of TRAP and ALP were signi
ficantly elevated in the anterior region of cases compared with the control
s (TRAP 55%, p=0.006; ALP 36%, p=0.003). For the posterior and inferior reg
ions there were no marked differences in cellular TRAP and ALP levels compa
red with control values. These data show that the increased cortical thinni
ng and increased porosity we have previously observed in the anterior corte
x in cases of hip fracture are associated with increased indices of Haversi
an remodeling. These findings are consistent with the hypothesis that, in c
ases of hip fracture, remodeling imbalance in the anterior cortex is a cont
inuing process up to the time of fracture and is due to increased osteoclas
tic cellular activity associated with an osteoblastic response that is inad
equate to prevent bone loss.