An ultrastructural study was carried out to investigate effects of initial osteoclastic bone resorption on the repair process after cortical bone defect. In the present study an incomplete defect was made in the tibial shaft of rats
using
a bone saw, and the repair process thereafter histologically examined under two conditions, When indomethacin, one of prostaglandin inhibitors, was administered dailyat a dose of 2mg/1kg/day. For the other condition, acetazolamide,
one
of
carbonic anhydrase inhibitors, was administered daily at a dose of 15mg/100g/day. The animals were sacrified at 2, 4, 7 and 14 days after bone defect. The tibial bones were extirpated and examined by light, scanning and trasmission
electron
microscopy.
@ES The results were summarized as follow:
@EN In the control groups,. on day 2, hemorrhage and a lose mesenchymal cell proliferation were observed in the room of bone defect. the osteoblasts converted from a flattened to a stellate shape and contracted. and then the bone
matrix
was
exposed. Osteoclastic bone resorption was often noticed in the cortical bone near the defect. With the advancement of repair after day 4. endosteal callus was formed and was maturing. On day 14, almost complete healing was
accomplished.
In the indomethacin group, on day 2, the osteoblasts did not observed shape change, and osteoclastic bone resorption was inconspicuous. With the advancement of repair after day 4, repair reaction was delayed on the endosteal surface
just
around the defect compared with that in the control. The new bone trabeculae were immature and bone marrow formation was observed in a small number of new trabeculae at 14 day after bone defect.
In the acetazolamide group, the osteoblasts converted from a flattened to a stellate shape and contracted, and then the bone matrix was exposed. Osteoclastic bone resorption, was minimal in the coritcal bone near the defect. The repair
reaction
was
also delayed compared with that in the control.
The results suggest that osteoclasts participate in bone repair mechanism by liberating some bone inductive factors normally burried in bone matrix, to trigger new bone formation. The prostaglandins may be important local factor for
induction
of bone repair process after fraculre.
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