The aim of this study was to evaluate a novel animal model
of bisphosphonates-associated osteonecrosis, which realistically
recapitulates the same pathological human
condition. Five Wistar rats were given intravenous zoledronic
acid 0.04 mgonce a week for 5 weeks. After 2 weeks,
the animals underwent the extraction of an upper molar,
producing a 4 mm-diameter bone defect on the same site.
After 7 weeks from the extraction, the animals were clinically
examined and a bone scintigraphy was carried out.
After an additional week, the rats were killed and both
Computerized Tomography and histological analysis were
performed. Five rats, not treated with zoledronic acid and
exposed to the same surgical treatment, were used as
controls. At 7 weeks after the extraction, all the rats
treated with zoledronic acid showed expansion of the defect
and bone exposure. These features were confirmed by
bone scintigraphy. The rats of the control group demonstrated
epithelialization of the bone defect and a normal
uptake of the contrast medium during the scan. The
Computerized Tomography scan disclosed irregularity of
the cortical margin and bone destruction, which were not
evident in the control group. On microscopy, the samples
showed necrotic bone, loss of osteocytes and peripheral
resorption without inflammatory infiltrate, while the
controls showed normal bone healing. The rat treated with
zoledronic acid can be considered a novel, reliable and
reproducible animal model to understand better the
pathophysiology of osteonecrosis of the jaw and to develop
a therapeutic approach.
