2 research outputs found
Expression of colony-stimulating factor 1 is associated with occurrence of osteochondral change in pigmented villonodular synovitis
Growth hormone treatment prevents osteoporosis in uremic rats
Introduction: Growth hormone (GH) is
responsible for longitudinal bone growth. GH-receptor
in the growth plate was found to be decreased in chronic
renal insufficiency. A therapeutic use of GH in chronic
renal insufficiency is not established. The current study
aims to clarify the effects of GH treatment on bone
metabolism in a uremic rat model. Methods: Sprague
Dawley rats were subjected to subtotal surgical renal
ablation (SNX) or sham operation. SNX rats were
randomized into 4 groups: treated with different doses of
GH (1.5, 4.0, or 10.0 mg/kg) or vehicle after 10 weeks of
uremia and treated for 6 weeks. Bone and renal
morphology was evaluated: bone density, thickness of
spongiosa, osteoblast surface, osteoid volume, osteoclast
quantity, and resorptive volume. Results: GH treatment
resulted in a decrease of resorption area and lower
number of osteoclasts. Osteoid volume, number of
osteoblasts, percentage of active osteoblasts, thickness of
the growth plate and mean cortical width increased. GH
receptor (GHR) protein expression increased in GH
treated rats. IGF-1 expression was decreased in
osteoblasts and chondroblasts of SNX-V rats and
increased following GH treatment. The TGF-ß
expression was down regulated in SNX+V group in
osteocytes and chondroblasts as compared to sham
operated animals. The down regulation was prevented in treated animals irrespective of the dose given.
Conclusions: Treatment with GH in uremic animals
increased bone density to the levels of non-uremic
controls. Thus GH seems to have a potential of
preventing renal osteodystrophy