scholarly journals Ankle Height Preservation with the Hind Foot Nail and Iliac Crest Bone Blocks in Patients with Sequelae of Partial or Complete Talus Bone Loss

2021 ◽  
Vol 15 (3) ◽  
pp. 91-98
Author(s):  
Gunasekeran C ◽  
Bhowmick K ◽  
Ramasamy B ◽  
Jepegnanam TS
Keyword(s):  
Bone Loss ◽  
Iliac Crest ◽  
Hind Foot

Prednisone-induced osteopenia in beagles: variable effects mediated by differential suppression of bone formation

1992 ◽  
Vol 263 (1) ◽  
pp. E136-E141 ◽  
Author(s):  
L. D. Quarles
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Iliac Crest ◽  
Matched Control ◽  
Prolonged Treatment ◽  
Normal Male ◽  
Dihydroxyvitamin D ◽  
Prednisone Treatment ◽  
Histological Abnormality ◽  
Dynamic Interplay

To examine the mechanism of glucocorticoid-induced osteopenia and the basis for variable bone loss after glucocorticoid administration, we gave prednisone (1.3 mg.kg-1.day-1) to normal male dogs (n = 15) for 29 wk to attempt induction of osteopenia. Compared with age-matched control dogs (n = 14), prednisone treatment rapidly decreased spinal bone density by 4.3%, as assessed by quantitative digital radiography, and reduced trabecular bone volume by 14.6%, as measured by quantitative histomorphology of iliac crest bone specimens. Bone loss was attenuated in prednisone-treated dogs after prolonged treatment (greater than 12 wk). Prednisone treatment resulted in diminished bone formation rates (15 +/- 3.4 vs. 47 +/- 4.5 microns/yr) and activation frequency (0.4 +/- 0.1 vs. 1.3 +/- 0.2/day). These findings indicate that suppression of osteoblastic function and recruitment is the primary histological abnormality mediating glucocorticoid-induced osteopenia in beagles. In contrast, prednisone administration had no effect on bone resorption or serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D, which suggests that these factors are not essential for prednisone-induced bone loss. Moreover, 33% of beagles were totally resistant to glucocorticoid-induced osteopenia. Such heterogeneity of bone loss was associated with variable suppressive effects of prednisone on osteoblastic function, as evidenced by greater bone formation rates and activation frequency in prednisone-resistant animals. Collectively, these observations suggest that glucocorticoid-induced bone loss results from a dynamic interplay between steroid-mediated suppression of osteoblastic function and recruitment and undefined compensatory factors that ameliorate the effects of glucocorticoids on osteoblastic precursors.

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