sodium-acetate--anhydrous and Bone-Diseases--Metabolic

Sodium acetate reportedly promotes bone atrophy by inducing resorption and inhibiting osteoprogenitor-cell proliferation, but little is known about its effects on bone-matrix deposition and mineralization by a population containing osteoprogenitor cells. The objective here was to assess the effects of 1-20 mM sodium acetate on the proliferation and differentiation of these cells and their resultant bone-nodule formation and mineralization in an in vitro assay. Exposure to 10 mM sodium acetate had no effect on cellular proliferation but significantly increased the production and mineralization of bone nodules (p < 0.01), suggesting that it affected osteoprogenitor differentiation and subsequent metabolism. However, 10 mM acetate did not increase net bone mass. Dilutions of 1-5 and 20 mM inhibited cellular proliferation and resultant bone-nodule formation and mineralization, significantly reducing the percentage bone area as compared to controls (p < 0.001). These data suggest that 1-5 and 20 mM sodium acetate significantly inhibit bone deposition, whereas 10 mM has no effects, which could contribute to iatrogenic metabolic bone disease in patients receiving either renal dialysis or total parenteral nutrition.

Topics: Analysis of Variance; Animals; Bone Diseases, Metabolic; Bone Matrix; Bone Resorption; Calcification, Physiologic; Cell Differentiation; Cell Division; Culture Techniques; Dose-Response Relationship, Drug; Female; Hemodialysis Solutions; Iatrogenic Disease; Osteoblasts; Osteogenesis; Parenteral Nutrition, Total; Rats; Rats, Sprague-Dawley; Renal Dialysis; Sodium Acetate