Epiphyseal Plate Development in the Zinc-Deficient Rat

Abstract

The effect of zinc deficiency on shearing strength, histological changes and proline utilization of the epiphyseal plate of the tibia of the weanling male rat was studied. A diet was fed based on sprayed egg white and containing less than 2 mg of zinc per kilogram. Over 27 day, the force required to displace the epiphysis of the zinc-deficient (ZD) rats was always less than that required for pair-fed (PF) controls. After 18 days, approximately 15% more force was required to displace the epiphysis of the PF rats than was required in the ZD rats. The thickness of the outside compact bone next to the epiphyseal plate region as determined by scanning electron microscopy was thicker in the ZD rats than in the PF controls of comparable age. The epiphyseal plates narrowed as the rats aged, and were clearly discernible in PF controls but not in ZD rats. The incorporation of L-[U-14C]proline into the epiphysis was significantly less in rats deprived of zinc for 16-22 days than in PF controls.

Dietary zinc reduces osteoclast resorption activities and increases markers of osteoblast differentiation, matrix maturation, and mineralization in the long bones of growing rats

“…When pair-feeding was used, the effects of Zn deficiency on bone were attributed to reduced osteoblast modeling activity only [3,38] or in combination with reduced osteoclast numbers [7]. In the present study, stepwise increases in dietary Zn produced incremental differences in metaphyseal trabecularization, consistent with previous comparisons between severely deficient and adequate groups [1,[4][5][6][7]. Here, graded levels of dietary Zn ranged from severely deficient (2.5 μg/g) to adequate (30 μg/g), and normal growth was maintained by 7.5 μg Zn/g diet.…”

“…Later, O'Dell et al [2] (1957) also reported defective hypertrophic chondrocyte proliferation related to low dietary Zn, providing additional evidence for an osteogenic Zn requirement. Bone formation in Zn-deficient animals is characterized by retarded growth plate activity [3][4][5][6] and is associated with reduced cancellous and trabecular volume [3,7,8]. The biophysical consequences of these events include decreased longitudinal and radial expansion of long bones, with increased susceptibility to breakage due to applied physical stress [3,9,10].…”

Zinc deficiency negatively affects alkaline phosphatase and the concentration of Ca, Mg and P in rats

“…In addition, Zn deficiency weakens protein synthesis (Giugiano & Millward, 1987), making Zn an essential factor for the synthesis of proteins (Hendy et al, 2001). Also, Zn is known to be necessary for normal collagen synthesis and mineralization of bone that has been demonstrated to be essential for normal growth of both human and animal skeletal systems (Bougle et al, 2004; Doherty et al, 2002; Eberle et al, 1999; Elmstachl et al, 1998; Hosea et al, 2004; Hyun et al, 2004; Ovesen et al, 2001; Peretz et al, 2001; Rossi et al, 2001; Seco et al, 1998; Suwarnasarn et al, 1982;). It therefore has been considered that Zn can be a critical factor to affect skeletal development and bone formation.…”

Moderate zinc deficiency negatively affects biomechanical properties of rat tibiae independently of body composition☆

“…Zinc (Zn) is a dietary essential trace mineral known to be necessary for normal collagen synthesis and mineralization of bone [1,2]. Zn has been demonstrated to be essential for normal growth of both human and animal skeletal systems [3][4][5][6][7][8][9][10][11][12].…”