ABSTRACT
Cage layer fatigue (CLF), which is commonly caused by calcium deficiency in the feed, leads to loss of structural bone and increase of bone fragility. In order to investigate the influence of low-calcium diets on bone quality and strength, histopathology, and egg quality, 72 laying hens were randomly allocated to 2 groups at 22 wk of age and received low calcium and control calcium until 34 wk, respectively. Egg production, feed consumption, BW, and egg quality were measured throughout. Bone mineral density, bone biomechanical properties, and histomorphology of femurs and tibias were assessed after birds were sacrificed in 26, 30, and 34 wk. The results showed that low-calcium (1.5%) diets decreased BW, feed consumption, and egg production. The broken eggs rate increased, and the eggshell strength and thickness were lower in treated birds than those in control birds at 30 wk and 34 wk. Femoral and tibial bone index and bone mineral density were lower, cortical thicknesses were thinner, and bone length were shorter over time when birds are in a low-calcium diet than those in control birds. In biomechanical properties, the values of stiffness, Young's modulus, and breaking strength were lower in both femurs and tibias in low-calcium hens at 30 wk and 34 wk than those in bones of control hens. In histomorphology of bone, the cortex turned thinner and there were more cavities in cortex and cancellous bone; the trabecular bone network was fewer, thinner, less cohesive, and generally fragmented; and trabeculae were less well-connected in low-calcium birds. Some cell nuclei in cancellous bone disappeared, and vacuolation was observed in bone cells. There appeared osteoid in cortex bone and cancellous bone in tibias. It was concluded that low-calcium diets could facilitate the development of osteoporosis characterized by an increase of osteoid and loss of structural bone and decrease the values of bone quality and strength, accompanied with a decrease in egg production and egg qualities, which may elucidate the developing mechanism of CLF.