Osteopontin and calbindin gene expression in the eggshell gland as related to eggshell abnormalities.

Eggshell quality is a major concern to the poultry industry: eggs with poor-quality shells hatch poorly and are rejected in the processing plant. The eggshell gland (ESG) proteins and the matrix proteins, which participate in crystallization, fulfill important functions during formation of the calcified tissues and contribute to the biomechanical properties of the mature product. We selected layers that consistently produced eggshells with specific abnormalities, and continued to do so after molting, and evaluated the expression of 2 genes-osteopontin (OPN) and calbindin-as related to particular eggshell abnormalities. These genes are synthesized by the ESG and appear to participate in the calcification process. When the ESG produces normal eggshells, OPN was expressed uniformly by all of the epithelial cells facing the lumen, and calbindin was expressed by the glandular epithelium. In contrast, in the layers producing pimpled eggs, OPN was expressed only in sections of the pseudostratified epithelium, separated by areas of cells devoid of OPN gene expression, whereas calbindin was expressed at much greater levels throughout the glandular epithelium. Almost no OPN gene expression was observed in the ESG of layers producing corrugated shells, but their pattern of calbindin expression was similar to but somewhat greater than that in ESG that produced normal eggshells. In cases in which eggs had cracks at the sharp or blunt poles, OPN was expressed only at the side opposite to the cracks, whereas calbindin was expressed at both sides equally independent of the cracks. The results suggest that synthesis of the proteins associated with the formation of eggshells with the various abnormalities is controlled by different mechanisms. This may imply that more than 1 strategy will be required to improve eggshell quality.

Egg shell quality responses of pullets given saline drinking water at different ages.

1. Saline drinking water given to pullets before sexual maturity had no effect on their subsequent egg shell quality. 2. Hens receiving saline drinking water from or after laying their first egg produced significantly more egg shell defects than hens receiving town water. 3. The production of eggs with defective shells occurred more rapidly when saline drinking water was given to 40-week-old hens than to hens during the first few weeks of lay. 4. The high incidence of egg shell defects resulting from the use of saline drinking water was reduced to control levels when hens in early lay were given town water for 5 weeks. This response was not observed with 40-week-old hens.

Responses in egg shell quality to sodium chloride supplementation of the diet and/or drinking water.

1. Supplementing the drinking water of 50-week-old laying hens with sodium chloride (NaCl) concentrations between 0.5 and 2 g/l for 7 weeks significantly increased the incidence of egg shell defects and significantly decreased egg shell quality. Dietary NaCl concentrations between 0 and 2 g/kg had little effect on this response. 2. At similar total NaCl intakes egg shell defects were much greater when the NaCl was obtained from the drinking water rather than from the diet. 3. Hens producing eggs with defective shells as a result of receiving saline drinking water failed to recover the ability to lay eggs with good shells after 8 weeks on normal water. 4. The increased incidence of shell damage was not related to decreased food intake or increased egg weight or production.

Physiological changes associated with the production of defective egg-shells by hens receiving sodium chloride in the drinking water.

1. Supplementing the drinking water of laying hens with 600 or 2000 mg sodium chloride/l induced large increases in egg-shell defects without corresponding changes in egg production, egg weight or food and water intakes. A supplement of 2000 mg NaCl/l resulted in a high incidence of shell-less eggs. 2. The increased incidence of egg-shell damage in hens receiving the NaCl was associated with a decrease in egg-shell quality measured objectively. These responses persisted even after the NaCl was removed from the drinking water. 3. The NaCl treatment had little effect on blood acid-base balance and electrolytes, but significant reductions were observed in the carbon dioxide tension, and bicarbonate and calcium concentrations in the fluid surrounding the egg in the shell gland. 4. The poor shell quality appeared to be associated with a reduced supply of bicarbonate, rather than with an effect on Ca, in the lumen of the shell gland, although a reduced residence time of eggs in the shell gland may also have contributed to the problem.

The relation between sodium chloride concentration in drinking water and egg-shell damage.

1. A significant linear increase in egg-shell defects from 60-week-old laying hens, and corresponding significant linear decreases in various egg-shell-quality measurements, were observed in response to increasing concentrations of sodium chloride in the drinking water, to the maximum concentration of 600 mg/l used in the present study. 2. The incidence of damaged egg shells was increased 3-fold by including NaCl in the drinking water at a concentration of 600 mg/l. 3. Shell defects declined when birds were placed on normal water for 5 weeks but were still 1.4- to 2.1-fold greater than control values. 4. After an induced rest from lay on normal water, shell defects were still 1.3- to 3.2-fold greater in birds which had previously received the NaCl in the drinking water. 5. The increased incidence of shell damage was not related to decreased food intake or increased egg weight or production.