Osteoporosis in Cage Layers

Osteoporosis (Caged Layer Fatigue) is a condition which manifests itself in several clinical signs. There is leg weakness and sometime paralysis. Affected birds are unable to stand and usually to move to the back area of the cage. They often fall onto their sides with leg outstretched. Birds which live for several days after going down may dehydrated or emaciate and are out of production. Although affected birds initially are alert and can continue to eat, they generally die from dehydration and starvation since they may not be able to reach a water or food source.

What is Caged Layer Osteoporosis?

Osteoporosis means literally 'porous bone', where the strong lattice-like structure of bone (comparable to a sponge like structure) thins and becomes literally porous and open, more like lace.

BONE REABSORPTION IS GREATER THAN BONE DEPOSITION

Egg-laying and the hen's bone structure:

Laying hens become sexually mature and therefore capable of laying eggs at bout 16-18 weeks. Before this time, they may be reared either in cages or in floor. In cage systems, the pullets transferred to cages where they remain for the whole of their laying life. The hens lay almost continuously from typically 20 weeks to 72 weeks of age and a high-producing modern laying hen can lay 310 eggs per year. The whole process of producing an egg takes a hen at least 24 hours. The shell deposited onto the egg in the uterus, where epithelial cells secrete calcium salts which bond to the egg membrane. Calcium carbonate is the major constituent of egg shells. By 72 weeks of age (known as 'end of lay') the egg production of the unit as a whole has fallen to about 70% of its theoretical maximum. The whole unit is then 'depopulated' and the 'spent hens' transported to the slaughterhouse.

The skeleton of a hen consists of structural bone (cortical and trabecular bone) which provides mechanical strength and supports the muscles, and a type of medullary (inner) bone special to birds, which has little mechanical function but acts as a reserve of calcium needed to form egg shells. The hen's medullary bone is formed just before the onset of sexual maturity and the start of egg laying and this coincides with a marked reduction in the volume of trabecular bone (the internal supporting framework of structural bone). 98% of body calcium and 80% of body phosphorus is present in the hen's skeleton, in the form of the mineral calcium hydroxyphosphate, which gives bones their strength and also acts as 7 a mineral reserve.

Calcium and phosphorus are each necessary for the absorption and utilisation of both of them from the diet and vitamin D3 is also necessary as it controls the absorption of calcium through the production of calcium binding protein. These nutrients should be provided in adequate quantity in the hen's diet. It is quite normal for high-producing hens to use the calcium reserves in their bones to produce egg shells.

Egg-shell formation is most intense in the period of darkness when the hen does not eat. She therefore has to use calcium from the medullary bone, by a process of resorption. When this process leads to disease, it is because the medullary bone has become depleted of calcium and the hen starts to break down the structural bone to use the calcium for the formation of egg shell and to replenish the minerals in the medullary bone. The result is a serious decrease in the amount of structural bone and the hen's skeleton becomes thin and brittle.

Nutritional Effects on Bone:

Normal bone growth/maintenance cannot occur without sufficient dietary intake of calcium and phosphate salts.
Calcium and phosphate are not absorbed in the intestine unless the hormone calcitriol is present. Calcitriol synthesis is dependent on the availability of the steroid cholecalciferol (Vitamin D) which may be synthesized in the skin or obtained from the diet.
Vitamins C, A, K, and B₁₂ are all necessary for bone growth as well.

Hormonal Effects on Bone:

Growth hormone, produced by the pituitary gland, and thyroxine, produced by the thyroid gland, stimulate bone growth.
- GH stimulates protein synthesis and cell growth throughout the body.
- Thyroxine stimulates cell metabolism and increases the rate of osteoblast activity.
- In proper balance, these hormones maintain normal activity of the epiphyseal plate
At puberty, the rising levels of sex hormones (estrogens in females and androgens in males) cause osteoblasts to produce bone faster than the epiphyseal cartilage can divide. This causes the characteristic growth spurt as well as the ultimate closure of the epiphyseal plate.
Estrogens cause faster closure of the epiphyseal growth plate than do androgens.
Estrogen also acts to stimulate osteoblast activity.
Other hormones that affect bone growth include insulin and the glucocorticoids.
- Insulin stimulates bone formation
- Glucocorticoids inhibit osteoclast activity.
Parathyroid hormone and calcitonin are 2 hormones that antagonistically maintain blood [Ca²⁺] at homeostatic levels.
- Since the skeleton is the body's major calcium reservoir, the activity of these 2 hormones affects bone resorption and deposition.

Calcitonin:

Released by the C cells of the thyroid gland in response to high blood [Ca²⁺].
Calcitonin acts to "tone down" blood calcium levels.
Calcitonin causes decreased osteoclast activity which results in decreased break down of bone matrix and decreased calcium being released into the blood.
Calcitonin also stimulates osteoblast activity which means calcium will be taken from the blood and deposited as bone matrix.

Calcitonin Negative Feedback Loop:

Parathyroid Hormone:

Released by the cells of the parathyroid gland in response to low blood [Ca²⁺]. Causes blood [Ca2+] to increase.
PTH will bind to osteoblasts and this will cause 2 things to occur:
The osteoblasts will decrease their activity and they will release a chemical known as osteoclast-stimulating factor.
Osteoclast-stimulating factor will increase osteoclast activity.
PTH increases calcitriol synthesis which increases Ca²⁺ absorption in the small intestine.
PTH decreases urinary Ca²⁺ excretion and increases urinary phosphate excretion.

Risk Factors for Osteoporosis:

Although the development of osteoporosis in birds is primarily related to

Aging
Genetic factors
Female sex
30 to 60 percent of cases of osteoporosis are associated with one or more secondary risk factors
Low calcium diet
Vitamin D₃ deficiency
High fiber diet
High protein diet
High blood homocysteine
Weight loss
Stress - Stress produces cortisol.
Too much sodium
Phosphorous imbalance

Causes of Osteoporosis:

Lack of estrogens

Declining estradiol levels in birds more strongly correlated with decreasing bone density than are declining testosterone levels.

Low level of androgens

Androgens required for developing peak bone mass and maintaining bone mass. Testosterone levels gradually decline with advancing age, but low levels in mature stage have not been found to correlate with low bone density.

Lack of exercise:

There is overwhelming evidence that the restriction of movement is the most important reason why the bones of caged hens are so fragile compared to hens in non-cage systems.

The caged hens took 72 steps an hour. The effect of increased exercise can be almost immediately beneficial that the only treatment for osteoporosis in its early stages is to remove hens from their cages.

Inadequate intake
Lack of vitamin D₃
Husbandry system and primarily the housing
High productive demands on modern laying hens
Enteric Disease condition (Digestive absorption problems)
Liver or thyroid problems
The development of bone strength:

An important cause of osteoporosis in laying hens seems to be that caging damages the normal process of developing the bone structure of the still growing pullets. It is well known that the mineralized bones of hens are depleted during their laying lives, so it should be seen as particularly

important that they can lay down enough bone during the rearing and growing period.

The structural bones of hens in lay have little or no osteoid (a collagenous material necessary for bone growth) and so they have little ability to form structural bone. However, modern layers are bred for early sexual maturity and they are not at their maximum adult body weight and development when they start laying.

When pullets are put into cages at the time of sexual maturity, this may inhibit them from developing sufficiently strong bones to withstand the inevitable calcium depletion that happens during their laying lives. There may even be a critical period in a hen's bone development, from sexual maturity to about one year, when exercise is particularly beneficial and lack of exercise particularly detrimental. "Placing pullets in cages prevents the skeletal system from developing sufficient strength to allow a gradual decrease in bone mass during the laying period and still remain strong enough to prevent shattering in the processing plant."

An egg a day - the demands of high productivity:

The output of eggs demanded from a laying hen has approximately doubled over the last half century and now stands at over 300 in the usual laying period of 52 weeks. This means that modern hens have few non-laying days. It is obvious that the high egg production puts great demands both on a hen's reserves of calcium and on her calcium metabolism. But once again we have to remember that only caged hens suffer from osteoporosis. Hens in non cage systems may lay as much as 97% of eggs laid by caged hens but still have stronger bones.

The high productivity, however, likely to contribute to the problem of brittle bones, because the hen has to provide calcium for the egg shells. In normal conditions about 40% of the calcium required for egg shells will come from her medullary bone but continuous egg-laying can also result in depletion of structural bone. Attempts to boost the hen's physiological machinery by feeding extra minerals have come up against the fact that there is a physiological limit to the amount of calcium and phosphorus that birds can absorb. The reality is that even with the best diet the high-producing hen's metabolism may not be able to keep up with the dual demand of egg shell production and bone maintenance. A hen has to move calcium from the blood to the egg at a rate of 115-130 mg per hour, so that she needs a complete turnover of blood calcium over 12 minutes.

Study found that calcium uptake from the intestine actually decreases quite rapidly when hens have been in lay about 4 months, but it increases again if they are given a rest from egg production by moult. Resting hens by moult after their normal laying cycle of 52 weeks has also been found to increase hens' bone strength quite significantly when they re-start laying, even 8 months after they would normally be considered to be 'spent'. The fact that a hen's health can be improved by a rest from laying confirms that long periods of laying are detrimental to a hens's bones and suggests strongly that laying hens are being worked beyond their physiological limit.

Diet, nutrition and breeding:

Improvement through breeding, since some individual hens are able to produce a large number of eggs and keep healthy bones or through improved nutrition during the hen's rearing period. A limited improvement in calcium uptake or bone strength has been achieved by feeding dietary supplements such as oystershell, 1,25-dihydroxyvitamin D₃ and 1α-hydroxyvitamin D₃ and carbonated water (Sodium-bicarbonate) during times of high temperature.

However, the scientific consensus that improved nutrition has little effect on slowing the loss of structural bone during the laying period and this bone loss that leads to osteoporosis. Consistently good nutrition is, however, essential for minimizing the impact of the disease on the hens.

Signs

Lameness.
Soft bones and beak.
Birds go off legs.
Drop in production.
Soft-shelled eggs.
Enlarged hocks.
Birds rest squatting

Pahtogenesis:

Metabolic Bone Disorder. Cage Layer Osteoporosis - Image 1

Post-mortem lesions:

Bones soft and rubbery
Epiphyses of long bones enlarged
Beading and fracture of ribs
Soft beak
Parathyroids enlarged

Treatment:

Treatment involves:

Correcting the diet as soon as possible before the bone deformities become too severe to be reversed.
Adjust the ration to fit the age and performance level of flock. If ration has been deficient in vitamin D₃, give Calcium with vitamin D₃ preparations like Calcicare or Merical or Solucal double the usual amount for a period of 1-2 weeks. (Remember, birds can only utilize vitamin D₃ not other forms of vitamin D packaged for mammals).
Vitamin AD₃EC and B-complex through drinking water.
Placing birds on a commercial diet designed for that age and species of bird
Supplementing the feed with calcium for example top-dressing the feed with dicalcium/phosphate or shell grit etc.
It is generally safe to assume that if the birds are developing rickets on a home-formulated diet, then they likely have other vitamin/mineral dietary problems as well, and so supplementation with multi-vitamin mineral packs may be helpful.
Proper diets are critical to raising healthy birds. Resist the temptation to buy cheap scratch grains and whole corn. Your investment in properly formulated and well balanced diets will pay dividends in good growth and healthy birds.

Control:

Feed a balanced ration with a adequate calcium, phosphorus and vitamin D₃. Chemical antioxidants (santoquin, ethoxyquin,BHT) can be added to help preserve the vitamin D₃. Rations should be carefully compounded to fit the age, purpose and performance of the flocks.
Provide oyster shell or course limestone free choice as a supplemental source of calcium.

Prevention of osteoporosis:

Prevention measures should aim at ensuring proper development of the structural skeleton (cortical and trabaculla bone) and medullary bone before the onset of egg production and the availability of dietary calcium, phosphorus and vitamin D₃.

Ensure the normal weight-for-age of pullet at sexual maturity. Underweight pullet should not be light stimulated to bring them into egg production. Underweight hens have smaller appetite which leads to reduced nutrient intake. Also the structural mass of the skeleton (trabecula and cortical bone) may not be fully developed in the early maturity, underweight birds, and this makes the bones more prone to osteoporosis.
Starting at two weeks before the anticipation of egg production, the hen must be fed layer ration to ensure proper development of medullary bone. The ration must contain 4% calcium, 0.45% available phosphorus and vitamin D₃ 500 IU per Kg. Avoid a feeding a high calcium diet for too long before the start of egg production, as this may cause damage of kidney.
Because the most intense calcification of egg shell occurs during the dark period, feeding the birds just before the next dark period will provide dietary calcium during egg shell formation.
Avoid the use of finely ground calcium particles. If finely ground particles (eg. Limestone or oystershell) are mixed with coarsely ground grain particles, the birds will pick up the large grain particles, leaving the fine calcium particles.
The use of coarsely ground calcium particles (larger than 0.75 mm) may help provide dietary calcium during the dark period. Some of the large particles are retained in the gizzard and passed to the intestine during the dark period.
Care must be taken to avoid the separation of calcium particles during the manufacture, delivery or feeding. This separation can take place in feed mash, especially if calcium particle size is rather large, leading to reduced calcium intake by the birds.
Starting at peak of egg production, the hens may be provided once or twice a week with additional calcium in the form of coarsely ground oystershell or limestone at the rate of 10 Kg per ton. Oystesrshell or limestone grit can be sprinkled on the feed in feeders. Supplementation of additional calcium should be continued for four months.
Provide good management, avoid adverse environmental conditions in the house, and the keep the birds healthy in order to maintain good feed consumption.
Maintain proper stocking density of cages.