The new broiler lines exhibit very rapid growth mainly due to genetic progress, improved nutrition, facilities, and biosecurity and health measures. All these factors have undergone considerable modernization in recent years. In addition, the chicken’s center of gravity has shifted forward due to selective breeding, especially for a higher proportion of breast muscle development.
These factors, along with others described in this article, influence the appearance of locomotor problems in broiler chickens.
These problems usually occur between the second and third week of the animal’s life, but may occur before or after this period.
In commercial laying hens, we must also focus on bone quality, as proper development will significantly influence eggshell quality and, therefore, the percentage of marketable eggs. Moreover, we must avoid problems such as cage layer fatigue, caused by excessive and premature wear of the structural bone.
As is known, bone grows from a cartilaginous growth plate, and its synthesis and resorption are regulated by the hormones calcitonin and parathyroid hormone. By examining this growth plate, we can identify certain problems affecting our animals.
For proper bone growth, adequate supplies of calcium, phosphorus, and magnesium are necessary, as well as trace elements such as copper, zinc, and manganese.
In addition, vitamin D3, which is a pre-hormone, regulates the absorption of phosphorus and calcium. This pre-hormone must be activated first in the liver and then mainly in the kidney to become the active metabolite.
Femoral Head Necrosis
emoral head necrosis is the most common infectious cause of lameness in broilers, responsible for approximately 60% of all cases.
Bacteria can enter the bloodstream through multiple routes: via the yolk sac if the infection comes from breeders or bacteria “leak” into the incubator, through the skin due to small cuts or scratches, through inhalation, or from the birds’ own intestines due to oral–cecal infection.
Once in the bloodstream, these bacteria can become trapped in the small blood vessels within the bone of the joint, causing infection and reducing bone quality.
Femoral head necrosis is mainly caused by Escherichia coli, Staphylococcus spp., and Enterococcus spp. Other bacteria may be involved, but rarely. The infection can be transmitted vertically.
Rickets
Rickets results from deficiencies in macromineral intake, causing several alterations that can be observed on the farm or during necropsy.
Rickets due to calcium or vitamin D3 deficiency causes macroscopic changes in bone structure. These bones present two completely distinguishable growth areas: the proliferation zone and the hypertrophy zone. In a normal bone, these zones are balanced. When animals suffer from a calcium or vitamin D3 deficiency, the proliferation zone is thickened.
Rickets due to phosphorus deficiency shows thickening of the hypertrophy zone.
Tibial dyschondroplasia is defined as a defect in the development of the growth plates, characterized by abnormal whitish cartilage masses beneath the growth plates of long bones.
In young animals with phosphorus-deficiency rickets, ossification is inadequate, making the bones easily bendable—commonly referred to as “rubber bones.” Causes include dietary phosphorus deficiency, incorrect phytase dosing, denaturation due to high pelleting or extrusion temperatures, or poor mixing homogeneity in the feed.
Tibial Dyschondroplasia
This condition can be detected easily in the tibia during necropsy but may also appear in the femur and humerus. It produces lameness and can also result in fractures. Causes include genetic factors, rapid growth in broilers, incorrect vitamin D3 metabolism, or feed contamination with mycotoxins. It is closely related to low calcium levels and zinc deficiencies.
Spondylolisthesis and Spondylitis
Spondylolisthesis is the displacement of one vertebra over the next. It is not infectious and is rare.
Spondylitis appears between the second and fifth week of age. It is a lumbar abscess that affects the bird’s mobility.
In the early phase (17–22 days), affected birds show lameness and sometimes tenosynovitis. From the fourth week, the late phase is characterized by birds with difficulty walking, legs spread in a “V” position, and sitting on their rear in a distinctive posture—known as “motorcycle chickens.” This condition quickly spreads through the flock, causing high variability.
It is attributed to Enterococcus, Streptococcus, and Staphylococcus species, and is often related to poor incubator hygiene or excessive numbers of dirty eggs.
Perosis (Chondrodystrophy)
Perosis occurs in young birds whose diets lack manganese, choline, niacin (B3), pyridoxine (B6), biotin (B7), or folic acid (B9).
It is a deformation of the leg bones in chicks due to delayed growth of long bones, with deformity of the tibiometatarsal joint. On the farm, affected birds show a typical prostrate position with one leg fully extended.
Malabsorption Syndrome
This multifactorial disease affects young birds and is caused by a combination of certain infectious agents—mainly reoviruses—along with environmental factors. It is closely linked to poor early growth (cold stress, lack of essential nutrients, etc.).
Affected flocks show low weight gain, unevenness, lameness, diarrhea, and poor feathering, characterized by wing feathers pointing forward (“helicopter feathers”).
Black Bone Syndrome
This syndrome is characterized by black discoloration of cooked bone and adjacent tissue, leading to consumer rejection. It is common in fast-growing broilers because bones must form in a short period and mineralization can be insufficient.
Storage temperature also influences its occurrence; frozen cuts tend to show higher incidence.
Other Causes of Lameness
Vitamin B6 (pyridoxine) deficiency, essential for sulfur amino acid metabolism, can cause lameness with inward (varus) or outward (valgus) leg curvature. Joint infections such as Mycoplasma synoviae, Staphylococcus spp., or articular gout (often due to excess dietary protein) can also cause lameness.
Bone Health in Commercial Layers
In layers, regular monitoring of bone health is important. Necropsies may reveal keel bone defects, such as an “S”-shaped curve. If not corrected promptly through diet adjustments, layers may develop cage layer fatigue. This occurs when hens use structural bone reserves to supply part of the daily calcium requirement for eggshell formation. Once medullary bone reserves are exhausted, hens begin to deplete structural bone, leading to premature exhaustion and recumbency.
It is important to note that structural bone always contributes a small amount of minerals, meaning it weakens gradually. For this reason, it is essential to maintain structural bone mineral reserves at high levels.
When minerals from medullary bone (mainly calcium and phosphorus) are mobilized, calcium can be used for eggshell formation, but phosphorus is excreted in urine. Therefore, an extra phosphorus supply is crucial, especially in the morning, after egg-laying.
