Tibial Dyschondroplasia in Chickens: Symptoms, Causes and Treatment

Tibial dyschondroplasia results from failure of the growth plate cartilage to vascularize and mineralize properly, leaving behind a structurally weak plug of avascular fibrocartilage.

• Rapid growth rate: Fast-growing broiler genetics create demand for rapid bone elongation that can outpace normal growth plate maturation. The growth plate is under maximum mechanical stress during peak growth periods.
• Calcium:phosphorus imbalance: The optimal Ca:P ratio for bone development is approximately 2:1. Excess phosphorus relative to calcium, or calcium deficiency, impairs cartilage mineralization and predisposes to TD.
• Vitamin D3 deficiency: Vitamin D3 is essential for intestinal calcium absorption and growth plate cartilage differentiation. Deficiency produces a clinical picture overlapping with TD and rickets.
• Chloride excess from feed acidifiers: High dietary chloride (from ammonium chloride or other acidifiers added to reduce urinary tract infections) acidifies the blood, impairing the alkaline environment needed for bone matrix mineralization. This is the most documented nutritional cause of TD in commercial broilers.
• Mycotoxins: Some Fusarium mycotoxins disrupt growth plate chondrocyte function and have been associated with increased TD incidence.

TD is confirmed by the characteristic gross finding of a white or translucent plug of cartilage in the proximal tibiotarsal growth plate at necropsy.

• Clinical signs: Bowing or twisting of the lower leg in 2-6 week old fast-growing birds. The deformity is progressive and most visible when viewing the bird from behind while standing.
• Necropsy: Section the tibia longitudinally to reveal the growth plate. TD presents as a white, waxy, avascular cartilage plug extending into the metaphysis. Normal growth plate cartilage is thin and pink-vascular.
• Differentials: Rickets (soft, rubbery bones throughout, not just growth plate plug), perosis/slipped tendon (tendon displacement without growth plate lesion), Mycoplasma synoviae arthritis (joint swelling with exudate, no growth plate lesion).

Established TD lesions in broilers are generally not treatable at flock level. Management is directed at reducing incidence in future flocks through nutritional correction.

Dietary correction for affected flocks: Adjust calcium to 1.0-1.1% (starter phase), phosphorus to 0.45-0.50% available phosphorus, and verify calcium:phosphorus ratio is 2:1. Supplement vitamin D3 to 2,000-4,000 IU/kg if deficiency is suspected.

Reduce dietary chloride: If ammonium chloride or other chloride-containing acidifiers are in the diet, reduce or eliminate them. Target dietary cation-anion balance (Na + K - Cl, in mEq/kg) of 250-300 mEq/kg.

For individual pet birds: Rest, soft bedding, and nutritional correction are supportive. Surgical intervention is not practical for broiler-class birds but may be considered in valuable breeding birds.

• Formulate starter diets with Ca:P ratio of 2:1 and verify available phosphorus is at target (0.45-0.50%). Have feed tested if TD incidence is elevated in a flock.
• Use vitamin D3 at 2,000-4,000 IU/kg in starter feed. Avoid vitamin D2 (ergocalciferol) as poultry utilize D3 (cholecalciferol) far more efficiently.
• Avoid excessive dietary chloride from acidifiers. Monitor the dietary cation-anion balance and target 250-300 mEq/kg.
• Consider feed restriction programs (skip-a-day or 6-hours-off) in fast-growing broiler breeds during weeks 1-3. Slower growth rate reduces mechanical stress on developing growth plates.
• Test feed for Fusarium mycotoxins (DON, fumonisin) if TD incidence rises despite correct nutrition. Mycotoxin binders may reduce TD rates in mycotoxin-challenged flocks.