Dyschondroplasia in poultry

A number of different skeletal disorders cause considerable welfare and production problems in commercial poultry production.Laying hens suffer from a generalized loss of structural bone mass characteristic of osteoporosis.In growing birds of meat-type strains, which have been selected over the past 50 years for fast growth, the most common skeletal defects occur in leg bones and joints.The welfare problem of broiler leg deformities was highlighted in a report of the Farm Animal Welfare Council (1992).Leg-bone deformities, frequently categorized under the heading of 'leg weakness', have been a cause for concern in the broiler industry for very many years.Many pathologies have been described but, despite much research, problems are still widespread.Research has been successful in identifying and eliminating some causes, such as chondrodystrophies caused by simple nutrient deficiencies.However, the types of problem that remain have grown in importance to the point that they are now seen as major causes of poor welfare for birds, as well as lost production for producers.Developmental disorders are characterized by angular and rotational deformities of the leg bones and are seen in both broilers and turkeys.They are typified by hock joint distortions commonly known as varus or valgus deformity.These distortions of the long bones and the joints may, in turn, lead to secondary soft tissue pathologies.Dyschondroplasia is the most commonly observed lesion in the bones of broilers showing these defects.It is usually referred to as tibia1 dyschondroplasia (TD) because it most severely affects the proximal tibia, which is the fastest-growing bone in young broilers, and has been shown to be a direct cause of clinical deformity and lameness (Lynch et al. 1992). CHARACTERISTICS OF TIBIAL DYSCHONDROPLASIAThe normal process of endochondral bone formation in the long bones of chickens involves growth plate chondrocytes passing through an orderly series of well-defined stages.Chondrocytes from the resting or reserve zone first commence proliferation to form a columnar zone of flattened cells.They then alter their phenotype as they start to differentiate into hypertrophic chondrocytes.In doing so, they first start to enlarge to form a zone of prehypertrophic chondrocytes which then secrete a matrix containing type X collagen as they mature to become fully hypertrophic.Mineralization starts within the matrix, capillary invasion occurs and bone formation takes place.The TD lesion takes the form of a plug of avascular cartilage underlying the bone growth plate.It is made up of an accumulation of prehypertrophic chondrocytes and can vary considerably in size from a small focal accumulation in one part of the growth plate to a large mass occupying the full width of the growth plate and extending to a depth of 10 mm or more.The lesion thus differs from both hypocalcaemic rickets, in which the thickening of the growth plate is due to an accumulation of proliferating chondrocytes, and hypophosphataemic rickets where hypertrophic chondrocytes accumulate.The lesion first becomes apparent at about 2 weeks of age and can be visualized by Xrays.Radiography can show the lesion typically increasing in size up to about 4 or 5 weeks of age and then regressing.Gross examination of the tibia in older birds can often reveal