May 2017

Turkey: Tibial dyschondroplasia


Turkey (Meleagris gallopavo), 80 days old.


Tibiotarsus: Tibial dyschondroplasia.


Sagittal section of tibiotarsus after decalcification. There is a plug of cartilage in the physeal region.


This animal was referred from a turkey flock that presented with chronic lameness problems and growth retardation. In-field necropsies showed occasional purulent arthritis in the femoro-tibial joints, but it was not a consistent finding. Skeletal system inspection of all the animals submitted revealed the persistence of cartilage in the physis. Additionally, the proximal tibiotarsal epiphysis was moderately enlarged.

Histologically, there was an extensive area of poorly vascularized persistent cartilage.  The chondrocytes in this area showed intense cytoplasmatic swelling and, multifocally, chondrocytes were apoptotic, with shrunken and karyorrhectic nuclei and  hypereosinophilic cytoplasm.

Dyschondroplasia is a skeletal disease of birds in which there is impairment of normal endochondral bone formation. It is characterized by an avascular plug of abnormal cartilage in the growth plate of long bones that extend into the metaphysis. It is most commonly recognized in the proximal tibiotarsus; hence, the condition is often described as tibial dyschondroplasia (TD).

In turkey flocks the incidence has been reported as high as 79%. Most birds show no clinical signs. If masses of cartilage are large, birds may exhibit reluctance to move, stilted gait and bilateral swelling of the femoro-tibial joints that is often associated with bowing of the legs. In turkeys, TD is recognized as early as 5 weeks, peaking between 12 and 14 weeks of age.

The occurrence of TD is influenced by genetic selection. However, the pathogenesis is not well understood. The current data indicates that is a consequence of an inability of the prehypertrophic chondrocytes to undergo terminal differentiation. It is essential to recognize the mechanisms involved in the maturation of chondrocytes to prevent TD; unfortunately, these processes are not fully understood.

Several nutrients or dietary supplements have been suggested as increasing the occurrence of TD. Among them, sorghum, some types of soybean and rations containing added cysteine, high level of vitamin A, copper-deficient diets and rations contaminated with the fungus Fusarium spp. have been identified.

Picture and author: Albert Canturri, ECVP Resident, Pathology Unit, Universitat Autònoma de Barcelona, Spain.