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ARS Home » Southeast Area » Fayetteville, Arkansas » Poultry Production and Product Safety Research » Research » Publications at this Location » Publication #226314

Title: Serum chemistry and histopathology of broiler femoral head necrosis and tibial dyschondroplasia

item Rath, Narayan
item CLARK, F

Submitted to: World Poultry Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 12/20/2007
Publication Date: 6/30/2008
Citation: Rath, N.C., Durairaj, V., Rasaputra, K.S., Okimoto, R., Clark, F.D. 2008. Serum chemistry and histopathology of broiler femoral head necrosis and tibial dyschondroplasia. In: Proceedings of the 23rd World Poultry Congress, June 30 - July 4, 2008, Queenslands, Brisbane, Australia. 2008 CDROM.

Interpretive Summary:

Technical Abstract: Femoral head necrosis (FHN) and tibial dyschondroplasia (TD) are two major leg problems in young meat type poultry which cause lameness, bone deformity and infections. Whereas FHN results from disarticulation of the femoral growth plate from the articular cartilage, TD lesions are characterized by incomplete bone development at the proximal growth plates of the tibia and tibio-tarsal bones. To understand the etiology of these problems we compared the serum chemistries and growth plate histology of six week-old broiler chickens with or without femoral head and TD lesions. Serum samples each from normal and disarticulated femoral heads without any lesion (DC), disarticulated femurs with gross lesions (FHN), and TD chickens were analyzed (n=12/ group). The FHN birds showed a differentially significant elevation in serum concentrations of cholesterol, triglyceride, and low density lipoprotein whereas the protein, albumin, and magnesium concentrations were increased in all problem groups compared with their normal counterparts. Neither serum transferrin nor interleukin-6 showed any increase indicating the absence of infection. There was no infiltration of granulocytes into either FHN or TD lesions. Although the TD lesions had many apoptotic cells, the FHN lesions showed no significant apoptosis. We surmise that FHN is associated with fat embolism related epiphysiolysis arising from problems of fat metabolism.