Effect of the addition of glycosaminoglycans on bone and cartilaginous development of broiler chickens.

Locomotion issues in broiler production may decrease performance (carcass yield and traits) and lead to high financial losses. This study evaluates the addition of glucosaminoglycans in broiler diets to minimize the lack of proper bone development and joint weakening. The experiment was conducted using 2,160 broilers randomly distributed in a factorial pattern (3 × 3) using 3 levels of glucosamine sulfate (0, 0.12, and 0.24%) and 3 levels of chondroitin sulfate addition (0, 0.08, and 0.16%). Eight repetitions were used for each treatment, distributed in 72 pens with 30 broilers each. There was a quadratic effect on feed conversion for broilers from 1 to 42 d old (P = 0.0123) for the addition of chondroitin, and better feed conversion was obtained by adding 0.08% of chondroitin. The relative tibia weight, the width of the proximal epiphysis and diaphysis presented a linear increased effect in broilers at 42 d old. An interaction was found between the amount of chondroitin × glucosamine and the number of chondrocytes in the proximal cartilage of the tibia (P = 0.0072). There was a quadratic effect of glucosamine levels (P = 0.0107) in the birds that had received the 0.16% addition of chondroitin, and the presence of 0.18% glucosamine increased the number chondrocytes in the cartilage of broilers. These results provide the first evidence that broilers may benefit from increased dietary chondroitin sulfate. These results indicate that the addition of glucosamine and chondroitin sulfates in broiler feed rations might alleviate leg conditions and decrease financial losses in the broiler industry.

Insulin-Like Growth Factor I Does Not Drive New Bone Formation in Experimental Arthritis.

INTRODUCTION: Insulin like growth factor (IGF)-I can act on a variety of cells involved in cartilage and bone repair, yet IGF-I has not been studied extensively in the context of inflammatory arthritis. The objective of this study was to investigate whether IGF-I overexpression in the osteoblast lineage could lead to increased reparative or pathological bone formation in rheumatoid arthritis and/or spondyloarthritis respectively. METHODS: Mice overexpressing IGF-I in the osteoblast lineage (Ob-IGF-I+/-) line 324-7 were studied during collagen induced arthritis and in the DBA/1 aging model for ankylosing enthesitis. Mice were scored clinically and peripheral joints were analysed histologically for the presence of hypertrophic chondrocytes and osteocalcin positive osteoblasts. RESULTS: 90-100% of the mice developed CIA with no differences between the Ob-IGF-I+/- and non-transgenic littermates. Histological analysis revealed similar levels of hypertrophic chondrocytes and osteocalcin positive osteoblasts in the ankle joints. In the DBA/1 aging model for ankylosing enthesitis 60% of the mice in both groups had a clinical score 1<. Severity was similar between both groups. Histological analysis revealed the presence of hypertrophic chondrocytes and osteocalcin positive osteoblasts in the toes in equal levels. CONCLUSION: Overexpression of IGF-I in the osteoblast lineage does not contribute to an increase in repair of erosions or syndesmophyte formation in mouse models for destructive and remodeling arthritis.

To Wnt or not to Wnt: the bone and joint health dilemma.

The Wnt signalling cascades have essential roles in development, growth and homeostasis of joints and the skeleton. Progress in basic research, particularly relating to our understanding of intracellular signalling cascades and fine regulation of receptor activation in the extracellular space, has provided novel insights into the roles of Wnt signalling in chronic arthritis. Cartilage and bone homeostasis require finely tuned Wnt signalling; both activation and suppression of the Wnt-ß-catenin cascade can lead to osteoarthritis in rodent models. Genetic associations with the Wnt antagonist encoded by FRZB and the transcriptional regulator encoded by Dot1l with osteoarthritis further corroborate the essential part played by Wnts in the joint. In rheumatoid arthritis, inhibition of Wnt signalling has a role in the persistence of bone erosions, whereas Wnts have been associated with the ankylosing phenotype in spondyloarthritis. Together, these observations identify the Wnt pathway as an attractive target for therapeutic intervention; however, the complexity of the Wnt signalling cascades and the potential secondary effects of drug interventions targeting them highlight the need for further research and suggest that our understanding of this exciting pathway is still in its infancy.