The effects of dietary fluoride on growth and bone mineralization in broiler chicks

Abstract

Fluoride has been shown to have varying degrees of beneficial effects on bone mineralization and bone strength, despite its toxic effects on growth and leg disorders. Some studies have demonstrated an increase in bone ash resulting from F supplementation. The purpose of the present study was to determine whether low levels of dietary F would have any beneficial effect on the bone strength and leg disorders of young chicks fed P-deficient diets. Effects on BW and feed efficiency were also observed to monitor for F toxicity. One-day-old straight-run Cobb × Cobb broiler chicks were weighed, randomly allocated to treatment groups, housed in electrically heated wire-floored battery brooders, and provided with water and feed for ad libitum consumption. Phosphorus-deficient diets were formulated to induce P rickets with 2 different P sources. Treatment 1 contained feed grade dicalcium phosphate to simulate a commercial diet. Treatment 2 contained purified dicalcium phosphate to represent a diet with minimal F (~0.46 mg/kg). Treatments 3 and 4 used purified dicalcium phosphate as the P source and contained 10 and 20 mg/kg of F from NaF, respectively. Four more treatments were added for experiment 2. Treatments 5, 6, 7, and 8 used purified dicalcium phosphate as the P source and contained 30, 40, 50, and 60 mg/kg of F from NaF, respectively. The analyzed F values in the diet were lower than the formulated values as a result of an unexplained lower than desired rate of recovery (72%) of an internal standard. Chicks fed purified calcium phosphate grew better in experiment 1 (P < 0.05) and had a lower incidence of P-deficiency rickets in experiment 2 (P < 0.01) than did birds fed feed grade dicalcium phosphate. Percentage of bone ash was increased by increasing the F level in the diets in experiment 1, but not experiment 2. It was concluded that even low levels of F, such as those used in the present study, have the potential to increase bone quality.

Increased sizes and improved qualities of tibia bones by myostatin mutation in Japanese quail

“…Especially, rapid growth of the body and bone during the early growth phase of a broiler is suggested as one of the main causes of poor bone quality in fast growing broilers ( Williams et al, 2000 , 2004 ; Tompkins et al, 2022a ; 2022b ). To minimize economic losses and concerns about animal welfare caused by the leg bone problems of broilers, genetic factors should also be considered and investigated in addition to other aspects including nutritional and environmental factors ( Shim et al, 2011 ; Liu et al, 2015 ; Huang et al, 2017 ).…”

Tibial dyschondroplasia is highly associated with suppression of tibial angiogenesis through regulating the HIF-1α/VEGF/VEGFR signaling pathway in chickens

“…Normal development of the bone is very important in meat-type broilers. Abnormal development of the bone (such as tibial dyschondroplasia, rickets, femoral head necrosis, and perosis) can lead to severe economic losses to the poultry industry and directly compromise poultry welfare 1 – 5 . Although these problems are of great concern for researchers around the world, the underlying etiology of tibial dyschondroplasia (TD) is not fully understood 5 – 8 .…”

Comparative Transcriptomics Reveals the Role of the Toll-Like Receptor Signaling Pathway in Fluoride-Induced Cardiotoxicity

“…It is well-known that low concentrations of fluoride are essential for the development of teeth and bones in humans and animals. − However, excessive fluoride ingestion has adverse effects and causes several health problems. Existing studies have shown that fluorosis causes damage to the heart through mechanisms that include induction of oxidative damage and induction of cardiomyocyte apoptosis. , However, the mechanism of fluoride cardiotoxicity in relation to inflammatory damage remains unclear.…”