Dyschondroplasia In Broilers Research Articles

Transcriptome analysis reveals the pathogenesis of spontaneous tibial dyschondroplasia in broilers.

Tibial dyschondroplasia (TD) is a severe bone disease that affects fast-growing broiler chickens and causes economic loss. Despite previous studies, the regulatory mechanism of TD remains unclear and is thought to be primarily based on thiram induction, which may differ from that of naturally occurring diseases. To better understand TD, a digital X-ray machine was used in the present study to determine its incidence in four hundred yellow-feathered broiler chickens. The results showed that the incidence of TD was 22% after 6weeks and gradually decreased after 8 and 10weeks. The body weight of broilers with TD decreased significantly compared to that of NTD broilers. In addition, the length and density of the tibia were reduced after eight and 10weeks, and the density of the tibia was reduced after 6weeks compared with the NTD chickens. This study also examined tibial quality parameters from TD (n = 12) and NTD broilers (n = 12) and found that bone mineral content, bone mineral density, bone ash content, calcium content, and phosphorus content were significantly reduced in TD broilers. Transcriptome analysis revealed 849 differentially expressed genes (DEGs) in the growth plate between TD (n = 6) and NTD groups (n = 6). These genes were enriched in ECM-receptor interaction, cytokine-cytokine receptor interaction, calcium signaling pathway, and TGF-β signaling. Genes encoding the alpha chain of type XII collagen, that is, COL1A1, COL5A1, and COL8A1) were identified as critical in the regulatory network of TD. Gene set enrichment analysis (GSEA) revealed that the pathways of cartilage development, circulatory system development, and nervous system development were changed in the growth plates of TD birds. In the blood transcriptome, 12 DEGs were found in TD (n = 4) and NTD chickens (n = 4), and GSEA revealed that the pathways from TD broilers' blood related to the phagosome, linoleic acid metabolism, monoatomic ion homeostasis, and calcium ion transport were downregulated. This study provides a comprehensive understanding of TD, including its effects on tibial quality, tibial changes, and the circulatory system, along with identifying important genes that may lead to the development of TD.

Thiram exposure induces tibial dyschondroplasia in broilers via the regulation effect of circ_003084/miR-130c-5p/BMPR1A crosstalk on chondrocyte proliferation and differentiation

Thiram, an agricultural insecticide, has been demonstrated to induce tibial dyschondroplasia (TD) in avian species. Circular RNA (circRNAs), a novel class of functional biological macromolecules characterized by their distinct circular structure, play crucial roles in various biological processes and diseases. Nevertheless, the precise regulatory mechanism underlying non-coding RNA involvement in thiram-induced broiler tibial chondrodysplasia remains elusive. In this study, we established a broiler model of thiram exposure for 10 days to assess TD and obtain a ceRNA network by RNA sequencing. By analyzing the differentially expressed circRNAs network, we id entify that circ_003084 was significantly upregulated in TD cartilage. Elevated circ_003084 inhibited TD chondrocytes proliferation and differentiation in vitro but promote apoptosis. Mechanistically, circ_003084 competitively binds to miR-130c-5p and prevents miR-130c-5p to decrease the level of BMPR1A, which upregulates the expression of apoptosis genes Caspase 3, Caspase 9, Bax and Bcl2, and finally facilitates cell apoptosis. Taken together, these findings imply that circ_003084/miR-130c-5p/BMPR1A interaction regulated TD chicken chondrocyte proliferation, apoptosis, and differentiation. This is the first work to reveal the mechanism of regulation of circRNA-related ceRNA on thiram-induced TD, offering a key reference for environmental toxicology.

Taurine is an effective therapy against thiram induced tibial dyschondroplasia via HIF-1α/VEGFA and β-catenin/ GSK-3β pathways in broilers

Thiram causes tibial dyschondroplasia in broilers, leading to a significant economic loss in the poultry industry. Our study explored the effects of taurine in thiram induced tibial dyschondroplasia (TD) through in vivo and in vitro approches. In in vivo study, thiram resulted in lameness disorder, low production parameters ALP, ACP, and a high level of NOS. While, the taurine exhibited promising effect by reducing lameness, increasing ALP, ACP levels, and significantly lowering NOS level with the restoration of the growth plate. In in vitro study, thiram caused distortion and disintegration of chondrocytes. The CCK-8 technique revealed the lower cell activity in TD as compared with the treatment group. Even, the treatment and taurine groups had higher cell activity than control group. Also, the chondrocyte morphology progressively reverted to normal after taurine treatment. It might effectively decreased the symptoms of TD in broilers and their production performance. Further research found that the taurine effectively improved chondrocytes' cell viability and recovered lameness disorder by regulation of HIF-1α, VEGFA, and Wnt/β-catenin signaling pathways. In summary, these results indicate that taurine has a protective effect on thiram-induced broilers and it can enhance the growth activity by directly affecting the development of chondrocytes and blood vessels.

Investigation of different levels of cholecalciferol and its metabolite in calcium and phosphorus deficient diets on growth performance, tibia bone ash and development of tibial dyschondroplasia in broilers

This experiment was conducted to examine the effects of 1-α(OH)D3 alone or in combination with different levels of cholecalciferol on performance, and tibia parameters of one-d–old male broilers fed a tibial dyschondroplasia (TD)-inducing diet. A total of three hundred male broilers were randomly allocated to 5 treatment groups with 4 replicates. The dietary treatments consisted of TD inducing diet, TD inducing diet supplemented with 5 μg per kg of 1-α(OH)D3; TD inducing diet supplemented with 5 μg per kg of 1-α(OH)D3 and 1,500; 3,000 or 5,000 IU cholecalciferol kg-1 of diet. At 42 d of age, broiler chickens fed diets containing 1-α(OH)D3 and 1,500 IU cholecalciferol kg-1 of diet had higher body weight (p < 0.05). In the complete experimental period the best FCR and the highest daily weight gain were obtained in broilers supplemented with 1-α(OH)D3 and 1,500 IU cholecalciferol kg-1 of diet. Broilers supplemented with 1-α(OH)D3 and 1,500 IU cholecalciferol kg-1 of diet had significantly lower incidence and severity of TD in comparison with other groups. In conclusion, the results indicated that the supplementation of 1-α(OH)D3 in combination of 1,500 IU cholecalciferol kg-1 of diet could maximize tibia bone ash, performance and prevent TD in broilers fed TD inducing diet.

Evaluation of a radiographic method to detect tibial dyschondroplasia lesions in broilers

This study aimed at developing radiographic techniques for the early detection of dyschondroplastic lesions in the tibia of broilers. The experiment was carried out at the facilities of UNIFOR/MG and Formiga and UNIFENAS/ Alfenas with 420 one-day-old male Cobb broilers. At 20 days of age, all birds were radiographed and identified with an alpha-numeric metal ring in the right leg. At 40 days of age, 42 broilers previously selected as a function of bone mineral density and lesion thickness scores were again radiographed and scored, and then sacrificed. Their right tibia was removed for gross and histological examination of the growth plate. The results showed that radiographic techniques are correlated with gross and histological examination and that there was no significant differences among techniques (P>0.05). it was concluded that the use of radiographic examination to identify tibial dyschondroplasia in broilers precludes the use of bone mineral density to diagnose this condition. The non-parametric statistical Chi-square test at 5% significance level was used to analyze the results.

Effects of high dietary vitamin A supplementation on tibial dyschondroplasia, skin pigmentation and growth performance in avian broilers

An experiment was conducted to study high dietary vitamin A on tibial dyschondroplasia, growth performance and skin pigmentation in broilers. One hundred and twenty Avian commercial broilers were randomly allotted to three treatments: group C (control group), in which broilers were fed basic diet containing vitamin A 5512 IU/kg diet; group A, in which broilers were fed basic diet with addition vitamin A 35 512 IU/kg; group B, broilers were fed basic diet with supplement vitamin A 65 512 IU/kg. The experiment lasted 35 d and at the end of the trial, broilers were killed and the right proximal tibiotarsi were dissected in longitudinal section for the assessment of TD incidence and TD index, skin from the same area of breast and tibia in broilers were collected to determine pigmentation. The results showed that a high level vitamin A significantly increased the rate of TD incidence and TD index, but middle level vitamin A did not have a significant effect on that. Both low and high retinoic acid decreased growth performance and skin pigmentation in broilers. It suggests that a high dietary vitamin A cause tibial dyschondroplasia in broilers, decreased growth performance and skin pigmentation. It is likely that the effect of vitamin A on TD is mediated through a depression of vitamin D status.

Effect of diet with thiram on liver antioxidant capacity and tibial dyschondroplasia in broilers

1. An experiment was conducted to study the effect of thiram on liver antioxidant capacity and incidence of tibial dyschondroplasia in broilers. 2. One hundred and twenty Avian commercial broilers were allotted at random to three treatments: control group, low thiram group (50 mg/kg) and high thiram group (100 mg/kg). 3. Blood samples were collected to determine the activity of AST (aspartate aminotransferase). At the end of the trial, broilers were killed and liver samples were collected to determine the activity of SOD (superoxide dismutase), GSH-Px (glutathione peroxidase) and MDA (malondialdehyde) content, while the right proximal tibiotarsi were dissected in longitudinal section for assessment of tibial dyschondroplasia (TD) incidence and TD score. 4. The results showed that thiram increased the incidence of TD and TD scores, increased serum AST activity and MDA content of liver, and decreased the activity of SOD and GSH-Px in the liver. 5. They suggest that thiram causes TD in broilers by reducing liver antioxidation capability and damaging liver function; this may be one of the mechanisms by which thiram causes TD in broilers.

Reliability and validity of a modified gait scoring system and its use in assessing tibial dyschondroplasia in broilers

1. The gait scoring system for broilers developed by Kestin et al . ( Veterinary Record , 131: 190-194, 1992) has been widely used to evaluate leg problems. The many factors and measures associated with this scale have empirically established its external (biological) validity. However, published test-retest (within-observer) reliabilities are poor, and inter-observer reliabilities are unknown. We evaluated several modifications to this scale aimed at improving its objectivity and reliability. 2. Eighteen naïve observers scored a standardised video of birds exhibiting varying degrees of lameness, either using Kestin et al .'s system, or our modified system. 3. Test-retest reliability (0.906) for Kestin et al .'s system was higher than previously reported. Interrater reliability was also good (0.892). The modified system offered significantly better test-retest (0.948) and inter-rater reliabilities (0.943), without incurring costs in terms of time taken or difficulty of use. The systems were consistent, assigning individual birds the same score on average. 4. It is concluded that the modified system offers the advantages of reduced error within and between studies. 5. In a second experiment, we used our modified scoring system to examine the relationship between tibial dyschondroplasia (TD) and gait score in 267 selected broilers. 6. Neither the presence nor severity of TD affected gait score, suggesting that, at least in this strain of broilers, other leg problems like slipped tendons or torsional deformities had more influence on gait impairment than did TD.

Influence of Stocking Density on Tonic Immobility, Lameness, and Tibial Dyschondroplasia in Broilers

This study assessed the effect of stocking density on the development of fear reaction (tonic immobility), lameness (gait), and tibial dyschondroplasia in broiler chicks of mixed sex. During 3 experiments, the study used 49,500 broiler chicks (Ross 208). Of these, 432 focal chicks were randomly selected and studied in 3 experiments (144 per experiment). The focal chicks were individually color-marked on the head and wings for identification. Series of stocking densities compared were 9 and 29, 13 and 25, 17 and 21, 18 and 30, and 20 and 28 chicks per m². From 8 to 42 days of age, the study tested focal chicks once a week for lameness (gait) using a scoring scale from 0 to 5 and for the duration of tonic immobility measured in seconds. Each trial terminated with the chicks' being humanely killed and examined for the expression of tibial dyschondroplasia, using a score from 0 to 3. For all series apart from 13 and 25 chicks per m², the average increase in the duration of tonic immobility per day was significantly higher, p < .05, for chicks kept at higher stocking densities. Tonic immobility durations also increased in chicks suffering from tibial dyschondroplasia, especially at 39 days of age, p < .01. The incidence of lameness was higher for high stocking densities among the series compared, p < .05 to p < .001. For most compared series, the growth rate also increased with a unit increase, p < .001. The incidence of tibial dyschondroplasia was significantly higher, p < .01, at stocking densities of 29, 25, 21, 30, and 28 birds per m² compared to those at 9, 13, 17, 18, and 20 birds per m², respectively. A total of 59.6% and 19.2%, respectively, of birds had tibial dyschondroplasia. The results show that high stocking densities adversely affect the welfare of broilers.

25-Hydroxycholecalciferol Fails to Prevent Tibial Dyschondroplasia in Broiler Chicks Raised in Battery Brooders

Two experiments were conducted to evaluate the effectiveness of high levels of 25-hydroxycholecalciferol (25-(OH)D3) in preventing tibial dyschondroplasia (TD) in broilers obtained from a commercial hatchery and grown in batter-brooder cages to 17 days of age. Levels of 25-(OH)D3 ranging from 0 to 250 μg/kg were added to diets adequate (0.95%) or low (0.65%) in calcium.There was no effect on body weight, feed:gain, plasma calcium or phosphorus, or bone ash. 25-(OH)D3 did not affect the incidence of TD or the number of severe lesions in these experiments. Although there was a decrease in overall severity in Experiment 1 when 46 μg/kg was fed, there was no response to dietary 25-(OH)D3 when higher levels were fed in either experiment. There was no consistent effect of 25-(OH)D3 on phytate phosphorus utilization. The results of these experiments indicate that 25-(OH)D3 did not prevent TD in commercial broiler chicks raised in battery-brooder cages when fed at levels as high as 250 μg/kg.

Effects of Dietary Calcium and 1,25-Dihydroxycholecalciferol on the Development of Tibial Dyschondroplasia in Broilers During the Starter and Grower Periods

Two experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3] can prevent tibial dyschon-droplasia in broiler chickens throughout the growing period when withdrawn from the grower diet. The birds were reared in floor pens with pine shavings to 6 wk in Experiment 1 and 5 wk of age in Experiment 2. Calcium was fed at .65 or 1.00% and 1,25-(OH)2 D3 was fed at 0 or 5 μ g/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2 D3 were then fed 0 μ g/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschon-droplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2 D3 increased bone ash at both levels of calcium at 3 wk and the end of the experiments when supplemented for the duration of the studies. When 1,25-(OH)2 D3 was fed, tibial dyschondroplasia was reduced in Experiment 2 only at 3 wk. Tibial dyschondroplasia was decreased at 5 wk in Experiment 2 when .65% calcium was fed with or without 1,25-(OH)2 D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2 D3 was decreased at 3 and 5 wk in Experiment 2 when 1.00% calcium was fed. The results of Experiment 2 suggest that 1,25-(OH)2 D3 can prevent tibial dyschondroplasia caused by inadequate calcium when fed for only 3 wk. The bone ash observed when 1.00% dietary calcium is fed is equal to that obtained when 5 μg/kg l,25-(OH)2 D3 is fed with .65% calcium for the entire growout period.

Correlated Responses to Selection for High or Low Incidence of Tibial Dyschondroplasia in Broilers

Selection for a high or a low incidence of tibial dyschondroplasia (TD) at 7 wk of age was practiced for four generations in broiler breeders keeping an unselected control (C) line and using low intensity X-ray imaging for TD diagnosis. The incidence of TD, BW at 4 and 7 wk of age, age at first egg, and egg production for the first 12 wk of production were determined in the four generations. Age at initial semen production and semen volume and concentration of males were determined only in Generations 3 and 4. The TD scores and BW at 7 wk were collected on 1,366, 1,301, and 1,389 broilers from the C, high (H), and low (L) incidence of TD lines. Incidence of TD at 7 wk in the fourth generation was 16.1, 61.9, and 3.5% for the C, H, and L lines, respectively. There were no significant differences in BW between the H and L lines in Generations 1, 3, or 4. However, in Generation 2, the H line was heavier (P < .01) than the L line. Second generation H line broilers with TD were heavier than those without TD at 4 and 7 wk of age (P < .01). There were no significant differences in age at first egg, age at semen production, or in semen volume between the H and the L lines. Egg production in the L line was greater (P < .01) than that of the H line in all four generations, and semen concentration was also greater (P < .01) in Generations 3 and 4. Correlated responses to selection in the H and the L line were estimated per generation and per weighted selection differential (WCSD) for the traits that were recorded in the four generations. Regression coefficients of cumulative response per generation and per unit of WCSD were not significant.

The effect of dietary 1,25-dihydroxycholecalciferol in preventing tibial dyschondroplasia in broilers fed on diets imbalanced in calcium and phosphorus

Three experiments were carried out to investigate the effects of supplemental dietary 1,25-dihydroxycholecalciferol (1,25(OH)2cholecalciferol) and a low dietary Ca:P ratio on the occurrence of tibial dyschondroplasia (TD) in 3-week-old broilers. Histopathology was used to diagnose TD. In the first experiment, feeding a diet containing 7.5 g Ca and 7.6 g P/kg gave a higher incidence of TD than a control diet containing normal amounts of Ca and P (12 and 6 g/kg respectively). Increasing the dietary supplement of cholecalciferol in the imbalanced diet prevented rickets but did not decrease the incidence of TD. In the second experiment, supplementing the imbalanced diet with 10 micrograms 1,25(OH)2cholecalciferol/kg prevented TD completely but also gave a slight growth depression. In the third experiment the imbalanced diet was supplemented with 0, 2.5, 5 or 10 micrograms 1,25(OH)2 cholecalciferol/kg. The supplement of 2.5 micrograms/kg depressed and the higher supplements prevented the occurrence of TD, this time without a growth depression. Feeding the 10 micrograms/kg supplement for the first week only did not prevent TD. Plasma total Ca, inorganic P and alkaline phosphatase (EC 3.1.3.1) were unaffected by diet but 1,25(OH)2cholecalciferol was higher on the imbalanced than on the control diet. Supplementation of the imbalanced diet with 1,25(OH)2cholecalciferol did not increase plasma levels. It is concluded that 1,25(OH)2cholecalciferol is exerting a powerful biological effect in this model of TD, but the mechanism is unclear.

Additive Amelioration of Tibial Dyschondroplasia in Broilers by Supplemental Calcium or Feed Deprivation

Two experiments were conducted to determine the effects of mineral nutrition and early growth rate on tibial dyschondroplasia (TD) in broiler chickens. A corn-soybean meal diet with .6% available P (aP) was fed from the day of hatching for 20 days. Experiment 1 had a 2 × 2 × 2 factorial arrangement of treatments with two dietary levels of Ca (1.1 or 1.8% of the diet), two levels of dietary Cl (.22 or .34%), and two feeding systems (ad libitum or deprived of feed for 8 h three times per week on Monday, Wednesday, and Friday beginning at 6 days of age). Experiment 2 was a 3 × 2 factorial arrangement with three levels of Ca (1.14, 1.50, or 1.80%) and two feeding systems (ad libitum or deprivation as in Experiment 1). Nineteen-day BW gain was not affected by treatments in the first experiment. Feed deprivation decreased gain in the second experiment, and gain was increased by the highest Ca level without affecting feed efficiency. Feed deprivation did not affect feed efficiency in either experiment. Dietary Cl level did not affect any variable studied. Supplemental Ca increased bone ash in the first experiment, but not in Experiment 2. Feed deprivation and increasing Ca levels decreased the incidence of TD and the amount of severe lesions. Increasing dietary Ca resulted in a greater accumulation of Ca into the epiphyseal growth plate cartilage. The results suggest that the dietary Ca:aP ratio required for bone integrity in starter chicks may be greater than 2.2:1.

Recent findings on tibial dyschondroplasia in broilers and osteoporosis in caged layers

The skeletal disorders causing the most severe welfare problems in different classes of poultry are bone growth disorders in young birds and bone fragility in older laying hens.Angular and rotational deformities of leg bones are widespread in young birds, especially in broilers but also in turkeys. Dyschondroplasia is a widely observed defect in the growth plates of leg bones. It occurs most noticeably in the growth plate of the proximal tibia, the fastest growing bone in the young broiler, and is frequently referred to as tibial dyschondroplasia (TD). Resulting from a failure of growth plate chondrocytes to differentiate fully, it leads to a build up of a mass of prehypertrophic chondrocytes. The lesions develop between the ages of 2 and 5 weeks and can regress thereafter.The importance of TD in causing bone deformity was assessed by carrying out sequential radiography of the proximal tibias of a group of 20 broilers growing up to 16 weeks of age. At this time the tibias were dissected and the angulation of the proximal end (tibial plateau angle, TP°) was measured. The severities and durations of the TD lesions, assessed by radiography, were found to be highly correlated with the TP°. Birds with abnormally large TP° were obviously lame. These observations confirm that TD can lead to distortion of bone growth and that this can contribute to lameness in broilers (Lynch et al., 1992).

Divergent Genetic Selection for Incidence of Tibial Dyschondroplasia in Broilers at Seven Weeks of Age

Selection for a high (H) or low (L) incidence of tibial dyschondroplasia (TD) at 7 wk of age was practiced for four generations in broiler breeders using low intensity x-ray imaging (Lixiscope) for TD diagnosis. As a result, broiler lines with H or L incidence of TD at 7 wk of age were developed keeping a randomly selected control (C) broiler line. A total of 4,232 chicks were hatched representing 172 sires and 612 dams over four generations for the H, L, and C lines. The TD scores at 7 wk were collected on 4,056 broilers. Incidence of TD at 4 and 7 wk of age were studied in the C, H, and L lines of broilers. Direct response to selection in the H and L lines were estimated per generation and per weighted cumulative selection differential (WCSD). Total WCSD deviation from the C line for incidence of TD at 7 wk of age was 1.496 and −.42 units for the H and the L lines, respectively. The response per generation for incidence of TD at 7 wk of age for the H line was .153 ± .028 units. The realized heritability for the H line for incidence of TD at 7 wk of age was .437 ± .065. The incidence of TD was not significantly decreased in the L line at 7 wk of age.

Effect of Dietary Calcium on Tibial Dyschondroplasia. Interaction with Light, Cholecalciferol, 1,25-Dihydroxycholecalciferol, Protein, and Synthetic Zeolite

A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 μg/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 μg/kg of 1,25-(OH)2 D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.

Effect of Diet on Growth and the Incidence of Tibial Dyschondroplasia in Broilers

Two experiments were conducted to study dietary factors affecting growth rate and the incidence of tibial dyschondroplasia (TD) in broiler cockerels grown to 3 wk of age. Chicks were fed corn-soy-bean meal-based diets containing one of the following: 3,145kcal ME/kg, 24% protein, and .50% available phosphorus (aP) (Diet 1); 2,900kcal ME/kg, 20% protein, and .35% aP (Diet 2); or 2,900 kcal ME/kg, 24% protein, and .50 aP (Diet 3). In experiment 1 chicks were fed Diets 1, 2, and 3ad libitum. During weeks 1 and 2, chicks fed Diet 1 were heavier and had better feed efficiency (g feed/g gain) than those fed Diets 2 and 3. Chicks fed Diets 2 and 3 had a lower incidence of TD (P<.05) than those fed Diet 1.In experiment 2 feed intake of Diet 1 was on an ad libitum and restricted basis (Diet 1-R) and Diet 2 was on an ad libitum basis. Beginning on day 2, chicks fed Diet 1-R were offered 90% of the amount of feed consumed the previous day by chicks fed Diet 1 free choice. Chicks fed Diet 1 were heavier than those fed Diet 1-R at 1 wk, and Diets 1-R and 2 at 2 and 3 wk. Chicks fed Diet 1 had higher incidence (P<.05) of TD lesions at 3 wk than those fed Diets 1-R and 2. No differences occurred (P>.05) in the incidence of TD lesions between chicks fed Diets 1-R and 2. The incidence of leg problems appeared to be related to rate of growth, rather than being a direct effect of dietary aP or calcium:aP ratio.

Hydrogenated oil decreases tissue concentrations of n‐6 polyunsaturated fatty acids and may contribute to dyschondroplasia in broilers

1. In a factorial design of dietary treatments, male Ross broilers were given diets containing soyabean oil, hydrogenated soyabean oil (as a source of trans-fatty acids) or feed fat with either 0 or 300 micrograms of added D-biotin/kg. 2. Growth to 28 d was not influenced by the dietary treatments. 3. Length of tibiotarsal bones was reduced (P less than 0.05) and severity of leg bone cartilage lesions, characteristic of dyschondroplasia, was highest (P less than 0.05) in broilers fed on diets containing hydrogenated soyabean oil. 4. Feeding hydrogenated soyabean oil lowered (P less than 0.05) the concentrations of C20:4n6 and the ratios of C20:4n6/C18:2n6 in liver and growth plate cartilage. 5. Growth plate cartilage from birds affected with dyschondroplasia contained lower proportions of prostaglandin precursor fatty acids compared with normal growth plate. 6. It is speculated that an inhibition of prostaglandin biosynthesis brought about by the presence of trans-fatty acids might contribute to the occurrence of lesions similar to dyschondroplasia.

Effects of vitamin A and D supplementation on tibial dyschondroplasia in broilers

A 2 × 2 factorial experiment was conducted to assess the effects of vitamin A and/of vitamin D 3 and their interaction on performance, the incidence and severity of tibial dyschondroplasia (TD), and serum mineral levels in broilers. The results showed that there were no significant effects with a high-chloride basal diet of supplementation with vitamin A (45 000 IU kg −1) on growth pe: ormance and TD lesions. Supplementation with vitamin D 3 (1000 IU kg −1) improved chick growate and lowered the incidence of TD significantly ( P < 0.01). The effects of dietary vitamin A and vitamin D 3 on serum calcium, molybdenum and sodium contents were interdependent. Dietary vitamin D 3 plays an anti-rachitic role by affecting the metabolism of calcium and magnesium. This study indicates that supplementation of vitamin D 3 can prevent TD in broilers.