Impact of the arginine silicate inositol complex on bone metabolism in broiler chickens with tibial dyschondroplasia caused by manganese deficiency.

1. Tibial dyschondroplasia (TD) is a skeletal disorder in broilers that has financial implications, necessitating dietary modifications to reduce the prevalence of this disease. This study explored how arginine silicate inositol complex (ASI) supplementation affected tibial growth plate (TGP) and overall bone health in broilers with manganese (Mn) deficiency-induced TD.2. A total of 240 broiler chicks were divided into four groups, each consisting of 60 birds (15 replicates of four broilers each) as follows: i) Control, with 60 mg Mn per kg of diet; ii) ASI, with 60 mg Mn and 1 g ASI per kg of diet; iii) TD, with 22 mg Mn per kg of diet, and iv) TD+ASI, with 22 mg Mn and 1 g ASI per kg of diet.3. It was found that ASI supplementation increased tibial bone length in Mn-deficient TD broilers (p = 0.007). There was no Mn x ASI interaction for other bone morphometry variables (p > 0.05). However, both tibial bone mineral content and density were affected by Mn and ASI (p < 0.05). With ASI supplementation, serum bone-specific alkaline phosphatase and osteocalcin levels were elevated in the TD+ASI group compared to the TD group (p < 0.001). In the TD group, osteoprotegerin (OPG) levels in the TGP decreased compared to the control groups (p < 0.001).4. In contrast, ASI supplementation in the TD broilers counteracted the decrease in OPG compared to TD broilers without ASI supplementation (p < 0.001). The Mn level and ASI supplementation significantly influenced the OPG/receptor activator of the nuclear factor-κB ligand ratio (p < 0.001).5. In conclusion, the results demonstrated that inclusion of ASI in broiler diets could enhance bone formation variables by controlling OPG levels in the TGP, potentially serving as an effective method to decrease the occurrence of TD.

Lactobacillus rhamnosus JYLR-005 Prevents Thiram-Induced Tibial Dyschondroplasia by Enhancing Bone-Related Growth Performance in Chickens.

Tibial dyschondroplasia (TD) is a leg disorder caused by the abnormal development of the tibia in fast-growing poultry. Lactobacillus rhamnosus (L. rhamnosus) strains have been reported to have effects on increasing bone growth and improving osteoporosis in animals. However, whether L. rhamnosus JYLR-005 can improve bone growth in TD chickens remains unclear. In this study, we noted that L. rhamnosus JYLR-005 could not reduce the suppression of the production performance of TD broilers (p > 0.05) but had a slight protective effect on the broiler survival rate (χ2 = 5.571, p = 0.062). However, for thiram-induced TD broiler chickens, L. rhamnosus JYLR-005 could promote tibia growth by increasing tibia-related parameters, including the tibia weight (day 11, p = 0.040), tibia length (day 15, p = 0.013), and tibia mean diameter (day 15, p = 0.035). Moreover, L. rhamnosus JYLR-005 supplementation improved the normal growth and development of the tibial growth plate by maintaining the morphological structure of the chondrocytes and restored the balance of calcium and phosphorus. Taken together, these findings provide a proof of principle that L. rhamnosus JYLR-005 may represent a therapeutic strategy to treat leg disease in chickens.

Treatment of tibial dyschondroplasia with traditional Chinese medicines: "Lesson and future directions".

Tibial dyschondroplasia (TD) is a metabolic tibiotarsal bone disease in rapidly growing birds throughout the world, which is characterized by gait disorders, reduced growth, and in an unrecoverable lameness in many cases. The short production cycle in chickens, long metabolism cycle in most of the drugs with the severe drug residue, and high treatment cost severely restrict the enthusiasm for the treatment of TD. Traditional Chinese medicine (TCM) has been used for the prevention, treatment, and cure of avian bone diseases. Previously, a couple of traditional Chinese medicines has been reported being useful in treating TD. This review will discuss the TCM used in TD and the alternative TCM to treat TD. Selecting a TCM approach and its pharmacologic effects on TD chickens mainly focused on the differentiation, proliferation, and apoptosis of chondrocytes, angiogenesis, matrix metabolism, oxidative damage, cytokines, and calcification of cartilage in tibia.

Dietary supplementation with glycosaminoglycans reduces locomotor problems in broiler chickens.

This study aimed to assess the influence of glycosaminoglycan (chondroitin and glucosamine sulfates) supplementation in the diet on the performance and incidence of locomotor problems in broiler chickens. A completely randomized design was carried out in a 3 × 3 factorial scheme (3 levels of chondroitin sulfate -0, 0.05, and 0.10%; and 3 levels of glucosamine sulfate -0, 0.15, and 0.30%). Each treatment was composed of 6 replications of 30 broilers each. The performance of broilers (average weight, weight gain, feed intake, feed conversion, and productive viability) was assessed at 7, 21, 35, and 42 d of age, whereas the gait score, valgus and varus deviations, femoral degeneration, and tibial dyschondroplasia were assessed at 21 and 42 d of age. Increasing levels of glucosamine sulfate inclusion linearly increased the weight gain from 1 to 35 and from 1 to 42 d of age of broilers (P = 0.047 and P = 0.039, respectively), frequency of broilers with no femoral degeneration in the right and left femurs, and the proliferating cartilage area of proximal epiphysis at 42 d of age (P = 0.014, P < 0.0001, and P = 0.028, respectively). The increasing inclusion of chondroitin and glucosamine sulfates led to an increase in the frequency of broilers on the gait score scale 0 (P = 0.007 and P = 0.0001, respectively) and frequency of broilers with no valgus and varus deviations (P = 0.014 and P = 0.0002, respectively) also at 42 d of age. Thus, chondroitin and glucosamine sulfates can be used in the diet of broiler chickens to reduce their locomotor problems.

Plastrum Testudinis Extract Mitigates Thiram Toxicity in Broilers via Regulating PI3K/AKT Signaling.

Tibial dyschondroplasia (TD) negatively affects broilers all over the world, in which the accretion of the growth plate (GP) develops into tibial proximal metaphysis. Plastrum testudinis extract (PTE) is renowned as a powerful antioxidant, anti-inflammatory, and bone healing agent. The current study was conducted to evaluate the efficacy of PTE for the treatment of thiram-induced TD chickens. Broilers (day old; n = 300) were raised for 3 days with normal feed. On the 4th day, three groups (n = 100 each) were sorted, namely, the control (normal diet), TD, and PTE groups (normal diet+ thiram 50 mg/kg). On the 7th day, thiram was stopped in the TD and PTE group, and the PTE group received a normal diet and PTE (30 mg/kg/day). Plastrum testudinis extract significantly restored (p < 0.05) the liver antioxidant enzymes, inflammatory cytokines, serum biochemicals, GP width, and tibia weight as compared to the TD group. The PTE administration significantly increased (p < 0.05) growth performance, vascularization, AKT (serine/threonine-protein kinase), and PI3K expressions and the number of hepatocytes and chondrocytes with intact nuclei were enhanced. In conclusion, PTE has the potential to heal TD lesions and act as an antioxidant and anti-inflammatory drug in chickens exposed to thiram via the upregulation of AKT and PI3K expressions.

Clinical efficiency and safety of Hsp90 inhibitor Novobiocin in avian tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is a bone defect of broilers and other poultry birds that disturbs growth plate and it causes lameness. Previously we evaluated differential expression of multiple genes involved in growth plate angiogenesis and reported the safety and efficacious of medicinal plant root extracted for controlling TD. In this study, clinical and protective effect of an antibiotic Novobiocin (Hsp90 inhibitor) and expression of Hsp90 and proteoglycan aggrecan was examined. The chicks were divided into three groups; Control, thiram-induced TD, and Novobiocin injected TD. After the induction of TD, the Novobiocin was administered through intraperitoneal route to TD-affected birds until the end of the experiment. The expressions and localization of Hsp90 were evaluated by qRT-PCR, immunohistochemistry (IHC) and western blot, respectively. Morphological, histological examinations, and serum biomarker levels were evaluated to assess specificity and protective effects of Novobiocin. The results showed that TD causing retarded growth, enlarged growth plate, distended chondrocytes, irregular columns of cells, decreased antioxidant capacity, reduced protein levels of proteoglycan aggrecan, and upregulated in Hsp90 expression (p < 0.05) in dyschondroplastic birds as compared with control. Novobiocin treatment restored growth plate morphology, reducing width, stimulated chondrocyte differentiation, sprouting blood vessels, corrected oxidative imbalance, decreased Hsp90 expressions and increased aggrecan level. Novobiocin treatment controlled lameness and improved growth in broiler chicken induced by thiram. In conclusion, the accumulation of the cartilage and up-regulated Hsp90 are associated with TD pathogenesis and irregular chondrocyte morphology in TD is along with reduced aggrecan levels in the growth plate. Our results indicate that Novobiocin treatment has potential to reduce TD by controlling the expression of Hsp90 in addition to improve growth and hepatic toxicity in broiler chicken.

Tibiotarsus bone characteristics and tibial dyschondroplasia incidence of broilers fed diets supplemented with leucine and valine.

Two experiments were conducted to study the effect of standardized ileal digestible (SID) leucine and valine levels on tibiotarsus bone characteristics and the incidence of tibial dyschondroplasia of broilers from day 1 to 21 (Experiment I) and day 21 to 42 post-hatch (Experiment II). Each experimental phase was evaluated independently. In both experiments, a total of 1,500 one-day-old Cobb 500 male broiler chickens were distributed in a completely randomized design 5 × 5 factorial arrangement for a total of 25 treatments. The SID leucine and valine levels were ranged from 10.0 to 19.6 g/kg, and 6.0 to 12.0 g/kg from day 1 to 21 post-hatch, respectively, while day 21 to 42 post-hatch ranged from 10.0 to 18.0 g leucine/kg, and 5.2 to 11.2 g valine/kg. Serum calcium and phosphorus, bone concentrations of calcium, phosphorus and ash, diameter and Seedor index of the tibiotarsus were not affected (p > .05) by the treatments at 21 or 42 days of age. There was an interaction (p ≤.06) between the SID levels of leucine and valine on tibiotarsus breaking strength at 21 days, but not at 42 days of age (p > .05). Tibiotarsus breaking strength was maximized in broilers from day 1 to 21 with the dietary levels of leucine and valine at 14.2 and 9.0 g/kg respectively. Dietary leucine levels reduced linearly (p < .05) the hypertrophic zone of tibiotarsus cartilage at 21 days of age. Therefore, leucine and valine supplementation interact positively on bone strength of broilers from day 1 to 21 post-hatch. Leucine can be a useful amino acid for reducing the hypertrophic cartilage zone in broilers from day 1 to 21, but not from day 21 to 42 post-hatch.

Hsp90 inhibitor celastrol reinstates growth plate angiogenesis in thiram-induced tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is an important long bone defect of broiler chickens that disturbs the proximal growth plate and is characterized by non-vascularized cartilage, a distended growth plate and lameness. Celastrol, a medicinal root extract from the plant Tripterygium wilfordii, is reported widely as a well-known heat-shock protein 90 (Hsp90) inhibitor. Recently, Hsp90 inhibition in chondrocyte differentiation and growth-plate vascularization were effective in restoring the morphology of the growth plate. The present study was aimed at investigating Hsp90 inhibition in TD using celastrol. The broiler chicks were divided into three groups; Control; TD induced (40 mg/kg thiram) and celastrol treatment. Hsp90, vascular endothelial growth factor and Flk-1 expressions were evaluated by quantitative real-time polymerase chain reaction and the protein levels of Hsp90 were measured by Western blot analysis. Antioxidant enzymes were determined to assess the liver damage caused by thiram and the protective effects of the medicine were evaluated by levels of serum biomarkers. The expression levels of Hsp90 and vascular endothelial growth factor mRNA transcripts were increased while Flk-1 receptor was decreased in TD-affected chicks. Celastrol therapy inhibited Hsp90 mRNA and protein levels and up-regulated the expressions of receptor Flk-1 in TD-affected tibial growth plates significantly (P < 0.05) in addition to rectifying the damaging effects of thiram on the liver by decreasing the levels of aspartate aminotransferase, alanine aminotransferase and malondialdehyde and correcting the oxidative imbalance. In conclusion, administering celastrol to dyschondroplastic chicks prevented un-vascularized growth plate, lameness and reinstated angiogenesis. Celastrol may be efficacious for the treatment of TD through the inhibition of Hsp90 expression and limiting the liver damage caused by thiram in broiler chickens.

Could a trace mineral deficiency be associated with congenital chondrodystrophy of unknown origin (CCUO) in beef cattle in Australia?

Congenital chondrodystrophy of unknown origin (CCUO) has been reported in beef cattle worldwide. A trace mineral deficiency in pregnant dams has been suggested as causing the deformities seen in CCUO calves. An extended outbreak of CCUO in Australia between 2002 and 2009 provided an opportunity to examine the pattern of trace mineral status in gestating cows and the effect of parenteral trace mineral supplementation on a herd at risk of CCUO calves. A property with a strong history of CCUO was identified from a previous case-control study. A randomly selected sample of multiparous (8 to 10 years old) Angus and Angus cross cows (n = 20) was assigned to control (no injection) or supplement group given three injections at the recommended dose rate of chelated mineral supplement (Mn, Zn, Cu and Se) at 6-week intervals in mid- to late gestation. Liver biopsies were performed to measure liver Mn, Zn, Cu and Fe at each injection time and 1 month post-calving. Pasture samples were also collected for analysis. Supplemented cows had higher liver Cu levels compared to control cows (p < 0.001), but there was no difference between supplement and control cows for liver Zn, Fe or Mn. Liver Cu (p < 0.001), Fe (p < 0.001) and Zn (p < 0.001) fell during gestation and liver Mn increased after calving (p < 0.001). Three cows from the control group and two from the supplement group had liver zinc levels below the normal values at the end of the trial. Two cows from the control group and one from the treatment group gave birth to cows with signs of CCUO including superior brachygnathia. All cows except one from the control group had rough dry coats with excessive dander. The role of trace mineral status in the birth of CCUO calves, especially the role of zinc deficiency, requires further investigation.

Effect of the level of cholecalciferol supplementation of broiler diets on the performance and tibial dyschondroplasia.

A study was conducted to evaluate four different cholecalciferol levels (NRC; modified), using diets supplemented with 200 (control), 1500, 2500 or 3500 IU/kg of cholecalciferol (VIT-D3). Each treatment was assigned to 3 pens of 17 broiler chicks of a commercial strain grown in an open-sided house with sidewall curtains. At 21 and 42 days, BW and feed conversion (FCR) were determined. At 42 days, five birds per pen were slaughtered to evaluate tibia and toe ash of the right leg, and incidence and severity of tibial dyschondroplasia (TD) of the left tibia and also measured dressing percentage and breast meat yield. Serum calcium and phosphorus concentrations were also determined. Haemagglutination inhibition antibody titre against Newcastle disease virus and lymphoid organs weight/body weight ratio were also determined. At both 21 and 42 days, the BW of birds fed 1500 IU/kg to 3500 IU/kg of VIT-D3 was significantly greater than birds fed 200 IU/kg. Similarly, better FCR was observed in birds those fed diets of high level of VIT-D3. No significant difference was observed for mortality at any age. Better dressing percentage and breast meat yield were noted in birds fed diets containing 2500 or 3500 IU/kg VIT-D3. Both tibia and toe ash contents were increased (p < 0.05) progressively with increased concentrations of cholecalciferol in feed. The incidence of TD (percentage of birds having TD scores greater than zero) was significantly (p < 0.05) influenced by level of 3500 IU VIT-D3/kg at 42 days. The severity of TD in birds fed diets containing 200 IU/kg VIT-D3 was apparently higher than birds fed diets with higher levels of VIT-D3. Concentrations of calcium and phosphorus minerals in the serum increased progressively with the high level of VIT-D3 supplementation to birds at both 21 and 42 days of age. Feeding levels of 1500 or 3500 IU of vitamin D3 did positively affect the immune system within the parameters measured. It may be concluded that performance, bone mineralization, blood chemistry and immunity against disease in broilers could be maintained when supplementing high level of VIT-D3 incorporated in broiler diets.

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 5512IU/kg diet; group A, in which broilers were fed basic diet with addition vitamin A 35512IU/kg; group B, broilers were fed basic diet with supplement vitamin A 65512IU/kg. The experiment lasted 35d 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.

Evaluation of the efficacy of vitamin D3 or its metabolites on thiram-induced tibial dyschondroplasia in chickens.

Two trials were conducted to determine if thiram-induced tibial dyschondroplasia (TD) in chickens was linked to a vitamin D deficiency and calcium homeostasis dysregulation, and whether feeding vitamin D fortified diets may prevent it. Day-old chickens were given grower diets containing different vitamin D products throughout the experiment until necropsy on day 16. Half of the birds in each feed group received thiram at levels of 100 ppm (trial 1) or 50 ppm (trial 2) between days 7-9 to induce TD. The birds were weighed, bled, and euthanized to determine TD incidences and severity by examining the growth plates. Tibial bones were used to measure biomechanical strength and ash content. Blood concentrations of 25-hydroxyvitamin D, Ca, P, alkaline phosphatase, and creatine kinase were measured in serum that showed no differences between different groups. Thiram reduced body weight and induced TD regardless of any vitamin D treatment to the same extent as untreated birds.

The effect of maternal dietary vitamin D3 supplementation on performance and tibial dyschondroplasia of broiler chicks.

A series of experiments was conducted to investigate the effects of maternal dietary vitamin D3 supplementation at 4 different times during the laying cycle, on the performance and bone quality of broiler chicks fed a diet that induced tibial dyschondroplasia (TD) or an adequate diet. Ross x Ross broiler breeder hens were fed a corn-soy diet with various levels of vitamin D3 from 24 to 66 wk of age. Eggs were collected at 39, 44, 53, and 64 wk of age and hatched. Chicks from hens fed 250 IU of D3/kg (low maternal D3 or LMD3) and 2,000 IU of D3/ kg (high maternal D3 or HMD3) levels were placed in battery brooders and fed the diets from 0 to 16 d. At 16 d, the chicks were weighed and killed; the left tibias were used for bone ash determinations, and the right tibias were used to score the incidence and severity of TD (0, 1, 2, or 3, where 3 is the most severe). Body weight gain and feed intake were significantly lower for the LMD3 chicks at wk 44 and 64, although there was no difference in weight at hatch. For the first 2 hatches (wk 39 and 44), the LMD3 and HMD3 chicks demonstrated high average TD scores (2.03 and 1.57 vs. 2.05 and 1.75 for the LMD3 vs. HMD3 chicks, respectively) and high average incidences of severe TD (50 and 35% vs. 45 and 34% for LMD3 vs. HMD3 levels, respectively). However, results from the last 2 hatches (wk 53 and 64) showed that HMD3 chicks, compared with LMD3 chicks, had reduced average TD scores (1.39 and 1.47 vs. 1.01 and 0.44 for LMD3 vs. HMD3 levels, respectively) and severe TD incidence (36 and 40% vs. 17 and 8% for the LMD3 vs. HMD3 levels, respectively). In this experiment, as egg production declined toward the end of the laying cycle, hens fed the HMD3 might have been able to deposit sufficient quantities of vitamin D3 in the egg to maintain excellent body weight gain at 16 d of age and reduce the incidence and severity of TD. Hens fed the LMD3 diet were unable to produce similar improvements.

Effects of different management factors on broiler performance and incidence of tibial dyschondroplasia.

(1) This study was to determine the effects of two lighting programmes (continuous--24L:0D or intermittent--12L:3(1L:3D)), two feeding programmes (continuous--ad libitum or meal Jeeding--3 h feed:3 h deprivation x 4 times per d) and two ascorbic acid (AA) supplementations (0 or 150 mg/l in water) on broiler performance and incidence of tibial dyschondroplasia (TD). (2) One-day-old male commercial (Ross PM3) broiler chicks (1600) were used. The chicks were randomly divided into 8 treatment groups (2 x 2 x 2) and their replicates (2) replicates per treatment). (3) Intermittent lighting increased body weight and improved feed conversion. Body weight of broilers was decreased by meal feeding. AA supplementation had no significant effect on the body weight and feed conversion ratio. There was no lighting x feeding x supplemental AA interaction for body weight, feed conversion ratio, mortality rate and carcase weight. (4) Supplemental AA improved the cortical thickness of tibiotarsus and decreased the incidence of TD. (5) It was concluded that the application of intermittent lighting in combination with supplementation of 150 mg/l AA is a useful method to reduce TD in broilers without loss of performance.

Effect of casein phosphopeptide and 25-hydroxycholecalciferol on tibial dyschondroplasia in growing broiler chickens.

1. An experiment was conducted to investigate the influence of dietary casein phosphopeptides and 25-hydroxycholecalciferol on the incidence of tibial dyschondroplasia (TD) in 14-d-old commercial broiler chickens. 2. Three hundred and twenty broiler chicks (one day old) were randomly allocated to one of 4 dietary treatments. A standard broiler diet was used as the control with the three experimental treatments receiving the control diet supplemented with 10 g casein phosphopeptide/kg, 14 g casein phosphopeptide/kg or 69 microg 25-hydroxycholecalciferol/kg. 3. Those birds fed the diets supplemented with 14g casein phosphopeptide/kg or 25-hydroxycholecalciferol had a lower incidence of TD than both the control and 10g casein phosphopeptide/kg treatments when assessed grossly. 4. The body weight of birds fed the 10 g casein phosphopeptide/kg diet or the 25-hydroxycholecalciferol diet was higher than birds fed the control diet. Although not significant, the body weight of birds fed the 14 g casein phosphopeptide/kg diet was also greater than the control birds. 5. The current experiment demonstrated that both casein phosphopeptide and 25-hydroxycholecalciferol can reduce the incidence of TD in the young broiler chicken. More research is required to explain the unexpected increase in body weight described above.

Effectiveness of twenty-five-hydroxycholecalciferol in the prevention of tibial dyschondroplasia in Ross cockerels depends on dietary calcium level.

Five experiments were conducted to evaluate the efficacy of 25-hydroxycholecalciferol [25-(OH)D3] to minimize the development of tibial dyschondroplasia (TD) and improve phytate phosphorus retention in Ross cockerels during the starter period. In experiment 1, chicks were fed a TD-inducing (0.67% calcium) diet with or without exposure to ultraviolet light and no supplemental cholecalciferol. Dietary 25-(OH)D3 was added at 0, 10, or 70 microg/kg for both light treatments. In experiment 2, 25-(OH)D3 was added at 0, 10, 40, or 70 microg/kg to a TD-inducing diet containing 27.5 microg/kg added cholecalciferol. Experiment 3 was similar to experiment 2 except a diet marginal (0.85%) in calcium was fed, and cholecalciferol was added at 55 microg/kg. In experiments 4 and 5, 25-(OH)D3 was added at 0, 18, 36, 54, 72, or 90 microg/kg to a diet marginal in calcium. Dietary 25-(OH)D3 decreased the incidence of TD similarly at 40 and 70 microg/kg 25-(OH)D3 and improved phytate phosphorus retention when the TD-inducing diet was fed. The incidence of TD was decreased when 70 microg/kg 25-(OH)D3 was added to a diet marginal in calcium in experiment 3 only. Phytate phosphorus retention was generally not affected by dietary 25-(OH)D3 when a diet containing marginal calcium, adequate phosphorus, and high cholecalciferol was fed. The effectiveness of 25-(OH)D3 to reduce the incidence of TD in young broilers was higher when the dietary calcium level was below 0.85%. The incidence of TD in Ross cockerels was low (< 25%) when dietary calcium was greater than 0.85%.

The expression of calbindin in chicks that are divergently selected for low or high incidence of tibial dyschondroplasia.

Three experiments were conducted with broiler chicks that were divergently selected for low or high incidence of tibial dyschondroplasia (LTD and HTD, respectively) to determine if the expression of intestinal calbindin-28 kD mRNA and protein differed between the 2 strains. In addition, levels of intestinal vitamin D receptor mRNA and plasma thyroid hormone concentrations were also examined. In experiment 1, LTD and HTD chicks were fed a corn-soybean meal diet that was adequate in all nutrients except cholecalciferol (D3), which was titrated to 5 or 40 microg/kg diet in a completely randomized 2 x 2 factorial arrangement. At 4 and 8 d of age, HTD chicks fed 5 microg of D3/kg of diet had a lower (P < 0.05) expression level of calbindin-28 kD mRNA than the LTD chicks fed the same diet. At 4 and 8 d of age, HTD chicks fed 5 microg of D3 had the lowest intestinal expression of calbindin-28 kD protein. Expression of vitamin D receptor mRNA did not differ for broiler strains at either level of D3 supplementation. In experiment 2, there was no significant difference in the expression of calbindin-28 kD mRNA or vitamin D receptor mRNA between day-of-hatch LTD, HTD, and commercial broiler chicks. Experiment 3 was similar in design to the first experiment except that the birds were fed for 18 d. Calbindin-28 kD and vitamin D receptor mRNA expression levels at 18 d were similar to those observed in experiment 1. Plasma triiodothyronine and free-triiodothyronine concentrations were greater for LTD chicks, regardless of dietary D3 supplementation levels. These results suggest that divergent selection of broilers for LTD or HTD alters the physiological response to nutritionally inadequate levels of dietary D3.

Role of dietary calcium and available phosphorus in the aetiology of tibial dyschondroplasia in growing turkeys.

1. Large White male turkeys from a heavy commercial male-line were fed 16 diets containing 4 concentrations of calcium (6, 10, 14 and 18 g/kg) and available phosphorus (3, 5, 7 and 9 g/kg) in a 4 x 4 factorial experiment. There were three replicates (pens) of each treatment and the skeletal health, morphology and mineral status of 4 turkeys from each pen were assessed at 7, 10 and 13 weeks of age. 2. The prevalence of tibial dyschondroplasia increased after 7 weeks of age and was present in 50 and 71% of turkeys respectively at 10 and 13 weeks. The lesion was localised in the caudal aspect of the proximal tibiae. Dietary calcium and available phosphorus did not affect the prevalence of the lesion except in turkeys on the diet containing 6 g calcium/kg, where body weight and the incidence of tibial dyschondroplasia were low. 3. Histological investigation showed no evidence of rachitic changes. 4. Low dietary calcium was associated with lower tibial plateau angles at 10 and 13 weeks of age. Tibial torsion and the angle of rotation were not affected by dietary treatments or age. Tibial torsion and the angle of rotation were not affected by dietary treatments or age. 5. Increasing dietary calcium increased tibial radiodensity, cortical density and the widths of the cortex and proximal tibiotarsus. Radiodensities increased to 10 weeks and were significantly lower at 13 weeks of age. 6. Bone ash, calcium and phosphorus declined with age, particularly between 10 and 13 weeks, whereas bone calcium: phosphorus ratios were not affected by dietary treatment or age. 7. Dietary calcium was positively associated with blood calcium and calcium ion concentrations and was without effect on blood phosphorus. Available phosphorus was associated positively with increased blood phosphorus and lower calcium ion concentrations but had no effect on total calcium. Alkaline phosphatase activity was low at high concentrations of dietary calcium with low available phosphorus and there was higher activity on diets containing low calcium and high available phosphorus.

Influence of dietary phytase supplementation on incidence and severity in broilers divergently selected for tibial dyschondroplasia.

A study was conducted to determine the effect of dietary supplementation of phytase on the incidence and severity of tibial dyschondroplasia (TD) in chickens selected for high (HTD) and low (LTD) incidences of TD for 11 generations. By feeding a phosphorus-deficient diet (0.1% nonphytate phosphorous; nPP), HTD and LTD chickens were further identified as high-sensitivity birds (HS) and low-sensitivity birds (LS) to phosphorus deficiency based on mortality. Two hundred forty 1-d-old chicks from HTD and LTD lines (five replications of four birds per treatment) were randomly assigned to a control diet with 0.5% nPP and two treatment diets (0.1% nPP) with and without 600 phytase units (FTU) Natuphos phytase/kg. Feed consumption and growth rate were measured for 3 wk, and both tibiae were scored for TD incidence, average TD score, and total number of TD lesions with the most severe form of the abnormality (lesions that were scored 3). The addition of phytase had no influence on TD incidence and lesion scores of 3 in HTD chicks. However, a nonsignificant reduction in TD incidence (P = 0.07), TD score, and no. 3 lesions (P < or = 0.01) were observed in LTD chicks. Interactions between sensitivity (to P deficiency) and phytase (P < or = 0.01) and sensitivity and nPP (P < or = 0.01) were observed for no. 3 scores in LTD chicks. These results indicate that phytase was effective in reducing TD incidence and severity in LTD chicks but not in HTD chicks.

Dietary effects on bone quality and turnover, and Ca and P metabolism in chickens.

The responses of skeletal health and blood calcium (Ca) and phosphorus (P) status to different dietary calcium and available P (avP) contents were examined in 2-week-old chickens. High avP content resulted in more inorganic P (P(i)) and less ionised Ca (Ca(2+)) in the blood. Birds on low Ca and high avP diets showed a higher incidence of tibial dyschondroplasia and hypocalcaemic rickets and were therefore assumed to be hypocalcaemic. However the molar Ca:P ratio in bone was closer to the expected 1.67:1 in diets high in avP. No significant dietary mineral content effect was found on bone mineral content, or breaking strength, within the range of diets used. Results suggest that variations in molar Ca:P ratios in bone have little effect on mechanical competence, and that diets for this strain should be higher in Ca, and could be lower in avP, than current recommendations.