High Incidence Of Tibial Dyschondroplasia Research Articles

High vitamin D3 requirements in broilers for bone quality and prevention of tibial dyschondroplasia and interactions with dietary calcium, available phosphorus and vitamin A

1. Two experiments were carried out to investigate responses in performance and bone compositional and structural characteristics in broilers fed diets containing 4 concentrations of vitamin D3 (5, 20, 125 and 250 µg cholecalciferol/kg) at different concentrations of calcium, available phosphorus and vitamin A. 2. In experiment 1, body weight and tibia breaking strength were maximised at 14 d with 250 µg vitamin D3/kg, tibia ash was maximised with 125 µg vitamin D3/kg. A high incidence of tibial dyschondroplasia (TD) was decreased to very low levels with 125 µg vitamin D/kg. 3. At 42 d, performance and bone characteristics showed no response to vitamin D3 concentrations above 20 µg/kg. 4. Dietary vitamin A within the range 2·4 to 4·5 mg retinol/kg did not show any interaction with vitamin D3 status at either age. 5. In experiment 2, responses to vitamin D3 were strongly influenced by dietary calcium/available phosphorus. With 13 g calcium and 5 g available phosphorus/kg, performance and bone characteristics responded to vitamin D3 concentrations up to 125 µg/kg but more was needed at less optimal concentrations of calcium and available phosphorus. TD incidence was minimised with 250 µg/kg. 6. This study shows that high dietary concentrations of vitamin D3 can prevent TD. It is concluded that the vitamin D3 requirement of broilers up to 14 d of age at optimal dietary calcium and available phosphorus concentrations may be in the range 35 to 50 µg/kg for cortical bone quality and up to 250 µg/kg for prevention of TD. The vitamin D3 requirement for cortical bone quality after 14 d is not higher than 20 µg/kg. These requirements are much higher than earlier estimates and may be related to higher calcium requirements of modern broiler genotypes. Current regulations limiting maximum vitamin D3 concentrations in broiler starter diets may need to be reviewed.

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 × 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.

Effect of Lesion Size on the Metabolic Activity of Tibial Dyschondroplastic Chondrocytes

Experiments were conducted to determine the influence of lesion size and method of producing tibial dyschondroplasia on metabolic activity of cultured chondrocytes. Genetic selection was one method used to produce a high incidence of tibial dyschondroplasia. Chondrocytes obtained from severe lesions exhibited reduced mitogenic activity (3 H-thymidine incorporation) and ability to synthesize matrix proteoglycans (35 SO4 incorporation) when compared with normal growth plate and smaller lesions. When a commercial broiler strain was used, all chondrocytes isolated from lesions induced by feeding thiram had reduced metabolic activity. Similar results were observed with severe lesions obtained from copper-deficient chicks. It is concluded that lesion size is an important factor in determining subsequent metabolic activity of chondrocytes isolated from tibial dyschondroplastic lesions.

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.

Effects of dietary chloride and magnesium on the incidence of tibial dyschondroplasia in chickens fed on Chinese practical diets.

1. The effects of varying the concentrations of dietary magnesium and chloride on the performance, incidence of tibial dyschondroplasia and tissue element contents of broilers fed on Chinese practical maize soya-bean meal diets was assessed. 2. Two concentrations of dietary chloride (1.5 and 3.5 g/kg) and 3 of dietary magnesium (2.0, 4.0 and 6.0 g/kg) were used to form 6 dietary treatments for a 21-d experimental period. 3. Results from this study indicated that the dietary ingredients of maize and soya-bean meals produced in the northeast of China may predispose or influence the susceptibility of chickens to tibial dyschondroplasia. 4. High dietary chloride induces a high incidence of tibial dyschondroplasia (P less than 0.05) which could be ameliorated by dietary magnesium supplementation. 5. Dietary magnesium plays an anti-rachitic role by improving the deposition of copper and zinc in the bone tissue. 6. Supplementation with magnesium to 4.0 g/kg is recommended for broiler diets in northeast China.

Efficacy of Several Vitamin D Compounds in the Prevention of Tibial Dyschondroplasia in Broiler Chickens

Studies were conducted to evaluate several cholecalciferol (D3 metabolites: 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], 1,24R,25-trihydroxycholecalciferol [1,24R,25-(OH)3D3], 1 alpha-hydroxy-cholecalciferol (1 alpha-OHD3), 24R,25-dihydroxycholecalciferol [24R,25-(OH)2D3], 1,25-dihydroxy-26,27 hexadeuterium cholecalciferol (1,25-(OH)2-26,27[2H]6D3) and 1,25-dihydroxy-24R-fluorocholecalciferol [1,25-(OH)2-24R-FD3] for their activity in preventing the development of tibial dyschondroplasia in broilers. The basal diet used is low in calcium, high in phosphorus and chlorine and is known to promote a high incidence of tibial dyschondroplasia. The chicks received ultraviolet radiation from fluorescent lights in addition to 1100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet. Supplementation of the diet with 10 micrograms/kg of all the metabolites except 24R,25-(OH)2D3 significantly lowered the incidence and severity of tibial dyschondroplasia and increased bone ash when compared to birds receiving the basal diet. None of the active D3 metabolites was effective when fed at 0.1 or 1.0 micrograms/kg of diet. Two active compounds tested [1,25-(OH)2D3 and 1,24R,25-(OH)3D3] at 5 micrograms/kg of diet were effective in reducing either the incidence or severity of tibial dyschondroplasia.

The Effect of Dietary Cholecalciferol, 25-Hydroxycholecalciferol and 1,25-Dihydroxycholecalciferol on the Development of Tibial Dyschondroplasia in Broiler Chickens in the Absence and Presence of Disulfiram

Four experiments were conducted to determine the effect of dietary cholecalciferol (vitamin D3), 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on the changes in growth, feed efficiency and bone ash, and the incidence, severity and number of #3 scores of tibial dyschondroplasia caused by the addition of disulfiram to the diet. The basal diet used was low in calcium and high in phosphorus and chlorine and known to promote a high incidence of tibial dyschondroplasia in broiler chickens. The chickens in all experiments received enough ultraviolet radiation from fluorescent lights in the pens to nearly satisfy their need for vitamin D. The addition of disulfiram to the diet caused an increase in most of the measurements indicating development of tibial dyschondroplasia in all of the experiments, and caused a decrease in bone ash in two of the experiments and a decrease in growth and gain:feed in one experiment. The addition of D3 to a diet containing no D3 caused higher bone ash and lower incidence of tibial dyschondroplasia in the absence or presence of disulfiram. The effects of the addition of 25-OHD3 to diets containing approximately five times the requirement of D3 in the absence and presence of disulfiram caused variable results. The addition of 1,25-(OH)2D3 to the D3-supplemented diet in the absence or presence of disulfiram caused dramatic increases in bone ash and a decrease in most of the criteria used to measure development of tibial dyschondroplasia. There was no indication of interaction of the effects of D3, 25-OHD3 and 1,25-(OH)2D3 with the action of disulfiram.

Effect of Dietary Calcium, Phosphorus, Chloride, and Zeolite on the Development of Tibial Dyschondroplasia

The effect of synthetic zeolite was investigated on the development of tibial dyschondroplasia in young broilers fed diets in which the dietary levels of calcium, phosphorus, and chloride ranged from adequate to deficient. In the first two experiments the calcium level was maintained at .65% and four combinations were fed of .30% and .15% chloride and .75 % and .50% phosphorus with and without 1% zeolite.Feeding the high phosphorus diet caused a high incidence of tibial dyschondroplasia that was lowered by feeding 1% zeolite. In both experiments the feeding of zeolite at a low level of dietary phosphorus caused a significant lowering of 16-day weight and bone ash. In the third experiment, when diets containing all combinations of .65% and .80% calcium and .50% and .60% phosphorus were fed, the addition of 1% zeolite caused a significant lowering of the 16-day weight, bone ash, and incidence, score, and percentage severe tibial dyschondroplasia. Once again as in the previous two experiments, there was a significant interaction between dietary phosphorus level and zeolite and 16-day weight and bone ash. Feeding zeolite significantly decreased phytate phosphorus retention.

Effects of Different Soybean Meals on the Incidence of Tibial Dyschondroplasia in the Chicken

Interexperimental variation in the incidence of tibial dyschondroplasia of chickens that occurred in studies on the effect of dietary calcium, phosphorus and cholecalciferol metabolites was apparent from previous reports from this laboratory. Since the source of commercial soybean meal used in the diets was known to change, studies were conducted to evaluate different sources of soybean meal on the incidence of tibial dyschondroplasia. A series of experiments demonstrated that the soybean meals from one source consistently produced a high incidence of tibial dyschondroplasia (34–69%); whereas soybean meals from a different source consistently produced low incidences (14–28%). This same relationship was found with soybean meals from these two plants produced a year apart. When the levels of two soybean meals that produced a high incidence of tibial dyschondroplasia were reduced in the diet from 35 to 24 to 12% the incidence of tibial dyschondroplasia was reduced from 60 and 69% to 25 and 20% to 15 and 10%, respectively. The most striking difference between the meals observed by chemical analysis was in the high antitrypsin and urease values of the meals that induced tibial dyschondroplasia. Chickens fed the soybean meal that reduced tibial dyschondroplasia also had reduced pancreas size in one experiment but not another. The soybean meals that induced tibial dyschondroplasia caused an increase in testes size but had no effect on liver, adrenal and thyroid size or plasma levels of calcium, phosphorus and triiodothyronine (T3). No difference in the utilization of the diets as measured by metabolizable energy values and lipid calcium, phosphorus or phytin phosphorus retention was found between the soybean meals that induced high or low incidence of tibial dyschondroplasia with chickens at 19–21 d of age.

Effect of Dietary Sodium Fluoride on Growth and Bone Development in Growing Turkeys

Large White male turkeys were fed rations containing 0, 12.5, 25, 50, 100, 200, 400, and 800 ppm added fluoride (F) from sodium fluoride in a corn-soybean assay diet containing tricalcium phosphate and 3 to 5 ppm F. The 800 ppm treatment was discontinued at 8 weeks because of low weight gains and a high incidence of leg disorders.Turkeys receiving defluorinated phosphate (32% calcium, 18% phosphorus) had significantly higher 4-week body weights than turkeys receiving tricalcium phosphate. Turkeys fed 0, 400, and 800 ppm F had significantly lower body weights at 8 weeks than turkeys fed 50 ppm F. A similar weight pattern was seen at 18 weeks, although the differences were not statistically significant. Based on growth response in this study, a requirement of 20 ppm F is proposed.Increasing levels of dietary F resulted in large increases in tibia F. Removal of high dietary F in certain groups at 8 weeks resulted in growth recovery and reduction in tibia F by 18 weeks.Elevated plasma alkaline phosphatase activity was observed with added dietary F of 400 and 800 ppm. At 4 weeks, tibiae from turkeys receiving high F had a trend (not statistically significant) toward lower percentage ash and a significantly lower breaking strength than controls. Compared to controls, tibiotarsi from turkeys on high F rations were significantly shorter, had thinner cortices, and had a narrower proliferative zone of proximal growth plates. A high incidence of tibial dyschondroplasia was observed, but it was not correlated with dietary treatment.

The Role of Calcium and Phosphorus in the Etiology of Tibial Dyschondroplasia in Young Chicks

By means of a central composite rotatable design with dietary calcium levels of 0.63, 0.70, 1.10, 1.50 and 1.67% and total phosphorus levels of 0.53, 0.61, 0.81, 1.01 and 1.09%, practical-type rations were fed for 2 weeks to commercial broiler-type chickens. The design involved three replicates for each rotatable point and 15 replicates for the central point with 10 cockerels per replicate or a total of 390 birds. When the experiment was terminated, the chickens were weighed and killed; one tibia was used to determine bone ash and the other tibia for scoring the incidence and severity of tibial dyschondroplasia. The incidence of tibial dyschondroplasia in chickens fed the various diets ranged from 0 to 37%. A high incidence of tibial dyschondroplasia was associated with diets containing high phosphorus and low calcium levels. Tibial dyschondroplasia score and percentage of bone ash were not correlated. No obvious relationships existed between tibial dyschondroplasia incidence and percentage retention of calcium and phosphorus. A second experiment confirmed the finding that increased dietary calcium levels would reduce the incidence of tibial dyschondroplasia when chcikens were fed diets high in phosphorus.

An Intermittent Problem with Tibial Dyschondroplasia

Broilers observed in the summer of 1978 had an excessively high incidence of tibial dyschondroplasia, causing both downgrading and loss of parts from broken legs. No etiological agent was determined. Birds held to 16 weeks of age retained the cartilaginous lesions. Bone ash was not diagnostic. Serology indicated no correlation with infectious bursal disease. No bacteria were isolated. The condition was not observed in the next placement of chicks.

The inheritance of tibial dyschondroplasia in broilers.

A breeding programme to develop a line of chickens with a high incidence of tibial dyschondroplasia (TD) from Australian broiler stock is described. Despite the absence of a control flock, this programme has demonstrated that selection in a broiler population can rapidly increase the incidence of TD. There was consistent circumstantial evidence of the presence of a major sex-linked gene, the recessive allele of which is associated with an increased incidence of TD. The realised heritability estimates (obtained in the absence of a control flock) consistently exceeded 1.00, suggesting the presence of an environmental trend favourable to the onset of TD over the four generations of this investigation. There was a high maternal component or dominance genetic component, or both, for the inheritance of TD in the final generation, suggesting that environmental factors associated with the female parent line may influence the incidence of TD in broilers.

Studies on tibial dyschondroplasia in ducks

A high incidence of tibial dyschondroplasia was present naturally in a variety of strains of ducks. The incidence was higher in heavy strains than in light strains and both incidence and severity were markedly reduced by early restriction of growth rate. The incidence and severity differed somewhat in groups of ducks of the same strain and growing at the same rate on two different commercial rations. The abnormality was not dramatically reduced by feeding a ration containing a high bicarbonate mineral mix. The histological development of the lesion is described and possible aetiologies discussed. Despite the high incidence, tibial dyschondroplasia seldom caused significant economic loss.