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At least 19 recordsLinked to original sources
PubMed1985

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 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.

Animal Feed↗
PubMed1985

Observations on several factors influencing the incidence of tibial dyschondroplasia in broiler chickens.

The effects of age vs. diet, potassium level, tetramethylthiuram disulfide (thiuram), and ionophores in the diet on the development of tibial dyschondroplasia in broilers was investigated. Changing broiler chicks from a diet that induced tibial dyschondroplasia to one that reduced the disease or vice versa caused a change in the incidence in the direction of the last-fed diet; however, in most cases the chicks did not develop as low or high an incidence of tibial dyschondroplasia as the birds fed the reducing or inducing diet, respectively, for the entire experimental period. Potassium supplementation of a corn-soybean meal diet that contained .88% potassium had no effect on the incidence of tibial dyschondroplasia. However, supplementation of a low potassium (.3%) corn-corn gluten meal-animal protein diet with potassium increased the incidence of tibial dyschondroplasia. The addition of thiuram to the diet caused an increase in tibial dyschondroplasia. When thiuram was added to the tibial dyschondroplasia-inducing diet, it also caused a decrease in bone ash and in the total and ultrafilterable plasma calcium. A significant negative correlation was obtained between incidence and score of tibial dyschondroplasia and bone ash of the ends and middles of the tibia when thiuram was fed. No consistent effects of the ionophores monensin and lasalocid on the development of tibial dyschondroplasia in broilers was noted in three experiments, although significant effects of the ionophores on the incidence or score of the disease was observed in two experiments.

Animals↗
PubMed1984

Studies on the etiology of tibial dyschondroplasia in chickens.

Experiments have been conducted to obtain information on the cause of tibial dyschondroplasia in chickens. All studies were conducted with corn-soybean meal practical-type diets and chicks from 1 day to 3 or 4 weeks of age. A high calcium and low phosphorus content of the diet and a wide calcium:phosphorus ratio in the diet decrease the incidence of tibial dyschondroplasia in broiler chickens. Increasing the chloride level of the diet increased the incidence of tibial dyschondroplasia. Increasing the magnesium content of the diet decreased tibial dyschondroplasia; however, the effect of magnesium was not as strong as that of calcium. The addition of sodium sulfate to the diet had no effect on the incidence of tibial dyschondroplasia. Five broiler strain crosses were all susceptible, although to a variable extent, to the development of tibial dyschondroplasia, whereas Single Comb White Leghorn chickens did not develop the disease. Male chicks developed tibial dyschondroplasia with a higher incidence than did female chicks. Supplementation of the chickens with 20 ng/day of either 1,25-dihydroxycholecalciferol [1,25(OH)2D3] or 24,25-dihydroxycholecalciferol [24,25(OH)2D3] had no effect on the incidence of tibial dyschondroplasia. J. Nutr . 114: 1001-1013, 1984.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

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 weighted 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 chickens were fed diets high in phosphorus.

Animals↗
PubMed1994

Molybdenum but not copper counteracts cysteine-induced tibial dyschondroplasia in broiler chicks.

Studies were conducted to evaluate the ability of copper and molybdenum to prevent cysteine-induced tibial dyschondroplasia in broiler chicks. Experiment 1 was a 3 x 3 factorial arrangement of treatments used to investigate the interaction between Cu (0, 150 or 300 mg/kg diet) and Mo (0, 10, or 100 mg/kg diet) on cysteine-induced tibial dyschondroplasia. Molybdenum at both supplemental levels, but not Cu, prevented cysteine-induced tibial dyschondroplasia. In Experiment 2 (a 3 x 3 factorial arrangement of treatments with 0, 5 or 10 g/kg diet of cysteine and 0, 10 or 100 mg/kg diet of Mo), Mo prevented cysteine-induced but not spontaneous tibial dyschondroplasia. Cysteine and Mo did not affect the mechanical properties of the tibiotarsus. In Experiment 3, cysteine (0 or 10 g/kg diet) and Mo (0 or 100 mg/kg diet) were used to study the tissue concentrations of mineral and hepatic sulfite oxidase activity. Supplemental Mo increased Mo concentrations in the plasma and liver. Cysteine prevented these increases; however, cysteine, in the absence of supplemental Mo, did not affect concentrations of Mo in these tissues. Dietary cysteine and/or Mo did not affect tissue levels of Cu. We conclude that Mo prevents cysteine-induced tibial dyschondroplasia and that the induction of tibial dyschondroplasia by cysteine is not related to the Mo and Cu deficiency.

Animals↗
PubMed1994

Plasma concentrations of growth hormone and insulin-like growth factor-I in chickens developing tibial dyschondroplasia.

The concentrations of plasma growth hormone (GH) and insulin-like growth factor-I (IGF-I) were measured in broilers during the initial development of tibial dyschondroplasia. Chicks were fed a standard starter ration, or a diet imbalanced in calcium and phosphorus to increase the incidence of dyschondroplasia. At 14 days of age four blood samples were collected and assayed for GH and IGF-I. The chicks were killed at three weeks of age and sections of bone were assessed histologically for evidence of dyschondroplasia. All the chicks displayed a pulsatile pattern of GH secretion. Eight of the group fed the imbalanced diet developed dyschondroplasia which was accompanied by a significant increase in the mean and peak GH concentrations compared with the control group but no increase in basal concentrations. The chicks fed the imbalanced diet which did not develop dyschondroplasia were not different from the control birds. There were no differences in IGF-I concentrations between the groups.

Animals↗
PubMed1987

Effect of short fasts on the development of tibial dyschondroplasia in chickens.

The length of time each day that feed is available to young broiler-type chickens significantly influenced the development of tibial dyschondroplasia. Birds that were fasted for 8 or 10 h per day had reduced incidences of tibial dyschondroplasia as compared to birds fed ad libitum (5-11% vs. 59-68%). When birds were fasted for only 2 or 4 h each day there was no significant effect on the development of tibial dyschondroplasia. Birds fasted for 8 h every other day or every 4th d had lower incidences of tibial dyschondroplasia compared to ad libitum fed controls. Fasting for 8 h on the 4th d or the 4th and 8th d of a 20-d experiment had no effect on the incidence of tibial dyschondroplasia as compared to controls. Except for the daily fasting there was little effect of fasting on 20-d body weight or gain per feed intake. Fasting increased the percent bone ash in the tibia in all experiments. Fasting had no effect on total calcium, ultrafilterable calcium, dialyzable phosphorus or growth hormone levels in plasma taken from the birds the 18th and 19th day. The hour of the day that the birds were bled had a significant influence on the plasma total calcium, dialyzable phosphorus and growth hormone levels.

Animals↗
PubMed1989

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.

Animals↗
PubMed1980

Evaluation of tibial dyschondroplasia during aflatoxicosis and feed restriction in young broiler chickens.

Graded levels of aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram of toxin per gram of feed) were incorporated into a broiler starter ration that was fed from day-old to 3 weeks of age. Both tibias were removed from the birds, tibial dyschondroplasia lesions were scored, and the incidence of lesions reported. Both the incidence and severity of tibial dyschondroplasia decreased significantly (P less than .05) at the aflatoxin levels of 2.5, 5.0, and 10.0 ppm. In a second experiment, birds received a broiler starter ration either ad libitum or feed restricted by 23% of the feed consumed by the controls. The feed-restricted birds' body weights and the severity and the incidence of tibial dyschondroplasia decreased to values comparable with those of birds receiving 5.0 ppm aflatoxin. These data suggest that either feed consumption or growth rate, or both, plays a major role in the initiation of tibial dyschondroplasia and tibial dyschondroplasia is not a result of direct intervention of aflatoxin in bone development.

Aflatoxins↗
PubMed1988

Effects of dietary zeolite and vitamin A on tibial dyschondroplasia in chickens.

Four experiments were conducted to determine the effects of dietary zeolites on tibial dyschondroplasia in chicks. All studies used a practical-type corn-soybean meal diet and male broiler chicks from 1 day to 14 or 16 days of age. Vitamin A was added to the diet in the first experiment at levels of 0 or 45,000 IU/kg in addition to full or half required levels of vitamin premix, and in the second experiment at levels of 0, 11,250, 22,500 and 45,000 IU/kg in addition to full requirement levels of vitamin premix. This was done in order to determine if vitamin levels affected expression of tibial dyschondroplasia and, if so, if this expression could be influenced by 1.0% dietary zeolite. A high level of dietary vitamin A caused a lower incidence of tibial dyschondroplasia in Experiment 1 but had no effect in Experiment 2. Zeolite at graded levels of 0, .25, .50, and 1.0% in Experiment 3 and at the 1.0% level in all other experiments consistently caused a higher bone ash and a lower incidence and number of birds exhibiting severe tibial dyschondroplasia. The addition of zeolite to the diet generally had no effect on body weight or gain:feed ratio but reduced tibial dyschondroplasia scores in two of the four experiments. In Experiment 4, the addition of dietary zeolite increased 47Ca absorption but did not influence biological half-life.

Aluminum Silicates↗
PubMed1992

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)2D3], 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 micrograms/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 micrograms/kg of 1,25-(OH)2D3 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.

Aluminum Silicates↗
PubMed1995

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)2D3] can prevent tibial dyschondroplasia 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)2D3 was fed at 0 or 5 micrograms/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2D3 were then fed 0 microgram/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschondroplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2D3 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)2D3 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)2D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2D3 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)2D3 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 micrograms/kg 1,25-(OH)2D3 is fed with .65% calcium for the entire growout period.

Age Factors↗
PubMed1978

Tibial dyschondroplasia (osteochondrosis) in the turkey. A morphologic investigation.

Sixty-seven Broadbreasted White Turkeys, 4 to 137 days old, were included in the investigation. Some were normal, while others were limping, and some had bowed legs. Immediately after destruction of the birds, the arteries of the legs were injected with Colorpaque, using a technique introduced by the author. The proximal part of one or both tibiae were examined radiographically, macroscopically, and microscopically. The microscopic examination included histology, microangiography, and microradiography. The normal development and morphology of the proximal tibia is presented. Thereafter an account is given of development and morphology of the tibia with dyschondroplastic lesions (retained cartilages). It was found that 39 of the 67 birds had some degree of tibial dyschondroplasia. The retained cartilage was seen in the posteromedial part of the proximal tibial metaphysis. The growth plate both of the normal and abnormal birds consisted of 3 layers of cells in order from the epiphysis--the one of proliferating cells, the one of transitional cells, and the one of hypertrophied cells. A main feature in tibial dyschondroplasia is accumulation of transitional cells, which do not have a vascular supply. By microangiographic means it was possible to demonstrate that the retained cartilage is surrounded by numerous vessels, which apparently cannot get into the cartilage. The reason for the loss of normal differentiation of the cartilage cells and concomitant disturbance of the endochondral ossification is obscure. It is speculated that changes on an ultrastructural and biochemical level are responsible for the pathologic condition. When the retained cartilage reaches a certain size, degenerative changes, necrosis, and fissures occur. Complete healing of the lesion was not seen in any of the birds, but partial disappearance of the proximal or distal part of the retained cartilage took place in some birds. It was concluded that the present investigation has shed light on the development and morphology of tibial dyschondroplasia, but it has also brought forward a number of questions about etiology. There seems to be good reason to believe that dyschondroplasia in the turkey is of similar nature as dyschondroplasia in broilers and osteochondrosis in domestic mammals.

Animals↗
PubMed1978

Skeletal lesions in the broiler, with special reference to dyschondroplasia (osteochondrosis). Pathology, frequency and clinical significance in two strains of birds on high and low energy feed.

The material consisted of 2,950 broilers of the variety Hybro Compact of two lines. An equal number of birds of both lines were given either a high energy feed (H) or a low energy feed (L), containing all nutrients known to be required by broilers. During the first 3 weeks, H and L starter feeds were given and thereafter H and L finishing feeds. At 21, 35, and 45 days of age, the birds were weighed in groups, and feed conversion calculated. At 21 days of age, the frequency of crooked toes and swollen hocks was registered. Birds were taken from each group for necropsy at regular intervals. Both clinically normal birds and those with locomotor disturbances were selected for necropsy, including radiographic examination. With the exception of 240 birds, which were kept for a long-term study, the birds on the H feed were slaughtered at 42 days of age and the ones on the L feed at 49 days of age. The long-term birds were slaughtered at regular intervals, weighed, and necropsied. The last birds were slaughtered at 134 days of age. A large number of skeletal lesions were found. They were: Twisted legs, slipped tendons, crooked toes, bowing of the proximal tibia, dyschondroplasia at different sites, fracture of the fibula, deformity of the spine, deviated sternum (with breast blisters), arthritis, and osteomyelitis. Leg weakness was found to be almost synonymous with skeletal deformities. Other causes were rare. The normal development and morphology of the skeleton and the morphology of tibial dyschondroplasia were the same as those previously described in the turkey. Dyschondroplasia was found not only in the proximal tibia but also in the distal tibia, proximal tarsometatarsus, proximal and distal femur, and to some extent also in the costochondral junction. Tibial dyschondroplasia was more common in the birds on the H feed than in the birds on the L feed. Hence, tibial dyschondroplasia was correlated with rapid growth. The other skeletal lesions did not differ in incidence in the birds on the H and L feeds. It was postulated that greater difference in growth rate is necessary for a demonstration of a possible correlation between skeletal deformities and growth rate.

Animal Feed↗
PubMedDate not supplied

Immune and bone properties of chicks consuming corn contaminated with a Fusarium that induces dyschondroplasia.

A study was conducted to contrast the dyschondroplasia-inducing capability of several species of Fusarium with that of the natural fungi found in poultry diets and litter. Day-old broiler chicks were fed pure corn cultures of specific fungal isolates for 3 weeks. Humoral immunity to sheep red blood cells (SRBC), body weight, valgus and varus leg deformities, incidence of dyschondroplasia, and mechanical properties of the tibiotarsi were examined. F. equiseti #15 was the only fungal isolate to induce dyschondroplasia to any significant degree, which confirmed previous work in Minnesota. This isolate also suppressed growth rate and humoral immunity, although dyschondroplasia sometimes did occur without associated immunosuppression and growth depression. Bone strength of the tibiotarsal diaphysis was normal, and gross lesions of valgus and varus leg deformities did not appear to be related to the incidence of dyschondroplasia in the 3-week-old chicks.

Animal Feed↗
PubMed1987

Effects of thiuram, disulfiram and a trace element mixture on the incidence of tibial dyschondroplasia in chickens.

Two experiments were conducted to determine the effect of dietary addition of 30 ppm of thiuram or disulfiram on the development of tibial dyschondroplasia (a large mass of cartilage in the proximal end of the tibia) in chicks in the presence and absence of trace element supplementation: B, Ni, Al, Sr, Br, V, Si, Sn, Cr, F, Mo, Li, Mn, Zn, Fe, Cu and I. In two experiments, the incidence and severity of tibial dyschondroplasia were lower in chicks fed the diet containing the trace element supplement than in those fed the basal diet. Adding thiuram or disulfiram to the diet caused a significantly higher incidence and severity of tibial dyschondroplasia in chicks regardless of the presence or absence of the trace element supplement. In a third experiment not involving thiuram or disulfiram the addition of trace elements had no significant effect on tibial dyschondroplasia. Adding thiuram or disulfiram to the diet in a fourth experiment lowered the absorption of 47Ca from the gastrointestinal tract but did not influence the biological half-life of 47Ca in the chick.

Absorption↗
PubMed1990

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.

24,25-Dihydroxyvitamin D 3↗
PubMed1994

Avian tibial dyschondroplasia: a morphological and biochemical review of the growth plate lesion and its causes.

Avian tibial dyschondroplasia is a disease found in fast growing strains of chickens, ducks, and turkeys worldwide in which growth plate cartilage accumulates in the metaphyseal region of the tibiotarsus; it is similar to mammalian osteochondrosis. Several biochemical and pathologic studies have shown that the growth plate chondrocytes do not reach their expected size in the hypertrophic zone and necroses prematurely. The chondrocytes also produce decreased amounts of extracellular proteins, such as collagen X and fibroblast growth factor-beta, that are necessary for cartilage maturation. This immature cartilage becomes highly cross-linked in the collagen molecules and apparently resistant to resorption and vascularization by the metaphyseal vessels. The dyschondroplastic cartilage remains in the metaphysis for several weeks. Not until the growth rate of the birds slows down is the cartilage able to be resorbed and replaced by trabecular bone. Many conditions have been found to induce tibial dyschondroplasia, including copper deficiency; fusarochromanone, thiram, and antabuse intoxication; excessive dietary levels of cysteine and homocysteine; metabolic acidosis; and bird rearing environment. However, the mechanism(s) by which these various methods induce tibial dyschondroplasia is presently not known. Current research is focusing on understanding the development of the disease and whether or not all these methods work by the same physiological chain of events. Recent biochemical evidence suggests that a copper deficiency might be caused by a different mechanism than genetically and thiram-induced tibial dyschondroplasia.

Animals↗