Nutritional, Genetic and Morphological Studies of an Abnormal Cartilage Formation in Young Chicks

Leach, R. M.; Nesheim, M. C.

doi:10.1093/jn/86.3.236

Cited by 233 publications

(106 citation statements)

References 4 publications

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“…TD, also called osteochondrosis, occurs in a variety of strains of domestic animals bred and raised for rapid growth (Olsson, 1978). There appear to be both genetic and nutritional factors involved but these have not been clearly defined (Poulos et al, 1978;Leach and Nesheim, 1965).…”

mentioning

confidence: 99%

Chicken tibial dyschondroplasia: A limb mutant with two growth plates and possible defects of collagen crosslinking

Chen

Gibney

Leach

et al. 1993

Developmental Dynamics

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In the cartilaginous epiphyseal growth plate, extracellular matrix molecules such as collagens are believed to play important roles during both normal and abnormal development. One defect of the epiphyseal plate occurs in chickens with a condition termed tibial dyschondroplasia (TD). This abnormality occurs in certain strains of juvenile chickens and other rapidly developing animals. It is characterized by the presence of a mass of avascular, uncalcified cartilage which is retained in the proximal metaphysis of the tibiotarsus. To elucidate the developmental events which may be involved in this lesion, we have performed both immunohistochemistry and in situ hybridizations for collagen types I1 and X, known components of the extracellular matrix of the growth plate. By immunohistochemical analyses, the TD lesion contains both of these collagen types; therefore, the presence of these molecules per se is not sufficient for calcification of vascularization to occur. Since type X collagen is expressed exclusively in hypertrophic cartilage, the chondrocytes in the lesion must have undergone hypertrophy before their developmental arrest. The matrix of the lesion also reacted with a monoclonal antibody which is directed against an epitope in the NH,-terminal telopeptide of the al(I1) chain. Our previous data suggest that this epitope is rendered unavailable in type 11 collagen which has undergone crosslink formation; its availability in the lesion suggests that crosslinking may be abnormal. Lastly, analyses by in situ hybridization failed to detect mRNA for either type I1 or type X collagen within the lesion, but chondrocytes distal to the lesion do contain mRNAs for these collagens in a spatial pattern suggesting the presence of a second growth plate. 0 1993 Wiley-Liss, Inc.

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confidence: 99%

Chicken tibial dyschondroplasia: A limb mutant with two growth plates and possible defects of collagen crosslinking

Chen

Gibney

Leach

et al. 1993

Developmental Dynamics

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“…This indicates that this hormone is effective in preventing TD induced by genetic selection and not only TD induced by a Ca/P imbalance (Edwards, 1989;Edwards, 1990;Rennie et al, 1993). Previous investigators (Leach & Nesheim, 1965;Riddell, 1975;Sheridan et al, 1978;Wong-Valle et al, 1992) have indicated that selective breeding can influence the incidence of TD. The results of this study, where two lines of broilers were selected for high or low frequency of TD, agree with this hypothesis.…”

Section: Discussionmentioning

confidence: 78%

“…For the purposes of the present study the growth plate was considered to consist of three distinct zones characterized by the morphological appearance of proliferative, transitional and hypertrophic chondrocytes. The assessment of dyschondroplasia by histological examination, was based on microscopic changes to the cells and matrix which are considered characteristic of TD (Leach & Nesheim, 1965;Siller, 1970;Poulos, 1980;Hargest et al, 1985): these include the accumulation of an avascular matrix in which rounded lacunae contain partially hypertrophied chondrocytes. In addition some chondrocytes demonstrate marked degenerative changes to their cytoplasm and nuclei (Thorp etal, 1991).…”

Section: Histological Assessmentmentioning

confidence: 99%

“…Avian tibial dyschondroplasia (TD) is characterized by a mass of opaque cartilage, extending from the growth plate (physis) into the metaphysis (Leach & Nesheim, 1965), which is composed of smaller lacunae and more matrix than normal hypertrophic cartilage (Leach & Nesheim, 1965;Siller, 1970;Itakura et al, 1973;Poulos, 1980;Hargest et al, 1985). Recent studies (Thorp et al, 1991;Farquharson et al, 1992c;Loveridge et al, 1992b;Thorp, 1992) have indicated that the accumulated cells are a consequence of a failure of transitional (prehypertrophic) chondrocytes to hypertrophy fully.…”

Section: Introductionmentioning

confidence: 99%

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Avian tibial dyschondroplasia: The interaction of genetic selection and dietary 1,25 ‐dihydroxycholecalciferol

et al. 1993

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SUMMARYThe effects of dietary 1,25-dihydroxycholecalciferol on the incidence and severity of tibial dyschondroplasia (TD) were assessed in broiler fowl selected for TD (high-TD line) and against TD (low-TD line). Assessment was by examination with a portable Lixiscope to identify lesions in live birds, gross pathology and histopathology. Eighty broilers in four groups of 20 were examined. When fed on standard diets the low-TD line had a 15% incidence whereas the high-TD line had a 63% incidence. The chicks in the high-TD line, when fed on a diet supplemented with 5 μg or with 10 μg 1,25-dihydroxycholecalciferol/kg diet, showed a marked reduction in the incidence of TD, to 21% and 0% respectively. The growth plate in the proximal tibiotarsi of the high-TD line showed accumulations of transitional chondrocytes, supporting the hypothesis that a failure of chondrocyte differentiation is the cause of dyschondroplasia. This hypothesis is further supported by studies which indicate 1,25-dihydroxycholecalciferol has a major role in chondrocyte differentiation.

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“…Tibial dyschondroplasia results from abnormal growth plate cartilage development and was first described in chickens by Leach & Nesheim (1965). It remains, despite intensive research, one of the major skeletal disorders of the modern broiler chicken .…”

Section: Introductionmentioning

confidence: 99%

Parathyroid hormone-related peptide expression in tibial dyschondroplasia

Farquharson¹,

Seawright²,

Jefferies³

2001

Avian Pathology

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Parathyroid hormone-related peptide (PTHrP) has a key role in the growth of long bones, as it is a negative regulator of growth plate chondrocyte terminal differentiation. We have examined the distribution and gene expression levels of PTHrP in the growth plates of broiler chickens with tibial dyschondroplasia (TD) in order to determine whether increased expression of PTHrP is responsible for the delayed chondrocyte differentiation that is characteristic of this skeletal disorder. PTHrP protein distribution and gene expression levels were assessed by immunocytochemistry and reverse transcriptase-polymerase chain reaction, respectively. In growth plates of normal birds, PTHrP was found to be distributed throughout all maturational zones of the growth plate. In cartilage proximal to the TD lesion, PTHrP immunostaining and the level of PTHrP gene expression were similar to that observed in normal birds. In contrast, many chondrocytes within the centre of the TD lesion stained poorly for PTHrP and this was reflected in the lower levels of PTHrP mRNA detected in lesion cells. These results suggest that alterations in PTHrP distribution and gene expression are not primarily responsible for the delayed chondrocyte differentiation and hypertrophy noted in dyschondroplasia, but are a result of secondary changes due to the pathology of the condition.

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Nutritional, Genetic and Morphological Studies of an Abnormal Cartilage Formation in Young Chicks

Cited by 233 publications

References 4 publications

Chicken tibial dyschondroplasia: A limb mutant with two growth plates and possible defects of collagen crosslinking

Chicken tibial dyschondroplasia: A limb mutant with two growth plates and possible defects of collagen crosslinking

Avian tibial dyschondroplasia: The interaction of genetic selection and dietary 1,25 ‐dihydroxycholecalciferol

Parathyroid hormone-related peptide expression in tibial dyschondroplasia

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