Avian Tibial Dyschondroplasia: A Morphological and Biochemical Review of the Growth Plate Lesion and Its Causes

Abstract

Abstract. 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 necrose prematurely. The chondrocytes also produce decreased amounts of extracellular proteins, such as collagen X and fibroblast growth factor-0, that are necessary for cartilage maturation. This immature cartilage becomes highly crosslinked 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 thiraminduced tibial dyschondroplasia.Key words: Chickens; copper deficiency; dyschondroplasia; growth plate; homocysteine; osteochondrosis.Endochondral ossification describes the processes by which bones grow longitudinally and several types of fractures heal. Longitudinal growth occurs in the growth plate that links the epiphyseal and the metaphyseal regions within bone. The main physiological events of endochondral ossification are chondrocyte proliferation, extracellular matrix production, chondrocyte hypertrophy, matrix calcification, vascular invasion, matrix degradation, and primary bone formation.The main components of the growth plate include metaphyseal bone, a fibrous peripheral structure, and a layer of cartilage called the physis. The metaphysis functions include 1) vascular penetration into the bottom of the physis, 2) bone formation, and 3) remodeling of calcified cartilage and bone to form trabecular bone.I4 The fibrous peripheral structure is composed of the ossification groove, which provides chondrocytes for latitudinal expansion of the growth plate, and the perichondrial ring, which provides mechanical support for the tenuous chondro-osseous j u n c t i~n . '~~> l~~ The growth plate cartilage is responsible for the rate of growth and actual length of the bone and can be divided into three principal zones: the reserve, proliferative, and hypertrophic zones. Reserve zoneThe reserve zone lies either adjacent to ...

Earlier hatching time predisposes Cobb broiler chickens to tibial dyschondroplasia

“…TD is known as a common developmental disease in several avian species that is related to rapid growth, particularly in early life (Orth and Cook, 1994;Praul et al, 2000;Leach and Monsonego-Ornan, 2007;Dan et al, 2009). …”

“…TD has similarities to mammalian osteochondrosis (Orth and Cook, 1994), including several skeletal diseases in humans and pigs involving described mutations in collagen and parathyroid hormone (Leach and Monsonego-Ornan, 2007). In TD, the usual procession in long bones of chondrocyte phenotypes through to a fully differentiated state within the resting zone of the epiphysis is disrupted (Farquharson and Jefferies, 2000).…”

“…The chondrocytes in the hypertrophic zone of long bones do not reach their expected size, remaining small and rounded (Thorp, 2008) and their lifespan is increased (Farquharson and Jefferies, 2000;Leach and Monsonego-Ornan, 2007). This results in an accumulation of immature cartilage in the metaphysis (Orth and Cook, 1994) and is most notable in the proximal tibia. The collagen in this cartilage is abnormal, the molecules being highly crosslinked (Orth and Cook, 1994), which impairs the resorption of cartilage by osteoclasts and makes the cartilage resilient to vascular invasion (Farquharson and Jefferies, 2000).…”

“…This results in an accumulation of immature cartilage in the metaphysis (Orth and Cook, 1994) and is most notable in the proximal tibia. The collagen in this cartilage is abnormal, the molecules being highly crosslinked (Orth and Cook, 1994), which impairs the resorption of cartilage by osteoclasts and makes the cartilage resilient to vascular invasion (Farquharson and Jefferies, 2000).…”

“…Many factors have been incriminated in the occurrence of TD, including genetic predisposition, an inappropriate calcium : phosphorus ratio in feed (i.e. a relative excess of phosphorus), metabolic acidosis resulting from an electrolyte imbalance in feed (excess chloride over the sum of sodium and potassium ions), copper deficiency, excess dietary cysteine or homocysteine and some mycotoxins (Orth and Cook, 1994;Thorp, 2008). Experimentally, TD has been induced by thiram treatment but the mechanisms involved in these studies may differ from the condition observed in the field (Orth and Cook, 1994).…”