Avian tibial dyschondroplasia (ATD) results from a defect in endochondral ossification and is characterised by an accumulation of non-mineralised avascular cartilage extended distally from the proximal tibiotarsal epiphysis

During longitudinal bone growth, chondrocytes within the epiphyseal plate pass through a series of well defined stages (see Brighton, 1978), characterised by changes in proliferation rate, shape and size, and synthesis and deposition of extracellular matrix components (Hunziker and Schenk, 1989). Consequently, the growth plate of the chick (Howlett, 1979) and other species can be divided into several distinct zones containing resting, proliferating, maturing/transitional and hypertrophic cells. Controversy exists concerning the molecular control and co-ordination of the mechanisms involved in the transition of cells from a proliferative to a differentiating state, partly due to the fact that studies on isolated cells may not reflect the responses of cells in their normal microenvironment in vivo (Nathan and Sporn, 1991). The spatial and temporal organisation of the growth plate makes it ideal for the in situ biochemical study (Zanelli and Loveridge, 1991) of the regulation of these mechanisms during bone growth. The morphological changes associated with chondrocyte maturation are well defined and we and others have recently reported that chondrocytes undergoing differentiation and hypertrophy express high levels of transforming growth factor-β (TGF-β) (Thorp et al., 1992; Jingushi et al., 1990) and the product of the proto-oncogene c-myc (Farquharson et al., 1992a) but the importance of these proteins in endochondral ossification has, thus far, not been defined. However, recent reports indicate that c-myc is essential in apoptosis (Evan et al., 1992; Shi et al., 1992) and it has been suggested that growth plate mineralisation involves this process (Kardos and Hubbard, 1982; Akisaka and Gay, 1985). Avian tibial dyschondroplasia (ATD) results from a defect in endochondral ossification and is characterised by an accumulation of non-mineralised avascular cartilage extended distally from the proximal tibiotarsal epiphysis (Leach and Nesheim, 1965; Riddell et al., 1971; Poulos, 1978). It occurs spontaneously, and may be similar to osteochondrosis (Poulos, 1978), a generalised cartilage defect that has been reported in rapidly growing mammals (Rejno and Stromberg, 1978) and metaphyseal chondroplasia in humans (Rimoin et al., 1974). Although the incidence of ATD is affected by a number of factors such as nutrition 949 Journal of Cell Science 105,949-956 (1993) Printed in Great Britain © The Company of Biologists Limited 1993