The vascularisation of cartilage, despite its importance in development and a number of disease processes has yet to be fully elucidated. The work presented here lends evidence for a major role for the vasculature in the erosion of cartilage. A soluble factor or factors produced by the endothelium is responsible for the degeneration and subsequent death of hypertrophic chondrocytes. The cartilage itself, however, may also have a role, as it is also shown that only a particular subset of hypertrophic chondrocytes can become invaded by the vasculature, and only at a specific time when placed on the chick chorio-allantoic membrane (CAM). Evidence is provided that the control of this may be periosteally derived, and further evidence suggests that the breakdown of cartilage hyaluronan may be an initiating factor in the process.;The collagen expression of the degenerate chondrocytes is not adversely affected qualitatively by the endothelium, except for a loss of type X collagen, though quantitatively, there is a large reduction in the amount of collagen produced. Of importance, is that throughout the degeneration process, and despite the loss of chondrocyte morphology, the cells maintain expression of type II collagen and there is no specific switch to type I collagen production that is associated with some morphological changes in chondrocytes The ultimate fate of these chondrocytes could not be convincingly elucidated.;Finally, the vascularisation of human OA cartilage was studied. Human OA cartilage loses its ability to remain avascular when placed into an in-vivo model of vascularisation, the chick CAM. The vascular invasion is associated with a loss of histochemical staining for proteoglycans and glycosaminoglycans and a deposition of type I and type X collagens around the invasive vessel