No abstract

The effects of human recombinant bone morphogenetic protein-2 (rhBMP-2) on rabbit fractures healing under both stable and unstable mechanical conditions were investigated. rhBMP-2 was administered (1) on bioerodible particles, (2) in a collagen gel, and (3) by injection. rhBMP-2 on bioerodible particles has no effect as the particles prevent the migration of cells that produce the callus. The collagen gel is resorbed more rapidly; the development of the callus of mechanically unstable fractures is similar to controls at 14 days. When rhBMP-2 is injected, the callus of mechanically unstable fractures develops more rapidly so that cortical union occurs by 21 days, as compared with 28 days in control fractures. The effects on fractures healing under stable mechanical conditions are minimal. It is argued that mechanical factors influence the size of the callus of normally healing fractures and, although BMP-2 accelerates the rate of development of the callus and cortical union, it does not affect the amounts of bone and cartilage produced.

The development of the articular cartilage of the rabbit knee joint from the 17-day fetus to the 2-year adult rabbit has been examined. At 17 days, the developing femur and tibia are separated by the interzone. Cavitation occurs around 25 days; the cells of the intermediate layer flatten and move onto those of the chondogenous layers to create the articular surfaces. After birth, growth of the cartilage is mainly the result of matrix production. Ossification of the epiphyses is complete by 6 weeks postpartum. Horizontal zones can be distinguished in the articular cartilage; the superficial cells are aligned parallel to the surface, but in the deep layers the cells are in columns. The tidemark is first seen at 12-14 weeks. The matrix of the interzone in the 17-day fetus contains types I, III and V collagens, but no type II. After cavitation at 25 days, the surface layer of the articular cartilage still contains type I, but no type II collagen. From 6 weeks postnatal onwards, type II collagen is present throughout the cartilage and type I disappears. Type III collagen is initially in the inter-territorial matrix, but later it is mainly pericellular. Type V collagen is pericellular both in the chondrogenous layers and later in the articular cartilage, but is not present in the epiphyseal cartilage below. From 6 weeks onwards, types III and V collagens create a capsule around all the chondrocytes above the tidemark. The relationship of types V and XI collagens is discussed. It is concluded that the articular chondrocytes form a unique subset of cells from the earliest stages of joint formation in the fetal rabbit.