Mechanically modulated cartilage growth may regulate joint surface morphogenesis

The development of normal joints depends on mechanical function in utero. E xperimental studies have shown that the normal surface topography of diarth rodial joints fails to form in paralyzed embryos. We implemented a mathemat ical model for joint morphogenesis that explores the hypothesis that the st ress distribution created in a functional joint may modulate the growth of the cartilage anlagen and lead to the development of congruent articular su rfaces. We simulated the morphogenesis of a human finger joint (proximal in terphalangeal joint) between days 55 and 70 of fetal life. A baseline biolo gical growth rate was defined to account for the intrinsic biological influ ences an the growth of the articulating ends of the anlagen. We assumed thi s rate to be proportional to the chondrocyte density in the growing tissue. Cyclic hydrostatic stress caused by joint motion was assumed to modulate t he baseline biological growth, with compression slowing it and tension acce lerating it. Changes in the overall shape of the joint resulted from spatia l differences in growth rates throughout the developing chondroepiphyses. W hen only baseline biological growth was included, the two epiphyses increas ed in size but retained convex incongruent joint surfaces. The inclusion of mechanobiological-based growth modulation in the chondroepiphyses led to o ne convex joint surface, which articulated with a locally concave surface. The articular surfaces became more congruent, and the anlagen exhibited an asymmetric sagittal profile similar to that observed in adult phalangeal bo nes. These results are consistent with the hypothesis that mechanobiologica l influences associated with normal function play an important role in the regulation of joint morphogenesis.