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The Journal of Bone and Joint Surgery, Vol 69, Issue 2 162-173, Copyright © 1987 by Journal of Bone and Joint Surgery, Inc
Quantitation of chondrocyte performance in growth-plate cartilage during longitudinal bone growth
EB Hunziker, RK Schenk and LM Cruz-Orive
The longitudinal growth of bone depends on the activities of individual
chondrocytes of the growth plate. Each chondrocyte remains in a fixed
location throughout its life, and there accomplishes all of its functions.
Although a cell may perform several or all of its activities
simultaneously, one of these will usually predominate during a particular
phase of its life. The two most prominent stages are those of cellular
proliferation and hypertrophy (including the mineralization of matrix)
before the resorption of tissue during vascular invasion. By applying
recently developed stereological procedures and improved methods for the
fixation of cartilage, we compared cellular shape modulation, various
ultrastructural parameters (surface areas or volumes of endoplasmic
reticulum, Golgi membranes, and mitochondria), the production of matrix,
and cellular turnover for proliferating and hypertrophic chondrocytes
within the proximal tibial growth plate of the rat. By the late
hypertrophic stage, fourfold and tenfold increases in the mean cellular
height and volume, respectively, and a threefold increase in the mean
volume of the matrix per cell were achieved. The high metabolic activity of
hypertrophic cells was reflected by a twofold to fivefold increase in the
mean cellular surface area of rough endoplasmic reticulum, the Golgi
membranes, and the mean cellular mitochondrial volume. Rates of
longitudinal growth were determined by fluorochrome labeling and
incident-light fluorescence microscopy. Using these values and the
stereological estimators describing cellular height, the rates of cellular
turnover were calculated. The rapid progression of the vascular invasion
front was found to eliminate, for each column of cells, one chondrocyte
every three hours; that is, eight cells a day. The maintenance of a
steady-state structure for growth-plate cartilage in rats in a steady state
of growth thus necessitates efficient compensation for these losses, which
is achieved by a high rate of cellular proliferation and rapid hypertrophy.
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