612
I L S E
L A S N I T Z K I
It is therefore possible that in irradiated skin hydrocortisone reduces
the output of lysosomal enzymes.
E . E F F E C T S
O N
C H I C K B O N E
R U D I M E N T S
Cortisone produces striking developmental abnormalities in cartilage
and bones of most laboratory animals including chick embryos (Follis,
1951). Bufio and Goyena (1955) were the first to show that this effect
was due to a direct action of the hormone on the bone. They explanted
femora of 7-day chick embryos in the presence of hydrocortisone and
cortisone (0-025 mg/ml). After 48 h growth with either hormone the
treated rudiments showed a growth inhibition of 37% of the controls.
The difference between experimental and control cultures increased
until the fifteenth day and then stayed constant. As with lymphocytes
the effect on the bone was reversible. Cultures maintained in normal
medium after a 96 h cultivation with the hormones recovered rapidly,
and reached the control size after 2 | days in normal medium. The
authors attribute the inhibition of growth to a reduced rate of proliferation of chondro- and osteoblasts under the influence of the hormone.
The retardation of bone growth by cortisone and hydrocortisone
was confirmed by Sobel and Freund (1958) on chick femora and by
Fell and Thomas (1961) on the long-bone rudiments of chick and mouse
embryos. Both groups of authors found, however, that the hormones
interfered with the differentiation of the cartilage and not with the
proliferation of cells. In the treated chick-bone rudiments the cells
in the epiphysis and diaphysis were smaller and did not hypertrophy
like those in the controls, and bone formation was absent. The intercellular partitions were narrower and gave a more intense metachromatic staining than those in the controls. Treated mouse-bone
rudiments showed the same growth-rate as their controls but the excavation of the cartilage normally occurring in untreated cultures was
arrested (Figs. 6 and 7). The disturbance of cartilage formation without
arrest of cell proliferation agrees well with results of Layton (1951) who
found that cortisone inhibited the synthesis of chondroitin sulphate in
vivo, and with those of Whitehouse and Lash (1961) who studied the
action of cortisone, hydrocortisone and related compounds on chondrogenesis in somites grown in vitro. The amount of cartilage was
severely reduced in the treated somites due to inhibited sulphonation of
chondroitin, while the increase of D N A was the same in treated and
control cultures.
Although cortisone disturbed the development of bone it enhanced
the differentiation of muscle cells. Sobel and Freund (1958) found that
I L S E
L A S N I T Z K I
It is therefore possible that in irradiated skin hydrocortisone reduces
the output of lysosomal enzymes.
E . E F F E C T S
O N
C H I C K B O N E
R U D I M E N T S
Cortisone produces striking developmental abnormalities in cartilage
and bones of most laboratory animals including chick embryos (Follis,
1951). Bufio and Goyena (1955) were the first to show that this effect
was due to a direct action of the hormone on the bone. They explanted
femora of 7-day chick embryos in the presence of hydrocortisone and
cortisone (0-025 mg/ml). After 48 h growth with either hormone the
treated rudiments showed a growth inhibition of 37% of the controls.
The difference between experimental and control cultures increased
until the fifteenth day and then stayed constant. As with lymphocytes
the effect on the bone was reversible. Cultures maintained in normal
medium after a 96 h cultivation with the hormones recovered rapidly,
and reached the control size after 2 | days in normal medium. The
authors attribute the inhibition of growth to a reduced rate of proliferation of chondro- and osteoblasts under the influence of the hormone.
The retardation of bone growth by cortisone and hydrocortisone
was confirmed by Sobel and Freund (1958) on chick femora and by
Fell and Thomas (1961) on the long-bone rudiments of chick and mouse
embryos. Both groups of authors found, however, that the hormones
interfered with the differentiation of the cartilage and not with the
proliferation of cells. In the treated chick-bone rudiments the cells
in the epiphysis and diaphysis were smaller and did not hypertrophy
like those in the controls, and bone formation was absent. The intercellular partitions were narrower and gave a more intense metachromatic staining than those in the controls. Treated mouse-bone
rudiments showed the same growth-rate as their controls but the excavation of the cartilage normally occurring in untreated cultures was
arrested (Figs. 6 and 7). The disturbance of cartilage formation without
arrest of cell proliferation agrees well with results of Layton (1951) who
found that cortisone inhibited the synthesis of chondroitin sulphate in
vivo, and with those of Whitehouse and Lash (1961) who studied the
action of cortisone, hydrocortisone and related compounds on chondrogenesis in somites grown in vitro. The amount of cartilage was
severely reduced in the treated somites due to inhibited sulphonation of
chondroitin, while the increase of D N A was the same in treated and
control cultures.
Although cortisone disturbed the development of bone it enhanced
the differentiation of muscle cells. Sobel and Freund (1958) found that