wn Bab oak thw ae ce
wb a Oe ee
63
tt
100%/year|
tf
for sever.
low rate
’
wnt and by
GN
-
~
at-4 (r>0.2 mer
l
2
!
4
1
7
lL
10
{
l
20
40
l
NN
70
sone turneriginal formation of the skeleton (assumed to occur at the
skeleto fey: of adolescence). Figures from Table 27,
.
five oe component as a lowlevel, relatively uniform,
sureme,eonsterm uptake of activity in existing bone. In men
Fwho take in their activity at an advanced age the
eral years.
na:
.
‘tdixtribution of bone ages within their skeleton is
irent resi;
.
ae
.
.
émuch wider than in 15- to 25-year-old men and in 1- to
> observa.
;
;
.
0.0!
I
100
emodcling at the rate X for a period of time 7 since the
.
0.02 |
:
spots, the
T-TIME OF INJECTION IN YEARS AFTER ADOLESCENCE
is of bon Fic. 52—The calculated value of the average augmentation
nger thar ate (lugs) in a region of bone that has been subject to random
Suremente ..
CALCULATED DIFFUSE/UNIFORM LABEL
oO
1
| 0%/ year
1% /year
X= 0.92% /year|
Jil
rr
prc
X= 69.3% “year
23.1
d bytetra
. &
rm caleiur,
neties. The
‘the model
0.7
2
5
10
!
20
50
100
T- YEARS AFTER ADOLESCENCE
(BONE AGE AT TIME OF INJECTION)
{ADOLESCENCE = 18 YEARS) -
Fic. 53—The calculated ratio of the diffuse specific activity
to the uniform label (average specific activity) for a region of
bone that has been remodeling randomly at the rate \ for a
time 7 after adolescence. The diffuse specific activity referred
to here is assumed to be that deposited by the augmentation
rate of the original, unremodeled bone which is of age 7. The
total activity of the bone is the sum of this diffuse activity,
the activity in hotspots in newly-forming bone, and the augmentational hotspots in bone of age less than T that has been
formed by remodeling since adolescence.
PPvcurold dogs, which have provided most of our
fautoradiographs. The volume of bone originally laid
ossible ta:
.
~
fdown during skeletal growth has been reduced by
respect
.
.
oe
of an in. resorption to a small fraction of the skeleton, butit is
ndividua his bone with its low augmentation rate that we have
(00
X= 69.3% /year
tion an is vounger bone with higher augmentation rates. The
.
most intense hotspotsstill correspond to sites of apposiever, are.
.
.
bone aoe at the time of tracer intake, but there should now
minutior be many hotspots of intermediate intensity which are
roughouProt associated with current bone formationor secondary
s thereaation These augmentational hotspots have
.
‘As, in %/year
probably associated with the diffuse component. In
riant bej*.
.
minutjo fsites that have been remodeled since
adolescence there
Ty Not previously been identified, but the above ealcula-
copea tinsx show
chow
i a third
1
that they should contain
or a half
fol the total activity in a skeletal system receiving its
tracer activity at an advanced age. The specific ac-
‘Uvities of some of these augmentational hotspots could
be x high as ten times thespecific activity of the diffuse
uptake in the remnant of adolescent bone. Figures 53
tic Migure 54 show that this realization solves a long
it stiunding discrepancy in our approach. It is important
of to locate these augmentational hotspots experi‘usion in’ Mentally by combined “Ca and tetracycline labeling
ze thet In older animals and man.
I
Lot
2
tail
5
10
[fp ittit
20
50
100
T (Years after Adolescence - Age of bone at injection)
Fic. 64—Calculated values of As as a function of \ and T.
The total activity represented by As is the sum of the diffuse
activity in original bone (aged T), the activity in newly forming
hotspots (75% »), and the activity in augmentational hotspots.
Figures from Table 27.