M. Svanberg et M. Knuuttila, THE EFFECT OF DIETARY XYLITOL ON RECALCIFYING AND NEWLY FORMED CORTICAL LONG-BONE IN RATS, Calcified tissue international, 53(2), 1993, pp. 135-138
Thirty-six 3-week-old male Wistar rats were labeled with a single intr
aperitoneal tetracycline injection. Twenty-four of them were then fed
a Ca-deficient basal diet for 3 weeks, while the control group receive
d the basal diet supplemented with CaCO3 (12 g/kg). The tetracycline l
abeling was then repeated and six animals in each group were decapitat
ed. The diet of the remaining formerly Ca-deficient animals was return
ed to normal, and half the test rats also received xylitol supplementa
tion (50 g/kg). After 4 weeks of rehabilitation the labeling was repea
ted and the animals were decapitated and their tibias were prepared. T
he tibias were measured in terms of weight and density and cross secti
ons were prepared for the examination of mineral content. Bone element
analysis was performed by scanning electron microscopy with electron-
probe microanalysis, examining separately the bone areas formed during
the various dietary periods. Areas of the former Ca-deficient and new
ly formed cortical bone were identified by tetracycline fluorescence u
nder ultraviolet light, and the amount of cortical bone in each group
was measured. The mineralization-promoting effect of dietary xylitol a
s compared with CaCO3 supplementation alone was seen more clearly in t
he newly formed periosteal bone than in remineralization of the former
ly Ca-deficient bone, the concentrations of Ca and P being significant
ly elevated (P < 0.05), as also was the total mineral content (P < 0.0
1). The cortical bone volume was similar following the CaCO3 and CaCO3
+ xylitol supplementations, suggesting unaltered formation of the org
anic matrix. The results show that the effect of xylitol on bone durin
g dietary Ca rehabilitation particularly concerns newly formed bone mi
neral. This may be due to the slow process of remodeling in the former
mineralized bone or to xylitol-induced effects on osteoblast and/or o
steoclast metabolism.