Chung-Ching Liu

Differential response in alveolar bone osteoclasts residing at two different bone sites

SummaryUsing a histochemical method for demonstrating acid phosphatase activity, we have studied osteoclasts residing at two different bone sites in rat incisor alveolar bone, one at the endosteum and the other at the tooth socket, and compared the response of these osteoclasts to systemic changes. After 12 days of calcium (0%) or phosphorus (0.2%) deprivation, the number of osteoclasts/cross section at the endosteum increased 463% (P<0.001) and 103% (P<0.002), respectively. After 10 days of calcium or phosphorus replenishment, the number of osteoclasts at this bone site decreased to levels not significantly different from those in the control. In contrast, the number of osteoclasts at the incisor socket remained insignificantly changed throughout the experimental period. A similar osteoclast differential response was also observed in the alveolar bone surrounding the first molar tooth. After 12 days of calcium deprivation, the number of osteoclasts/mm bone surface increased 371% (P<0.001) at the endosteum but remained insignificantly changed at the first molar socket. These results suggest that an osteoclast differential response exists in alveolar bone and that the response may be of significance inasmuch as the major function of alveolar bone is to support the teeth. The work described here supports the concept of local as well as systemic regulation of bone metabolism to simultaneously perform the dual functions of mineral homeostasis and mechanical support.

Acute reduction in 0steoclast number during bone repletion

Growing rats were fed a calcium-deficient diet for 12 days to induce bone loss and were subsequently placed on a calcium-replacement diet for 1 to 3 days to evoke bone repletion. Control animals were fed the calcium-replacement diet continuously. Twelve days of calcium deprivation resulted in a 21-fold increase in the number of endosteal osteoclasts in the tibial diaphysis as compared with controls. These osteoclasts, however, rapidly disappeared from the endosteum after restoration of dietary calcium. Only 14% of these endosteal osteoclasts remained after 1 day, and no osteoclasts were present after 3 days of calcium replenishment. During this time, plump osteoblasts replaced osteoclasts on the endosteal surface. The number of osteoclasts in the marrow space also changed strikingly. An 11-fold increase in the number of osteoclasts in the marrow space occurred during the calcium-deprivation phase. However, the greatest increase (39-fold) was observed during the first day of calcium replenishment. Thereafter, the number of osteoclasts in the marrow space declined and, after 3 days of calcium replenishment, returned to the control level. During calcium replenishment, acid phosphatase-positive fragments in the marrow space appeared concomitantly with osteoclast disintegration and fragmentation. The kinetic changes and acid phosphatase staining of these fragments suggest that the fragments are the products of disintegrating osteoclasts, a finding consistent with the hypothesis that the fate of some osteoclasts in vivo is cell death. At the end of calcium deprivation, serum iPTH levels and the production of 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D3 were significantly increased compared to controls. After 3 days of calcium replenishment, serum iPTH had decreased to control levels, but the production of 1,25-dihydroxyvitamin D3 was still elevated. Changes in serum iPTH and the production of 1,25-dihydroxyvitamin D3 cannot, therefore, be totally responsible for the observed decrease in osteoclast number during bone repletion. Bone repair after calcium deprivation may be a locally controlled phenomenon.

Stimulation of Bone Formation and Bone Resorption by Fluoride in Thyroparathyroidectomized Rats

In TPTX as well as sham-operated rats, F increased periosteal bone formation, decreased endosteal bone formation and endosteal osteoid maturation rate, and increased endosteal bone resorption. Serum iPTH was not affected by F treatment. Thus, the effects of F on bone are not mediated by PTH.

Immobilization and its effect on bone repletion in calcium-deficient rats fed a high calcium diet

Abstract In past work we demonstrated that, in growing rats, endosteal bone loss during a low calcium diet (depletion) was replaced when the animals were fed a normal calcium diet (repletion). Because past work showed that bone mechanical stress associated with weight bearing was increased les a result of bone depletion, the present study was undertaken to determine if immobilization during the repletion period would prevent bone repletion. In rats fed a 0% calcium diet (containing normal dietary phosphorus) for 12 days, there was a 460% increase in endosteal resorbing surface and a 38% increase in medullary area. When such animals were then fed a 1.2% calcium diet (normal phosphorus) for 15 days, the amount of endosteal resorbing surface decreased below the basal level to 0. Much of the endosteal resorbing surface was actually converted to forming surface, and les a result there was a 75% increase in the rate of endosteal bone formation compared with control (bone replete) animals. Bone replete animals subjected to immobilization of the left hind limb for 15 days by nerve transection had decreases of 31% and 33% in periosteal and endosteal bone formation rates, respectively, in the immobilized tibia. However, immobilization instituted at the start of the bone repletion period did not prevent or diminish the increment in the endosteal bone formation response during bone repletion over the intervening 15 days. Thus, the immobilized tibia from bone repleting rats exhibited an endosteal bone formation rate 128% greater than that in the immobilized limb of control (bone replete) rats. This increase was not less than that seen in bone repleting rats not subjected to immobilization. Thus, calcium repletion, even without mechanical stress, was sufficient to cause a marked increase in endosteal bone formation.

The Effect of Vitamin D Deficiency on Bone Repletion

Abstract The present study was undertaken to determine the effects of vitamin D deficiency, serum calcium, and PTH on the two major bone changes associated with bone repletion: the increase in endosteal matrix formation and the decrease in endosteal bone resorption. Following a period of bone depletion induced by calcium deficiency, vitamin D-deficient repleting rats demonstrated a marked increase in endosteal bone matrix formation over that seen in pair-weighted nonrepleting control rats. Further, in repleting rats deficient in vitamin D, bone matrix deposition was equivalent to that seen in pair-weighted vitamin D-treated repleting rats, indicating that vitamin D is not essential for matrix repletion. Analysis of serum parameters showed that the repleting vitamin D-deficient rats were severely hypocalcemic and exhibited an eightfold elevation in serum iPTH. Thus, neither the normalizing of the hypocalcemia nor of the high PTH levels incurred during bone depletion is necessary for matrix repletion. On the other hand, in the absence of vitamin D, there was a severe impairment of mineralization of the repleting bone matrix. Bone resorption was depressed during repletion in both vitamin D-deficient and vitamin D-treated rats. The depression of resorption in the vitamin D-deficient rats occurred despite a sustained increase in serum PTH, suggesting that some aspect of the repletion state is capable of suppressing PTH-mediated bone resorption.

Pore Size Measurements and Some Age-Related Changes in Human Alveolar Bone and Rat Femur

Pore size was not changed and bone density was consistently decreased in alveolar bone from patients with periodontal disease. Bone density increased with age in normal alveolar bone, and lacunar-canalicular volume decreased with age in both normal and diseased alveolar bones. Normal rat femur showed similar age-related changes.

In Vivo Calvarial Bone Cell Responses to Dietary Perturbations and the Implications for Mineral Homeostasis

Abstract Calvariae from small animals have been an important source for in vitro studies of bone. However, few in vivo studies have been undertaken on quantitative cell changes in calvariae. In the present study of mineral perturbations, rats were first deprived of calcium. After 18 days endosteal osteoclasts and nuclei/osteoclast in the parietal bone had increased 120% (P < 0.001) and 26% (P < 0.001), respectively, the marrow space had increased 141% (P < 0.001), and the bone area experienced a 49% decrease (P < 0.001). This thinning and weakening of the calvaria was accompanied by a compensatory increase in the number of endosteal osteoblasts (297%, P < 0.001). These rats were then replenished with calcium, and after 14 days the number of endosteal osteoclasts had decreased to 86% (P < 0.001) below the control and the endosteal surface was almost completely covered by osteoblasts (866% above the control, P < 0.001). Bone area was increased by 51% (P < 0.01). Similarly, in calcium-deficient rats in the tibial diaphysis at the fibular junction, the number of endosteal osteoclasts and the medullary space increased 1606% (P < 0.001) and 63% (P < 0.001), respectively, which were accompanied by a 32% decrease (P < 0.001) in cortical bone area. After calcium replenishment, most endosteal osteoclasts in the tibial diaphysis disappeared from the endosteal surface and were replaced by osteoblasts (increased 487%, P < 0.001). These results indicate that changes in bone cell activity in response to calcium deficiency are similar in calvariae and long bones, and that mobilization of calcium from the calvaria during calcium deficiency occurs at the expense of the protective action of the calvaria. Therefore, long bones as well as membranous bones are apparently important for the maintenance of mineral homeostasis.