Fluoride profiles in the cementum and root dentine of human permanent anterior teeth extracted from adult residents in a naturally fluoridated and a non-fluoridated area.

OBJECTIVES: To determine the effect of water fluoride concentration on the fluoride profile across the entire thickness of the cementum and root dentine of human permanent anterior teeth in adults. SUBJECTS: Twenty-eight human permanent anterior teeth from individuals aged from 30 to over 60 years were studied. SETTING: Teeth were obtained from a natural high-fluoride area (West Hartle-pool, UK; 1.0-1.3 ppm F in drinking water, WHP) and the other from a non-fluoridated naturally low fluoride area (Leeds, UK; 0.1 ppm F in drinking water, LDS). DESIGN: Cementum and root dentine were sampled using an abrasive micro-sampling technique from the cementum surface to the pulpal surface of root dentine. RESULTS: Fluoride concentration was higher in tooth roots (the cementum and dentine) taken from the naturally fluoridated area (WHP) than from the non-fluoridated area (LDS). Age and average fluoride concentration showed a positive correlation in WHP dentine, middle region of the root (r = 0.78, P < 0.001) and in the apical region of the root (r = 0.61, P < 0.05). WHP cementum had the strongest fluoride concentration correlation with age in the cervical region of the root (r = 0.67, P < 0.01). An analysis of variance (ANOVA) showed that the area (water fluoride content), age and number of years lived in the area combined with total age were significant. CONCLUSIONS: The fluoride content of cementum and root dentine in adult residents is related to fluoride content in drinking water.

Morphological differences in the skull of ascorbic acid-deficient ODS rats.

The physiological importance of ascorbic acid (AsA) in bone formation has been thought to be due mainly to its effects on collagen production and, consequently, matrix formation. However, effects of AsA deficiency on growing animals are poorly understood. The purpose of this experiment was to find how AsA deficiency affects craniofacial growth cephalometrically, and the periodontal ligament and the bone density of alveolar septum histologically. Five-week-old growing male rats with hereditary defects in AsA synthesis (ODS rats) placed on an AsA-deficient or minimally supplemented diet for 4 weeks showed a marked reduction in plasma AsA level and a negative or slight increment in body weight. Cephalometric evaluation revealed that craniofacial growth was influenced by AsA deficiency. Histological observations of periodontal structure and bone density in AsA-deficient animals showed no difference from controls, whereas the periodontal ligament of the upper first molar in the deficient animals was narrower than that of controls. These observations indicate that AsA deficiency reduces craniofacial size and the width of the periodontal ligament significantly in growing rats, whereas bone density is not affected. Thus, AsA, through collagen production, may be important to the increase in size of the craniofacial structures in growing animals.

Effect of HEBP (1-hydroxyethylidene-1,1-bisphosphonate) on experimental osteoporosis induced by ovariectomy in rats.

The present study was undertaken to test whether long term administration of HEBP could prevent the progress of bone loss induced by ovariectomy in rats. Administration of HEBP was started from day 111 after ovariectomy. The animals received subcutaneous injections of HEBP, at a dose of 0, 2, 4, or 8 mg/kg, every other day for 92 days. Tibiae, femora and incisor teeth were investigated by chemical analyses and by contact microradiography. Effects on calcium, phosphorus, and alkaline phosphatase activity in the plasma were also examined. Progress in the loss of bone density and ash content caused by ovariectomy was prevented by the administration of 2 mg/kg HEBP for 92 days and was partially prevented by the administration of 4 mg/kg. At a dose of 8 mg/kg, however, HEBP did not prevent the bone loss but, rather, potentiated it. These chemical findings were qualitatively confirmed by contact microradiography. A dose-dependent inhibition was observed in the mineralization of incisor dentin. These results suggest that HEBP, at least at low dose levels in which the inhibition of mineralization is not predominant, has a potency to prevent the progress of bone loss induced by ovariectomy. At higher doses, however, this compound seems not to be effective, because of the severe inhibition of mineralization.

Effects of retinoic acid on bone formation and resorption in cultured mouse calvaria.

1. The effects of retinoids on bone metabolism were examined in newborn mouse calvaria. 2. Incubation of calvaria with 0.01-1 microM retinoic acid for 4 days decreased their alkaline phosphatase (ALP) activity, mineral content and collagen content in a concentration-dependent fashion. 3. With treatment for 2 days, retinoic acid (1 microM) decreased the ALP activity and collagen content, but not the mineral content. 4. All these inhibitory effects were observed in calvaria from 0-day-old mice, but no inhibition of ALP activity was observed in calvaria from 14-day-old mice. 5. 1-Hydroxyethylidene-1,1-bisphosphonate (HEBP, 1 mM), which inhibits bone resorption, prevented the effect of retinoic acid (1 microM) on the bone mineral content, but not the effects on ALP and collagen (synthesized by osteoblasts). HEBP (1 mM) alone had no effect on the calvarial mineral and collagen contents. 6. These findings indicate that retinoic acid both stimulates bone resorption and inhibits osteoblastic activity by different mechanisms, and that stimulation of bone resorption by retinoic acid is inhibited by HEBP.

Elevation of blood pressure in young rats fed a low calcium diet. Effects of nifedipine and captopril.

Hypertension was developed in 5-week-old male rats fed a low calcium diet, which evokes hypocalcemia and nutritional hyperparathyroidism, for 2 weeks. Blood pressure returned to normal after changing to a normal calcium diet. These changes of blood pressure were preceded by changes of calcium levels in plasma. In parathyroidectomized rats receiving a normal calcium diet, blood pressure did not rise, though the plasma calcium level decreased to a similar extent as in rats fed the low calcium diet. These findings seem to indicate that hyperparathyroidism, not hypocalcemia, is involved in the elevation of blood pressure in rats fed a low calcium diet. The elevated blood pressure was reduced by a calcium antagonist, nifedipine, but not by an inhibitor of angiotensin-converting enzyme, captopril. This may indicate that hypertension due to nutritional hyperparathyroidism responds to the calcium antagonist nifedipine and calcium supplementation, and is not dependent on renin.