Effect of leptin on the development of primary ossification centers in mouse fetuses.

Leptin may be considered a significat cartilage/bone growth factor

Leptin effect on rat primary ossification centers during bone histogenesis.

During the early phases of endochondral ossification, Leptin positive effects are shown in growith of rat ossification centers

Leptin increases growth of primary ossification centers in fetal mice

The effect of peripheral leptin on fetal primary ossification centers during the early phases of bone histogenesis was investigated by administration of leptin to pregnant mice. Fourteen pregnant mice were divided into two groups. The treated pregnant group was subcutaneously injected in the intrascapular region with supraphysiologic doses (2 mg kg(-1)) of leptin (Vinci Biochem, Firenze, Italy) in a volume of 0.1 mL per 10 g body weight, at the 7th, 9th and 11th day of gestation. The control group was treated with physiological solution in the same manner and same times as the treated group. The new-born mice were killed 1 day after birth and the primary ossification centers were stained with Alizarin Red S after diaphanizing the soft tissues in 1% potassium hydroxide. The development of both endochondral and intramembranous ossification centers was morphometrically analysed in long bones. The results showed that the ossification centers of mice born by mothers treated with leptin grow more rapidly in both length and cross-sectional area compared with mice born by the untreated mothers. As the development of long bones depends on endochondral ossification occurring at proximal and distal epiphyseal plates as well as on intramembranous ossification along the periosteal surface, it appears that leptin activates the differentiation and proliferation of both chondrocytes and osteoblasts. The role of leptin as a growth factor of cartilage and bone is discussed in the light of the data reported in the literature

Osteocyte-bone lining cell system at the origin of steady ionic current in damaged anphibian bone.

A wound-generated steady electric current was measured by a two-dimensional vibrating probe system in the metatarsal banes of 22 adult frogs (Xenopus laevis) placed in amphibian Ringer. Inward currents were recorded entering a micrometric hole drilled through the cortex at middiaphyseal level. These steady state currents (mean +/- SD 8.50 +/- 2.77 mu A/cm(2)) last approximately 2 hours, were dependent on the presence of sodium in the incubation medium, were no more detectable after fixation, and were reduced to background level when the cell membranes were solubilized. These results agree with previous recordings of metatarsal bones of weanling mice, under identical conditions. Both results suggest that the measured ionic currents have a cellular origin. Metatarsal bones of adult amphibian were purposely selected for this study because, unlike mammalian bones, their shafts are avascular and only contain an osteocyte-bone lining fell system, as documented by scanning and transmission electron observations. Thus, unlike the data from previous investigations on mammals, the results succeeded in giving the first convincing evidence that the osteocyte-bone lining cell system is the origin of damage-generated ionic currents. As damage exposes bone ionic compartment to plasma, damage-generated ionic currents are representative of ion fluxes at bone plasma interface, and cells at the origin of the current generate the driving force of such fluxes. By demonstrating that osteocytes and bone lining cells are at the origin of the current, this study suggests that the osteocyte-bone lining cell system, though operating as a cellular membrane partition, regulates ionic flow between bone and plasma. Since strain-related adaptive remodeling could also depend on ionic characteristics and flow of the bone fluid through the osteocyte lacuno-canalicular network, the results reported here support the view that osteocyte and bone lining cells may constitute a functional syncytium involved in mineral homeostasis as well as in bone adaptation to mechanical loading

Effect of the phytoestrogen ferutinin in preventing and recovering osteoporosis: histomorphometric analysis of bone mass in ovariectomized rats.

Ferutinin seems to display the same effects on bone mass obtained with estradiol in OVX rats

New aspects of Ferutinin effect in preventing osteoporosis

The results of the study suggest that ferutinin role, in preventing osteoporosis due to estrogen deficiency, is expressed in inhibiting osteoclast erosion rather than in enhancing osteoblast deposition (as previously suggested); moreover, in all F-OVX groups the bone turnover is very low and seems correlated to the trivial body weight increase, which, in turn, depends on ferutinin treatment

Phytoestrogen effects on bone mass in ovariectomized rats: preliminary histomorphometric analysis.

Phytoestrogens ferutinine could prevent in rats the risk of osteoporosis in estrogen deficient conditions and it could enhance the recover of bone mass in osteoporotic OVX rats

Influence of ferutinin on bone metabolism in ovariectomized rats. I: role in preventing osteoporosis

Phytoestrogens play a role in maintaining bone mass in the post-menopausal period for their putative function as osteoprotective agents. The aim of the present study was to investigate the influence of Ferutinin, a phytoestrogen found in the plants of Ferula genus, on bone loss in ovariectomized rats. Such an animal model can simulate the various clinical syndromes deriving from osteoporosis. The effect of the daily oral administration of ferutinin to ovariectomized rats (dosed at 2 mg/kg per day for 30 and 60 days) was compared to that of estradiol benzoate (subcutaneously administered at the dose of 1.5 microg/rat twice a week). After the sacrifice, histomorphometrical analyses were performed on trabecular bone of L4-L5 vertebrae and distal femoral metaphysis, as well as on cortical bone of femoral diaphysis; biochemical parameters (bone mineral components and markers) were also evaluated from the rat serum. The histomorphometrical analyses of trabecular and cortical bone from lumbar vertebrae and femur showed that ferutinin has the same antiosteoporotic effect of estradiol benzoate on bone mass, and in some cases is even stronger. This fact suggests that it could prevent osteoporosis caused by severe estrogen deficiency in ovariectomized rats. The possibility of using ferutinin as an alternative to the commonly employed hormonal replacing therapy in post-menopausal women is discussed

Influence of ferutinin on bone mass and its side effects in ovariectomized rats.

Ferutinin seems to display the same effects on bone mass recorded with estradiol, but with respect to estrogens it seems to extert a protection against uterine carcinoma