Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0276640 (
TEM
)
20,729
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The results of previous investigations examining the association between corticosteroids and bone resorption in vitro have been conflicting. Recent studies have shown that application of a triamcinolone-containing medicament to the dental pulp cavity inhibits dentinoclast-mediated tooth resorption in vivo and in vitro. The aims of this study were to quantitate early ultrastructural changes in osteoclasts in vivo in response to a single steroid dose, and to examine the attachment of dentinoclasts grown in steroid-supplemented cultures in vitro. Resorbing bone around erupting rat molars was examined using
TEM
and morphometrically quantitated for changes in ruffled border and clear zone areas 1 and 4 h after injections of NaCl, calcitonin, hydrocortisone and prednisolone. Dentinoclasts were harvested from resorption areas in mature rat molars, grown in cultures with calcitonin, hydrocortisone or prednisolone, and fixed and viewed with SEM after 30 min and 2 h. Results of
TEM
studies showed a significant reduction in areas of resorbing structures in osteoclasts treated with calcitonin at 1 and 4 h, and prednisolone at 4 h. At 1 and 4 h, hydrocortisone showed an increase in resorbing structure areas. SEM results indicated all experimental substances reduced dentinoclast spreading and attachment. It was concluded that the direct effect of steroids on clastic cells may be one of inhibition (the degree of which depends on the nature and dose of the steroid) whereas, in vivo, systemic administration may cause more secondary effects (such as
PTH
stimulation) to compete with this inhibition. The efficacy of steroid-containing medicaments in inhibiting dentinoclastic resorption may be due to their relatively localized area of application.
...
PMID:Early responses by osteoclasts in vivo and dentinoclasts in vitro to corticosteroids. 279 Jul 32
The mechanism of transduction of mechanical strains into biological signals remains one of the more baffling problems of skeletal homeostasis. The updated literature ascribes to osteocytes the function of sensing the strains induced into the bone matrix by mechanical stresses. Whether the osteocytes perform such function by themselves or they are helped by other cells is also unknown. Indeed
TEM
investigations carried out in our laboratory pointed out the existence of a functional syncytium among all the cells of the osteogenic lineage (COL; stromal cells, osteoblasts or bone lining cells, osteocytes). On the basis of this finding, we suggested that COL may reciprocally modulate their function not only by volume transmission (paracrine and autocrine stimulation) but also by wiring transmission, namely in a neuronal like manner. Thanks to their location, osteocytes should theoretically be the first cells of COL functional syncytium to sense mechanical strains, whereas stromal cells should be the first to be activated by hormonal molecules diffusing across the endothelial lining. Since
PTH
and Estrogen receptors have also been localized on osteocytes, and considering that such hormones have been suggested to modulate the sensitivity to strain of the bone mechanosensor, we suggested that the osteocyte syncytium may constitute the microscopic bone structure that sense both mechanical strain and biochemical factors and, at any moment, after having combined the two types of stimuli, issues the appropriate signals to the other bone cells by volume and/or wiring-transmission. Stromal cells, on the other hand, besides transmitting signals from vascular endothelium to bone cells, may control the differentiation and then direct the course of the osteoblasts around the vascular framework.
...
PMID:The osteocyte as a wiring transmission system. 1575 6
Oral formulation of human parathyroid hormone 1-34 (
PTH
1-34) is an alternative patient compliant route in treating osteoporosis.
PTH
1-34 loaded chitosan nanoparticles were PEGylated (PEG-CS-
PTH
NPs) and characterized by DLS, SEM,
TEM
and FTIR. PEG-CS-
PTH
NP aggregates of 200-250 nm which in turn comprised 20 nm individual nanoparticles were observed in SEM and
TEM
images respectively. The PEG-CS-
PTH
NP with 40% encapsulation efficiency was subjected to an in vitro release in simulated rat body fluids. PEG-CS-
PTH
NP treated human primary osteoblast cells, upon
PTH
1-34 receptor activation, produced second messenger-cAMP, which downstream stimulated intracellular calcium uptake, production of bone specific alkaline phosphatase, osteocalcin etc., which substantiates the anabolic effect of the peptide. PEG-CS-
PTH
NPs showed an oral bioavailability of 100-160 pg/mL
PTH
1-34 throughout 48 h, which is remarkable compared to the bare
PTH
1-34 and CS-
PTH
NPs. The NIR image of gastrointestinal transit of ICG conjugated PEG-CS-
PTH
NPs supports this significant finding.
...
PMID:In vitro and in vivo evaluation of osteoporosis therapeutic peptide PTH 1-34 loaded pegylated chitosan nanoparticles. 3079 7