Parathyroid hormone 1–34 enhances titanium implant anchorage in low-density trabecular bone: A correlative micro-computed tomographic and biomechanical analysis

Bone ◽  
2006 ◽  
Vol 39 (2) ◽  
pp. 276-282 ◽  
Author(s):  
Yankel Gabet ◽  
Ralph Müller ◽  
Jay Levy ◽  
Richard Dimarchi ◽  
Michael Chorev ◽  
...  
Blood ◽  
2012 ◽  
Vol 119 (11) ◽  
pp. 2489-2499 ◽  
Author(s):  
Laura M. Calvi ◽  
Olga Bromberg ◽  
Yumie Rhee ◽  
Jonathan M. Weber ◽  
Julianne N. P. Smith ◽  
...  

Abstract Microenvironmental expansion of hematopoietic stem cells (HSCs) is induced by treatment with parathyroid hormone (PTH) or activation of the PTH receptor (PTH1R) in osteoblastic cells; however, the osteoblastic subset mediating this action of PTH is unknown. Osteocytes are terminally differentiated osteoblasts embedded in mineralized bone matrix but are connected with the BM. Activation of PTH1R in osteocytes increases osteoblastic number and bone mass. To establish whether osteocyte-mediated PTH1R signaling expands HSCs, we studied mice expressing a constitutively active PTH1R in osteocytes (TG mice). Osteoblasts, osteoclasts, and trabecular bone were increased in TG mice without changes in BM phenotypic HSCs or HSC function. TG mice had progressively increased trabecular bone but decreased HSC function. In severely affected TG mice, phenotypic HSCs were decreased in the BM but increased in the spleen. TG osteocytes had no increase in signals associated with microenvironmental HSC support, and the spindle-shaped osteoblastic cells that increased with PTH treatment were not present in TG bones. These findings demonstrate that activation of PTH1R signaling in osteocytes does not expand BM HSCs, which are instead decreased in TG mice. Therefore, osteocytes do not mediate the HSC expansion induced by PTH1R signaling. Further, osteoblastic expansion is not sufficient to increase HSCs.


Neurosurgery ◽  
1987 ◽  
Vol 20 (4) ◽  
pp. 577-583 ◽  
Author(s):  
David W. Johnson ◽  
David Parkinson ◽  
Samuel M. Wolpert ◽  
David L. Kasdon ◽  
Eddie S. K. Kwan ◽  
...  

Abstract After radiotherapy, 20 patients, 18 with documented progression of malignant glioma and 2 with Grade II astrocytoma, received a total of 52 courses of intracarotid 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) at a dose of 150 mg/m2 dissolved in 5% dextrose in water. The patients were treated at 6-week intervals for a maximum of five courses of chemotherapy per patient. Response to treatment was analyzed on computed tomographic scans by measuring the volume of the enhancing tumor and any central low density. From these data, tumor doubling times ranging from 110 to 968 days were obtained. An 11 to 60% reduction in enhancing tumor volume was noted in 8 patients, 2 of whom had a greater than 50% decrease in tumor volume. One patient had no change in tumor volume 110 weeks after the initiation of BCNU chemotherapy. Four patients had tumor in more than one vascular territory; tumor growth was arrested in the perfused territory, but continued in the nonperfused area. In 1 of the 4 patients, tumor also grew along a shunt catheter tract and spread over the surface of the ipsilateral hemisphere. One patient developed clinically asymptomatic leukoencephalopathy after five courses of BCNU. Two patients had postradiation leukoencephalopathy before BCNU treatment. Seventeen patients had peritumoral low density with mass effect after BCNU; thus, the true incidence of BCNU-related leukoencephalopathy could not be determined. All patients experienced transient unilateral orbital pain during the infusion and scleral erythema that lasted for several hours afterward. Loss of vision was noted in 2 patients, although it seemed to be related to the therapy in only 1 patient. In our group of patients, there was no significant myelosuppression or indication of other systemic toxicity.


2019 ◽  
Vol 30 (1) ◽  
pp. 43-46 ◽  
Author(s):  
Carlos Eduardo Secco Mafra ◽  
Marcelo Sirolli ◽  
Marília Cabral Cavalcanti ◽  
Rodrigo Basílio Albuquerque dos Santos ◽  
Cláudio Mendes Pannuti ◽  
...  

Abstract The aim of this study was to evaluate the effect of a lower dose of parathyroid hormone- PTH (1-34) on osteogenic potential of bone healing around titanium implants inserted into the tibia of rats. A blind parallel study was conducted in 45 adult male Wistar rats. Each rat received one titanium implant (4.5 x 2.2 mm) and was randomly assigned to receive subcutaneous injections, three times/week for 30 days, of the following treatments: group 1 - 40 µg/kg of PTH (1-34) (n=15); group 2 - 2 µg/kg of PTH (1-34) (n=15) and; group 3 - only the vehicle required for hormone dissolution (n=15). Thirty days after surgery, the animals were sacrificed and specimens containing the implant and the surrounding bone were removed and processed for non-decalcified sections. The sections were evaluated according to the following histometric parameters: proportion of mineralized tissue (PMT) adjacent to the implant threads (500 µm band); bone filling within the limits of the threads (BF) and; bone-to-implant contact (BIC). For the cortical region, both hormone dosages (groups 1 and 2) promoted better results, for all parameters, when compared to control group (p<0.05). Similar results were observed for the BF parameter in the cancellous region (p=0.0394). Therefore, systemic administration of PTH (1-34) stimulates bone formation around titanium implants, even at low doses.


Bone ◽  
2012 ◽  
Vol 50 (3) ◽  
pp. 733-738 ◽  
Author(s):  
Davide Ruffoni ◽  
Andreas J. Wirth ◽  
Juri A. Steiner ◽  
Ian H. Parkinson ◽  
Ralph Müller ◽  
...  

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