Search Results (4)

Previous studies on microtaphonomy have identified multiple types of organic microstructures in fossil vertebrates from a variety of time periods and past environmental settings. This study investigates potential taphonomic, paleoenvironmental, and paleoclimatic controls on soft tissue and cellular preservation in fossil bone. To this end, fifteen vertebrate fossils were studied: eight fossils collected from the Oligocene Sharps Formation of the Arikaree Group in Badlands National Park, South Dakota, and seven fossils from formations in the underlying White River Group, including the Oligocene Brule Formation of Badlands National Park, and the Eocene Chadron Formation of Flagstaff Rim, Wyoming; Toadstool Geologic Park, Nebraska; and Badlands National Park, South Dakota. A portion of each fossil was demineralized to identify any organic microstructures preserved within the fossils. We investigated several factors which may have influenced cellular/soft tissue decay and/or preservation pathways, including taxonomic identity, paleoclimatic conditions, depositional environment, and general diagenetic history (as interpreted through thin section analysis). Soft tissue microstructures were preserved in all fossil samples, and cellular structures morphologically consistent with osteocytes were recovered from 11 of the 15 fossil specimens. Preservation of these microstructures was found to be independent of taxonomy, paleoclimate regime, apatite crystallinity, depositional environment, and general diagenetic history, indicating that biogeochemical reactions operating within microenvironments within skeletal tissues, such as within individual osteocyte lacunae or Haversian canals, may exert stronger controls on soft tissue and biomolecular decay or stabilization than external environmental (or climatic) conditions. Full article

Background and Objectives: The gold standard for a successful prosthetic approach is the osseointegration of an implant. However, this integration can be a problem in cases where the implant needs to be removed. Removing the implant with minimal damage to the surrounding tissues is important. Osteocytes cannot survive below −2 °C, but epithelial cells, fibroblasts, and other surrounding tissue cells can. Remodeling can be triggered by cryotherapy at temperatures that specifically affect osteocyte necrosis. In this study, we aimed to develop a method for reversing the osseointegration mechanism and for protecting the surrounding tissues by bone remodeling induced by CO₂ cryotherapy. Materials and Methods: In this study, eight 2.8 mm diameter, one-piece mini implants were used in New Zealand rabbit tibias. Two control and six implants were tested in this study. After 2 months of osseointegration, a reverse torque force method was used to remove all osseointegrated implants at 5, 10, 20, and 30 Ncm. The osseointegration of the implants was proven by periotest measurements. Changes in bone tissue were examined in histological sections stained with toluidine blue after rabbit sacrifice. The number of lacunae with osteocyte, empty lacunae, and lacunae greater than 5 µm and the osteon number in a 10,000 µm² area were calculated. Cryotherapy was applied to the test implants for 1 min, 2 min, and 5 min. Three implants were subjected to cryotherapy at −40 °C, and the other implants were subjected to cryotherapy at −80 °C. Results: Empty lacunae, filled osteocytes, lacunae >5 µm, and the osteon count around the implant applied at −40 °C were not significantly different from the control implants. The application of −40 °C for 1 min was found to cause minimal damage to the bone cells. The implants, which were applied for 1 min and 2 min, were successfully explanted on the 2nd day with the 5 Ncm reverse torque method. Test implants, which were applied cold for 5 min, were explanted on day 1. Tissue damage was detected in all test groups at −80 °C. Conclusions: The method of removing implants with cryotherapy was found to be successful in −40 °C freeze–thaw cycles applied three times for 1 min. To prove implant removal with cryotherapy, more implant trials should be conducted. Full article

Osteocytes are terminally differentiated osteoblasts embedded within the bone matrix and key orchestrators of bone metabolism. However, they are generally not characterized by conventional bone histomorphometry because of their location and the limited resolution of light microscopy. OI is characterized by disturbed bone homeostasis, matrix abnormalities and elevated bone matrix mineralization density. To gain further insights into osteocyte characteristics and bone metabolism in OI, we evaluated 2D osteocyte lacunae sections (OLS) based on quantitative backscattered electron imaging in transiliac bone biopsy samples from children with OI type I (n = 19) and age-matched controls (n = 24). The OLS characteristics were related to previously obtained, re-visited histomorphometric parameters. Moreover, we present pediatric bone mineralization density distribution reference data in OI type I (n = 19) and controls (n = 50) obtained with a field emission scanning electron microscope. Compared to controls, OI has highly increased OLS density in cortical and trabecular bone (+50.66%, +61.73%; both p < 0.001), whereas OLS area is slightly decreased in trabecular bone (−10.28%; p = 0.015). Correlation analyses show a low to moderate, positive association of OLS density with surface-based bone formation parameters and negative association with indices of osteoblast function. In conclusion, hyperosteocytosis of the hypermineralized OI bone matrix associates with abnormal bone cell metabolism and might further impact the mechanical competence of the bone tissue. Full article

Osteocytic osteolysis/perilacunar remodeling is thought to contribute to the maintenance of mineral homeostasis. Here, we utilized a reversible, adult-onset model of secondary hyperparathyroidism to study femoral bone mineralization density distribution (BMDD) and osteocyte lacunae sections (OLS) based on quantitative backscattered electron imaging. Male mice with a non-functioning vitamin D receptor (VDR^Δ/Δ) or wild-type mice were exposed to a rescue diet (RD) (baseline) and subsequently to a low calcium challenge diet (CD). Thereafter, VDR^Δ/Δ mice received either the CD, a normal diet (ND), or the RD. At baseline, BMDD and OLS characteristics were similar in VDR^Δ/Δ and wild-type mice. The CD induced large cortical pores, osteomalacia, and a reduced epiphyseal average degree of mineralization in the VDR^Δ/Δ mice relative to the baseline (−9.5%, p < 0.05 after two months and −10.3%, p < 0.01 after five months of the CD). Switching VDR^Δ/Δ mice on the CD back to the RD fully restored BMDD to baseline values. However, OLS remained unchanged in all groups of mice, independent of diet. We conclude that adult VDR^Δ/Δ animals on an RD lack any skeletal abnormalities, suggesting that VDR signaling is dispensable for normal bone mineralization as long as mineral homeostasis is normal. Our findings also indicate that VDR^Δ/Δ mice attempt to correct a calcium challenge by enhanced osteoclastic resorption rather than by osteocytic osteolysis. Full article