“…Interestingly, we also found that the focal BMC loss was independently increased in the low BMD cases. This result is in agreement with previous histological studies on human cancellous bones 56,57 . In the ex vivo study, microstructure parameters, including trabecular bone separation and trabecular bone thickness, were rapidly changed when the bone volume fraction was <15%, 56 further indicating that the structural integrity would be rapidly decreased in the population with low bone density.…”
Section: Discussionsupporting
confidence: 91%
“…This result is in agreement with previous histological studies on human cancellous bones. 56,57 In the ex vivo study, microstructure parameters, including trabecular bone separation and trabecular bone thickness, were rapidly changed when the bone volume fraction was <15%, 56…”
Introduction: Focal osteoporosis defect has shown a high association with the bone fragility and osteoporotic fracture prevalence. However, no routine computed tomography (CT)-based vertebral focal osteoporosis defect measurement and its association with vertebral compression fracture (VCF) were discussed yet. This study aimed to develop a routine CT-based measurement method for focal osteoporosis defect quantification, and to assess its association with the VCF prevalence. Materials and Methods: A total of 205 cases who underwent routine CT scanning, were retrospectively reviewed and enrolled into either the VCF or the control group. The focal bone mineral content loss (focal BMC loss), measured as the cumulated demineralization within bone void space, was proposed for focal osteoporosis defect quantification. Its scan-rescan reproducibility and its correlation with trabecular bone mineral density (BMD) and apparent microarchitecture parameters were evaluated.The association between focal BMC loss and the prevalence of VCF was studied by logistic regression.
Results:The measurement of focal BMC loss showed high reproducibility (RMSSD = 0.011 mm, LSC = 0.030 mm, ICC = 0.97), and good correlation with focal bone volume fraction (r = 0.79, P < 0.001), trabecular bone separation (r = 0.76, P < 0.001), but poor correlation with trabecular BMD (r = 0.37, P < 0.001). The focal BMC loss was significantly higher in the fracture group than the control (1.03 ± 0.13 vs. 0.93 ± 0.11 mm; P < 0.001), and was associated with prevalent VCF (1.87, 95% CI = 1.31-2.65, P < 0.001) independent of trabecular BMD level.Discussion: As a surrogate measure of focal osteoporosis defect, focal BMC Loss independently associated with the VCF prevalence. It suggests that focal osteoporosis defect is a common manifestation that positively contributed to compression fracture risk and can be quantified with routine CT using focal BMC Loss.
“…Interestingly, we also found that the focal BMC loss was independently increased in the low BMD cases. This result is in agreement with previous histological studies on human cancellous bones 56,57 . In the ex vivo study, microstructure parameters, including trabecular bone separation and trabecular bone thickness, were rapidly changed when the bone volume fraction was <15%, 56 further indicating that the structural integrity would be rapidly decreased in the population with low bone density.…”
Section: Discussionsupporting
confidence: 91%
“…This result is in agreement with previous histological studies on human cancellous bones. 56,57 In the ex vivo study, microstructure parameters, including trabecular bone separation and trabecular bone thickness, were rapidly changed when the bone volume fraction was <15%, 56…”
Introduction: Focal osteoporosis defect has shown a high association with the bone fragility and osteoporotic fracture prevalence. However, no routine computed tomography (CT)-based vertebral focal osteoporosis defect measurement and its association with vertebral compression fracture (VCF) were discussed yet. This study aimed to develop a routine CT-based measurement method for focal osteoporosis defect quantification, and to assess its association with the VCF prevalence. Materials and Methods: A total of 205 cases who underwent routine CT scanning, were retrospectively reviewed and enrolled into either the VCF or the control group. The focal bone mineral content loss (focal BMC loss), measured as the cumulated demineralization within bone void space, was proposed for focal osteoporosis defect quantification. Its scan-rescan reproducibility and its correlation with trabecular bone mineral density (BMD) and apparent microarchitecture parameters were evaluated.The association between focal BMC loss and the prevalence of VCF was studied by logistic regression.
Results:The measurement of focal BMC loss showed high reproducibility (RMSSD = 0.011 mm, LSC = 0.030 mm, ICC = 0.97), and good correlation with focal bone volume fraction (r = 0.79, P < 0.001), trabecular bone separation (r = 0.76, P < 0.001), but poor correlation with trabecular BMD (r = 0.37, P < 0.001). The focal BMC loss was significantly higher in the fracture group than the control (1.03 ± 0.13 vs. 0.93 ± 0.11 mm; P < 0.001), and was associated with prevalent VCF (1.87, 95% CI = 1.31-2.65, P < 0.001) independent of trabecular BMD level.Discussion: As a surrogate measure of focal osteoporosis defect, focal BMC Loss independently associated with the VCF prevalence. It suggests that focal osteoporosis defect is a common manifestation that positively contributed to compression fracture risk and can be quantified with routine CT using focal BMC Loss.
“…Sp is a critical bone parameter used to evaluate the trabecular structure of subchondral bone, and higher Tb. Sp indicates stronger bone resorption activity 34 . Our results showed that GW4064 decreased Tb.…”
Section: Resultsmentioning
confidence: 52%
“…Sp indicates stronger bone resorption activity. 34 Our results showed that GW4064 decreased Tb. Sp in subchondral bone of ACLT mice, while guggulsterone reversed this inhibition (Figure 3E).…”
Osteoarthritis (OA) is a prevalent degenerative disease of the joint, featured by articular cartilage destruction and subchondral bone marrow lesions. Articular cartilage and subchondral bone constitute an osteochondral unit that guarantees joint homeostasis. During OA initiation, activated osteoclasts in subchondral bone ultimately result in impaired capacities of the subchondral bone in response to mechanical stress, followed by the degradation of overlying articular cartilage. Thus, targeting osteoclasts could be a potential therapeutic option for treating OA. Here, we observed that farnesoid X receptor (FXR) expression and osteoclast fusion and activity in subchondral bone were concomitantly changed during early‐stage OA in the OA mouse model established by anterior cruciate ligament transection (ACLT). Then, we explored the therapeutic effects of FXR agonist GW4064 on the osteochondral pathologies in ACLT mice. We showed that GW4064 obviously ameliorated subchondral bone deterioration, associated with reduction in tartrate‐resistant acid phosphatase (TRAP) positive multinuclear osteoclast number, as well as articular cartilage degradation, which were blocked by the treatment with FXR antagonist Guggulsterone. Mechanistically, GW4064 impeded osteoclastogenesis through inhibiting subchondral bone osteoclast fusion via suppressing c‐Jun N‐terminal kinase (JNK) 1/2/nuclear factor of activated T‐cells 1 (NFATc1) pathway. Taken together, our results present evidence for the protective effects of GW4064 against OA by blunting osteoclast‐mediated aberrant subchondral bone loss and subsequent cartilage deterioration. Therefore, GW4064 demonstrates the potential as an alternative therapeutic option against OA for further drug development.
“…Next, trabecular architecture analysis was performed to evaluate bone strength. 31 Trabecular architecture, including trabecular thickness (Tb.Th), trabecular bone volume (BV/TV), trabecular number (Tb.N), and trabecular separation (Tb.Sp) of different treatment groups, was examined on day 21. As shown in Figure 4C,D, higher Tb.Th and BV/TV were found in alveolar bone defects treated with ILGel compared to that treated with PBS or IL-10, indicating that the microstructures of the trabecular bone in the alveolar bone defects regenerated better with ILGel treatment.…”
The development of a biodegradable and shape-adaptable bioscaffold that can enhance local cytokine retention and bioactivity is essential for the application of immunotherapy in periodontal diseases. Here, we report a biodegradable, anti-inflammatory, and osteogenic ILGel that uses a physically cross-linked DNA hydrogel as a soft bioscaffold for the long-term sustained release of cytokine interleukin-10 (IL-10) to accelerate diabetic alveolar bone rebuilding. Porous microstructures of ILGel favored the encapsulation of IL-10 and maintained IL-10 bioactivity for at least 7 days. ILGel can be gradually degraded or hydrolyzed under physiological conditions, avoiding the potential undesired side effects on dental tissues. Long-term sustained release of bioactive IL-10 from ILGel not only promoted M2 macrophage polarization and attenuated periodontal inflammation but also triggered osteogenesis of mesenchymal stem cells (MSCs), leading to accelerated alveolar bone formation and healing of alveolar bone defects under diabetic conditions in vivo. ILGel treatment significantly accelerated the defect healing rate of diabetic alveolar injury up to 93.42 ± 4.6% on day 21 post treatment compared to that of free IL-10 treatment (63.30 ± 7.39%), with improved trabecular architectures. Our findings imply the potential application of the DNA hydrogel as the bioscaffold for cytokine-based immunotherapy in diabetic alveolar bone injury and other periodontal diseases.
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