OPG is Required for the Postnatal Maintenance of Condylar Cartilage

Chen, Danying; Liu, Yi; Liu, Zongxiang; Wang, Penglai

doi:10.1007/s00223-018-00510-z

Cited by 12 publications

(10 citation statements)

References 43 publications

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“…Stainless-steel wire-induced traumatic occlusion is a wellestablished mouse model in which the periodontal tissues and temporomandibular joint are disrupted within 14 days after stainless-steel wire bonding [24,25,30]. Based on the approaches that were used in previous studies, we developed a novel in vivo mouse model of ONJ, which was induced by experimental hyperocclusion and high-dose N-BP treatment.…”

Section: Discussionmentioning

confidence: 99%

“…The dosages and duration of treatment were chosen on the basis of a previous study that described ONJ-like lesion development in mice [22,23]. One week after starting the experiment, a hyperocclusive state was created as previously described with minor modifications [24,25]. Anesthesia was induced in the mice using a combination of 0.3 mg/kg of medetomidine, 4 mg/kg of midazolam, and 5 mg/kg of butorphanol, and a stainless steel wire (0.5 mm diameter, 4 mm length) was bent into a U-shape and bonded to the occlusal surface of each mouse's left first maxillary molar using methyl methacrylate resin (Super-Bond; Sun Medical Inc., Shiga, Japan; Fig.…”

Section: In Vivo Bisphosphonate-medicated Model With Experimental Hyperocclusionmentioning

confidence: 99%

“…For histological analysis, the ROI was defined at 0.5 mm from the alveolar crest; all measurements were performed in that area of alveolar bone and PDL space. In this study, the root furcation, which is most affected by traumatic occlusion in the experimental hyperocclusion mouse model [24,25], was chosen as the osteonecrosis evaluation site. The bone area ROI on digital images was measured using ImageJ software (version 1.53, National Institutes of Health, Bethesda, MD, USA).…”

Section: Histological Assessmentsmentioning

confidence: 99%

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Occlusal Trauma and Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

et al. 2021

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Osteonecrosis of the jaw (ONJ) is a serious adverse event that is associated with antiresorptive agents, and it manifests as bone exposure in the maxillofacial region. Previous clinical reports suggest that mechanical trauma would trigger ONJ in a manner that is similar to tooth extractions. To the best of our knowledge, there have been few detailed pathophysiological investigations of the mechanisms by which occlusal/mechanical trauma influences ONJ. Here, we developed a novel mouse model that exhibits ONJ following experimental hyperocclusion and nitrogen-containing bisphosphonate (N-BP) treatment. This in vivo model exhibited ONJ in alveolar bone, particularly in the mandible. Moreover, the experimental hyperocclusion induced remarkable alveolar bone resorption in both mouse mandible and maxilla, whereas N-BP treatment completely prevented alveolar bone resorption. In this study, we also modeled trauma by exposing clumps of mesenchymal stem cells (MSCs)/extracellular matrix complex to hydrostatic pressure in combination with N-BP. Hydrostatic pressure loading induced lactate dehydrogenase (LDH) release by calcified cell clumps that were differentiated from MSCs; this LDH release was enhanced by N-BP priming. These in vivo and in vitro models may contribute further insights into the effect of excessive mechanical loading on ONJ onset in patients with occlusal trauma.

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Section: Discussionmentioning

confidence: 99%

Section: In Vivo Bisphosphonate-medicated Model With Experimental Hyperocclusionmentioning

confidence: 99%

Section: Histological Assessmentsmentioning

confidence: 99%

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Occlusal Trauma and Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

et al. 2021

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“…The OPG/OPGL/RANK system is a key path connecting cartilage and subchondral bone. The balance of OPG and OPGL plays a decisive role in the remodeling of subchondral bone [15]. Both OPG and OPGL can be secreted by chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

The Mechanism of Mitochondrial Fatty Acid Oxidation’s Involvement in Osteoporosis in Aggravating Cartilage Degeneration of Rabbit Knee Osteoarthritis

Jia¹,

Deng²,

Wen³

et al. 2021

Preprint

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Objective: To observe whether the oxidative metabolism of mitochondrial fatty acids is involved in osteoporosis by detecting the changes in the contents of interleukin 1β, osteoprotegerin (OPG) and osteoprotegerin ligand（OPGL) and carnitine palmitoyl transferase I B （CPT1B）in rabbit OA cartilage Regulation of experimental rabbit knee OA. Methods: 30 female New Zealand rabbits were randomly divided into 3 groups with 10 in each group: Normal group ,OP+OA group and OA group. After successful modeling, the knee articular cartilage of each group were taken; The BMC and BMD of each group were measured; Observe the results of HE staining of cartilage; immunohistochemical method Detection of IL-1β; The Q-PCR method and Western blot method were used to detect IL-1β, OPG, OPGL and CPT1B mRNA and protein expression in cartilage.Results: Compared with the normal group, the expression of IL-1β, OPGL and CPT1B in the OP+OA group and the OA group was significantly increased (P<0.01), while the expression of OPG decreased (P<0.01); Compared with OP+OA group ,The expression of OPG and the ratio of OPG/OPGL was significantly higher in the OA group (P<0.01). Compared with OA group, The expression of IL-1β, OPGL and CPT1B in the OP+OA group was significantly higher (P<0.01); Conclusion: Mitochondrial fatty acid oxidation metabolism can be involved in the effect of osteoporosis on osteoarthritis by up-regulating the expression of CPT1b, which can mediate changes in the OPG/OPGL ratio, increase the expression of IL-1β, and aggravate the Degeneration of OA cartilage and subchondral bone.

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“…Necrosis of the femoral head (NFH) is an orthopedic disease that results in a decrease in blood supply to the femoral head under the joint action of numerous factors. This leads to the apoptosis or death of cartilage cells and a decrease in the number of osteocytes, which reduces the mechanical strength of the femoral head ( 1 , 2 ). Finally, the femoral head collapses, resulting in functional disorders of the hip joint ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of osteoprotegerin inhibits tert‑butyl hydroperoxide‑induced apoptosis of human chondrocytes

Ren

Zhang

et al. 2022

Exp Ther Med

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Necrosis of the femoral head (NFH) is an orthopedic disease characterized by a severe lack of blood supply to the femoral head and a marked increase in intraosseous pressure. NFH is associated with numerous factors, such as alcohol consumption and hormone levels. The present study focused on the expression levels of osteoprotegerin (OPG) in NFH and the effect of OPG overexpression on chondrocyte apoptosis. The results demonstrated that OPG expression was markedly decreased in the femoral head of patients with NFH compared with normal femoral heads. Lentivirus-mediated overexpression of OPG in human chondrocytes reversed the decrease in cell viability and the increase in reactive oxygen species production induced by an oxidative stress-inducing factor, tert -butyl hydroperoxide. Flow cytometry and TUNEL assays revealed that OPG overexpression inhibited the apoptosis of chondrocytes. In addition, it was revealed that OPG exerted its anti-apoptotic effect mainly by promoting Bcl-2 expression and Akt phosphorylation and inhibiting caspase-3 cleavage and Bax expression. The present study revealed that OPG may be an important regulator of NFH.

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OPG is Required for the Postnatal Maintenance of Condylar Cartilage

Cited by 12 publications

References 43 publications

Occlusal Trauma and Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

Occlusal Trauma and Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

The Mechanism of Mitochondrial Fatty Acid Oxidation’s Involvement in Osteoporosis in Aggravating Cartilage Degeneration of Rabbit Knee Osteoarthritis

Upregulation of osteoprotegerin inhibits tert‑butyl hydroperoxide‑induced apoptosis of human chondrocytes

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