scholarly journals Role of the SDF-1/CXCR4 signaling pathway in cartilage and subchondral bone in temporomandibular joint osteoarthritis induced by overloaded functional orthopedics in rats

2020 ◽  
Author(s):  
jing yang ◽  
Yazhen Li ◽  
Ying Liu ◽  
Qiang Zhang ◽  
Qi Zhang ◽  
...  
Keyword(s):  
Temporomandibular Joint ◽  
Signaling Pathway ◽  
Subchondral Bone ◽  
Cartilage Damage ◽  
Mandibular Advancement ◽  
Micro Computed Tomography ◽  
Cxcr4 Signaling ◽  
Skeletal Class Ii ◽  
Temporomandibular Joint Osteoarthritis

Abstract Objectives: To: (i) use a mandibular-advancement appliance in rats to investigate the role of the stromal cell-derived factor/ CXC receptor 4 (SDF-1/CXCR4) signaling pathway in temporomandibular joint osteoarthritis (TMJ OA) induced by overloaded functional orthopedics (OFO); (ii) provide a cellular and molecular basis for efficacious treatment of skeletal class-II malocclusion and avoidance of TMJ OA.Method: Male Sprague–Dawley rats (6 weeks) were divided randomly into control+normal saline (NS), EXP+ADM3100 (SDF-1 antagonist), EXP+NS, and control+ADM3100 groups. Changes in articular cartilage and subchondral bone after TMJ OA in these four groups were observed by hematoxylin and eosin (H&E), Immunofluorescence double staining (IDS), Safranin-O staining, immunohistochemical (IHC) staining, real-time polymerase chain reaction, and micro-computed tomography at 2, 4, and 8 weeks.Results: OFO led to increased expression of SDF-1, CXCR4, and matrix metalloproteinase (MMP)13 and decreased expression of collagen II. The thickness of the hypertrophic cartilage layer was reduced at 4 weeks in the EXP+NS group, and damage to subchondral bone was observed at 2 weeks. Using ADM3100 to inhibit SDF-1 signaling could attenuate expression of MMP13, cartilage damage, and osteoblast differentiation. IDS showed that the areas of expression of SDF-1 and OSX in subchondral bone overlapped.Conclusions: Overloaded functional orthopedics (OFO) induced TMJ-OA. The destruction of subchondral bone in TMJ OA caused by OFO occurred before damage to cartilage. SDF-1/CXCR4 may induce the osteogenic differentiation and cause cartilage degradation in TMJ OA caused by OFO.

scholarly journals Role of the SDF-1/CXCR4 signaling pathway in cartilage and subchondral bone in temporomandibular joint osteoarthritis induced by overloaded functional orthopedics in rats

2020 ◽  
Author(s):  
jing yang ◽  
Yazhen Li ◽  
Ying Liu ◽  
Qiang Zhang ◽  
Qi Zhang ◽  
...  
Keyword(s):  
Temporomandibular Joint ◽  
Signaling Pathway ◽  
Subchondral Bone ◽  
Cartilage Damage ◽  
Mandibular Advancement ◽  
Micro Computed Tomography ◽  
Cxcr4 Signaling ◽  
Skeletal Class Ii ◽  
Temporomandibular Joint Osteoarthritis

Abstract Objectives To: (i) use a mandibular-advancement appliance in rats to investigate the role of the stromal cell-derived factor/ CXC receptor 4 (SDF-1/CXCR4) signaling pathway in temporomandibular joint osteoarthritis (TMJ OA) induced by overloaded functional orthopedics (OFO); (ii) provide a cellular and molecular basis for efficacious treatment of skeletal class-II malocclusion and avoidance of TMJ OA.Method: Male Sprague–Dawley rats (6 weeks) were divided randomly into control + normal saline (NS), EXP + ADM3100 (SDF-1 antagonist), EXP + NS, and control + ADM3100 groups. Changes in articular cartilage and subchondral bone after TMJ OA in these four groups were observed by hematoxylin and eosin (H&E), Immunofluorescence double staining (IDS), Safranin-O staining, immunohistochemical (IHC) staining, real-time polymerase chain reaction, and micro-computed tomography at 2, 4, and 8 weeks.Results OFO led to increased expression of SDF-1, CXCR4, and matrix metalloproteinase (MMP)13 and decreased expression of collagen II. The thickness of the hypertrophic cartilage layer was reduced at 4 weeks in the EXP + NS group, and damage to subchondral bone was observed at 2 weeks. Using ADM3100 to inhibit SDF-1 signaling could attenuate expression of MMP13, cartilage damage, and osteoblast differentiation. IDS showed that the areas of expression of SDF-1 and OSX in subchondral bone overlapped.Conclusions The destruction of subchondral bone in TMJ OA caused by OFO occurred before damage to cartilage. An increase in expression of the SDF-1/CXCR4 signaling pathway in TMJ OA induced by OFO enabled osteoblasts in subchondral bone to up-regulate expression of SDF-1.

scholarly journals Role of Hyaluronic Acid in the Homeostasis and Therapeutics of Temporomandibular Joint Osteoarthritis

2017 ◽  
Vol 35 (3) ◽  
pp. 870-876 ◽  
Author(s):  
Veronica Iturriaga ◽  
Bélgica Vásquez ◽  
Carlos Manterola ◽  
Mariano del Sol
Keyword(s):  
Hyaluronic Acid ◽  
Temporomandibular Joint ◽  
Temporomandibular Joint Osteoarthritis

scholarly journals Roles for B[a]P and FICZ in subchondral bone metabolism and experimental temporomandibular joint osteoarthritis via the AhR/Cyp1a1 signaling axis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuri Yoshikawa ◽  
Takashi Izawa ◽  
Yusaku Hamada ◽  
Hiroko Takenaga ◽  
Ziyi Wang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Mouse Model ◽  
Bone Metabolism ◽  
Temporomandibular Joint ◽  
Subchondral Bone ◽  
Dependent Manner ◽  
Bone Homeostasis ◽  
Wild Type ◽  
Temporomandibular Joint Osteoarthritis ◽  
Signaling Axis

AbstractBone loss due to smoking represents a major risk factor for fractures and bone osteoporosis. Signaling through the aryl hydrocarbon receptor (AhR) and its ligands contributes to both bone homeostasis and inflammatory diseases. It remains unclear whether the same AhR signaling axis affects the temporomandibular joint (TMJ). The aim of this study was to investigate possible mechanisms which mediate bone loss in the TMJ due to smoking. In particular, whether benzo[a]pyrene (B[a]P), a carcinogen of tobacco smoke, induces expression of the AhR target gene, Cyp1a1, in mandibular condyles. Possible functions of an endogenous ligand of FICZ, were also investigated in a TMJ-osteoarthritis (OA) mouse model. B[a]P was administered orally to wild-type and AhR−/− mice and bone metabolism was subsequently examined. TMJ-OA was induced in wild-type mice with forceful opening of the mouth. Therapeutic functions of FICZ were detected with μCT and histology. Exposure to B[a]P accelerated bone loss in the mandibular subchondral bone. This bone loss manifested with osteoclastic bone resorption and upregulated expression of Cyp1a1 in an AhR-dependent manner. In a mouse model of TMJ-OA, FICZ exhibited a dose-dependent rescue of mandibular subchondral bone loss by repressing osteoclast activity. Meanwhile, in vitro, pre-treatment with FICZ reduced RANKL-mediated osteoclastogenesis. B[a]P regulates mandibular subchondral bone metabolism via the Cyp1a1. The AhR ligand, FICZ, can prevent TMJ-OA by regulating osteoclast differentiation.

Mesenchymal Stromal Cell Transplantation Induces Regeneration of Large and Full-Thickness Cartilage Defect of the Temporomandibular Joint

Cartilage ◽  
2020 ◽  
pp. 194760352092671 ◽  
Author(s):  
Marcos Gomez ◽  
Olga Wittig ◽  
Dylana Diaz-Solano ◽  
José E. Cardier
Keyword(s):  
Temporomandibular Joint ◽  
Subchondral Bone ◽  
Histological Analysis ◽  
Cellular Therapy ◽  
Platelet Rich Plasma ◽  
Articular Surface ◽  
Cartilage Damage ◽  
Cartilage Regeneration ◽  
Osteochondral Lesions ◽  
Field Evidence

Objective Cartilage damage (CD) in the temporomandibular joint (TMJ) continues being a major problem in maxillofacial field. Evidence suggests that cellular therapy may be used for repairing CD in the TMJ. Design A murine model of condyle CD (CCD) was generated in the TMJ to evaluate the capacity of mesenchymal stromal cells (MSCs) to induce cartilage regeneration in CCD. A large CCD was surgically created in a condyle head of the TMJ of C57BL/6 mice. Human MSC embedded into preclotted platelet-rich plasma (PRP) were placed on the surface of CCD. As controls, untreated CCD and exposed TMJ condyle (sham) were used. After 6 weeks, animals were sacrificed, and each mandibular condyle was removed and CCD healing was assessed macroscopically and histologically. Results Macroscopic observation of CCD treated with MSC showed the presence of cartilage-like tissue in the CCD site. Histological analysis showed a complete repair of the articular surface with the presence of cartilage-like tissue and subchondral bone filling the CCD area. Chondrocytes were observed into collagen and glycosaminoglycans extracellular matrix filling the repaired tissue. There was no evidence of subchondral bone sclerosis. Untreated CCD showed denudated osteochondral lesions without signs of cartilage repair. Histological analysis showed the absence of tissue formation over the CCD. Conclusions Transplantation of MSC induces regeneration of TMJ-CCD. These results provide strong evidence to use MSC as potential treatment in patients with cartilage lesions in the TMJ.

scholarly journals A comparative analysis of NLRP3-related inflammatory mediators in synovial fluid in temporomandibular joint osteoarthritis and internal derangement

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mengying Jia ◽  
Yaoguang Lv ◽  
Yingjie Xu ◽  
Zhongcheng Gong
Keyword(s):  
Synovial Fluid ◽  
Temporomandibular Joint ◽  
Signaling Pathway ◽  
Inflammatory Mediators ◽  
Nlrp3 Inflammasome ◽  
Internal Derangement ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Clinical Effects ◽  
Temporomandibular Joint Osteoarthritis

Abstract Background The nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome signaling pathway is a highlighted topic in the field of inflammation. However, there is little research on the relationship between the NLRP3 inflammasome pathway and temporomandibular joint osteoarthritis (TMJOA). The aim of this study was to examine the expression of inflammatory mediators related to the NLRP3 inflammasome in the synovial fluid of patients with condylar cartilage degeneration and verify the clinical effects of sodium hyaluronic acid (HA) treatment on TMJOA. Methods Patients diagnosed with temporomandibular joint internal derangement (TMJID) without condylar defects and TMJOA with condylar defects were divided into two groups. There were thirty patients in each group, and inflammatory mediators related to the NLRP3 inflammasome, including interleukin-1 beta (IL-1β), IL-18, NLRP3, and cysteinyl aspartate specific proteinase 1 (CASP1), in synovial fluid were measured by enzyme-linked immunosorbent assay (ELISA). Eighteen patients in the TMJOA group were retested after two HA treatments to evaluate the therapeutic effects of HA. Results IL-1β, IL-18, NLRP3 and CASP1 were all positive in the two groups, and TMJOA patients with condylar defects had higher expression of these molecules than TMJID patients (P < 0.05). IL-1β, IL-18, and NLRP3 were decreased after two HA treatments (P<0.05), but there was no significant difference in CASP1 after two HA injections (P = 0.549). Conclusions The NLRP3 inflammasome signaling pathway may be involved in condylar degeneration. HA could reduce some inflammatory molecules to alleviate inflammation.

scholarly journals Hypoxia-inducible Factor Expression Is Related to Apoptosis and Cartilage Degradation in Temporomandibular Joint Osteoarthritis

2022 ◽  
Author(s):  
Jun Zhang ◽  
Yu Hu ◽  
Zihan Wang ◽  
Xuelian Wu ◽  
Chun Yang ◽  
...  
Keyword(s):  
Temporomandibular Joint ◽  
Expression Patterns ◽  
Cartilage Damage ◽  
Hypoxia Inducible Factor ◽  
Cartilage Degeneration ◽  
Chondrocyte Apoptosis ◽  
Control Group ◽  
Condylar Cartilage ◽  
Hypoxic Conditions ◽  
Temporomandibular Joint Osteoarthritis

Abstract Background: It remains unclear whether hypoxic conditions affect apoptosis and contribute to degradation of cartilaginous tissues in osteoarthritis (OA) lesions. In this study, we hypothesized that hypoxic conditions induced the accumulation of hypoxia-inducible factor (HIF) and activated apoptosis to contribute to OA cartilage degeneration in vivo.Methods: Malocclusion stress was applied for 2 weeks, 4 weeks and 8 weeks to induce an OA-like lesion animal model (OD) in rats. Histological analysis was performed by H&E staining and safranin O/fast green staining. The expression levels of protein in condylar cartilage were examined by immunostaining to evaluate cartilage degeneration.Results: We found apparent histological phenotypes associated with degeneration in the occlusion disorder stress (OD) group. The OD group at 4 weeks and 8 weeks had obviously reduced expression of Acan and Col II in cartilage. In contrast, the OD groups had higher levels of Col X, ADAMTS5 and MMP13 in the condylar cartilage than the control group. Moreover, the OD group cartilage had prominent degenerative changes with reduced levels of HIF1α and increased levels of HIF2α and the apoptosis factor Caspase3 in condylar cartilage at 8 weeks.Occlusion disorder stress results in cartilage degeneration. HIF1α and HIF2α are involved in temporomandibular joint (TMJ) cartilage homeostasis by regulating chondrocyte apoptosis, which contributes to TMJ cartilage degeneration. Conclusion: Thus, abnormal hypoxic conditions inducing opposite expression patterns of HIF1α and HIF2α could be involved in the pathogenesis of condylar cartilage degeneration. HIF2α may provide a potential negative feedback mechanism for HIF1α during cartilage damage.

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