Role of Subchondral Bone in the Initiation and Progression of Cartilage Damage

1986 ◽  
Vol &NA; (213) ◽  
pp. 34???40 ◽  
Author(s):  
ERIC L. RADIN ◽  
ROBERT M. ROSE
Keyword(s):  
Subchondral Bone ◽  
Cartilage Damage

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 Genetic Deletion of Interleukin-15 Is Not Associated with Major Structural Changes Following Experimental Post-Traumatic Knee Osteoarthritis in Rats

2021 ◽  
Vol 11 (15) ◽  
pp. 7118
Author(s):  
Ermina Hadzic ◽  
Garth Blackler ◽  
Holly Dupuis ◽  
Stephen James Renaud ◽  
Christopher Thomas Appleton ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Structural Changes ◽  
Cartilage Damage ◽  
Wild Type ◽  
Significant Difference ◽  
Post Traumatic ◽  
Interleukin 15 ◽  
Joint Trauma ◽  
Surgically Induced

Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease, leading to articular cartilage breakdown, osteophyte formation, and synovitis, caused by an initial joint trauma. Pro-inflammatory cytokines increase catabolic activity and may perpetuate inflammation following joint trauma. Interleukin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its roles in PTOA pathophysiology are not well characterized. Here, we utilized Il15 deficient rats to examine the role of IL-15 in PTOA pathogenesis in an injury-induced model. OA was surgically induced in Il15 deficient Holtzman Sprague-Dawley rats and control wild-type rats to compare PTOA progression. Semi-quantitative scoring of the articular cartilage, subchondral bone, osteophyte size, and synovium was performed by two blinded observers. There was no significant difference between Il15 deficient rats and wild-type rats following PTOA-induction across articular cartilage damage, subchondral bone damage, and osteophyte scoring. Similarly, synovitis scoring across six parameters found no significant difference between genetic variants. Overall, IL-15 does not appear to play a key role in the development of structural changes in this surgically-induced rat model of PTOA.

scholarly journals Systematic Analysis of Transcriptomic Profile of Chondrocytes in Osteoarthritic Knee Using Next-Generation Sequencing and Bioinformatics

2018 ◽  
Vol 7 (12) ◽  
pp. 535 ◽  
Author(s):  
Yi-Jen Chen ◽  
Wei-An Chang ◽  
Ling-Yu Wu ◽  
Ya-Ling Hsu ◽  
Chia-Hsin Chen ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Family Member ◽  
Subchondral Bone ◽  
Joint Pain ◽  
Expression Patterns ◽  
Cartilage Damage ◽  
Phenotypic Change ◽  
Next Generation ◽  
Arthritic Joint ◽  
Generation Sequencing

The phenotypic change of chondrocytes and the interplay between cartilage and subchondral bone in osteoarthritis (OA) has received much attention. Structural changes with nerve ingrowth and vascular penetration within OA cartilage may contribute to arthritic joint pain. The aim of this study was to identify differentially expressed genes and potential miRNA regulations in OA knee chondrocytes through next-generation sequencing and bioinformatics analysis. Results suggested the involvement of SMAD family member 3 (SMAD3) and Wnt family member 5A (WNT5A) in the growth of blood vessels and cell aggregation, representing features of cartilage damage in OA. Additionally, 26 dysregulated genes with potential miRNA–mRNA interactions were identified in OA knee chondrocytes. Myristoylated alanine rich protein kinase C substrate (MARCKS), epiregulin (EREG), leucine rich repeat containing 15 (LRRC15), and phosphodiesterase 3A (PDE3A) expression patterns were similar among related OA cartilage, subchondral bone and synovial tissue arrays in Gene Expression Omnibus database. The Ingenuity Pathway Analysis identified MARCKS to be associated with the outgrowth of neurite, and novel miRNA regulations were proposed to play critical roles in the pathogenesis of the altered OA knee joint microenvironment. The current findings suggest new perspectives in studying novel genes potentially contributing to arthritic joint pain in knee OA, which may assist in finding new targets for OA treatment.

scholarly journals The role of subchondral bone, and its histomorphology, on the dynamic viscoelasticity of cartilage, bone and osteochondral cores

2019 ◽  
Vol 27 (3) ◽  
pp. 535-543 ◽  
Author(s):  
N.L.A. Fell ◽  
B.M. Lawless ◽  
S.C. Cox ◽  
M.E. Cooke ◽  
N.M. Eisenstein ◽  
...  
Keyword(s):  
Subchondral Bone ◽  
Dynamic Viscoelasticity

scholarly journals Selonsertib Alleviates the Progression of Rat Osteoarthritis: An in vitro and in vivo Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiyuan Yan ◽  
Yingchi Zhang ◽  
Gaohong Sheng ◽  
Bowei Ni ◽  
Yifan Xiao ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Cartilage Damage ◽  
Cartilage Degradation ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Therapeutic Effects ◽  
Exact Role

Osteoarthritis (OA) is a prevalent degenerative joint disease. Its development is highly associated with inflammatory response and apoptosis in chondrocytes. Selonsertib (Ser), the inhibitor of Apoptosis Signal-regulated kinase-1 (ASK1), has exhibited multiple therapeutic effects in several diseases. However, the exact role of Ser in OA remains unclear. Herein, we investigated the anti-arthritic effects as well as the potential mechanism of Ser on rat OA. Our results showed that Ser could markedly prevent the IL-1β-induced inflammatory reaction, cartilage degradation and cell apoptosis in rat chondrocytes. Meanwhile, the ASK1/P38/JNK and NFκB pathways were involved in the protective roles of Ser. Furthermore, intra-articular injection of Ser could significantly alleviate the surgery induced cartilage damage in rat OA model. In conclusion, our work provided insights into the therapeutic potential of Ser in OA, indicating that Ser might serve as a new avenue in OA treatment.

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