scholarly journals Cartilage degeneration and excessive subchondral bone formation in spontaneous osteoarthritis involves altered TGF-β signaling

2015 ◽  
Vol 34 (5) ◽  
pp. 763-770 ◽  
Author(s):  
Weiwei Zhao ◽  
Ting Wang ◽  
Qiang Luo ◽  
Yan Chen ◽  
Victor Y. L. Leung ◽  
...  
Keyword(s):  
Bone Formation ◽  
Subchondral Bone ◽  
Cartilage Degeneration

scholarly journals Effect of differences in mechanical stress in vivo on the onset and progression of knee osteoarthritis

2021 ◽  
Author(s):  
Kohei Arakawa ◽  
Kei Takahata ◽  
Yuichiro Oka ◽  
Kaichi Ozone ◽  
Sumika Nakagaki ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Bone Formation ◽  
Mechanical Stress ◽  
Compressive Stress ◽  
Subchondral Bone ◽  
Shear Force ◽  
Joint Instability ◽  
Cartilage Degeneration ◽  
Articular Cartilage Degeneration

Objective: The effect of the type of mechanical stress on OA onset has not been clarified. The aim of this study was to establish a new model that reproduces the type and increase and decrease of mechanical stress in vivo and to clarify the differences in the mechanism of knee OA onset and progression among the models. Design: To reproduce the difference in mechanical stress, we used the anterior cruciate ligament transection (ACL-T) model and the destabilization of the medial meniscus (DMM) model. In addition, we created a controlled abnormal tibial translation (CATT) model and a controlled abnormal tibial rotation (CATR) model that suppressed the joint instability of the ACL-T and DMM model, respectively. These four models reproduced the increase and decrease in shear force due to joint instability and compressive stress due to meniscal dysfunction. We performed joint instability analysis with soft X-ray, micro computed tomography analysis, histological analysis, and immunohistological analysis in 4 and 6 weeks. Results: Joint instability decreased in the CATT and CATR groups. The meniscus deviated in the DMM and CATR groups. Chondrocyte hypertrophy increased in the ACL-T and DMM groups with joint instability. In the subchondral bone, bone resorption was promoted in the ACL-T and CATT groups, and bone formation was promoted in the DMM and CATR groups. Conclusions: Increased shear force causes articular cartilage degeneration and osteoclast activation in the subchondral bone. In contrast, increased compressive stress promotes bone formation in the subchondral bone earlier than articular cartilage degeneration occurs.

scholarly journals Inhibition of Semaphorin 4D/Plexin-B1 Signal Inhibits the Subchondral Bone Loss in Early-Stage Osteoarthritis of Temporomandibular Joint

2021 ◽  
Author(s):  
Zhaoyichun Zhang ◽  
Lei Lu ◽  
Tao Ye ◽  
Shibin Yu ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Temporomandibular Joint ◽  
Subchondral Bone ◽  
Early Stage ◽  
Cartilage Degeneration ◽  
Pathological Feature ◽  
Semaphorin 4D ◽  
New Therapeutic Approaches

Subchondral bone loss is an important pathological feature of early-stage temporomandibular joint (TMJ) osteoarthritis (OA). Previous studies focused mainly on the bone resorption by osteoclasts in early-stage OA, but the bone formation feature has not drawn enough attention. Sema4D/Plexin-B1 is a pair of molecules expressed by osteoclast/osteoblast, which is capable of inhibiting bone formation by osteoblasts. The present study found that subchondral bone loss in early-stage TMJ OA was accompanied by up-regulated expression of Sema4D in cartilage and subchondral bone and Plexin-B1 in subchondral bone. Reducing Sema4D level could inhibit the subchondral bone loss and cartilage degeneration of early-stage TMJ OA. In vitro, results revealed that Sema4D could reduce the expression of osteocalcin (OCN) and alkaline phosphatase (ALP), and increase the migrating capability of Plexin-B1-positive osteoblasts. Our results revealed that elevated Sema4D expression in early-stage TMJ OA might decrease the bone formation activity of osteoblasts in the subchondral bone by binding to Plexin-B1 expressed by osteoblasts. Inhibiting Sema4D/Plexin-B1 signaling in the early-stage OA holds promise as a strategy for new therapeutic approaches to osteoarthritis.

scholarly journals Early patellofemoral articular cartilage degeneration in a rat model of patellar instability is associated with activation of the NF-κB signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wei Lin ◽  
Huijun Kang ◽  
Yike Dai ◽  
Yingzhen Niu ◽  
Guangmin Yang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Signaling Pathway ◽  
Subchondral Bone ◽  
Patellofemoral Joint ◽  
Patellar Instability ◽  
Cartilage Degeneration ◽  
Control Group ◽  
And Control ◽  
Articular Cartilage Degeneration ◽  
And Cartilage

Abstract Background Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The molecular mechanism of early articular cartilage degeneration during patellofemoral osteoarthritis (PFOA) still requires further investigation. However, it is known that the NF-κB signaling pathway plays an important role in articular cartilage degeneration. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration. Methods We established a rat model of PI-induced PFOA. Female 4-week-old Sprague-Dawley rats (n = 120) were randomly divided into two groups: the PI (n = 60) and control group (n = 60). The distal femurs of the PI and control group were isolated and compared 4, 8, and 12 weeks after surgery. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomography and histology. The expression of NF-κB, matrix metalloproteinase (MMP)-13, collagen X, and TNF-ɑ were evaluated by immunohistochemistry and quantitative polymerase chain reaction. Results In the PI group, subchondral bone loss and cartilage degeneration were found 4 weeks after surgery. Compared with the control group, the protein and mRNA expression of NF-κB and TNF-ɑ were significantly increased 4, 8, and 12 weeks after surgery in the PI group. In addition, the markers of cartilage degeneration MMP-13 and collagen X were more highly expressed in the PI group compared with the control group at different time points after surgery. Conclusions This study has demonstrated that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss and cartilage degeneration. In addition, the degeneration of articular cartilage may be associated with the activation of the NF-κB signaling pathway and can deteriorate with time as a result of PI.

Electroacupuncture Ameliorates Subchondral Bone Deterioration and Inhibits Cartilage Degeneration in Ovariectomised Rats

2018 ◽  
Vol 36 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Jun Zhou ◽  
Peirui Zhong ◽  
Ying Liao ◽  
Jing Liu ◽  
Yuan Liao ◽  
...  
Keyword(s):  
Subchondral Bone ◽  
Type I Collagen ◽  
Cartilage Degeneration ◽  
Cross Linking ◽  
Control Group ◽  
Sham Operation ◽  
Type I ◽  
Trabecular Thickness ◽  
Ovx Rats ◽  
Time Point

Objectives To investigate the effects of electroacupuncture (EA) on subchondral bone mass and cartilage degeneration in an experimental animal model of osteoarthritis (OA) induced by ovariectomy (OVX). Methods Ninety 3-month-old female Sprague-Dawley rats were randomly divided into the following three groups (n = 30 each): sham operation without treatment (control group); OVX without treatment (OVX group);, and ovariectomy with EA treatment (EA group). Rats in the EA group received EA treatment from the day of OVX. Ten rats in each group were randomly killed at 4, 8 and 12 weeks after operation. Results EA reduced urine C-terminal cross-linking telopeptide of type I collagen from 4 weeks after OVX, reduced C-terminal cross-linking telopeptide of type II collagen and body weight from 8 weeks after OVX, and increased serum 17β-oestradiol from 4 weeks after OVX compared with the OVX group (all p<0.01). In the EA group, trabecular bone volume ratio, trabecular thickness and trabecular number increased, and trabecular separation were reduced at each time point compared with the OVX group (p<0.05, p<0.01, respectively). In the EA group, osteoprotegerin (OPG) expression was increased and receptor activator of nuclear factor kappa-B ligand (RANKL) expression was reduced at each time point compared with the OVX group (p<0.05, p<0.01, respectively). Mankin scores and mRNA expression of matrix metalloproteinase-13 (MMP-13) were lower in EA versus OVX groups at 12 weeks after OVX (both p<0.01). Conclusion The results suggest that EA inhibits subchondral bone loss by regulating RANK/RANKL/OPG signalling and protects articular cartilage by inhibiting MMP-13 in OVX rats.

Relationship Between Bone Marrow Lesions on MRI and Cartilage Degeneration in Osteochondral Lesions of the Talar Dome

2018 ◽  
Vol 39 (8) ◽  
pp. 908-915 ◽  
Author(s):  
Tomoyuki Nakasa ◽  
Yasunari Ikuta ◽  
Mikiya Sawa ◽  
Masahiro Yoshikawa ◽  
Yusuke Tsuyuguchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Subchondral Bone ◽  
Cartilage Degeneration ◽  
Osteochondral Lesions ◽  
Talar Dome ◽  
Mankin Score ◽  
Osteochondral Fragment ◽  
The Mean ◽  
And Cartilage ◽  
Ct And Mri

Background: In the evaluation of osteochondral lesions of the talar dome (OLT), bone marrow lesions (BML) are commonly observed in the subchondral bone on magnetic resonance imaging (MRI). However, the significance of BML, such as the histology of the overlying cartilage, is still unclear. The purpose of this study was to investigate the relationship between the BML and cartilage degeneration in OLT. Methods: Thirty-three ankles with OLT were included in this study. All ankles underwent CT and MRI and had operative treatment. The ankles were divided into 2 groups, depending on the presence of bone sclerosis (ie, with or without) in the host bone just below the osteochondral fragment (nonsclerosis group and sclerosis group). The area of BML was compared between the 2 groups. Biopsies of the osteochondral fragment from 20 ankles were performed during surgery, and the correlation between the BML and cartilage degeneration was analyzed. The remaining 13 ankles had the CT and MRI compared with the arthroscopic findings. Results: The mean area of BML in the nonsclerosis group was significantly larger than that in the sclerosis group. In the histologic analysis, there was a significant and moderate correlation between the Mankin score and the area of BML. The mean Mankin score in the nonsclerosis group was significantly lower than that in the sclerosis group. Conclusions: This study revealed that a large area of BML on MRI exhibited low degeneration of cartilage of the osteochondral fragment, while a small area of BML indicated sclerosis of the subchondral bone with severe degeneration of cartilage. The evaluation of BML may predict the cartilage condition of the osteochondral fragment. Level of Evidence: Level III, comparative series.

scholarly journals Noggin Inhibits IL-1β and BMP-2 Expression, and Attenuates Cartilage Degeneration and Subchondral Bone Destruction in Experimental Osteoarthritis

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 927 ◽  
Author(s):  
Szu-Yu Chien ◽  
Chun-Hao Tsai ◽  
Shan-Chi Liu ◽  
Chien-Chung Huang ◽  
Tzu-Hung Lin ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Signaling Pathways ◽  
Bone Remodeling ◽  
Subchondral Bone ◽  
Bone Destruction ◽  
Cartilage Degeneration ◽  
Cartilage Degradation ◽  
Mitogen Activated Protein Kinase ◽  
Bone Morphogenetic Protein 2 ◽  
Joint Disease

Osteoarthritis (OA) is a chronic inflammatory and progressive joint disease that results in cartilage degradation and subchondral bone remodeling. The proinflammatory cytokine interleukin 1 beta (IL-1β) is abundantly expressed in OA and plays a crucial role in cartilage remodeling, although its role in the activity of chondrocytes in cartilage and subchondral remodeling remains unclear. In this study, stimulating chondrogenic ATDC5 cells with IL-1β increased the levels of bone morphogenetic protein 2 (BMP-2), promoted articular cartilage degradation, and enhanced structural remodeling. Immunohistochemistry staining and microcomputed tomography imaging of the subchondral trabecular bone region in the experimental OA rat model revealed that the OA disease promotes levels of IL-1β, BMP-2, and matrix metalloproteinase 13 (MMP-13) expression in the articular cartilage and enhances subchondral bone remodeling. The intra-articular injection of Noggin protein (a BMP-2 inhibitor) attenuated subchondral bone remodeling and disease progression in OA rats. We also found that IL-1β increased BMP-2 expression by activating the mitogen-activated protein kinase (MEK), extracellular signal-regulated kinase (ERK), and specificity protein 1 (Sp1) signaling pathways. We conclude that IL-1β promotes BMP-2 expression in chondrocytes via the MEK/ERK/Sp1 signaling pathways. The administration of Noggin protein reduces the expression of IL-1β and BMP-2, which prevents cartilage degeneration and OA development.

Osteoarthritis

2018 ◽  
Author(s):  
Michael Doherty
Keyword(s):  
Risk Factors ◽  
Bone Formation ◽  
Subchondral Bone ◽  
Environmental Risk ◽  
Hyaline Cartilage ◽  
Bone Remodelling ◽  
Interphalangeal Joint ◽  
New Bone Formation ◽  
Clinical Phenotypes ◽  
Knee Oa

Osteoarthritis (OA) is a disorder of synovial joints and is characterized by the combination of focal hyaline cartilage loss and accompanying subchondral bone remodelling and marginal new bone formation (osteophyte). It has genetic, constitutional, and environmental risk factors and presents a spectrum of clinical phenotypes and outcomes. OA commonly affects just one region (e.g. knee OA, hip OA). However, multiple hand interphalangeal joint OA, usually accompanied by posterolateral firm swellings (nodes), is a marker for a tendency towards polyarticular ‘generalized nodal OA’.

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