A CURRENT REVIEW ON THE BIOLOGY AND TREATMENT OF ARTICULAR CARTILAGE DEFECTS (PART I & PART II)

2003 ◽  
Vol 07 (03n04) ◽  
pp. 157-181 ◽  
Author(s):  
Craig Willers ◽  
David J. Wood ◽  
Ming H. Zheng
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
18Th Century ◽  
Later Life ◽  
Fibrin Clot ◽  
Joint Disease ◽  
Cartilage Defects ◽  
Adult Males ◽  
Chondrocyte Implantation ◽  
Osteochondral Injury

Osteochondral injury occurs predominantly in physically active young adult males. Injury to the articular cartilage and/or subchondral bone may not only cause acute joint disease resulting in osseous intracapsular (synovitis) or extracapsular pain, but may also act to spawn arthritic conditions in later life. Since the 18th century, such injury has proven difficult to treat clinically, and much therapy has been essentially palliative. Past treatments such as abrasion arthroplasty, drilling, microfracture and arthroscopic lavage have been useful in removing articular debris and promoting the formation of the fibrin clot used in most native repair mechanisms. However, the limitation of these techniques is their inability to restore the damaged cartilage and subchondral bone to their normal tissue architecture. Recent developments in tissue engineering have concentrated on the utilization of autologous chondrocyte implantation, biomaterials and growth factors to promote the regeneration of biomechanically superior hyaline articular cartilage. This paper reviews the etiology, repair biology and therapeutic techniques of cartilage and/or osteochondral injury over the previous decades, and attempts to provide insight into interesting new research directions which offer much potential for improved treatment of these troublesome lesions.

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.

scholarly journals Peptide-biofunctionalization of biomaterials for osteochondral tissue regeneration in early stage osteoarthritis: challenges and opportunities

2019 ◽  
Vol 7 (7) ◽  
pp. 1027-1044 ◽  
Author(s):  
D. Bicho ◽  
S. Ajami ◽  
C. Liu ◽  
R. L. Reis ◽  
J. M. Oliveira
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Tissue Regeneration ◽  
Early Stage ◽  
Degenerative Joint Disease ◽  
Synovial Inflammation ◽  
Joint Disease ◽  
Progressive Deterioration ◽  
Challenges And Opportunities ◽  
Osteochondral Tissue

Osteoarthritis is a degenerative joint disease characterized by the progressive deterioration of articular cartilage, synovial inflammation and changes in periarticular and subchondral bone, being a leading cause of disability.

scholarly journals Surgical Preparation for Articular Cartilage Regeneration in the Osteoarthritic Knee Joint

Cartilage ◽  
2016 ◽  
Vol 8 (4) ◽  
pp. 365-368 ◽  
Author(s):  
Joerg Mika ◽  
Thomas O. Clanton ◽  
Catherine G. Ambrose ◽  
Raimund W. Kinne
Keyword(s):  
Subchondral Bone ◽  
Cartilage Regeneration ◽  
Fibrin Clot ◽  
Bone Plate ◽  
Subchondral Bone Plate ◽  
Large Area ◽  
Smooth Edge ◽  
Chondrocyte Implantation ◽  
Surgical Preparation

Purpose: Autologous chondrocyte implantation (ACI) is a treatment option even in early osteoarthritis (OA). Surgical preparation for ACI should avoid penetration of the subchondral bone plate to prevent hemorrhage, fibrin clot formation, and subsequent activation of the inflammatory response. Hypothesis: Current surgical procedures with ring curettes preserve the integrity of the subchondral bone plate, even in patients with OA. Methods: Subchondral femoral bone plates ( n = 40) of OA knees undergoing total knee arthroplasty were prepared in vivo using standard, non–brute-force debridement for ACI. To approach regular wear/early OA, only cartilage with maximally grade 3A International Cartilage Repair Society score was prepared. Effects were analyzed by light microscopy. Results: In 87.5% of the specimens (35/40), standard debridement did not violate the tide mark, except for occasional minor openings with a smooth edge (diameter approximately 20 µm). In contrast, 5/40 samples (12.5%) showed one large area with a missing bone plate and an open bone marrow space. Twenty-eight specimens (70%) showed at least remnants of uncalcified cartilage. Conclusion: On the basis of size/fine structure, the occasional minor openings are likely due to increased vascular penetration through the tide mark in the pathologically altered bone-cartilage interface in OA. The consequences of limited hemorrhage through minor openings or selected large defects following in vivo debridement are still unknown. Thus, standard debridement appears suitable for cartilage regeneration even in OA defects.

A review of the treatment methods for cartilage defects

2012 ◽  
Vol 25 (04) ◽  
pp. 263-272 ◽  
Author(s):  
R. M. Thiede ◽  
Y. Lu ◽  
M. D. Markel
Keyword(s):  
Growth Factors ◽  
Articular Cartilage ◽  
Radio Frequency ◽  
Cartilage Defects ◽  
Review Of The Literature ◽  
Treatment Methods ◽  
Chondrocyte Implantation ◽  
Major Treatment ◽  
Osteochondral Tissue ◽  
Articular Cartilage Defects

SummaryThe purpose of this article is to provide a broad review of the literature related to the treatment of cartilage defects and degenerated cartilage in animals with some inferences to the treatment in humans. Methods range from the insertion of osteochondral tissue or cells to the application of radio frequency or insertion of scaffolds and growth factors alone or in combination. Debridement, microfracture, radio frequency, and chondrocyte implantation are all methods normally utilized when treating smaller articular cartilage defects. Scaffolds and mosaicplasty are examples of methods to treat larger defects. This review will cover all major treatment methods currently used to treat articular cartilage defects.

scholarly journals Baicalein Alleviates Osteoarthritis Progression in Mice by Protecting Subchondral Bone and Suppressing Chondrocyte Apoptosis Based on Network Pharmacology

2022 ◽  
Vol 12 ◽  
Author(s):  
Nanxing Yi ◽  
Yilin Mi ◽  
Xiaotong Xu ◽  
Naping Li ◽  
Fan Zeng ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Articular Cartilage ◽  
Signaling Pathway ◽  
Subchondral Bone ◽  
Caspase 3 ◽  
Synovial Inflammation ◽  
Joint Disease ◽  
Network Pharmacology ◽  
Chondrocyte Apoptosis ◽  
Apoptotic Signaling

As life expectancy increases, Osteoarthritis (OA) is becoming a more frequently seen chronic joint disease. The main characteristics of OA are loss of articular cartilage, subchondral bone sclerosis, and synovial inflammation. Baicalein (Bai), a traditional Chinese medicine extracted from Scutellaria baicalensis Georgi, has been demonstrated to exert notable anti-inflammatory effects in previous studies, suggesting its potential effect in the treatment of OA. In this study, we first predicted the action targets of Bai, mapped target genes related to OA, identified potential anti-OA targets for Bai, performed gene ontology (GO) enrichment, and KEGG signaling pathway analyses of the action targets, and analyzed the molecular docking of key Bai targets. Additionally, the effect and potential mechanism of Bai against OA were verified in mouse knee OA models induced by destabilized medial meniscus (DMM) surgery. GO and KEGG analyses showed that 19 anti-OA targets were mainly involved in the response to oxidative stress, the response to hypoxia and apoptosis, and the PI3K-Akt and p53 signaling pathways. Molecular docking results indicated that BAX, BCL 2, and Caspase 3 enriched in the apoptotic signaling pathway have high binding affinity with Bai. Validation experiments showed that Bai can significantly attenuate the loss of articular cartilage (OARSI score), suppress synovial inflammation (synovitis score), and ameliorate subchondral bone resorption measured by micro-CT. In addition, Bai notably inhibited the expression of apoptosis-related proteins in articular cartilage (BAX, BCL 2, and Caspase 3). By combining network pharmacology with experimental validation, our study identifies and verifies the importance of the apoptotic signaling pathway in the treatment of OA by Bai. Bai may have promising application and potential therapeutic value in OA treatment.

scholarly journals Effect of Vertical or Beveled Chondral Defect Creation on Rim Deformation and Contact

Cartilage ◽  
2018 ◽  
Vol 10 (2) ◽  
pp. 222-228 ◽  
Author(s):  
Adam B. Yanke ◽  
Megan L. Konopka ◽  
Davietta C. Butty ◽  
Maximilian A. Meyer ◽  
Eric J. Cotter ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Rank Test ◽  
Cartilage Defects ◽  
Micro Computed Tomography ◽  
Bone Contact ◽  
Defect Center ◽  
Tibial Cartilage ◽  
Contact Width ◽  
Articular Cartilage Defects

Objective To determine biomechanical effects of knee cartilage defect perimeter morphology based on cartilage strain and opposing subchondral bone contact. Design Articular cartilage defects were created in 5 bovine femoral condyles: group 1, 45° inner bevel with 8-mm rim; group 2, vertical with 8-mm rim; and group 3, 45° outer bevel with 8-mm base. Samples were placed into a custom-machined micro–computed tomography tube and subjected to 800 N of axial loading. DICOM data were used to calculate cartilage thickness 4 and 6 mm from the center, distance between tibial cartilage surface and femoral subchondral bone, and contact width between tibial cartilage and subchondral bone. Strain 4 mm from the center and both absolute and change in distance (mm) to subchondral bone were compared between groups 1 and 2 using paired t tests. Strain at 6 mm and distance changed, loaded distance, and contact width (mm) were compared between groups using the Friedman test with post hoc analysis using Wilcoxon signed rank test. Results No significant differences in rim strain were noted between groups 1 and 2 at 4 mm ( P = 0.10) and between groups 1, 2, and 3 at 6 mm ( P = 0.247) from the defect center. The loaded distance was significantly different between groups 1 and 3 ( P = 0.013). No significant change in distance to the subchondral bone was found between groups ( P = 0.156). The difference in subchondral bone contact area approached but did not reach significance ( P = 0.074). Conclusion When debriding focal articular cartilage defects, establishment of an inner bevel decreases tissue deformation and contact with opposing subchondral bone.

scholarly journals The Effects of Annatto Tocotrienol Supplementation on Cartilage and Subchondral Bone in an Animal Model of Osteoarthritis Induced by Monosodium Iodoacetate

2019 ◽  
Vol 16 (16) ◽  
pp. 2897 ◽  
Author(s):  
Kok-Yong Chin ◽  
Sok Kuan Wong ◽  
Fadhlullah Zuhair Japar Sidik ◽  
Juliana Abdul Hamid ◽  
Nurul Hafizah Abas ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Sham Group ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Sprague Dawley ◽  
Joint Protection ◽  
Sprague Dawley Rats ◽  
Monosodium Iodoacetate ◽  
Inflammatory Component

Osteoarthritis is a degenerative joint disease which primarily affects the articular cartilage and subchondral bones. Since there is an underlying localized inflammatory component in the pathogenesis of osteoarthritis, compounds like tocotrienol with anti-inflammatory properties may be able to retard its progression. This study aimed to determine the effects of oral tocotrienol supplementation on the articular cartilage and subchondral bone in a rat model of osteoarthritis induced by monosodium iodoacetate (MIA). Thirty male Sprague-Dawley rats (three-month-old) were randomized into five groups. Four groups were induced with osteoarthritis (single injection of MIA at week 0) and another served as the sham group. Three of the four groups with osteoarthritis were supplemented with annatto tocotrienol at 50, 100 and 150 mg/kg/day orally for five weeks. At week 5, all rats were sacrificed, and their tibial-femoral joints were harvested for analysis. The results indicated that the groups which received annatto tocotrienol at 100 and 150 mg/kg/day had lower histological scores and cartilage remodeling markers. Annatto tocotrienol at 150 mg/kg/day significantly lowered the osteocalcin levels and osteoclast surface of subchondral bone. In conclusion, annatto tocotrienol may potentially retard the progression of osteoarthritis. Future studies to confirm its mechanism of joint protection should be performed.

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