Articular Cartilage Proteoglycan Metabolism in Avian Degenerative Joint Disease: Effects of Strain Selection and Body Weight

1999 ◽  
Vol 40 (3) ◽  
pp. 199-208 ◽  
Author(s):  
N. Venkatesan ◽  
B. H. Thorp ◽  
D. J. S. Hulmes
Keyword(s):  
Body Weight ◽  
Articular Cartilage ◽  
Degenerative Joint Disease ◽  
Strain Selection ◽  
Joint Disease ◽  
Cartilage Proteoglycan

scholarly journals Effects of chondroitin sulfate and sodium hyaluronate on chondrocytes and extracellular matrix of articular cartilage in dogs with degenerative joint disease

2008 ◽  
Vol 60 (1) ◽  
pp. 93-102 ◽  
Author(s):  
G. Gonçalves ◽  
E.G. Melo ◽  
M.G. Gomes ◽  
V.A. Nunes ◽  
C.M.F. Rezende
Keyword(s):  
Articular Cartilage ◽  
Chondroitin Sulfate ◽  
Sodium Hyaluronate ◽  
Nucleolar Organizer ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Control Group ◽  
Nucleolar Organizer Regions ◽  
Morphological Evaluation ◽  
Cell Counts

Samples of articular cartilage of femur, tibia and patella of 15 dogs with experimentally induced degenerative joint disease (DJD) were microscopically analyzed. Animals were distributed into three groups (n=5): the control group received no medication; the second group was treated with chondroitin sulfate and the third received sodium hyaluronate. Samples were processed and stained with HE and toluidine blue for morphological evaluation. The metabolic and proliferative activity of the chondrocytes was evaluated by the measurement of nucleolar organizer regions (NORs) after impregnation by silver nitrate. Significant differences were not observed (P>0.05) in the morphology among the groups, however, the group treated with sodium hyaluronate had a higher score suggesting a trend to a greater severity of the lesions. Significant differences were not observed (P>0.05) in the measurement of NORs, cells and NORs/cells among the groups. Although differences were not significant, sodium hyaluronate group showed higher NOR and cell counts which suggested an increase of the proliferation rate of chondrocytes. In addition, a higher NOR/cell ratio in the group treated with chondroitin sulfate suggested that this drug may have stimulated the metabolic activity of the chondrocytes, minimizing the lesions resulting from DJD.

scholarly journals New Therapeutic Strategies for Osteoarthritis by Targeting Sialic Acid Receptors

Biomolecules ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 637 ◽  
Author(s):  
Paula Carpintero-Fernandez ◽  
Marta Varela-Eirin ◽  
Alessandra Lacetera ◽  
Raquel Gago-Fuentes ◽  
Eduardo Fonseca ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Ex Vivo ◽  
Molecular Model ◽  
Cartilage Degradation ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Novel Therapy ◽  
Human Cartilage ◽  
Sialic Acid Receptors ◽  
Cartilage Breakdown

Osteoarthritis (OA) is the most common degenerative joint disease characterized by articular cartilage degradation and joint degeneration. The articular cartilage is mainly formed by chondrocytes and a collagen-proteoglycan extracellular matrix that contains high levels of glycosylated proteins. It was reported that the shift from glycoproteins containing α-2,6-linked sialic acids to those that contain α-2,3 was associated with the onset of common types of arthritis. However, the pathophysiology of α-2,3-sialylation in cartilage has not been yet elucidated. We show that cartilage from osteoarthritic patients expresses high levels of the α-2,3-sialylated transmembrane mucin receptor, known as podoplanin (PDPN). Additionally, the Maackia amurensis seed lectin (MASL), that can be utilized to target PDPN, attenuates the inflammatory response mediated by NF-kB activation in primary chondrocytes and protects human cartilage breakdown ex vivo and in an animal model of arthritis. These findings reveal that specific lectins targeting α-2,3-sialylated receptors on chondrocytes might effectively inhibit cartilage breakdown. We also present a computational 3D molecular model for this interaction. These findings provide mechanistic information on how a specific lectin could be used as a novel therapy to treat degenerative joint diseases such as osteoarthritis.

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 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.

Frictional Characteristics and Tissue Loss of Articular Cartilage Under a Novel Wear Regime

2007 ◽  
Author(s):  
Kelly J. Shields ◽  
John R. Owen ◽  
Jennifer S. Wayne
Keyword(s):  
Articular Cartilage ◽  
Articular Surface ◽  
Cartilage Damage ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Tissue Loss ◽  
Joint Function ◽  
Repair Technique ◽  
Repair Techniques

Degenerative joint disease, age, and trauma lead to progressive articular cartilage damage due to the tissue’s limited repair capabilities. Numerous clinical repair techniques with varying degrees of success have been developed in order to repair damaged tissue and restore joint function. One approach is the development of articular cartilage repair tissue to implant into the damaged or diseased articular surface. Determining the viability of an articular repair technique or tissue under in vivo stresses and wear is crucial to predict its success.

scholarly journals Osmotic Swelling Responses are Conserved Across Cartilaginous Tissues with Varied Sulfated-Glycosaminoglycan Contents

2018 ◽  
Author(s):  
Eva G. Baylon ◽  
Marc E. Levenston
Keyword(s):  
Articular Cartilage ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Confined Compression ◽  
Osmotic Swelling ◽  
Swelling Properties ◽  
Sulfated Glycosaminoglycan ◽  
Low Concentrations ◽  
Sgag Content ◽  
Phosphate Buffered Saline

AbstractThe interactions between the negatively charged sulfated glycosaminoglycan (sGAG) chains and the ionic interstitial fluid in articular cartilage and meniscal fibrocartilage give rise to an osmotic swelling stress that is critical for the load-bearing capability of both tissues. This osmotic swelling stress is altered when the sGAG content is changed, as during progression of degenerative joint disease; understanding the influence of sGAG concentration on the osmotic swelling stress of cartilage and meniscus is important to enhance our understanding of physiology and disease. This study compared the effect of altered osmotic environments on the confined compression swelling behavior of bovine tissues spanning a range of sGAG concentrations: juvenile articular cartilage, juvenile and adult meniscus, and juvenile cartilage degraded to reduce sGAG content. The transient response to changes in bath conditions was evaluated for explants assigned to one of three compressive offsets (5%, 10%, or 15% strain) and one of three bath conditions (0.1X, 1X, or 10X Phosphate Buffered Saline). Our results show that relative responses to alterations to the osmotic environment are consistent across tissue types, demonstrating that the role of sGAG in the swelling properties of the tissues tested is conserved, even when sGAG is present at low concentrations. Additionally, this study found unexpected correlations across tissue types between sGAG and collagen contents and between the aggregate modulus and both sGAG and collagen contents. These results suggest some conservation of composition-function relationships across a range of tissue types.

scholarly journals Proof-of-concept for the detection of early osteoarthritis pathology by endomicroscopy

2019 ◽  
Author(s):  
Mathäus Tschaikowsky ◽  
Sofia Brander ◽  
Bizan N. Balzer ◽  
Bernd Rolauffs ◽  
Thorsten Hugel
Keyword(s):  
Articular Cartilage ◽  
Spatial Patterns ◽  
Spatial Organization ◽  
Degenerative Joint Disease ◽  
Optical Methods ◽  
Joint Disease ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
Proof Of Concept ◽  
Early Oa

AbstractOsteoarthritis (OA) is a degenerative joint disease and the leading cause of global disability. Clinical trials to date have been unable to pinpoint early and potentially reversible disease states with current clinical technology and hence disease-modifying OA drug candidates cannot be tested early in the disease. To overcome this obstacle, we correlate articular cartilage stiffness changes and cellular spatial organization. The former is a well-understood and functionally relevant OA pathology, while the latter allows discriminating between healthy vs early OA, based on distinct cellular spatial patterns. We demonstrated that an extensive loss of atomic force microscopy-detected stiffness can be seen in cartilage tissues with spatial patterns exhibiting the earliest identifiable OA. In addition, the translation of commercially available clinically usable probe-based confocal laser-endomicroscopy allows us to detect these early OA spatial patterns. This study resolves a major clinical trial obstacle by presenting the proof-of-concept that early OA pathology can be detected by already available clinical technology.One Sentence SummaryWe report a correlation between articular cartilage surface nanoscale stiffness and chondrocyte spatial organization; using this correlation enables early pathology detection by currently available clinical optical methods.

scholarly journals Chondrocytes apoptosis in osteoarthritis

2018 ◽  
Vol 72 ◽  
pp. 875-883
Author(s):  
Sabina Galiniak ◽  
Izabela Krawczyk-Marć ◽  
Agata Wawrzyniak ◽  
Stanisław Orkisz
Keyword(s):  
Cell Death ◽  
Articular Cartilage ◽  
Mechanical Damage ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Chondrocyte Apoptosis ◽  
Free Oxygen Radicals ◽  
Motor Disability ◽  
Chondrocyte Death ◽  
Underlying Causes

Osteoarthritis (OA) is a type of degenerative joint disease where the balance between the degradation and the regeneration of articular cartilage is impaired, which leads to its progressive loss. This disease is the most common chronic musculoskeletal disease that leads to premature motor disability. Risk factors for developing OA include age, obesity, sex, past traumas and arthritis, genetic factors, diet and ethnicity. Typical OA symptoms are arthralgia, restriction of movement, cracking and secondary inflammatory lesions. In recent years, the underlying causes of this disease include chondrocyte death by apoptosis, necrosis or combinations of these types of cell death. Apoptosis, called programmed cell death, has clear morphological features, and is a highly regulated process. Apoptosis is involved in maintaining homeostasis; however, its severity is observed in many pathological conditions. Articular cartilage chondrocyte death by apoptosis disrupts the proper maintenance of cartilage structure by reducing cell density. Chondrocyte apoptosis causes mechanical damage, manifested by increased synthesis of free oxygen radicals and disturbance of the integrity of the extracellular matrix. An increasing amount of reports regarding the potential pharmacological substances that have been used as inhibitors of apoptosis have improved the quality of life in OA patients. This article presents the current state of knowledge on apoptosis and apoptotic death of chondrocytes in the course of osteoarthritis.

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