glycogen and Osteoarthritis

Topics: Animals; Apoptosis; Autophagy; Cartilage, Articular; Chondrocytes; Dental Implants; Glycogen; Male; Osteoarthritis; Rats; Rats, Sprague-Dawley; Temporomandibular Joint

Kashin-Beck disease (KBD) is a chronic endemic osteoarthritis in China. Previous studies have suggested a role of metabolic dysfunction in causation of this disease. In this investigation, the metabolomics approach and cell experiments were used to discover the metabolic changes and their effects on KBD chondrocytes. Nuclear magnetic resonance ((1)H NMR) spectroscopy was used to examine serum samples from both the KBD patients and normal controls. The pattern recognition multivariate analysis (OSC-PLS) and quantitative analysis (QMTLS iterator) revealed altered glycometabolism in KBD, with increased glucose and decreased lactate and citrate levels. IPA biological analysis showed the centric location of glucose in the metabolic network. Massive glycogen deposits in chondrocytes and increased uptake of glucose by chondrocytes further confirmed disordered glycometabolism in KBD. An in vitro study showed the effects of disordered glycometabolism in chondrocytes. When chondrocytes were treated with high glucose, expression of type II collagen and aggrecan were decreased, while TNF-α expression, the level of cellular reactive oxygen species and cell apoptosis rates all were increased. Therefore, our results demonstrated that disordered glycometabolism in patients with KBD was linked to the damage of chondrocytes. This may provide a new basis for understanding the pathogenesis of KBD.

Topics: Aged; Aggrecans; Case-Control Studies; China; Chondrocytes; Collagen Type II; Female; Glucose; Glycogen; Humans; Kashin-Beck Disease; Male; Metabolic Networks and Pathways; Metabolomics; Middle Aged; Osteoarthritis; Reactive Oxygen Species; Tumor Necrosis Factor-alpha

The statement that blood in the articular cavity is cause of cartilage degradation is widely accepted as an axiom. Although the causes of the different articular diseases were explained in numerous studies, none of them has clarified the pathomechanism of haemarthrosis. Our aims were: 1/ to give a morphological description of the blood induced changes in the cartilage, 2/ to verify that the haemarthros is the cause of the cartilage degradation. 10 white rabbits were used in our experimental model. Artificial haemarthros was produced in their left hind knees by intraarticular injection of their own blood. The right hind served as control. The rabbits were divided into to five groups based on the time of the haemarthros (22-50 days). Samples of the condylar cartilage were taken for light, polarization, transmission and scanning electron microscopy examinations. Signs of the disorganization of the matrix structure were showed by polarisation microscope and serious lesions were detected in the perichondrium by scanning electron microscope. Similarity have been suggested amongst the pathomechanism of haemarthrosis and other degenerative cartilage diseases (e. g.: osteoarthrosis, rheumatoid arthritis), so we made the same comparison. In many cases similar morphological changes were observed, as described by other authors in case of degenerative diseases.

Topics: Animals; Arthritis, Rheumatoid; Cartilage Diseases; Cartilage, Articular; Cytoplasm; Disease Models, Animal; Extracellular Matrix; Glycogen; Glycosaminoglycans; Hemarthrosis; Hindlimb; Menisci, Tibial; Microscopy, Electron; Microscopy, Electron, Scanning; Microscopy, Polarization; Osteoarthritis; Porosity; Proteoglycans; Rabbits

Investigations aiming to establish the content of glycogen and of some biochemical characteristics (pH, peroxidase, ammonia, sulfurated hydrogen and reaction in bouillon with copper sulfate) of the muscles (m. gracilis, m. longissimus dorsi, caput longum of m. triceps brachii and the muscules of the neck between the 5th and 7th neck vertebrae) and liver of 16 fattened calves of the Bulgarian brown cattle breed suffering fro degenerative osteoarthrosis, were carried out. It was established that in glycogen content and in biochemical characteristics investigated the muscle and liver samples of calves suffering from degenerative osteoarthrosis differ from those of healthy animals.

Topics: Animals; Cattle; Cattle Diseases; Glycogen; Liver Glycogen; Muscles; Osteoarthritis

Normal canine hip cartilage was compared with cartilage from the degenerative lesions found in young dogs with canine hip dysplasia. The upper 0.5 mm of normal cartilage was characterized. Four distinct layers or zones were found: a layer of fine fibrous material covering the surface, a layer (surface layer) of small (32 nm diameter or less) collagen fibrils tightly packed in bundles and oriented parallel to the surface, a layer (upper layer) or less tightly packed collagen fibrils oriented mostly parallel to the surface with about 33% of the fibrils 64 nm or more, and a layer (intermediate layer) of randomly oriented fibrils with more than 50% of the fibrils 64 nm or larger. Fibril density was high in the surface layer and decreased with depth into the cartilage. In a moderately advanced lesion of degenerative cartilage, there was a layer of amorphous material over the surface. The tightly packed surface layer of small fibrils was absent. The surface itself was uneven and fissued. At depths from the surface comparable to the upper and the intermediate layers in normal cartilage, the proportion of large fibrils was less than in normal cartilage. The overall density of fibrils in degenerative cartilage increased with depth into the tissue. Cells flattened parallel to the surface, with relatively large nuclei, were found in the upper layer of normal cartilage. Cells in the intermediate layers were larger and round. The oblong cells of the upper layer of normal cartilage were not found in any layer of degenerative cartilage. Differences between cells in other layers of normal and degenerative cartilages were minimal. A model for the arrangement of chondrocytes and collagen fibrils for normal and degenerative cartilage was proposed. Ultrastructural changes in degenerative cartilage were prominent in the upper 0.5 mm of cartilage. These changes were changes in the number of collagen fibrils/mum-2 and a change from a characteristic pattern of collagen fibril diameters and orientation found in normal tissue.

Topics: Animals; Cartilage, Articular; Cell Nucleus; Cytoplasmic Granules; Dog Diseases; Dogs; Endoplasmic Reticulum; Glycogen; Golgi Apparatus; Hip Joint; Histocytochemistry; Mitochondria; Osteoarthritis; Pinocytosis; Proteoglycans

Topics: Aging; Animals; Autopsy; Cartilage, Articular; Collagen; Decalcification Technique; Disease Models, Animal; Female; Femur Head; Glycogen; Hindlimb; Hypopituitarism; Joints; Male; Mice; Mice, Inbred Strains; Microscopy, Electron; Organoids; Osteoarthritis; Sex Factors; Staining and Labeling