Fractionation of protein components of the human synovial fluid was carried out with paper and disc electrophoresis, and isoelectric focusing. The mean ranges of total protein content of synovial fluid obtained in the thirty patients suffering from nonspecific and traumatic synovitis, degenerative osteoarthritis or rheumatoid arthritis were 3.8 to 4.6g/dl. There was no significant difference between each from of arthritis. The pattern of protein fractionation of synovial fluid by paper electrophoresis was similar to that of serum protein. On disc electrophoresis, 20 fractions were identified in synovial fluid and the main fraction was albumin. Isoelectric focusing of the human serum with Ampholine carrier ampholyte in thin layer polyacrylamide gel revealed 27 protein fractions and five isoenzymes of amylase and two of them were the main fractions. In the synovial fluid 22 protein fractions and two isoenzymes of amylase, which had the same isoelectric points as the main fractions of serum, were noted. It is suggested that the isoamylases in the synovial fluid are a dialysate of plasma enzymes.
Arthritis, Rheumatoid/metabolism ; Human ; Osteoarthritis/metabolism ; Proteins/metabolism* ; Synovial Fluid/metabolism* ; Synovitis/metabolism

OBJECTIVE: To summarize the role of chondrocyte mitochondrial homeostasis imbalance in the pathogenesis of osteoarthritis (OA) and analyze its application prospects. METHODS: The recent literature at home and abroad was reviewed to summarize the mechanism of mitochondrial homeostasis imbalance, the relationship between mitochondrial homeostasis imbalance and the pathogenesis of OA, and the application prospect in the treatment of OA. RESULTS: Recent studies have shown that mitochondrial homeostasis imbalance, which is caused by abnormal mitochondrial biogenesis, the imbalance of mitochondrial redox, the imbalance of mitochondrial dynamics, and damaged mitochondrial autophagy of chondrocytes, plays an important role in the pathogenesis of OA. Abnormal mitochondrial biogenesis can accelerate the catabolic reaction of OA chondrocytes and aggravate cartilage damage. The imbalance of mitochondrial redox can lead to the accumulation of reactive oxygen species (ROS), inhibit the synthesis of extracellular matrix, induce ferroptosis and eventually leads to cartilage degradation. The imbalance of mitochondrial dynamics can lead to mitochondrial DNA mutation, decreased adenosine triphosphate production, ROS accumulation, and accelerated apoptosis of chondrocytes. When mitochondrial autophagy is damaged, dysfunctional mitochondria cannot be cleared in time, leading to ROS accumulation, which leads to chondrocyte apoptosis. It has been found that substances such as puerarin, safflower yellow, and astaxanthin can inhibit the development of OA by regulating mitochondrial homeostasis, which proves the potential to be used in the treatment of OA. CONCLUSION The mitochondrial homeostasis imbalance in chondrocytes is one of the most important pathogeneses of OA, and further exploration of the mechanisms of mitochondrial homeostasis imbalance is of great significance for the prevention and treatment of OA.
Humans ; Reactive Oxygen Species/metabolism* ; Chondrocytes/metabolism* ; Osteoarthritis/metabolism* ; Homeostasis ; Mitochondria/metabolism* ; Cartilage, Articular/metabolism*

Interleukin (IL)-36 is a family of cytokines that belongs to the larger IL-1 superfamily. IL-36 agonist/antagonist binds to the interleukin-36 receptor involving in physiological inflammation regulation and pathogenesis of many inflammatory diseases. In inflammatory joint diseases, the expression of IL-36 changes, and some studies have initially explored the role of IL-36 in these diseases. In psoriatic arthritis, IL-36 signal mediates plasma cell and fibroblast-like synoviocyte crosstalk presenting IL-36 agonist/antagonist imbalance. In rheumatoid arthritis, IL-36 agonists induce fibroblast-like synoviocyte to produce pro-inflammatory factors, while IL-36 antagonist deficiency leads to lesion progression. In osteoarthritis, IL-36 agonists induce chondrocytes to produce catabolic enzymes and pro-inflammatory factors. This article reviews the expression and function of IL-36 in different inflammatory joint diseases to provide a reference for revealing their pathogenic mechanisms and discovering therapeutic targets.
Humans ; Interleukins ; Arthritis, Rheumatoid ; Osteoarthritis/pathology* ; Arthritis, Psoriatic/metabolism* ; Cytokines

It is very difficult to diagnosis osteoarthritis in the early stage, due to the slow development of the disease, no symptoms occures, and no X-ray findings in the early stage, it is difficult to early diagnosis with the traditional diagnostic methods, resulting in the poor treatment outcome, and even some patients develop joint deformity, activity limitation, and must take an operation, it brought great pain and heavy financial burden to patients. How to early diagnosis of articular cartilage injury become difficult now. Some scholars suggest that to those suspected patients, the arthroscopic diagnosis must be taken. Although the small trauma and quick recover, the method of operation has trauma, not only increase the suffering of the patients, but the treatment is very expensive, make the patients finch. A large number of domestic and foreign scholars to study patients with OA to find the ideal fluid biological markers (BM) to reflect articular cartilage metabolism, and revealed disease activity or prognosis. The CTX-II can reflect degradation of the articular cartilage.
Biomarkers ; metabolism ; Collagen Type I ; metabolism ; Humans ; Osteoarthritis ; diagnosis ; metabolism ; Peptides ; metabolism

With the effects of the mechanics and biological factors, the imbalance between the degradation and synthesis of chondrocyte, extracelluar matrix and subchondral bone leads to the osteoarthritis. The imbalance between MMPs and TIMPs caused by biomechanical abnormality is the key factor of osteoarthritis. This review will focus on the stress and their roles in the metabolism of the cartilage matrix.
Cartilage ; metabolism ; Humans ; Matrix Metalloproteinases ; metabolism ; Osteoarthritis ; metabolism ; Stress, Mechanical ; Tissue Inhibitor of Metalloproteinases ; metabolism

OBJECTIVE: To detect the changes of mitochondrion DNA (mtDNA) sequence in articular chondrocytes of cartilage affected by osteoarthritis and to clarified the pathogenetic mechanism of osteoarthritis. METHODS: We analyzed the mtDNA 4,977 bp deletion mutations of articular chondrocytes in 10 patients with osteoarthritis and 3 normal cartilages using the gap-PCR amplification method. We designed a two round PCR detection method, in which total DNA was isolated from articular chondrocytes as the template of the first round PCR reaction and products from the first round were the template in the second round reaction. RESULTS: The results of the first rounds of PCR reaction showed the mtDNA 524 bp amplified products in the osteoarthritis group and in the corresponding peripheral blood samples were not detected, but the 533 bp products were detected. However,the results of the second round reaction revealed that the 524 bp zones were detected in 2 of the 10 osteoarthritis patients and the corresponding peripheral blood samples were not detected. The 533 bp products were detected in all specimens. The mtDNA 524 bp amplified products in all the normal articular chondrocytes and the corresponding peripheral white blood cells contrast were not detected in both rounds PCR. CONCLUSION This was the first study to evaluate the mtDNA 4799 bp large fragment deletion mutational accumulation between nt8,470 - nt13,447 of articular chondrocytes in osteoarthritic cartilage. Osteoarthritis may be related to mtDNA mutation of articular chondrocytes.
Adult ; Cartilage, Articular ; metabolism ; pathology ; Chondrocytes ; metabolism ; DNA, Mitochondrial ; genetics ; Female ; Gene Deletion ; Humans ; Male ; Middle Aged ; Osteoarthritis ; genetics ; Osteoarthritis, Hip ; genetics ; Osteoarthritis, Knee ; genetics ; Sequence Analysis, DNA

OBJECTIVETo determine the concentrations of interleukin-18 (IL-18), IL-6, IL-8, and prostaglandin E2 (PGE2) in the synovial fluid in patients with osteoarthritis (OA), and explore the role of IL-18 in the pathogenesis of OA.

METHODSThe synovial fluid was collected from 30 patients with knee OA, and the concentrations of IL-18 and the other cytokines were measured using enzyme-linked immunosorbent assay (ELISA). A linear regression was performed between IL-18 and the other cytokines.

RESULTSThe average IL-18 and PGE2 concentrations were 220-/+304 pg/ml and 89-/+104 pg/ml in the synovial fluid, respectively, and the two cytokines showed a positive correlation in the synovial fluid (r=0.628, P=0.001). The IL-18 concentration was also correlated to the concentrations of IL-6 (1200-/+1587 pg/ml, n=22; r=0.590, P=0.008) and IL-8 (5190-/+6024 pg/ml, n=9; r=0.776, P=0.014).

CONCLUSIONIL-18 can promote PGE2 production, which causes cartilage degradation in OA, thus therapies targeting this cytokine may prove an effective approach to early OA treatment.

Aged ; Dinoprostone ; biosynthesis ; Female ; Humans ; Interleukin-18 ; metabolism ; Male ; Middle Aged ; Osteoarthritis ; metabolism ; Synovial Fluid ; metabolism

The Wnt signaling exists in every kinds of species and regulates a variety of biological processes including cell fate, proliferation and function, immunity, stress, apoptosis and so on. During the researching, Wnt signaling also plays an important role in chondrocyte differentiation and maturation. So it has been the new spot in pathogenesis of osteoarthritis study.
Animals ; Chondrocytes ; metabolism ; pathology ; Humans ; Osteoarthritis ; metabolism ; pathology ; Signal Transduction ; Wnt Proteins ; metabolism

OBJECTIVES: Mutation of p53 may play a role in manifestation of rheumatoid arthritis synovium, but several studies on p53 expression in synovial tissues of rheumatoid arthritis showed conflicting results. We investigated the amount and pattern of p53 positive cells in rheumatoid arthritis synovium, in comparison with osteoarthritis synovium, by using immunohistochemistry with two other monoclonal antibodies for p53. METHODS: Synovial tissues from 9 patients with rheumatoid arthritis and 5 patients with osteoarthritis were examined for p53 expression by immunohistochemistry with 2 monoclonal antibodies for p53, DO-1 and DO-7. Histologic features of inflammation were also scored and compared with p53 expression. RESULTS: There was no significant difference between inflammatory scores in both groups. In the synovial tissues of rheumatoid arthritis patients, p53 positive cells were detected in 3 out of 9 samples(33%) and p53 expressions were restricted to inflammatory mononuclear cells, but synovial lining cells, subsynovial fibroblast-like cells and vascular endothelial cells were p53 negative. p53 expressions in osteoarthritis synovial tissues as control were observed in 2 out of 5 samples(40%) and the amount and pattern of p53 positive cells were comparable to those seen in rheumatoid arthritis synovial tissues. There was no demonstrable correlation between the synovial tissues of both groups with respect to inflammation scores and expression of p53 protein. CONCLUSION: Our findings suggest that altered p53 expression may not play a significant role in the manifestation of rheumatoid arthritis synovium. However these data need to be strengthened by increasing the number of samples and molecular biology approaches.
Arthritis, Rheumatoid/metabolism* ; Arthritis, Rheumatoid/genetics ; Comparative Study ; Gene Expression ; Genes, p53 ; Human ; Immunohistochemistry ; Osteoarthritis/metabolism ; Osteoarthritis/genetics ; Protein p53/metabolism* ; Protein p53/genetics ; Synovial Membrane/metabolism

To investigate the estrogen receptor (ER) expression in cartilage cell in the development of osteoarthritis induced by bilateral ovariectomy in guinea pig and to find their relationship. 30 two-month-old female guinea pigs were randomly divided into two groups (n = 15 each): sham operation (control) group and ovariectomized group (OVX); Scanning electorne microscope (SEM) and transmission electron microscope (TEM) were obtained to analysis the cartilage degeneration of the hind limb knee joint after 6 and 12 weeks of ovariectomy. Dextran-Coated-Charcoal (DCC) was taken to quantitively detect the expression of ER. The serum levels of estrogen and gestone were detected by immune contest assay. The results showed that ER do exist in the cartilages of the guinea pigs, with higher expression in the control group than in OVX group at the same time point (P < 0.05). It was increased also at 12 th week after operation than that of preoperation. The blood serum levels of estrogen and gestone showed a similar tendency to the expression of ER. Joint cartilage degeneration detected by SEM and TEM could be found at 6 th week, but severe degenerative lesions at 12 th week in the OVX group compared with the control group (P < 0.01). The data suggested that bilateral ovariectomy in guinea pig lead to severe osteoarthritis which mighgt be related to the lower serum level of estrogen and the downregulation of the expression of ER in the cartilage also.
Cartilage, Articular/cytology ; Cartilage, Articular/*metabolism ; Chondrocytes/metabolism ; Estrogens/*blood ; Osteoarthritis/*etiology ; Osteoarthritis/metabolism ; Ovariectomy ; Random Allocation ; Receptors, Estrogen/*biosynthesis ; Receptors, Estrogen/genetics