| PrefaceOsteoarthritis (OA) is the most prevalent chronic joint disease. One prominent feature is the change of collagen and proteoglycan in articular cartilage, resulting in degeneration and loss of articular cartilage. Type Ⅱ collagen (80% -90% of total collagen) forms the fibrous framework of the tissue. Type Ⅱ collagen denaturation were seen in OA early, but very little known about its mechanism of formation.The study of OA interfered with many inflammatory cytokines, the research of nitric oxide (NO) influence articular cartilage began from 1991. NO have small molecular weight and short half - life, it character is activity. As an important signaling molecule, NO participate in many physiology and pathology reaction. Some research shows NO concern with the occur and progress of cartilage degeneration. NO could inhibit the proliferate of chondrocyte and promote it ap-optosis, and activate cyclo - oxygenase ( COX) to enhancing PGE2 production and causing inflammation. But someone thought NO could modulation matrix ca-tabolism which caused by IL -1 and inhibit PGE2 synthesis in early stage of inflammation. It may act as protective function. This is still disputed until now. We investigated the content of NO, iNOS and collagen Ⅱ in OA cartilage of different trauma degree, studied they're change direction and analyzed the correlation between NO and collagen type Ⅱ. We want to make sure the effect of NO in OA and get more knowledge about the pathogenesis of OA.Materials and methodsCommonly materials; Human cartilages were obtained at arthroplasty from25 patients with OA diagnosed according to the criteria of the American College of Rheumatology in 1991. Corresponding articular cartilages were obtained at arthroplasty or amputation for trauma, tumour or infection from 5 patients with no history of arthritis.Cartilage primarily preparation: Cartilage samples were chopped into 1.0 × 1.0×0. 2cm,fixed in 10% paraformaldehyde and decalcification with 15% ED-TA. Then samples were dehydrated, lucidificated, embedded in paraffin, and cut into 5μm sections. Each tissue sample was stained with HE and Safranin -O, graded histologically by the method of Mankin.After weighted up 100mg each tissue sample, broke into pieces, and added natrium chloride, we got 10% tissue liquid, then measure concentrations of NO according to the demand of reagent case.Each tissue sample was immunohistochemistried with collagen Ⅱ and iNOS, and dealed with micrograph analyze instrument. Each slice was random mensu-rated 10 high fields of eyeshot, and made half quantitative analysis of ash degree.The data was analyzed with Spearman rank correlation analysis and analysis of variance, performed in SPSS Stat software. P values less than 0.05 were considered statistically significant.Results1. Mankin grade: normal 5; mild OA 8; middle OA 11; severe OA 6.2. There were no expression of NO and iNOS in normal articular cartilage, but they were increase with trauma grade. The amount of type II collagen in mild OA were more than in normal, but decreased in middle OA and little in severe OA.3. Analysis of Spearman rank correlation of NO with type Ⅱ collagen, r3 = -0. 85 ,P <0.05. There is a negative correlation between NO and type Ⅱ collagen in OA. Analysis of variance show there are discrepancy among NO, iNOS and type Ⅱ collagen in OA cartilage of various trauma grade.DiscussionArticular cartilage contains the chondrocytes and extracellular matrix. Chondrocytes have the ability of synthesize extracellular matrix which composed of water, collagens, proteoglycans, and noncollagenous proteins. The collagen network resembles the endoskeleton of cartilage. Type Ⅱ collagen (80% -90% of total collagen) forms the fibrous network and provides the basic architecture of cartilage. Type Ⅱ collagen degeneration means cartilage structure were destroyed, function were wrecked and pathological changes were happened. From our study, we indicted the amount of type II collagen in mild OA are more than in normal, but decreased in middle OA and little in severe OA.NO is a free radical with no partnership electron. NO has a simple structure and half - life of 4 - 10 seconds. A serious of study showed NO could inhibit the proliferation of chondrocyte and promote it apoptosis, inhibit the synthesis of proteoglycans, and activate COX to enhancing PGE2 production and causing inflammatory reactions. NO also causes cartilage degradation by activating matrix metalloproteinase ( MMP). NO may act as an important biological mediator, and participate in induce many physiological and pathological reaction. NO originates from oxidation of a guanidine nitrogen of L - arginine, catalysed by the NO synthase (NOS). NOS has three isoenzymes, iNOS is act in articular cartilage. The expression of NO and iNOS were not observed in normal cartilage, while increased significantly in OA.Using immunohistochemical technique, we detected the content of NO, iNOS and type Ⅱ collagen of articular cartilage in normal and OA different stages. NO changed with iNOS, this means NO were produced in local cartilage and belong endogenesis cytokine. With the serious of cartilage trauma, type Ⅱ collagen were declined, but NO and iNOS increased. There is negative correlation between NO and type Ⅱcollagen, and discrepancy among NO, iNOS and type Ⅱ collagen in OA cartilage of various trauma grade.NO plays an important role in pathogenesis of OA. It may inhibit the proliferation of chondrocyte and promote it apoptosis, inhibit the synthesis of matrix. |
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