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At least 271 records · Page 15Linked to original sources
PubMed1998

Nitric oxide and inflammatory joint diseases.

Nitric oxide (NO) is synthesized from L-arginine by the NO synthases. At present, mainly three NO synthase isoenzyme groups are differentiated: two constitutive NO synthases, responsible for homeostatic cardiovascular and neuronal functions of NO, and an inducible NO synthase. After induction by certain cytokines or endotoxin, this latter isoform produces large quantities of NO with cyto- and bacteriotoxic effects. High amounts of NO, synthesized systemically and intra-articularly, play an important role in inflammatory joint diseases, as shown in animal models of arthritis and in patients with rheumatoid arthritis or spondyloarthropathies. In experimental arthritis, administration of NO synthase inhibitors profoundly reduced disease activity. In humans, beneficial effects of NO synthesis inhibition are inferred from indirect evidence: glucocorticoids, inhibiting induction of the inducible NO synthase, reduce enhanced NO synthesis and disease activity. Thus, selective inhibition of the pathologically enhanced NO synthesis emerges as a new experimental therapeutic approach in the treatment of inflammatory joint diseases.

Arthritis↗
PubMed2002

Evaluation of a radiographic caudolateral curvilinear osteophyte on the femoral neck and its relationship to degenerative joint disease and distraction index in dogs.

OBJECTIVE: To determine prevalence of a radiographic caudolateral curvilinear osteophyte (CCO) on the femoral neck in various breeds and age groups of dogs and to evaluate its contemporaneous relationship with degenerative joint disease (DJD) and distraction index (DI). DESIGN: Cross-sectional prevalence study. ANIMALS: 25,968 dogs, including 3,729 German Shepherd Dogs, 4,545 Golden Retrievers, 6,277 Labrador Retrievers, and 1,191 Rottweilers. PROCEDURE: Data from the University of Pennsylvania Hip Improvement Program database were analyzed, including ventrodorsal hip-extended, compression, and distraction radiographs. The CCO and radiographic signs of DJD were considered independent events and were interpreted as either present or absent. Statistical methods were used to evaluate the CCO as a possible risk factor for DJD and assess its association with DI, as measured by use of distraction radiography. RESULTS: When all breeds were pooled, DJD was detected in 8.6% of dogs, and the CCO was detected in 21.6% of dogs. Among dogs with a CCO, 25.1% had radiographic evidence of DJD. Among dogs without a CCO, only 4% had DJD. Dogs with a CCO were 7.9 times as likely to have DJD as were those without a CCO. Additionally, DI, weight, and age were significant risk factors for the CCO. CONCLUSION AND CLINICAL RELEVANCE: Results confirm the contemporaneous association between the CCO and DJD and that passive hip laxity, as measured by use of the DI, is associated with both the CCO and DJD.

Age Factors↗
PubMed1982

Current concepts in equine degenerative joint disease.

Current concepts of pathogenesis, diagnosis, and treatment of equine degenerative joint disease are presented on the basis of recently acquired experimental and clinical knowledge. A number of concepts of pathogenesis need modification and the rationale of some of the newer treatments requires definition. Synovitis and other soft tissue changes are important components of the pathogenesis in addition to direct trauma to the articular cartilage. Loss of glycosaminoglycans constitutes an important biochemical "lesion" in the articular cartilage, making it weak and susceptible to trauma. Recognition of these early changes and appropriate treatment of them are important. Treatment methods include physical therapy, use of anti-inflammatory drugs, joint lavage, sodium hyaluronate, and synovectomy. When there are cartilage and bony changes, the use of articular cartilage curettage, osteophyte removal, radiation therapy, and surgical arthrodesis remain appropriate in some cases. Studies continue to develop agents capable of promoting the synthesis of the important biochemical components of the articular cartilage and its subsequent healing.

Adrenal Cortex Hormones↗
PubMed1983

Chronic repetitive trauma: a cause of atypical degenerative joint disease.

Six cases of amateur athletes who have severe atypical degenerative joint disease (DJD) are presented; their histories suggest that chronic, repetitive trauma was causative in the development of their arthropathy. Although many examples of this process have been reported in professional athletes, it has not been reported in amateurs. As participation in athletic activities increases we can, perhaps, expect to see more of this type of DJD in the future.

Adult↗
PubMed1985

Six-week, double-blind, placebo-controlled and long-term, open-label multicenter study of isoxicam in treatment of degenerative joint disease.

A new nonsteroidal anti-inflammatory drug, isoxicam (Maxicam), was studied in patients with degenerative joint disease of the knee or hip. During a six-week, double-blind, placebo-controlled phase involving 176 patients, isoxicam at a dosage of 200 mg once daily was significantly superior to placebo in parameters (knee) of night pain, pain on walking, starting pain, pain on motion, swelling, tenderness, maximal extension, maximal flexion, and limitation of range of motion, and in the parameter (hip) of pain on walking. In patients with knee involvement and those with hip involvement, isoxicam was superior to placebo in overall and global assessments of its efficacy by physicians and patients. When 165 patients continued in a long-term, open-label phase and received isoxicam, a further alleviation of symptoms was noted in those patients who had received isoxicam in the double-blind phase, and a marked and sustained improvement was seen in patients who had received placebo in the double-blind phase.

Adult↗
PubMed2002

Fibroblast growth factor-2 determines severity of joint disease in adjuvant-induced arthritis in rats.

Rheumatoid arthritis (RA), a systemic inflammatory disease of unknown etiology, mainly affects synovial joints. Although angiogenic growth factors, including fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), may play a critical role in the development and progression of RA joint disease, little information is now available regarding their exact role in initiation and/or progression of RA. In this study, we show that both polypeptides were up-regulated in the rat joint synovial tissue of an adjuvant-induced model of arthritis (AIA), as well as human subjects with RA. FGF-2 overexpression via Sendai virus-mediated gene transfer significantly worsened clinical symptoms and signs of rat AIA, including hind paw swelling and radiological bone destruction, as well as histological findings based on inflammatory reaction, synovial angiogenesis, pannus formation, and osteocartilaginous destruction, associated with up-regulation of endogenous VEGF. FGF-2 gene transfer to non-AIA joints was without effect. These findings suggested that FGF-2 modulated disease progression, but did not affect initiation. Reverse experiments using anti-FGF-2-neutralizing rabbit IgG attenuated clinical symptoms and histopathological abnormalities of AIA joints. To our knowledge, this is the first report indicating direct in vivo evidence of disease-modulatory effects of FGF-2 in AIA, as probably associated with endogenous VEGF function. FGF-2 may prove to be a possible therapeutic target to treat subjects with RA.

Adjuvants, Immunologic↗
PubMed1993

[Serum keratan sulfate studies and their significance in the evaluation of cartilage degradation in degenerative and inflammatory joint diseases].

Fragments of high density cartilage proteoglycan (aggrecan) are released during either the normal or pathological turnover of cartilage proteoglycans, which fragments diffuse into the synovial fluids and then appear in the serum. The keratan sulphate (KS; a glycosaminoglycan side chain of aggrecan) is resistant to enzymatic degradation, it has a relatively low clearance and has a "standard" serum level indicating the actual level of cartilage (proteoglycan) breakdown. Using anti-KS monoclonal antibody in ELISA (enzyme-linked immunosorbent assay), we measured serum KS levels in patients with different joint diseases. The highest KS content (595 ng/ml) was measured in the sera of patients with articular chondrocalcinosis (calcium pyrophosphate crystal deposition disease/pseudogout). Slightly lower KS levels were determined in osteoarthrosis (OA; 578 ng/ml) and much less in rheumatoid arthritis (RA; 421 ng/ml). All these patient groups (either with degenerative or inflammatory joint diseases) expressed slightly higher KS levels compared to control blood donors (295 ng/ml). However, there were remarkable variations between these diseased groups, i. e., KS levels in patients with RA were significantly lower than in patients with OA (p < 0.001) and this difference was more pronounced in rheumatoid patients with I-II Steinbrocker stage (370 ng/ml) or in those treated with non-steroid anti-inflammatory drugs (NSAIDs) (382 ng/ml). Keratan sulphate levels in RA patients chronically treated with corticosteroid (460 ng/ml) or auro-thiomalat (473 ng/ml) indicate that these drugs may influence the cartilage metabolism more effectively than the NSAIDs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Prostanoids in children with joint diseases].

The radiological method was used to study the level of prostaglandins E + E, GF2 alpha and LTB4 in the blood plasma and the synovial fluid in 138 children with rheumatoid and other arthritis and noninflammatory diseases of the joints. The role of PGE + A and LTB4 in the pathogenesis of arthritis and low participation of PGF2 have been established. Determination of prostanoids in biological fluids can be used as an additional laboratory index to reveal the general and local activity of the pathological process in rheumatoid and other arthritis and distinguish them from noninflammatory diseases of the joints.

Adolescent↗
PubMed1986

Is running associated with degenerative joint disease?

Little information is available regarding the long-term effects, if any, of running on the musculoskeletal system. We therefore compared the prevalence of degenerative joint disease among 17 male runners (mean age, 56 years; height, 180 cm [5 ft 11 in]; and weight, 73.02 kg [161 lb] with 18 male nonrunners (mean age, 60 years; height, 178 cm [5 ft 10 in]; and weight, 78 kg [171 lb]). Running subjects (53% marathoners) ran a mean of 44.8 km (28 miles)/wk for 12 years. Pain and swelling of hips, knees, ankles, and feet and other musculoskeletal complaints among runners were comparable with those among nonrunners. Radiologic examinations (for osteophytes, cartilage thickness, and grade of degeneration) also were without notable differences among groups. We did not find an increased prevalence of osteoarthritis among the runners. Our observations suggest, within the limits of our study, that long-duration, high-mileage running need not be associated with premature degenerative joint disease in the lower extremities.

Aged↗
PubMed1983

Serum copper and ceruloplasmin levels in rheumatoid arthritis and degenerative joint disease and their pharmacological implications.

Serum copper concentration and ceruloplasmin activity were measured in patients with clinically established rheumatoid arthritis (R.A.) during the active phase, in patients with degenerative joint disease (D.J.D.) and in normal subjects. Copper and ceruloplasmin serum levels are significantly increased (P less than 0.01) in the arthritic group, but not in the degenerative joint disease group. Copper and ceruloplasmin levels are high significantly correlated in all the groups. This parallel enhancement of serum copper and ceruloplasmin in R.A. is commented in view of a possible protective role of endogenous copper and/or ceruloplasmin in inflammation.

Arthritis, Rheumatoid↗
PubMed1997

CR1, CD35 in synovial fluid from patients with inflammatory joint diseases.

OBJECTIVE: To investigate synovial fluid (SF) for the presence of CR1 and to study its relationship to SF leukocytes and to serum levels of soluble CR1 (sCR1) in patients with rheumatic diseases. METHODS: Synovial fluids were collected from 35 patients with rheumatoid arthritis (RA) and 26 patients with other inflammatory joint diseases. Total CR1 in the SF and serum were measured with a sandwich enzyme-linked immunosorbent assay (ELISA) that recognized both soluble and transmembrane forms of CR1. The characteristics of CR1 in SF were analyzed by ultracentrifugation and by a second ELISA specific for transmembrane CR1. RESULTS: CR1 was found in all SF samples tested (range 5-281 ng/ml). SF CR1 was higher in patients with RA (mean +/- SD 81 +/- 66 ng/ml) than in those with other inflammatory joint diseases (31.8 +/- 23.8 ng/ml) (P < 0.001). Serum sCR1 was not significantly increased in the patients compared with the normal subjects. There was no correlation between serum sCR1 and SF CR1. In 44% of the patients, the SF CR1 level was higher than the serum sCR1 level. A fraction (30-80%) of SF CR1 was pelleted by ultracentrifugation and, unlike serum sCR1, it reacted in an ELISA specific for transmembrane CR1. Thus, SF contained 2 forms of CR1: a membrane-associated and a soluble form, which was confirmed by sucrose density-gradient ultracentrifugation. SF CR1 levels correlated directly with the number of SF total leukocytes and polymorphonuclear leukocytes (PMN). These 2 forms of CR1 were also found in the supernatant of in vitro-activated PMN from normal subjects. SF CR1 exhibited the capacity to act as a cofactor for the factor I degradation of C3b. CONCLUSION: CR1 is found in the SF of patients with joint inflammation. The data suggest that SF CR1 originates from the infiltrating leukocytes, which shed both a soluble and a membrane-associated form. Whether SF CR1 participates in the local regulation of complement activation remains to be examined.

Arthritis↗
PubMed2001

[Diagnostic imaging of inflammatory rheumatic joint diseases. Part II: techniques and axial joints].

Imaging of inflammatory disorders of the spine and sacro-iliac joints is important for the diagnosis, prognosis, and evaluation of therapy. Conventional radiography still constitutes the basic imaging modality, but supplementary computed tomography (CT) and especially magnetic resonance imaging (MR-scanning) may provide additional important information. The radiation dose by CT must be taken into account. It is therefore expected that MR-scanning, which is without known risks, will increasingly become the method of choice when the information obtained by conventional radiography is inadequate.

Arthritis, Rheumatoid↗
PubMed2001

The effects on knowledge of the systematic education of patients with joint diseases treated with NSAIDs and diuretics.

In a randomised, controlled trial, patients with joint diseases and concomitant treatment with NSAIDs and diuretics received systematic education. The intervention group was given information by a self-conducted, interactive Kodak Photo-CD program in addition to personal drug information and non-commercial drug leaflets. Awareness of drug interactions and encouragement of self-adjustment of treatment was focused on. Control patients received conventional information. Three months after randomisation, knowledge was tested by means of a questionnaire. At 3 months there was a significant difference in attained score between the intervention group and the control group. Greater knowledge was achieved, especially on drug interaction, in the intervention group. In conclusion, less than 1 h of systematic education significantly improved patients' knowledge on essential issues of concomitant treatment with NSAIDs and diuretics. Knowledge of effects, side-effects and interactions of drugs is essential for self-adjustment of treatment. The method employed, which is standardised and produces a reproducible quantity of education, might be applicable to several other medical conditions.

Adult↗