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PubMed1989

Joint disease.

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Diagnostic Imaging↗
PubMed1992

Development and application of a radioimmunoassay for interleukin-8: detection of interleukin-8 in synovial fluids from patients with inflammatory joint disease.

A sensitive and specific radioimmunoassay for human interleukin-8 (IL-8) was developed using isotopically labeled homogenous natural protein. The detection limit (20% inhibition of 125I-IL-8 binding) was 30 pg/100 microliters; 50% displacement occurred at 140 pg/100 microliters. There was no cross-reactivity with the structurally and functionally related neutrophil-activating peptides 2 and 3 up to 500 ng/100 microliters. The intra- and inter-assay coefficients of variation were 4 and 7%, respectively. In vitro experiments showed that human fibroblasts triggered by interleukin-1, double-stranded RNA or virus release immunoreactive and biologically active IL-8 in a dose- and time-dependent manner. Monocytes produce immunoreactive IL-8 in the 100 ng/ml range when exposed to plant mitogen, bacterial endotoxin, virus or IL-1. Although the radioimmunoassay was more sensitive than the chemotaxis assay (detection limit 0.6 ng/ml versus 10 ng/ml) a correlation between concentrations of immunoreactive IL-8 and neutrophil chemotactic activity in the supernatants from stimulated monocytes and fibroblasts was observed. In synovial fluids from patients with inflammatory joint disease, IL-8 was clearly demonstrable, but there was no correlation between IL-8 levels and general parameters of disease activity (erythrocyte sedimentation rate and serum levels of C-reactive protein). Synovial fluids from patients with rheumatoid arthritis, seropositive for rheumatoid factor, contained significantly higher concentrations of IL-8 than synovial fluids from seronegative rheumatoid arthritis patients and patients with non-rheumatoid arthritis joint inflammation. There was a highly significant correlation between IL-8 levels and serum titers of rheumatoid factor. These findings suggest that the molecular mechanisms underlying joint inflammation may be distinct in different types of arthritis.

Adult↗
PubMed1990

Conservative management of temporomandibular joint disease: a case study.

Although temporomandibular joint (TMJ) problems are difficult to diagnose and evaluate, treatment today centers on conservative methods, not surgery. Many dentists lack the knowledge to adequately diagnose and treat TMJ, and many insurers as well as managed care plans have often refused to pay for conservative therapy, now known as Phase 1 TMJ treatment. This treatment consists of appliance or intraoral splint placement, along with physical therapy. Ultimately, this therapy is far less expensive than either joint or orthognathic surgery. Since there is no recognized specialty in TMJ disease, managed care programs need to establish discernible criteria for the selection of providers to diagnose and treat their TMJ patients. By carefully selecting providers and monitoring the outcome of treatment rendered to patients, costs and time of treatment could be drastically reduced, benefiting the patient and the managed care program.

Adolescent↗
PubMed2002

Small-molecule inhibitors of NF-kappaB for the treatment of inflammatory joint disease.

Recent advances in our understanding of the role of cytokine networks in inflammatory processes have led to the development of novel biological agents for the treatment of chronic inflammatory diseases. At the present time, significant efforts are focused on characterizing the complex signal transduction cascades that are activated by these cytokines and, in turn, regulate their expression. The transcription factor NF-kappaB is a pivotal regulator of the inducible expression of key proinflammatory mediators, and activated NF-kappaB has been observed in several debilitating inflammatory disorders, including rheumatoid arthritis and osteoarthritis. In light of its central role in inflammation, the identification of inhibitors of NF-kappaB should provide novel therapeutics for the treatment of chronic joint disease.

Animals↗
PubMed1997

Development of in vitro model systems for destructive joint diseases: novel strategies for establishing inflammatory pannus.

OBJECTIVE: To establish a novel 3-dimensional (3-D) in vitro model for the investigation of destructive processes in rheumatoid arthritis (RA). METHODS: Two distinct culture systems were developed, consisting of RA synovial membrane and articular cartilage explants or interactive RA synovial cell/chondrocyte cultures embedded in 3-D fibrin matrices. The expression of proteolytic enzymes, chondrocyte matrix architecture, and matrix degradation parameters was analyzed by immunohistochemistry. RESULTS: Of 28 RA explant cultures, 16 displayed an invasion of synovial tissue into the cartilage explants, compared with 1 of 8 osteoarthritis explants. The expression of collagenase and vascular cell adhesion molecule 1 could be demonstrated at the cartilage-pannus junction. Of 20 interactive cell cultures, 18 revealed invasive behavior and remained vital for extended periods of time. CONCLUSION: The models presented allow us to study distinct aspects of destructive joint diseases under in vitro conditions that resemble human pathology. Moreover, our model is able to supplement animal experiments in basic research and drug testing.

Animals↗
PubMed1994

Mice lacking alpha 1 (IX) collagen develop noninflammatory degenerative joint disease.

Type IX collagen is a nonfibrillar collagen composed of three gene products, alpha 1(IX), alpha 2(IX), and alpha 3(IX). Type IX molecules are localized on the surface of type II-containing fibrils and consist of two arms, a long arm that is crosslinked to type II collagen and a short arm that projects into the perifibrillar space. In hyaline cartilage, the alpha 1(IX) collagen transcript encodes a polypeptide with a large N-terminal globular domain (NC4), whereas in many other tissues an alternative transcript encodes an alpha 1(IX) chain with a truncated NC4 domain. It has been proposed that type IX molecules are involved in the interaction of fibrils with each other or with other components of the extracellular matrix. To test this hypothesis, we have generated a mouse strain lacking both isoforms of the alpha 1(IX) chain. Homozygous mutant mice are viable and show no detectable abnormalities at birth but develop a severe degenerative joint disease resembling human osteoarthritis.

Animals↗
PubMedDate not supplied

[Serum hyaluronic acid and aminoterminal procollagen III peptide in inflammatory and degenerative joint diseases].

Serum levels of hyaluronic acid (HA) and the amino-terminal type III procollagen peptide (NP-III-P) were determined simultaneously by specific immunoassays in patients with rheumatoid arthritis (n = 41), osteoarthritis (n = 43), ankylosing spondylitis (n = 7), psoriatic arthritis (n = 6), and reactive arthritis (n = 6). Increased serum levels of both HA and NP-III-P, were found in rheumatoid arthritis and - although less pronounced - in osteoarthritis, differing significantly from age- and sex-matched controls (n = 77). Furthermore, patients suffering from active rheumatoid arthritis showed higher serum levels of both antigens than patients with inactive disease, and significant correlations were found in rheumatoid arthritis between acute phase plasma proteins, HA and NP-III-P, respectively. In contrast, determination of low molecular weight fractions of NP-III-P by Fab- assay proved not to be useful in regard to clinical application. No significant effects of anti-inflammatory treatment were evident in any of the parameters. In rheumatoid patients, the serum concentrations of HA were found to correlate positively with the serum reactivity of NP-III-P related antigens (r = 0.692) and with the excretion of urinary pyridinoline (r = 0.455). Thus, both parameters seem to reflect similar mechanisms of connective tissue activation and may be related to inflammatory activity in joint diseases.

Adult↗
PubMed1989

Anti-type II collagen antibody in naturally occurring canine joint diseases.

Autoimmunity to collagen was investigated in several naturally occurring arthropathies of the dog. Increased levels of serum anti-native collagen type II antibody, as assessed by ELISA, were shown in 72.4% of dogs with rheumatoid arthritis (RA), 88% of dogs with infective arthritis (IA) and 52% of dogs with osteoarthritis (OA) (p less than 0.001). The mean levels of antibody in cruciate disease patients (CR) were also significantly increased compared to control dogs (p less than 0.01). Serum anti-collagen antibody in OA dogs correlated with that in precipitated serum immune complexes. There was also a correlation between anti-collagen antibody level in synovial fluid and in synovial fluid complexes in dogs with rupture of the cranial cruciate ligament. In all patient groups, collagenase digestion of polyethylene glycol (PEG) precipitates from sera and synovial fluids caused a significant rise in specific antibody levels to collagen, indicating the presence of collagen-anti-collagen complexes in all arthropathies. In dogs with RA, the levels of collagen-specific antibody in synovial fluid complexes correlated with the total IgG in these complexes. These findings implicate collagen-anti-collagen complexes in the pathogenesis of naturally occurring joint diseases in the dog, but they are unlikely to be the primary aetiological mechanism.

Animals↗
PubMed2004

Pulsed-field gradient-nuclear magnetic resonance (PFG NMR) to measure the diffusion of ions and polymers in cartilage: applications in joint diseases.

Since cartilage contains neither blood nor lymph vessels, diffusion is the most important transport process for the supply of cartilage with nutrients and for the removal of metabolic waste products. Therefore, diffusion measurements are of high interest in cartilage research. Different techniques of diffusion measurements exist. Here we describe methods based on pulsed-field gradient nuclear magnetic resonance (PFG NMR). This technique offers the considerable advantage that neither concentration gradients nor labeling of the diffusing species are required. In addition to the description of the fundamentals and the applicability of PFG NMR studies in cartilage research, emphasis is on the influence of the observation time, Delta, on the diffusion coefficient, D: at short times, diffusion is primarily determined by the water content of the sample, and great care is needed to keep this parameter constant. However, by varying the diffusion time, data on the internal structure of cartilage, e.g., the distance of the collagen fibrils, can also be obtained. In addition to classical water diffusion, the diffusion behavior of selected ions and polymers in cartilage is described. The capabilities, the limitations, and the clinical relevance of diffusion measurements for the assessment of joint diseases are discussed.

Animals↗