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At least 181 records · Page 10Linked to original sources
PubMed1994

Upregulation of complement regulators MCP (CD46), DAF (CD55) and protectin (CD59) in arthritic joint disease.

CD46, CD55 and CD59 are cell surface glycoproteins which are widely distributed on normal tissue, where they function in the prevention of complement-mediated damage. In this study we have investigated the altered expression of these molecules under inflammatory conditions both in vitro and in vivo. By using immunocytochemical techniques we demonstrated marked but disparate upregulation of these molecules in IL1-treated cartilage and in diseased cartilage from arthritic joints compared to normal cartilage in both humans and pigs. Expression of these proteins was restricted to the chondrocyte surface, and was also demonstrated on isolated chondrocytes grown in monolayer culture and stimulated with IL1. It is suggested that the elevated levels of these regulatory proteins may be necessary to ameliorate the multiple damaging effects of the inflammatory processes associated with destructive joint diseases.

Adult↗
PubMed1982

[Long term results of radiotherapy of degenerative joint diseases (author's transl)].

At the Radiologic Department of The Städtisches Krankenhaus Passau, 473 patients with degenerative diseases in the big joints and the spine were irradiated with the caesium unit between 1971 and 1979. Among these patients, 249 could be followed up during a prolonged period (1/2 to 9 years, i.e. 4.2 years on an average). According to the categories of v. Pannewitz, 11% were pain-free at this moment, 21% showed an essential improvement, 29% showed an improvement, and 39% were not influenced by the treatment. 13.5% showed recurrent pains; these were mentioned as "not influenced" in the statistical analysis. It is proved that the relief of pain does not depend on the age of the patients, but on the anamnesis period, the results of the X-ray examination, and the degree of the restriction of mobility. Due to the delay of irradiation, a preliminary treatment mostly produces a less favorable radiotherapeutic result. Compared with other therapeutic methods, the long term results or radiotherapy of degenerative joint diseases are generally favorable. This conclusion is also confirmed by the results of patients checked up more than five years after the treatment.

Adult↗
PubMed1982

Erythrocyte sedimentation rate in women with different manifestations of joint disease.

A comprehensive population study of women aged 44-46 was carried out in Göteborg, Sweden in 1974-75. The mean erythrocyte sedimentation rate (ESR) and the rate of high ESR values (defined as ESR greater than or equal to 30 mm) were higher in women with manifestations of joint diseases than in other women, the differences being statistically significant for women with swollen or deformed finger joints and symptoms from the wrists. Women with manifestations of active joint disease at the time of the examination had even higher ESR values, the differences being statistically significant also for women with symptoms from the finger joints. High ESR values were more common in women with a positive serological test for rheumatoid factor and joint manifestations indicating arthritis and osteoarthrosis. The "arthritis" and "osteoarthrosis" groups each included about one-third of the subjects with rheumatoid factor. It is concluded that although ESR values are moderately increased in subjects with different manifestations of joint disease, the vast majority of such subjects have ESR values less than 30 mm.

Adult↗
PubMed2006

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease.

Bacterial arthritis is a progressive joint disease which includes rapid destruction of articular cartilage even after clearance of the causal factor. The resulting post-infectious arthropathy is mainly characterized by self-perpetuating joint destruction and extensive angiogenesis in the emerging pannus-like synovial membrane, but the underlying molecular mechanisms of the bacteria-initiated process remain incompletely understood. This study was conducted to elucidate the expression and regulation of angiogenic and cartilage-destructive vascular endothelial growth factor (VEGF) in septic arthritis. For that purpose, aspirates of synovial fluid from patients with pyogenic arthritis were examined for VEGF levels by ELISA. In vitro studies with primary and immortalized chondrocytes were performed to determine whether Gram-positive and Gram-negative bacteria induce VEGF expression, by using real-time RT-PCR, ELISA, and immunohistochemistry. Activation of the transcription factor AP-1 was assessed by EMSA experiments. The necessity of the Toll-like receptor-2 (TLR-2), ERK-1/-2, and AP-1 pathway for infectious VEGF induction in chondrocytes was examined by using specific blocking reagents. ELISA experiments revealed that aspirates of synovial fluid from patients with pyogenic arthritis contain elevated levels of VEGF. The in vitro results confirmed the transcriptional induction of VEGF in chondrocytes after bacterial challenge by real-time RT-PCR, ELISA, and immunohistochemistry. This activation was mediated by a TLR-2-, ERK-1/-2-, and AP-1-dependent pathway. The findings demonstrate the expression of Toll-like receptors on mesenchymal articular chondrocytes and reveal TLR-2-mediated VEGF induction in human chondrocytes after Gram-positive bacterial sensing. Since VEGF is a potent angiogenic and tissue remodelling factor, evidence that Toll-like receptors contribute to destructive arthropathy after microbial joint infection is provided. VEGF may be a therapeutic target in the future for the prevention of post-infectious cartilage degradation in articular joints.

Arthritis, Infectious↗
PubMed1998

Oxidative stress and degenerative temporomandibular joint disease: a proposed hypothesis.

The molecular events that underlie degenerative temporomandibular joint diseases are poorly understood. Recent studies have provided evidence that a variety of molecular species, including cytokines, matrix degrading enzymes, neuropeptides, and arachidonic acid catabolites may be involved. This paper advances the theory that mechanical stresses lead to the accumulation of damaging free radicals in affected articular tissues of susceptible individuals. This condition is called oxidative stress. The authors postulate mechanisms that may be involved in the production of free radicals in the temporomandibular joint and in the subsequent induction of molecular events that may amplify damage of articular tissues initiated by free radicals. If the proposed model is correct, then future therapeutic strategies directed at the control of oxidative stress could be effective in the management of degenerative temporomandibular joint diseases.

Arachidonic Acids↗
PubMed1994

Site-specific cartilage changes in murine degenerative knee joint disease induced by iodoacetate and collagenase.

Degenerative joint disease was induced in the knee joints of mice by intraarticular injection of two different stimuli: iodoacetate and highly purified collagenase. Proteoglycan synthesis was measured in vivo at different time points in four topographical areas of the knee joint (central and peripheral parts of the patella and central parts of the medial and lateral tibial plateaus) and was compared with histological observations of localized damage to the joint. In vitro incubation with iodoacetate had a direct effect on proteoglycan metabolism. Intra-articular injection of iodoacetate in vivo inhibited the proteoglycan synthesis in cartilage from the central part of the patella. In the peripheral part of the patella, inhibition on day 1 was followed by stimulation of synthesis on days 3-30. Proteoglycan synthesis also was inhibited in the central parts of the medial and lateral tibial plateaus. The areas with inhibited synthesis had loss of safranin O staining on histology. In vitro incubation with collagenase did not have a direct effect on the proteoglycan metabolism of intact cartilage; this led to the assumption that osteoarthritis after injection of collagenase is caused by ligamentous injury, which leads to an unstable joint. Injection of collagenase in vivo stimulated the proteoglycan synthesis in cartilage from the central and peripheral parts of the patella. In an early stage of the process, the cartilage from the tibial plateaus also was slightly stimulated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Neuropathic bone and joint disease.

The pathogenesis of the neuropathic joint has been a subject of controversy for many years. Two main theories of pathophysiologic pathways have evolved: (1) the neurotraumatic, which states that the changes result from mechanical trauma and repetitive injuries to an insensitive extremity or joint and (2) the neurovascular, which states that the changes result from a neurally initiated vascular reflex that leads to hyperemia, angiogenesis, and very active bone resorption by osteoclasts. Through clinical, radiographic, and pathologic observation, it appears evident that both pathways contribute to neuropathic bone and joint disease. Initially, the alteration of sympathetic control triggers a persistent hyperemia, leading to active bone resorption. There may or may not be associated pathologic fractures and subsequent repair. This depends upon the degree of joint insensitivity and whether or not it is subjected to continued weightbearing. If so, the neurotraumatic mechanisms come into play, but only secondarily.

Arthropathy, Neurogenic↗
PubMed1990

Arthroscopic evaluation of the synovial lining before and after open synovectomy of the knee joint in patients with chronic inflammatory joint diseases.

Twenty-eight patients with chronic inflammatory joint diseases had arthroscopy immediately before synovectomy of the knee joint and 6 and 12 months postoperatively. In patients with moderate and/or severe synovitis of the knee joint all of the synovial membrane is involved in the disease process. Resynovitis (synovitis of the regenerated synovial membrane after synovectomy), however, is patchy and if biopsy should be indicated, arthroscopic guidance is advocated. Following synovectomy there is a recurrence of mild synovitis of varying degree in some cases with an increase in resynovitis between 6 and 12 months. The level of synovitis at 12 months was, however, markedly less than at synovectomy (p less than 0.01). Similar development was found both in histopathology and immunohistopathology after synovectomy. Arthroscopic examination of the synovial membrane in chronic inflammatory disease of the knee joints gives valuable information of the severity and the longitudinal changes of synovitis. A simple method of scoring is described and is imperative when comparing patients or groups of patients and when doing longitudinal arthroscopic studies. The method was used both at arthroscopy and at subsequent synovectomy giving a highly significant correlation (p less than 0.001).

Arthroscopy↗
PubMed1975

Temporomandibular degenerative joint disease. Part II. Diagnostic procedure and comprehensive management.

The diagnostic procedure is given in the detail necessary to arrive at an accurate diagnosis of temporomandibular degenerative joint disease (TDJD). The differentiating clinical findings of degenerative joint disease (DJD) and rheumatoid arthritis of the temporomandibular joint (TMJ) are described. Principles and modalities of comprehensive management of TDJD are presented in the manner and sequence needed to allow practical clinical application. Methods of treatment are applied to the management of patients with acute and chronic TDJD. The surgical procedure for TDJD, intracapsular high condylectomy with a preauricular incision, is described in the detail required for individual application. Case reports are presented to illustrate the comprehensive management of TDJD.

Adult↗
PubMed1992

A hyaluronan-loading test applied to patients with liver and joint diseases.

The serum hyaluronan disappearance data, after an intravenous bolus injection of hyaluronan, were evaluated in terms of model-based parameters. The loading test was performed in 10 healthy persons (basal serum hyaluronan concentration, C0, 24.9 +/- 8.9 micrograms/l [mean +/- S.D.]), 6 patients with joint disease (62.3 +/- 41.1 micrograms/l) and 19 patients with liver disease (206 +/- 214 micrograms/l). The highest maximum Michaelis-Menten elimination rate (Vmax = 287 +/- 86 micrograms/min) was found in patients with joint disease, significantly higher than in healthy persons (Vmax = 179 +/- 16, P = 0.0015) and in patients with liver disease (Vmax = 149 +/- 59, P = 0.0002). C0 and Vmax were evaluated as discriminants for assessment of residual liver function. In patients with liver disease C0 correlated with liver function score (r = 0.875, P < 0.0001) and serum albumin concentration (r = -0.813, P < 0.0001). The Vmax parameter did not correlate with conventional liver function tests or with the liver score but a significantly negative correlation of Vmax with C0 was found in patients with liver disease. A combination of the C0 level and the Vmax parameter was found to discriminate between healthy persons, patients with joint disease and patients with liver disease and should be of benefit in separating patients, with or without elevated serum hyaluronan levels, into groups having increased influx or reduced elimination, respectively, of circulating hyaluronan.

Adult↗
PubMed1992

Radiologic manifestations of rheumatic joint diseases in the plain radiograph.

In the assessment of radiologic manifestations of joint diseases, rheumatoid arthritis (RA) is the disease to which all others are compared. Knowledge of its characteristics form the basis of the other conditions. To understand the changes seen on the plain radiograph, it is essential to understand its pathophysiology first so that the manifestations of each disease can be appreciated more fully. Due to space constraint, I shall only discuss the main forms of rheumatic joint disease. Other examples of erosive arthropathies, although not rheumatic in origin, will also be included as they form part of the differential diagnosis of an erosive arthropathy, eg gout and psoriasis.

Arthritis, Rheumatoid↗
PubMed1999

The osteogenic properties of the interface membrane at the site of orthopedic implants: the impact of underlying joint disease.

Osseointegration at the site of orthopedic implants is dependent on the recruitment, attachment, and differentiation of osteogenic cells. Data concerning the effect of a patient's underlying joint disease on the modulation of the cellular activity and the long-term survival of joint prostheses is limited. In this study, immunocytochemistry was used to investigate the osteogenic cell phenotype within the bone-implant interface fibrous membrane in 60 patients with different underlying joint disease. Tissue specimens were removed during revision operations performed at variable times following implantation. The results provided histological evidence of the presence of fibrocartilage tissue and calcified bone within the interface. TGF-beta, metalloproteinases (MMP1 and MMP2) and their inhibitors (TIMP1 and TIMP2) were immunolocalized within fibroblasts, chondrocytes, and osteoblasts throughout the interface, indicating that signals modulating the osteogenic cell phenotype at these sites are highly regulated. Finally, the study identified a significant difference in the histological changes elicited by implant particulate debris in patients of different diagnostic categories. Such observations imply that the activity of the original joint disorder could augment specific cellular activation/immune signals that subsequently affect the degree of the local inflammatory responses to implant wear particles. The negative balance between the rate of bone growth and resorption around the prosthetic joint is central to the pathogenesis of aseptic loosening of implants.

Adult↗