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ID PMID Title PublicationDate abstract
9645409 Treatment of amyloidosis and the rheumatologist. State of the art and perspectives for the 1998 The rheumatologist must be prepared to face diagnostic and therapeutic problems related to different categories of amyloidosis. This applies to the systemic AA amyloidosis that complicates chronic inflammatory arthropathies like adult and juvenile rheumatoid arthritis, causing nephropathy and various internal manifestations. Other types of amyloidosis are essential because they may localize to structures of the locomotor system and cause rheumatic complaints. At present, there is no cure for amyloidosis. But adequate and especially early therapeutic intervention is helpful in many cases. This review focuses on treatment of the categories of amyloidosis which are most relevant to the rheumatologist. In addition to treatments that are available today, more effective therapeutic modalities which hopefully will be available in the near future are also reviewed.
9035544 [Tendinopathies of the foot]. 1997 Jan 1 Tendinitis of the foot is frequent and is generally due to mechanical overload or inflammatory rheumatic disorders. It most often involves the posterior tibial tendon when obesity and calcaneus valgus combine to contribute to mechanical overwork, or in the early stages of rheumatoid arthritis. More rarely, the anterior tibial tendon or the fibular tendons are involved. The anatomic-clinical stages proceed from oedema to fissuration necrosis and ruptured tendon. The long-term risk is of a sinking internal arch and a fixed calcaneus valgus. A simple but effective treatment is the correction of the calcaneus valgus, but surgical arthrodesis may be necessary.
21340920 Rat Aortic Ring : 3D Model of Angiogenesis In Vitro. 2001 Angiogenesis is a necessary component of normal tissue repair, tumor growth and dissemination, and a wide variety of other inflammatory and pathological processes as well, including diabetic retinopathy, rheumatoid arthritis, and psoriasis. Consequently, the last two decades have seen extensive research into the regulation of neovascularization, particularly in tumors. Partly due to the emphasis on tumor angiogenesis, much of this effort has been devoted to the detection and characterization of angiogenic growth factors and inhibitory molecules. Thus assays have commonly been developed to measure the amount of vascular growth in vivo, or the modulation of endothelial cell (EC) proliferation, or migration in simple 2D culture systems (1).
24276731 A fatal pseudallescheria boydii brain abscess. 2000 Apr We present the clinical and radiological features of pseudallescheria boydii infection in a middle aged woman who presented with right frontal pseudallescheria abscess after two years use of prednisolone for rheumatoid arthritis. Despite early surgical excision and intravenous antifungal treatment she died after 7 weeks despite aggressive therapy.
10471124 Human peripheral blood T lymphocyte proliferation after activation of the T cell receptor: 1999 May Oils enriched in certain polyunsaturated fatty acids suppress joint pain and swelling in rheumatoid arthritis patients with active synovitis. Because T lymphocyte activation is important for propagation of joint tissue injury in patients with rheumatoid arthritis, we examined the effects of fatty acids added in vitro on proliferation of human T lymphocytes stimulated with monoclonal antibodies to CD3 and CD4. Unsaturated fatty acids reduced T cell proliferation in a dose dependent manner (dihomogammalinolenic acid > gammalinolenic acid > eicosapentaenoic acid > arachidonic acid). Removal of fatty acids from cultures before cell stimulation did not change the effects, but addition of fatty acids after cell stimulation failed to reduce T cell responses. The saturated palmitic acid did not influence T cell growth. These studies indicate that small changes in cellular fatty acids can have profound effects on early events in T cell signaling and on T cell function.
9930071 Association of pure red cell aplasia with T large granular lymphocyte leukaemia. 1998 Sep AIM: To define the relation between T large granular lymphocyte (T-LGL) leukaemia and pure red cell aplasia in Chinese patients. METHODS: Patients with T-LGL leukaemia were identified from a consecutive series of Chinese patients with chronic lymphoproliferative disorders. The diagnosis of T-LGL leukaemia was based on typical morphological and immunophenotypical features, and confirmed by the detection of clonal T cell receptor gene rearrangement. The clinicopathological features, response to treatment, and long term follow up were also examined. RESULTS: Five patients were identified as having T-LGL leukaemia from a consecutive series of 33 Chinese patients with chronic lymphoproliferative disorders. The median follow up time was 45 months. An obvious lymphocytosis was present in only two cases, although an increase in large granular lymphocytes in the peripheral blood was found in four. In one case, the LGL count was within the normal range. Epstein-Barr virus encoded early nuclear RNA was negative in all the cases. There was no evidence of rheumatoid arthritis, and none of the patients presented with recurrent infections. On follow up, pure red cell aplasia occurred at some stage of the disease in all the patients. This responded to treatment with cyclosporin A in two and with antithymocyte globulin in one. Two patients remained transfusion dependent. CONCLUSIONS: In contrast to Western patients, Chinese patients with T-LGL leukaemia do not appear to suffer from rheumatoid arthritis and recurrent infections, but pure red cell aplasia is a major cause of morbidity in this ethnic group.
9648917 Dedifferentiated chondrocytes cultured in alginate beads: restoration of the differentiate 1998 Aug Chondrocytes cultivated in monolayer rapidly divide and lose their morphological and biochemical characteristics, whereas they maintain their phenotype for long periods of time when they are cultivated in alginate beads. Because cartilage has a low cellularity and is difficult to obtain in large quantities, the number of available cells often becomes a limiting factor in studies of chondrocyte biology. Therefore, we explored the possibility of restoring the differentiated properties of chondrocytes by cultivating them in alginate beads after two multiplication passages in monolayer. This resulted in the reexpression of the two main markers of differentiated chondrocytes: Aggrecan and type II collagen gene expression was strongly reinduced from day 4 after alginate inclusion and paralleled protein expression. However, 2 weeks were necessary for total suppression of type I and III collagen synthesis, indicators of a modulated phenotype. Interleukin-1beta, a cytokine that is present in the synovial fluid of rheumatoid arthritis patients, induces many metabolic changes on the chondrocyte biology. Compared with cells in primary culture, the production of nitric oxide and 92-kDa gelatinase in response to interleukin-1beta was impaired in cells at passage 2 in monolayer but was fully recovered after their culture in alginate beads for 2 weeks. This suggests that the effects of interleukin-1beta on cartilage depend on the differentiation state of chondrocytes. This makes the culture in alginate beads a relevant model for the study of chondrocyte biology in the presence of interleukin-1beta and other mediators of cartilage destruction in rheumatoid arthritis and osteoarthrosis.
9561339 Lipid mediators in inflammatory disorders. 1998 Apr During the past few decades, intensive collaborative research in the fields of chronic and acute inflammatory disorders has resulted in a better understanding of the pathophysiology and diagnosis of these diseases. Modern therapeutic approaches are still not satisfactory and shock, sepsis and multiple organ failure remain the great challenge in intensive care medicine. However, the treatment of inflammatory diseases like rheumatoid arthritis, ulcerative colitis or psoriasis also represents an unresolved problem. Many factors contribute to the complex course of inflammatory reactions. Microbiological, immunological and toxic agents can initiate the inflammatory response by activating a variety of humoral and cellular mediators. In the early phase of inflammation, excessive amounts of interleukins and lipid-mediators are released and play a crucial role in the pathogenesis of organ dysfunction. Arachidonic acid (AA), the mother substance of the pro-inflammatory eicosanoids, is released from membrane phospholipids in the course of inflammatory activation and is metabolised to prostaglandins and leukotrienes. Various strategies have been evaluated to control the excessive production of lipid mediators on different levels of biochemical pathways, such as inhibition of phospholipase A2, the trigger enzyme for release of AA, blockade of cyclooxygenase and lipoxygenase pathways and the development of receptor antagonists against platelet activating factor and leukotrienes. Some of these agents exert protective effects in different inflammatory disorders such as septic organ failure, rheumatoid arthritis or asthma, whereas others fail to do so. Encouraging results have been obtained by dietary supplementation with long chain omega-3 fatty acids like eicosapentaenoic acid (EPA). In states of inflammation, EPA is released to compete with AA for enzymatic metabolism inducing the production of less inflammatory and chemotactic derivatives.
9654618 Phospholipase A2 sensitivity of the dorsal root and dorsal root ganglion. 1998 Jun 15 STUDY DESIGN: This study was designed to characterize the effects of phospholipase A2 on the neural response of dorsal root and dorsal root ganglion in the anesthetized New Zealand White rabbit. OBJECTIVES: To examine the effects of phospholipase A2 on the neural response of somatosensory neurons at the dorsal root ganglion level. SUMMARY OF BACKGROUND DATA: Phospholipase A2 may be an irritating component of disc tissue that is present in high concentration in painful herniated discs, in synovial fluids, and in sera of rheumatoid arthritis patients. Phospholipase A2 is inflammatory; however, its effects on dorsal roots and dorsal root ganglion response have never been demonstrated. METHODS: Surgically isolated dorsal roots and dorsal root ganglia from New Zealand White rabbits were investigated by electrophysiologic techniques. Phospholipase A2 doses ranging from 100 to 400 U were applied on the mechanically sensitive segments of the dorsal root ganglia, and responses to varying doses were evaluated in relation to elapsed time. RESULTS: The application of phospholipase A2 on the dorsal root ganglion resulted in possible neurotoxicity at doses more than 375 U, with no significant effect at lower doses except for recruitment of "silent units" at doses ranging from 200 to 340 U. CONCLUSIONS: Phospholipase A2 doses comparable to serum concentrations in human rheumatoid arthritis appeared to be neurotoxic when applied to dorsal root ganglia. At lower doses, silent units become activated that were not active before the phospholipase A2 application. These results suggest that dorsal roots and dorsal root ganglion may be impaired by phospholipase A2, leading to sciatica and low back pain.
9105428 Autoantibody production in healthy elderly people is not promoted by interleukin-10 althou 1997 Apr Healthy elderly people tend to have autoantibodies in their sera. These antibodies, not being associated with any clinical manifestation, have been considered as natural autoantibodies. In systemic lupus erythematosus, as well as in rheumatoid arthritis, the presence of autoantibodies characteristic of these disease (anti-dsDNA and rheumatoid factor, respectively) depends on the endogeneous production of IL-10. The same could hold true for autoantibodies found in healthy elderly individuals. In the present work, the authors analysed whether an increased production of IL-10 contributed to the production of autoantibodies in elderly people. The authors found that there is neither increased in vivo gene expression nor augmented production of IL-10 by peripheral blood mononuclear cells from elderly women even if they do produce autoantibodies. The authors further sought to determine if the production of autoantibodies is inhibited in vitro by adding an anti-IL-10 MoAb to cell cultures and found that it is not. Despite these negative findings of a role for IL-10 in the production of autoantibodies in elderly people, the authors investigated which cells produce IL-10. In so doing they found that intracellular IL-10 expression occurred exclusively in monocytes in young female controls, but in elderly females it involved also CD8+CD3+ large granular cells. These results indicate that autoantibody production in healthy aged individuals is IL-10 independent.
15992159 ISIS 2302, an antisense inhibitor of intercellular adhesion molecule 1. 1999 Sep ISIS 2302 is a 20 base phosphorothioate oligodeoxynucleotide (ODN) that inhibits intercellular adhesion molecule 1 (ICAM-1) expression through an antisense mechanism. Murine and rat analogues have been effective at doses of 0.06 - 10 mg/kg in a spectrum of models of human inflammatory diseases and allograft transplantation, and ISIS 2302 inhibits the upregulation of ICAM-1 expression in a variety of human cells in vitro. In animals, including primates, plasma distribution half-life ranges from 30 - 60 min, but tissue elimination half-lives range from 1 - 5 days, and the compound is metabolised as other nucleic acids. In a Phase I iv. study, the pharmacokinetic behaviour of ISIS 2302 was similar to that in other primates, and single and multiple every other day doses from 0.06 - 2 mg/kg infused over 2 h were well-tolerated. Phase IIa studies have been completed in Crohn's disease, rheumatoid arthritis, and psoriasis, and a combined Phase I/II renal allograft acute rejection prophylaxis study has just completed enrolment. In these studies, ISIS 2302, 0.5 - 2 mg/kg, or placebo was administered iv. every 2 - 3 days over 14 - 26 days (7 - 13 infusions) to 17 - 52 patients, with follow up for 6 months. In the Crohn's study, evidence of highly durable (5+ month) remission-inducing and steroid-sparing properties were demonstrated, without clinically important adverse events. A 300-patient, pivotal quality trial investigating the steroid-sparing and remission-inducing qualities of ISIS 2302 in patients with steroid-dependent Crohn's disease is completely enrolled, with results expected in the first half of 2000. Modest efficacy and excellent tolerability were demonstrated in the psoriasis and rheumatoid arthritis trials. A Phase IIa trial of a topical formulation in patients with psoriasis is expected to commence in late 1999, as is a trial of an enema formulation in distal ulcerative colitis. Administration by nebulisation for asthma is undergoing preclinical evaluation. Execution of future plans in organ transplantation will await the results of the ongoing Phase I/II trial.
9379065 Fas ligand expression and function in systemic lupus erythematosus. 1997 Nov 1 Mutations in the Fas receptor or its ligand (FasL) lead to lupus-like systemic autoimmune diseases in mice and in some humans. To determine whether a significant number of patients with systemic lupus erythematosus (SLE) have impaired FasL function, we compared T cell effector function by superantigen-activated CD4+ T cell lines or by anti-CD3- and IL-2-generated cytotoxic T cells. No differences were observed between SLE and normal control superantigen-derived CD4+ T cells in either the ability of these cells to up-regulate Fas expression or to induce apoptosis of the Fas-sensitive target B cells. When anti-CD3/IL-2-activated T cells were examined, SLE T cells had a modest reduction (-8%) in T cell cytotoxicity compared with normal controls, but the reduction was similar to the rheumatoid arthritis disease controls. A modest reduction in cytotoxicity was evident in both the Fas and perforin/granzyme pathways as determined by testing Fas-positive and -negative targets as well as by selective blockade of the perforin/granzyme pathway with concanamycin. These results indicate that no specific defects in FasL function are evident in the majority of SLE patients under the in vitro conditions tested. The proportional reduction in FasL and perforin/granzyme function in SLE and rheumatoid arthritis patients following anti-CD3/IL-2 stimulation most likely reflects subtle differences in activation in patient-derived vs normal control T cells.
10855951 Effects of methotrexate on nucleotide pools in normal human T cells and the CEM T cell lin 2000 It has been proposed that the clinical utility of methotrexate (MTX) in the treatment of rheumatoid arthritis may be due, in part, to inhibition of 5-amino imidazole-4-carboxamide ribonucleotide formyltransferase (AICARFT) by polyglutamated forms of MTX. AICARFT is the second folate dependent enzyme in de novo purine biosynthesis. In this study, the effects of MTX on de novo purine biosynthesis as well as total nucleotide pools were evaluated in both the human T cell line, CEM, and phytohemagglutinin-activated normal human T lymphocytes. De novo synthesized purines were metabolically labeled with 14C-glycine after MTX treatment and analyzed by HPLC. In normal T cells, MTX produced a dose-dependent reduction in de novo adenosine and guanosine pools with maximal effects (>50%) at 1 microM MTX. In CEM cells, de novo purine synthesis was almost completely blocked by 1 microM MTX. Total purine pools were also reduced in both cell types after MTX treatment. Since 1 microM MTX caused almost complete growth inhibition in CEM cells, we evaluated whether growth could be reconstituted with exogenous purine bases and pyrimidine nucleosides which can be utilized via salvage pathways. The combination of hypoxanthine and thymidine substantially reversed growth inhibition with 1 microM MTX in CEM cells. Taken together, these results demonstrate that MTX inhibits de novo nucleotide synthesis in T cells and suggest that AICARFT inhibition may be one aspect of the multi-site mechanism of MTX action in the treatment of rheumatoid arthritis.
10371276 Effects of soluble interleukin-1 type II receptor on rabbit antigen-induced arthritis: cli 1999 May OBJECTIVES: To investigate the effects of soluble interleukin-1 (IL-1) type II receptor (sIL-1RII) on a number of clinical, biochemical and histological parameters in rabbit antigen-induced arthritis. METHODS: Arthritis was induced by intra-articular injection of methylated bovine serum albumin (mBSA) into rabbits pre-sensitized to the same antigen. An initial i.v. bolus of sIL-1RII was administered, followed by s.c. mini-pump dosing for 14 days, starting at the time of the arthritis induction. Animals received vehicle (saline 500 microl + 5 microl/h), low-dose sIL-1RII (13.4 microg + 1.34 microg/h) or high-dose sIL-1RII (40.2 microg + 4.02 microg/h). RESULTS: Marked, dose-related inhibition of joint diameter, plasma prostaglandin E2 (PGE2), and synovial fluid IL-1alpha and IL-1beta concentrations were seen after administration of sIL-1RII. However, synovial fluid PGE2 concentrations and synovial fluid cell counts were not affected. A significant inhibitory effect was also seen histologically on soft-tissue swelling and joint damage with high-dose sIL-1RII. CONCLUSIONS: These results demonstrate that IL-1 plays an important role in the pathogenesis of rabbit antigen-induced arthritis, thus confirming it as an excellent animal model with respect to evaluating anti-cytokine therapies for rheumatoid arthritis.
10524676 V2 regions of 16S ribosomal RNA used as a molecular marker for the species identification 1999 Oct OBJECTIVE: To detect the 16S ribosomal RNA (rRNA) of 3 streptococcal species in the peripheral blood and synovial fluid of patients with psoriatic arthritis (PsA). METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) detection targets bacterial 16S rRNA, which is present in bacteria at high copy numbers. The 3 species-specific primers for group A streptococci (GAS; Streptococcus pyogenes), group B streptococci (GBS; Streptococcus agalactiae), and Streptococcus pneumoniae were designed from the fragments of highly variable V2 regions of 16S rRNA. Total RNA was prepared from whole peripheral blood and joint fluid obtained from patients with PsA and rheumatoid arthritis (RA). All positive PCR reactions were then sequenced with a Pharmacia ALF DNA sequencing system. RESULTS: Our data in 19 PsA patients showed that 7 peripheral blood samples were positive for GAS (P = 0.006 versus GAS-positive RA patients [n = 0], by Fisher's exact test), and 2 were also positive for GBS. One synovial fluid sample from a PsA patient was positive for GAS. S pneumoniae was absent from all specimens. Seventeen patients with RA were PCR negative for the 3 streptococcal species. Peripheral blood from a patient with inflammatory bowel disease was positive for GAS. CONCLUSION: The presence of GAS 16S rRNA in the peripheral blood and synovial fluid of patients with PsA supports the concept that PsA is a reactive arthritis to certain streptococci.
12461578 [Recombinant adenovirus-mediated gene transfer suppresses experimental arthritis]. 2001 Collagen Induced Arthritis (CIA) is a widely studied animal model to develop and test novel therapeutic approaches for treating Rheumatoid Arthritis (RA) in humans. Soluble Cytotoxic T-Lymphocyte Antigen 4 (CTLA4-Ig), which binds B7 molecule on antigen presenting cells and blocks CD28 mediated T-lymphocyte activation, has been shown to ameliorate experimental autoimmune diseases such as lupus, diabetes and CIA. Objective of our research was to investigate in vivo the effectiveness of blocking the B7/CD28 T-lymphocyte co-stimulatory pathway, utilizing a gene transfer technology, as a therapeutic strategy against CIA. Replication-deficient adenoviruses encoding a chimeric CTLA4-Ig fusion protein, or beta-galactosidase as control, have been injected intravenously once at arthritis onset. Disease activity has been monitored by the assessment of clinical score, paw thickness and type II collagen (CII) specific cellular and humoral immune responses for 21 days. The adenovirally delivered CTLA4-Ig fusion protein at a dose of 2x10^8 pfu suppressed established CIA, whereas the control beta-galactosidase did not significantly affect the disease course. CII-specific lymphocyte proliferation, IFNgamma production and anti-CII antibodies were significantly reduced by CTLA4-Ig treatment. Our results demonstrate that blockade of the B7/CD28 co-stimulatory pathway by adenovirus-mediated CTLA4-Ig gene transfer is effective in treating established CIA suggesting its potential in treating RA.
11246668 Association between vitiligo and spondyloarthritis. 2001 Feb OBJECTIVE: To establish if spondyloarthritis (SpA) and vitiligo occur together more frequently than by chance. METHODS: All consecutive patients with SpA seen in a 6 month period were evaluated for vitiligo by an experienced dermatologist. The control group included the 2 consecutive patients without SpA seen after each patient with SpA. RESULTS: Two hundred thirty-four patients with SpA (131 men, 103 women; mean age 59 +/- 18.3 yrs) were seen in the study period. Of these, 43 had ankylosing spondylitis (AS), 112 psoriatic arthritis (PsA), 14 SpA associated with inflammatory bowel disease, 64 undifferentiated SpA, and one reactive arthritis. The 468 control patients (360 women, 108 men; mean age 68.5 +/- 2 yrs) had various degenerative and inflammatory rheumatic diseases. Eight (3.4%) patients out of 234 with SpA had type A vitiligo. In the control group, 5 (1.06%) out of 468 had type A vitiligo. The difference was statistically significant (p < 0.05). Of the 8 patients with coexisting vitiligo and SpA, 4 had PsA, 2 primary AS, one AS associated with Crohn's disease, and one undifferentiated SpA. Of the 5 patients with vitiligo in the control group, one had rheumatoid arthritis, one S ogren's syndrome, one palindromic rheumatism, one crystal arthropathy, and one osteoarthritis. CONCLUSION: Our results suggest that vitiligo and SpA do not coexist by chance and that vitiligo should be included in the list of diseases associated with SpA.
9041870 Long-term psychosocial outcome in typical absence epilepsy. Sometimes a wolf in sheeps' cl 1997 Feb OBJECTIVES: To determine whether young adults in whom typical absence epilepsy has been diagnosed in childhood have greater psychosocial difficulties than those with a non-neurologic chronic disease and to decide which seizure-related factors predict poor psychosocial outcome. DESIGN: Population-based, inception cohort study. SETTING: The only tertiary care pediatric hospital in the province of Nova Scotia. PATIENTS: All children in whom typical absence epilepsy or juvenile rheumatoid arthritis (JRA) was diagnosed between January 1, 1997, and December 31, 1985, who were aged 18 years or older at follow-up in March 1994 to April 1995. Patients with typical absence epilepsy were identified from centralized electroencephalographic records for Nova Scotia, and those with JRA were identified from discharge diagnoses from the only children's hospital in Nova Scotia. MAIN OUTCOME MEASURE: Patients participated in a structured interview that assessed psychosocial function. RESULTS: Fifty-six (86%) of the 65 patients with absence epilepsy and 61 (80%) of the 76 patients with JRA participated in the interview. The mean age of the patients at the interview was 23 years. Terminal remission occurred in 32 (57%) of the patients with typical absence epilepsy but in only 17 (28%) of the patients with JRA. Factor analysis identified 5 categories of outcome: academic-personal, behavioral, employment-financial, family relations, and social-personal relations. Patients with typical absence epilepsy had greater difficulties in the academic-personal and in the behavioral categories (P < .001) than those with JRA. Those with ongoing seizures had the least favorable outcome. Most seizure-related factors showed minimal correlation with psychosocial functioning. CONCLUSION: Young adults with a history of typical absence epilepsy, particularly those without remission of their seizures, often have poor psychosocial outcomes, considerably worse than those with JRA.
11275972 Quantitation of the changes in vascularity during arthritis in the knee joint of a mouse w 2001 Apr 1 Many joint and bone diseases are caused by, or associated with vascular changes. Particularly in rheumatoid arthritis, vascular sprouting of synovial vessels plays a major role in the generation of joint pathology. To assess the effects of pharmaceuticals that are designed to inhibit neovascularization, we developed a quantitative procedure to measure vascular changes in cross-sections of the mouse knee joint during arthritic inflammation. Arthritis was induced in the knee joint of C57Black6 mice by a single subpatellar injection of methylated BSA after previous immunization. Total vascularity was visualized with a specific monoclonal rat anti-mouse antibody (9F1). Functional vessels were detected with the fluorescent perfusion marker Hoechst 33342. The localization of Hoechst and the vascular marker 9F1 were analyzed in separate images with an automated digital image processing system. By combining the two images, total vascularity and the perfusion status of the vessels during arthritis could be established. The digital image system measures synovial area (SA), number of all blood vessels (NBV) and the number of perfused blood vessels (NpBV). From these parameters the percentage of perfused vessels (perfusion fraction; PF), the vessel density (VD = NBV/SA) and the density of perfused vessels (VDp = NpBV/SA) can be calculated. The measurements showed that the area of synovial tissue had increased during arthritis. Moreover, both the number of blood vessels (NBV) and the number of perfused vessels (NpBV) in the synovial area had increased significantly on Days 4 and 7 after arthritis induction. This procedure enabled quantitation of total vascularity and of functional blood vessels in cross-sections of synovial tissue. It is expected to be a powerful tool, not only to analyze the effects of anti-angiogenic therapies in animal models of arthritis, but could also be applicable to study vascular and perfusion changes in vascular related diseases of the skeleton.
11426029 Radiographic signs of bone destruction in the arthritic temporomandibular joint with speci 2001 Jun OBJECTIVE: To investigate the progression of radiographic changes of the temporomandibular joint (TMJ) with reference to plasma levels of interleukin-1beta (IL-1beta), C-reactive protein (CRP) and disease duration. METHODS: Twenty-one patients with chronic inflammatory joint disease and TMJ involvement were included. Individualized tomography of the TMJ was performed twice with an interval of at least 12 months. Blood samples were analysed for IL-1beta and CRP. RESULTS: Significant progression of the overall grade of radiographic changes occurred during the observation period, whereas erosions showed great interindividual variability. Progression of TMJ bone loss was correlated to raised levels of CRP and, in patients with a diagnosis of rheumatoid arthritis, or with shorter duration, also to plasma IL-1beta. CONCLUSION: Progression of overall grade of radiographic changes in the TMJ occurs in patients with chronic inflammatory joint disease. Raised levels of serum CRP are associated with progression of TMJ bone loss.