fibrin and Arthritis

Fibrinogen is a unique protein that is converted into an insoluble fibrin in a single enzymatic event, which is a characteristic feature of fibrinogen due to its susceptibility to fibrinolytic degradation and dissolution. Although thrombosis is a result of activated blood coagulation, no explanation is being offered for the persistent presence of fibrin deposits in the affected organs. A classic example is stroke, in which the thrombolytic therapy is effective only during the first 3-4 h after the onset of thrombosis. This phenomenon can now be explained in terms of the modification of fibrinogen structure induced by hydroxyl radicals generated during the period of ischemia caused, in turn, by the blocking of the blood flow within the obstructed vessels. Fibrinogen modification involves intra-to intermolecular disulfide rearrangement induced by the reductive power of hydroxyl radicals that result in the exposition of buried hydrophobic epitopes. Such epitopes react readily with each other forming linkages stronger than the peptide covalent bonds, thus rendering them resistant to the proteolytic degradation. Also, limited reduction of human serum albumin (HSA) generates hydrophobic polymers that form huge insoluble complexes with fibrinogen. Consequently, such insoluble copolymers can be deposited within the circulation of various organs leading to their dysfunction. In conclusion, the study of protein hydrophobic interactions induced by a variety of nutritional and/or environmental factors can provide a rational explanation for a number of pathologic conditions including cardiovascular, neurologic, and other degenerative diseases including cancer.

Topics: Animals; Arthritis; Cardiovascular Diseases; Diabetes Mellitus; Fibrin; Fibrinogen; Fibrinolysis; Humans; Hydrophobic and Hydrophilic Interactions; Kidney Diseases; Lung Diseases; Models, Biological; Neoplasms; Nervous System Diseases; Polymerization; Protein Interaction Domains and Motifs; Serum Albumin, Human; Solubility; Thrombosis

Topics: Arthritis; Blood Coagulation Factors; Blood Platelets; Chronic Disease; Complement System Proteins; Connective Tissue; Disseminated Intravascular Coagulation; Endotoxins; Factor XII; Fibrin; Fibrinogen; Fibrinolysin; Glomerulonephritis; Humans; Inflammation; Kinins; Leukocytes; Nephritis; Shwartzman Phenomenon

Functional tissue engineering has emerged as a potential means for treatment of cartilage defect. Development of a stable cartilage composite is considered to be a good option. The aim of the study was to observe whether the incorporation of cultured chondrocytes on porous tantalum utilizing fibrin as a cell carrier would promote cartilage tissue formation.. Rabbit articular chondrocytes were cultured and seeded onto tantalum with fibrin as temporary matrix in a composite, which was divided into three groups. The first group was kept in vitro while a total of 12 constructs were implanted into the dorsum of mice for the second and third groups. The implanted tissues were harvested after 4 weeks (second group) and after 8 weeks (third group). Specific characteristic of cartilage growth were studied by histological and biochemical assessment, immunohistochemistry, and quantitative PCR analysis.. Histological and biochemical evaluation of the formed cartilage using hematoxylin and eosin and Alcian blue staining showed lacunae chondrocytes embedded in the proteoglycan rich matrix. Dimethylmethylene blue assay demonstrated high glycosaminoglycans content in the removed tissue following 8 weeks of implantation. Immunohistochemistry results showed the composites after implantation expressed high collagen type II. Quantitative PCR results confirmed a significant increase in cartilage associated genes expression (collagen type II, AggC, Sox 9) after implantation.. Tantalum scaffold with fibrin as cell carrier promotes chondrocyte proliferation and cartilaginous tissue formation. Producing hyaline cartilage within a stable construct of tantalum and fibrin has a potential for treatment of cartilage defect.

Topics: Animals; Arthritis; Chondrocytes; Fibrin; Glycosaminoglycans; Immunohistochemistry; Mice; Rabbits; Real-Time Polymerase Chain Reaction; Tantalum; Tissue Scaffolds

A 50-year-old man was treated with trimethoprim-sulfamethoxazole (TMP-SMX) for acute arthritis of his right big toe. Within a few days, he developed dyspnoea, hypoxaemia and diffuse pulmonary infiltrates. Symptoms improved with discontinuation of the antibiotic but worsened again with its reintroduction. An open lung biopsy was performed. We describe the workup performed and the factors that pointed to a final diagnosis of TMP-SMX-related pulmonary toxicity in the form of acute fibrinous organising pneumonia.

Topics: Alveolar Epithelial Cells; Anti-Bacterial Agents; Arthritis; Biopsy; Fibrin; Humans; Lung; Male; Middle Aged; Pneumonia; Trimethoprim, Sulfamethoxazole Drug Combination

Topics: Arthritis; Biopsy; Collagen; Female; Fibrin; Humans; Inclusion Bodies; Knee Joint; Magnetic Resonance Imaging; Middle Aged; Synovial Membrane

C4b-binding protein (C4BP) is a plasma oligomeric glycoprotein that participates in the regulation of complement and haemostasis. Complement-regulatory activity depends on the C4BPalpha-polypeptide, whereas the C4BPbeta-polypeptide inactivates protein S, interfering with the anti-coagulatory protein C-dependent pathway.. To investigate the expression of C4BPbeta in the rheumatoid joint.. Expression of C4BP was studied in synovial explants from patients with rheumatoid arthritis, osteoarthritis and healthy controls, using immunohistochemistry and in situ hybridisation. C4BP isoforms and free C4BPbeta were studied in synovial effusions from patients with rheumatoid arthritis, osteoarthritis and microcrystalline arthritis (MCA) by immunoblotting; total and free protein S levels were studied by enzyme immunoassay.. C4BPbeta was overexpressed in the synovial membranes of patients with rheumatoid arthritis, in close association with the severity of synovitis and the extension of interstitial fibrin deposits. As many as 85% fluids from patients with rheumatoid arthritis contained free C4BPbeta, whereas this unusual polypeptide was present in 50% fluids from patients with MCA and 40% fluids from patients with osteoarthritis. Free protein S at the effusions was pathologically reduced in patients with rheumatoid arthritis and MCA, and remained normal in patients with osteoarthritis.. C4BPbeta is expressed by the inflamed synovial tissue, where it can participate in processes of tissue remodelling associated with invasive growth.

Topics: Adult; Arthritis; Arthritis, Rheumatoid; Complement C4b-Binding Protein; Fibrin; Histocompatibility Antigens; Humans; Immunoenzyme Techniques; Osteoarthritis, Knee; Protein Isoforms; Protein S; Synovial Fluid; Synovial Membrane; Synovitis

The ability of calcium phosphate (CaP) and calcium pyrophosphate (CaPPi) to mediate matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9) binding to fibrin was evaluated. Substrate gel electrophoresis (gelatin zymography) revealed that CaP bound MMP-2 and MMP-9, forming a high molecular weight aggregate with lowered electrophoretic mobility. Formation of the CaP : MMP aggregate was necessary for fibrin binding. In contrast, CaPPi did not aggregate MMPs and did not promote uptake of MMPs into fibrin. Scatchard analysis (Ca/P ratio) revealed that CaPPi (1.96) was chemically similar to calcium pyrophosphate dihydrate (2.00) compared to amorphous CaP (1.50) or crystalline CaP, hydroxyapatite (1.66). MMP : CaP interaction appeared to be electrostatic in nature as high salt concentration (NaCl > 150 mm) reduced binding. In contrast, two non-ionic detergents (Brij-35 and Tween-20) did not prevent MMP : CaP binding. MMP : CaP interaction did not involve the C-terminal MMP region because the specific tissue inhibitor of metalloproteinases (TIMPs) also did not block MMP : CaP interaction and fibrin binding. Although MMP : CaP binding could be decreased with albumin, this effect appeared non-specific due to the high albumin concentration required. High albumin concentration could also partially dissociate preformed MMP : CaP complexes. Interestingly, type I and type IV collagen substantially increased MMP : fibrin-binding activity, whereas denatured collagen, gelatin, did not. Inflammatory joint fluid from five patients also demonstrated similar MMP fibrin-binding activity consistent with CaP mediation. The relevance of these findings to CaP and CaPPi in the pathogenesis of crystal arthropathies such as basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate crystal disease (CPPD) is discussed.

Topics: Adult; Aged; Arthritis; Calcium Phosphates; Calcium Pyrophosphate; Female; Fibrin; Humans; In Vitro Techniques; Male; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Matrix Metalloproteinases; Synovial Fluid

Activation of coagulation and fibrinolysis play a role in the pathophysiology of experimental arthritis.. To determine the extent of activation of the coagulation and fibrinolytic pathways in different joint diseases in humans and to ascertain the factors that may influence fibrin deposition within the joint.. Plasma from normal subjects (controls, n= 21) and plasma and synovial fluid samples from patients with rheumatoid arthritis (RA; n = 64), osteoarthritis (OA; n = 29), spondyloarthropathy (SpA; n = 22) and crystal arthritis (CA; n = 25) were analyzed for the levels of TF (tissue factor) and tissue factor pathway inhibitor (TFPI) activities, thrombin-antithrombin III (TAT) complexes, and F1 + 2 (thrombin fragment), fibrin d-dimer and thrombin-activated fibrinolysis inhibitor (TAFI) antigenic levels. The measurements were analyzed by pairwise correlation with each other as well as with standard parameters of inflammation [C-reactive protein (CRP), joint leukocyte count]. Inter-group comparisons were performed to look for disease-specific differences.. Compared with healthy controls, patients with joint diseases had higher levels of TAT, F1 + 2 and d-dimers in their plasma. In the synovial fluid, TF activity, TAT, d-dimers, and TAFI were significantly higher in inflammatory arthritides than in OA. The levels were highest in RA patients. In the plasma, TF activity was correlated with TAT and d-dimer levels with CRP, TFPI, and TAT. In the synovial fluid, TF activity correlated with plasma CRP levels, synovial fluid leukocyte count, and synovial TAT and TAFI levels. In addition, synovial d-dimers correlated with CRP, and synovial TAFI levels were correlated with synovial F1 + 2 and TAT.. Activation of the coagulation and fibrinolytic cascades in the joint and in the circulation is evident in both inflammatory and degenerative joint diseases. Within the joint, inflammatory mechanisms leading to TF-mediated activation of the coagulation pathway and subsequent fibrin deposition is the most likely explanation for the observed findings. In the plasma, the link between inflammation (CRP increase) and TF activation is weak, and a non-TF-mediated mechanism of coagulation activation could explain these findings. RA is characterized by significantly higher levels of TAT in the synovial fluid and plasma than other arthritides. Although fibrinolytic activity is linked to inflammation, the increased amounts of TAFI in the joint, particularly in RA, may explain why fibrin formation is so prominent in this condition compared with other joint diseases.

Topics: Adult; Aged; Arthritis; Arthritis, Rheumatoid; Biomarkers; Blood Coagulation; Carboxypeptidase B2; Case-Control Studies; Female; Fibrin; Fibrinolysis; Humans; Inflammation; Linear Models; Male; Middle Aged; Osteoarthritis; Spondylitis, Ankylosing; Synovial Fluid

The deleterious role of fibrin deposition in arthritic joints prompted us to explore the effect of the thrombin inhibition on the course of collagen-induced arthritis (CIA) in the mouse. CIA was induced in male DBA/1J mice using native chicken type II collagen. The thrombin inhibitor polyethyleneglycol-hirudin (PEG-hirudin) was given for 16 days, starting 20 days after the first immunization (preventive treatment) or at the onset of clinical signs of arthritis (curative treatment). All the mice treated with PEG-hirudin had a significantly prolonged clotting time compared with control mice. PEG-hirudin, administered in a preventive way, led to significantly reduced incidence and severity of CIA during most of the treatment period, as assessed by clinical scoring. Accordingly, histological features showed a significant diminution of synovial hyperplasia in PEG-hirudin-treated mice compared with untreated mice. There was also a significant downmodulation of the synovial proinflammatory IL-1beta and IL-12p35 cytokine mRNAs in treated mice. Intra-articular fibrin, evaluated by immunohistochemistry, was significantly reduced in treated mice compared with control mice and correlated with both clinical and histological scorings. Most importantly, once arthritis was established, PEG-hirudin also showed a curative effect. In conclusion, PEG-hirudin can both prevent the onset of CIA in a dose-dependent manner and ameliorate established arthritis, suggesting that thrombin inhibition may offer a new therapeutic approach in arthritis.

Topics: Animals; Antithrombins; Arthritis; Collagen; Cytokines; Fibrin; Hirudin Therapy; Hirudins; Immunoglobulin G; Knee Joint; Male; Mice; Mice, Inbred DBA; Receptor, PAR-1; Receptors, Thrombin; Synovial Membrane; Thrombin; Thrombosis; Transcription, Genetic; Whole Blood Coagulation Time

Extravascular coagulation and diminished fibrinolysis are processes that contribute to the pathology of both inflammatory arthritis and atherosclerosis. We hypothesized that, given its homology with plasminogen, apolipoprotein (apo) (a), the distinctive glycoprotein of the atherogenic lipoprotein (Lp) (a), may be equally implicated in inflammatory arthritis. We detected the presence of apo(a) as part of Lp(a) in human arthritic synovial fluid. The abundance of apo(a) in synovial fluid rose in proportion to plasma apo(a) levels and was higher in inflammatory arthritides than in osteoarthritis. In addition, apo(a) immunoreactive material, but not apo(a) transcripts, was detected in inflammatory arthritic synovial tissues. These data indicated that synovial fluid apo(a) originates from circulating Lp(a) and that diffusion of Lp(a) through synovial tissue is facilitated in inflammatory types of arthritis. In synovial tissues, apo(a) co-localized with fibrin. These observations could be reproduced in a model of antigen-induced arthritis, using transgenic mice expressing human Lp(a). Although in this mouse model the presence of apo(a) did not change the severity of arthritis, the co-localization of apo(a) with fibrin in synovial tissue suggests that, in humans, apo(a) may modulate locally the fibrinolytic activity and may thus contribute to the persistence of intra-articular fibrin in inflammatory arthritis.

Topics: Animals; Antigens; Apolipoproteins A; Arthritis; Arthritis, Rheumatoid; Fibrin; Humans; Joints; Lipoprotein(a); Mice; Mice, Transgenic; Osteoarthritis; Particle Size; Synovial Fluid; Synovial Membrane

In rheumatoid arthritis, synovial expression of urokinase (uPA) activity is greatly increased (Busso, N., V. Péclat, A. So, and A. -P. Sappino. 1997. Ann. Rheum. Dis. 56:550- 557). We report the same effect in murine antigen-induced arthritis. uPA-mediated plasminogen activation in arthritic joints may have deleterious effects via degradation of cartilage and bone matrix proteins as well as beneficial effects via fibrin degradation. We evaluated these contrasting effects in vivo by analyzing the phenotype of uPA-deficient (uPA-/-) and control mice during antigen-induced arthritis. Joint inflammation was comparable in both groups up to day 3 and subsequently declined in control mice, remaining significantly elevated in uPA-/- mice on days 10 and 30 after arthritis onset. Likewise, synovial thickness was markedly increased in uPA-deficient mice persisting for up to 2 mo, whereas it subsided in control animals. Bone erosion was exacerbated in uPA-/- mice on day 30. By contrast, no difference in articular cartilage proteoglycan content was found between both groups. Significantly increased accumulation of fibrin was observed by day 30 in arthritic joints of uPA-/- mice. We hypothesized that synovial fibrin deposition plays a role in joint inflammation. Accordingly, defibrinogenation of uPA-/- mice by ancrod significantly decreased the sustained joint inflammation. All the above observations were reproducible in plasminogen-deficient (Pln-/-) mice. In conclusion, synovial fibrin deposition plays a role as a nonimmunological mechanism which sustains chronic arthritis.

Topics: Animals; Antigens; Arthritis; Fibrin; Fibrinogen; Interleukin-1; Mice; Mice, Inbred C57BL; Synovial Membrane; Urokinase-Type Plasminogen Activator

To study the antiinflammatory effect of different doses of intraarticular somatostatin in experimental arthritis in rabbits.. Chronic arthritis was induced by a single injection of fibrin into the knee joint of rabbits previously sensitized to this antigen. The effects of sequential intraarticular injections of somatostatin into the rabbit knee, at doses of 500, 750, and 1,000 micrograms, were monitored by measuring knee joint circumferences and hematologic parameters. The measurements were compared with those obtained following use of triamcinolone acetonide and placebo. At the end of the experiments, the knee joints were examined histologically.. Somatostatin treatment induced a statistically significant and dose-related reduction of knee joint swelling. This effect was shorter than that produced by triamcinolone acetonide; however, the antiinflammatory activity elicited by successive doses of triamcinolone acetonide declined both in extent and duration, while the effects of somatostatin remained unchanged at each successive treatment. Histopathologic observations showed that both somatostatin and triamcinolone acetonide reduced the inflammatory signs in the joint structures, although triamcinolone acetonide appeared to be more effective.. These findings suggest that somatostatin exerts an antiinflammatory effect in this model of experimental arthritis and may represent a valid and safer alternative to corticosteroids for intraarticular therapy of arthritis.

Topics: Animals; Arthritis; Blood Sedimentation; Disease Models, Animal; Fibrin; Injections, Intra-Articular; Knee Joint; Leukocyte Count; Male; Rabbits; Somatostatin

Antigen arthritis in rabbits was associated with induction of bradykinin B1 receptors in isolated aorta smooth muscle 24 h following intra-articular injection of antigen in sensitized animals. Control tissues developed responsiveness to desArg9-bradykinin or bradykinin during 3 h incubation, but failed to respond to either kinin at the beginning of experiments. Aorta from rabbits 24 h after induction of arthritis not only developed responsiveness to kinins more rapidly than controls, but also responded at the outset of experiments. Antigen arthritis was characterized by acute phase protein synthesis and joint swelling. This is the first demonstration of induction of smooth muscle responsiveness to desArg9-bradykinin during an immune complex disease.

Topics: Animals; Antigens; Aorta; Arthritis; Bradykinin; Fibrin; Male; Muscle Contraction; Muscle, Smooth, Vascular; Phenylephrine; Rabbits; Receptors, Bradykinin; Receptors, Neurotransmitter

The synovial-like structure lining the cavity of a subcutaneous air pouch in rats was examined macroscopically and microscopically for changes during the induction and progression of adjuvant polyarthritis. The earliest event observed was the infiltration of the lining by inflammatory cells which occurred about 6 days after inoculation with adjuvant. Deposition of fibrin and proliferation of blood vessels and connective tissue soon followed, associated with an even greater infiltration by inflammatory cells and the formation of oedema in the hyperplastic fibrous tissue. These changes resulted in a substantial thickening of the pouch wall (and consequently in air pouch skin thickness) that was most marked on day 9, when few rats had visible signs of joint swelling. As arthritis developed and became established (day 12-14), pouch wall thickness declined to below pre-adjuvant thickness. Histological changes were still evident but at a much reduced intensity. Challenge of pouches with tuberculin at various times showed reactivity of the delayed type, beginning not earlier than day 5 post-adjuvant inoculation. Pouches however failed to respond to tuberculin or to the non-specific irritant carrageenan as arthritis developed.

Topics: Animals; Arthritis; Arthritis, Experimental; Connective Tissue; Female; Fibrin; Hypersensitivity, Delayed; Rats; Skin; Skinfold Thickness; Synovial Membrane; Time Factors; Tuberculin

In an attempt to produce a superior model of rheumatoid arthritis, experiments have been performed to investigate the ease of induction of experimental arthritis in marmosets by immunological means. Marmosets were sensitised with the following combinations of antigen and adjuvant: ovalbumin in Freund's complete adjuvant (FCA), ovalbumin in FCA + Bordetella pertussis, methylated-BSA in FCA + B. pertussis or human fibrin in FCA + B. pertussis, and subsequently injected with the corresponding antigen in saline into one knee joint. Animals receiving ovalbumin, with or without B. pertussis, produced only a weak transient monoarticular synovitis. Animals receiving Met-BSA + B. pertussis produced a chronic synovitis but only mild erosive changes were apparent even 21 weeks after intraarticular injection. Animals receiving human fibrin produced a transient monoarticular synovitis of moderate intensity. These results indicate that the marmoset offers no obvious advantages over the rabbit for the induction of experimental rheumatoid arthritis.

Topics: Animals; Arthritis; Arthritis, Experimental; Callithrix; Fibrin; Freund's Adjuvant; Immunization; Injections, Intra-Articular; Knee Joint; Ovalbumin; Pertussis Vaccine; Rheumatoid Factor; Serum Albumin, Bovine

Topics: Animals; Arthritis; Fibrin; Humans; Rats; Tendons

The infrapatellar fat pad, fibrous synovium, and cartilage joint surfaces of the tibia, patella, and femur of the knee joints of 17 normal rats and 38 rats with type II collagen-induced arthritis were examined by light and electron microscopy. In the normal animals, the synovium covering the fat pad was structurally variable in that the mesothelium was flattened and two to three cell layers thick in the central region but rounded and three to five layers thick at the tibial and patellar ends. Large vacuoles were more numerous in the synovial cells at either end of the fat pad, and these cells contained less endoplasmic reticulum than those in the central region. The fibrous synovium consisted of a flattened mesothelium composed of cells similar to those found in the central region of the fat pad. The normal cartilage was not covered by a mesothelium. Knees from animals immunized with collagen showed no structural changes until 5 days after immunization, when fibrin could be detected in the synovium by immunofluorescence. By day 12, fibrin deposition was found throughout the synovium covering the fat pad and fibrous tissue, as well as over the cartilage. In addition, hyperplasia of the synovium over the soft tissues was present, and synovial cells extended over the cartilage. On day 19, in approximately 20 per cent of the animals, inflammatory infiltrates, composed of mixtures of polymorphonuclear leukocytes and mononuclear cells, were observed within the synovium covering the soft tissues. Infiltrates were also seen at the edges of the cartilage. When the 80 per cent of the animals that did not have cellular infiltrates were examined 30 days after immunization, neither hyperplasia nor fibrin deposition were seen by light microscopy. By day 45, in 20 per cent of the animals, the synovium was hyperplastic, and granulation tissue, scarring, and granulomata were found in the soft tissues. It is concluded that there are two distinct stages in the development of this synovial disease--the first is characterized by hyperplasia and fibrin deposition, and the second by the presence of inflammatory infiltrates.

Topics: Animals; Arthritis; Arthritis, Experimental; Cartilage, Articular; Collagen; Female; Femur; Fibrin; Hindlimb; Patella; Rats; Rats, Inbred Strains; Synovial Membrane; Tibia

The effects of a number of steroids administered intra-articularly in a chronic model of fibrin-induced monoarticular arthritis in the rabbit have been investigated. Org 6216 hydrocortisone acetate, prednisolone tertiary butyl acetate and triamcinolone hexacetonide each suppressed the joint swelling produced 14 days after antigen challenge. These anti-inflammatory effects lasted for at least 7 days. Hydrocortisone semisuccinate was inactive in this model. In addition, the effects of the same compounds and several other anti-inflammatory steroids and indomethacin administered locally with adjuvant was assessed on the resultant paw oedema produced in the rat. The local anti-inflammatory activity, the duration of action and the systemic effects of these drugs varied considerably and only Org 6216, hydrocortisone acetate, prednisolone tertiary butyl acetate and indomethacin produced anti-inflammatory effects throughout the 4 days of the experiments and were devoid of significant adrenolytic and thymolytic activity.

Topics: Administration, Topical; Animals; Anti-Inflammatory Agents; Arthritis; Arthritis, Experimental; Disease Models, Animal; Dose-Response Relationship, Drug; Fibrin; Hydrocortisone; Indomethacin; Knee Joint; Male; Organ Size; Prednisolone; Pregnadienes; Rabbits; Rats; Time Factors; Triamcinolone

Psoriatic arthritis (PA) is included in the seronegative arthritis group, though it is now generally considered to represent a clinical entity. In PA, in contrast to psoriasis vulgaris and to other types of rheumatoid arthritis, only a few immunological studies have been reported. In the present report synovial joint membranes from patients with PA and control groups have been studied for the presence of (a) vascular changes, (b) fibrin, (c) immunoglobulins and complement factor C3.

Topics: Arthritis; Arthritis, Rheumatoid; Complement C3; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulins; Psoriasis; Synovial Membrane; Vasculitis

Topics: Arthritis; Cell Membrane; Cell Physiological Phenomena; Endocytosis; Exudates and Transudates; Fibrin; Humans; Inclusion Bodies; Microscopy, Electron; Multiple Sclerosis; Pseudopodia; Psoriasis; Synovial Fluid; Synovial Membrane

Topics: Adolescent; Adult; Anemia, Sickle Cell; Arthritis; Bone and Bones; Child; Child, Preschool; Erythrocytes, Abnormal; Female; Fibrin; Hemoglobin C Disease; Humans; Infarction; Joint Diseases; Male; Middle Aged; Mucins; Necrosis; Osteoporosis; Radiography; Sclerosis; Synovial Fluid; Synovial Membrane; Thalassemia; Uric Acid

Topics: Adolescent; Adult; Arthritis; Arthritis, Rheumatoid; Biopsy; Child; Diagnosis, Differential; Female; Fibrin; Follow-Up Studies; Histocytochemistry; Humans; Knee; Knee Joint; Male; Middle Aged; Prognosis; Retrospective Studies; Rheumatoid Factor; Synovial Membrane; Synovitis

Topics: Animals; Arthritis; Disease Models, Animal; Female; Fibrin; Formaldehyde; Histiocytes; Inflammation; Injections, Intra-Articular; Knee; Leukocytes; Lymphocytes; Necrosis; Plasma Cells; Rabbits; Serum Albumin, Bovine

Topics: Adolescent; Adult; Aged; Arthritis; Dermatitis, Exfoliative; Eczema; Female; Fibrin; Fluorescent Antibody Technique; Humans; Male; Middle Aged; Photosensitivity Disorders; Psoriasis; Skin; Time Factors

Topics: Adult; Aged; Albumins; Arthritis; Arthritis, Rheumatoid; Complement System Proteins; Female; Fibrin; Fibrinogen; Fibrinolysin; Fluorescent Antibody Technique; Humans; Immune Sera; Immunoglobulins; Male; Middle Aged; Osteoarthritis; Synovial Membrane

Topics: Animals; Arthritis; Fibrin; Fibrinogen; Freund's Adjuvant; Male; Rats; Time Factors

Topics: Arthritis; Blood Coagulation Factors; Calcium; Factor IX; Factor V; Factor VII; Factor VIII; Factor X; Factor XI; Factor XII; Factor XIII; Fibrin; Inflammation; Kinins

Topics: Animals; Arthritis; Carrageenan; Fibrin; Germ-Free Life; Hypertrophy; Lymphocytes; Phagocytosis; Rabbits; Swine; Swine Diseases; Synovial Fluid; Synovial Membrane

Topics: Acute Disease; Animals; Arthritis; Blood Coagulation; Blood Proteins; Chemotaxis; Dogs; Fibrin; Fibrinogen; Humans; Inflammation; Leukocytes; Skin; Skin Window Technique; Synovial Fluid

Topics: Animals; Arthritis; Blood Protein Electrophoresis; Fibrin; Freund's Adjuvant; Haplorhini; Humans; Macaca mulatta; Pathology; Radiography; Research

Topics: Animals; Antigens; Arthritis; Arthritis, Experimental; Arthritis, Rheumatoid; Autoimmune Diseases; Fibrin; Hypersensitivity, Delayed; Injections, Intra-Articular; Pathology; Rabbits; Research

Topics: Allergy and Immunology; Antibodies; Arthritis; Arthritis, Rheumatoid; Collagen; Fibrin; gamma-Globulins; Humans; Rheumatoid Factor

Topics: Allergy and Immunology; Animals; Antigen-Antibody Reactions; Arthritis; Arthritis, Rheumatoid; Fibrin; Haplorhini; Humans; Pathology; Rheumatic Diseases; Rheumatoid Factor; Rheumatoid Nodule

Topics: Arthritis; Fibrin; Fluorescent Antibody Technique; Pathology; Rabbits; Research; Serum Globulins

Topics: Arthritis; Arthritis, Rheumatoid; Blood Sedimentation; Fibrin; Humans; Rheumatic Heart Disease; Tonsillitis

Topics: Aniline Compounds; Arthritis; Arthritis, Rheumatoid; Blood Sedimentation; Diagnosis; Diphenylamine; Fibrin; Leukocytosis; Leukopenia; Rheumatic Diseases; Tonsillitis

Topics: Animals; Arthritis; Arthritis, Experimental; Fibrin; Lagomorpha; Rabbits

Topics: Arthritis; Arthroplasty; Fibrin; Humans; Tuberculosis; Tuberculosis, Osteoarticular

Topics: Arthritis; Arthroplasty; Fibrin; Humans; Tuberculosis; Tuberculosis, Osteoarticular

Topics: Arthritis; Arthritis, Rheumatoid; Fibrin; Humans; Rheumatic Diseases

Topics: Arthritis; Arthritis, Rheumatoid; Fibrin; Humans

Topics: Adrenocorticotropic Hormone; Arthritis; Arthritis, Rheumatoid; Fibrin; Fibrinogen; Protamines

Topics: Arthritis; Blood Coagulation; Chronic Disease; Fibrin; Fibrinolysis; Humans; Joint Diseases