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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Collagen-induced arthritis (CIA) in mice is a model of inflammatory polyarthritis that has many features similar to human rheumatoid arthritis. In rheumatoid arthritis, pregnancy leads to amelioration of the disease while exacerbation develops after delivery. We used the CIA model to elucidate the role of pregnancy on disease and vice versa. The onset of arthritis in pregnant mice was delayed in the B10.RIII strains immunized with native porcine type II collagen 7-12 days prior to syngeneic [B10.RIII (susceptible to CIA) X B10.RIII] and allogeneic (B10.RIII female X B10.K male that are CIA resistant) pregnancy. In contrast, when mice were immunized on days 1-6 of pregnancy, the onset of arthritis was earlier as compared with controls. In addition, once the mice developed CIA after delivery, the disease showed markedly rapid progression as compared to the control immunized group. Humoral immune responses to type II collagen showed significantly decreased levels on day 14 (at late stage of pregnancy) both in syngeneic and allogeneic postmating immunized pregnant mice. The same effect was also seen in allogeneic premating immunized pregnant mice on day 21 (at mid-stage of pregnancy). The levels of these antibodies increased after delivery. Subclasses of IgG1 and IgG2a antibodies to type II collagen were suppressed during pregnancy. In the pseudopregnant group, these antibodies showed decreased levels on day 14, but did not differ from the control groups on day 21 and 28. Some immunoregulatory changes may play a role in these alterations in pregnant arthritic mice. In comparison to the effects of syngeneic (susceptible X susceptible) pregnancy on CIA, allogeneic (susceptible female X resistant male) pregnancy seemed to be beneficial for the affected individuals. Litter size and mean birth weight were not affected by immunization of type II collagen. After onset of CIA, both syngeneic and allogeneic matings failed to produce offspring in arthritic female mice. The estrus cyclicity was highly disturbed in arthritic female mice and gonadotropin stimulation in arthritic mice induced significantly less ova in oviducts and maturing follicles as compared to nonarthritic controls. Immunological factors yet to be elucidated may be involved in this ovarian dysfunction.
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PMID:Collagen-induced arthritis and pregnancy in mice: the effects of pregnancy on collagen-induced arthritis and the high incidence of infertility in arthritic female mice. 374 Mar 48

Collagen-induced arthritis (CIA) in rodents is an experimental animal model that shares many clinical and pathologic findings with rheumatoid arthritis in man. Our previous findings suggested that the amelioration of CIA in mice by a fish oil diet was associated with macrophage accumulation and metabolism of eicosapentaenoic acid and a subsequently altered prostaglandin (PG) profile. In these experiments, we examined the role of gender and found that macrophages from female arthritis-susceptible B10.RIII or B10.G mice synthesized more PG and thromboxane than macrophages isolated from the males. Compared with males, female mice had higher circulating anti-type II collagen antibodies but were less likely to develop CIA. Females, especially those on a fish oil diet, developed a much less severe disease than the males. This supports our hypothesis that the type and/or amount of eicosanoid produced from the macrophage may alter the course of experimentally induced arthritis.
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PMID:Gender differences in eicosanoid production from macrophages of arthritis-susceptible mice. 379 38

The effect of the aminopropeptide of type I procollagen, Col 1(I), on collagen synthesis by normal and scleroderma fibroblasts was investigated. Collagen synthesis was inhibited by about 42% when normal fibroblasts were labeled with 3H-proline in the presence of 4 microM Col 1(I). In contrast, collagen synthesis by scleroderma fibroblasts was inhibited to a lesser degree, about 19%. Furthermore, scleroderma fibroblasts with elevated rates of collagen synthesis (2.5-5 times normal) were inhibited by only about 10%. The data suggest that the increased accumulation of collagen in the skin of scleroderma patients may be related to a defect in the regulation of collagen synthesis by the aminopropeptide.
Arthritis Rheum 1985 Jun
PMID:Collagen synthesis regulation by the aminopropeptide of procollagen I in normal and scleroderma fibroblasts. 400 75

Collagen arthritis has been passively transferred with a serum concentrate from immunized donors to immunologically naive recipients as well as cyclosporin-treated, type II collagen-tolerant rats. These findings point to an important role for anticollagen antibody and appear to rule out a role for cellular immunity to type II collagen in the initiation of this disease. The passively transferred arthritis was a transient lesion in the majority of naive recipients and in the cyclosporin-treated, type II collagen-tolerant rats as well when a serum concentrate was transferred after the cessation of cyclosporin treatment. When cyclosporin-treated, type II collagen-tolerant rats received transfer concentrate while cyclosporin was administered continuously, arthritis was significantly enhanced, and lasted as long as cyclosporin was administered and in the majority of rats up to 2 weeks after the cessation of cyclosporin treatment. These results, together with a rapid clearance of anticollagen antibody from the serum, suggest that anticollagen antibody is not the sole regulatory factor and that a cellular suppressor system, sensitive to cyclosporin, might participate in the regulation of this disease process.
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PMID:Serum transfer of collagen arthritis to cyclosporin-treated, type II collagen-tolerant rats. 407 91

Collagen-induced arthritis (CIA) developed in 70 to 90% of rats immunized with heterologous type II collagen. CIA was reduced to 0 to 18% when rats were injected i.v., i.e., pretreated, with 1 mg of soluble native type II collagen before immunization. Concomitant with the suppression of CIA were significant suppression of IgM, IgG, and delayed-type hypersensitivity (DTH) responses to type II collagen. Suppression of CIA and immunity to collagen was antigen-specific, related to dose and route of administration, and occurred only when 1 mg of collagen was injected i.v. either 32, 7, or 4 days before, or 7 days after immunization. Once CIA was established, however, neither arthritis nor immunity could be suppressed. To determine if adjuvant-induced arthritis (AIA), like CIA, could be suppressed by i.v. pretreatment with type II collagen, rats were given 1 mg of type II collagen or PBS i.v. before injection with mycobacteria and oil. AIA was not suppressed, and arthritis appeared in both groups at a similar incidence and severity. Sera from 26 rats with severe AIA that was collected between days 14 and 35 after injection were assayed for IgG to homologous rat type II collagen and were found to be negative. These findings further support the hypothesis that CIA in rats is mediated by immunity to type II collagen and also suggest that CIA and AIA have different primary pathogenic mechanisms.
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PMID:Collagen-induced arthritis in rats: antigen-specific suppression of arthritis and immunity by intravenously injected native type II collagen. 619 9

Hydroxyapatite crystals in spheroid-shaped masses 1.9-15.6 micrometer in diameter were found in 12 of 13 synovial fluids obtained from the shoulder joints of 4 patients with rotator cuff tears and glenohumeral osteoarthritis. Two of 16 control joint fluids also showed these particles. Collagen types I, II and III were identified in the joint fluid pellets from 3 of the 4 patients, and fibers with typical collagen periodicity were also seen on transmission electronmicroscopy. Collagenase and neutral protease activities were found in fluids from 5 joints in 3 patients, whereas active collagenase was found in only 1 of 10 fluids from rheumatoid arthritis patients and in none of 3 fluids from patients with osteoarthritis. Neutral protease activities were present in several rheumatoid joint fluids. These findings are compatible with the hypothesis of an enzymatic release of hydroxyapatite crystals from the synovium and endocytosis by synovial macrophage-like cells with subsequent crystal-stimulated release of collagenase and neutral protease into the joint fluid, completing a pathogenetic cycle.
Arthritis Rheum 1981 Mar
PMID:"Milwaukee shoulder"--association of microspheroids containing hydroxyapatite crystals, active collagenase, and neutral protease with rotator cuff defects. II. Synovial fluid studies. 626 Jan 21

Forty-nine specimens of human cartilage were taken from 3 sites on the tibial plateau (center of osteoarthritic lesion, edge of lesion, and remote site) and graded histologically by the scale of Mankin. The tissue was homogenized and centrifuged to obtain an insoluble pellet. This was resuspended in buffer and incubated at 37 degrees C, pH 7.5. Collagen digestion was quantitated by the release of hydroxyproline-containing peptides. The highest collagenolytic activity (4.6%) was found in the center of lesions, declining in remote sites to 2.4% and in controls to 1.1%. Moderately severe disease of grade 6--9 had the highest collagenolytic activity. Approximately 55% of the metal-dependent collagenolytic activity was in a latent form, activatable by amino-phenylmercuric acetate; the remainder was self-active. A method was developed for the extraction of collagenase from cartilage; the extracted enzyme produced the typical 75:25 cleavage products of type I collagen.
Arthritis Rheum 1983 Jan
PMID:Collagenase and collagenolytic activity in human osteoarthritic cartilage. 629 8

The timing and molecular profile of cartilage destruction in Escherichia coli and Staphylococcus aureus infectious arthritis and killed Mycobacterium butyricum adjuvant arthritis are presented. Infectious arthritis was studied for 3 weeks; cartilage samples were analyzed at 2, 10, and 21 days. At 48 h postinfection, glycosaminoglycan content was reduced by 20% (p less than 0.05) in E. coli infected knees and by 42% (p less than 0.05) in tibial plateau cartilage of S. aureus infected knees. By the 3rd week of infection, glycosaminoglycan losses amounted to as much as 73% (p less than 0.005). In comparison, collagen losses were not significant prior to the 3rd week of infection, at which time 42% (p less than 0.05) was lost. Adjuvant arthritic tibial plateau cartilage was examined at 1, 3 and 12 weeks. Glycosaminoglycans decreased by 42% the 1st week, plateauing at 62% by the 3rd and 12th weeks. Collagen degradation began at 3 weeks (28% loss, p less than 0.10) and by the 12th week was reduced by 49% (p less than 0.005). Analysis of the individual species of glycosaminoglycan showed a parallel loss of chondroitin sulfate and keratan sulfate. Fractionation of glycosaminoglycans with respect to size produced no evidence of shortened chains in cartilage from infected joints. Hyaluronic acid losses were greatest when collagen was significantly decreased. The pattern by which chondroitin and keratan sulfates are lost demonstrates that a prominent feature of infectious and noninfectious inflammatory arthritis is a rapid loss of proteoglycan subunits that precedes collagen loss.
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PMID:Comparison of cartilage destruction between infectious and adjuvant arthritis. 643 56

Collagen arthritis in rats has a well defined humoral and cellular immunologic response to type II collagen, the inciting antigen. Like other chronic models of inflammation, considerable variation exists in terms of severity and incidence. We have attempted to correlate the inflammatory response as measured by paw volume, with serum type II collagen antibody and skin delayed hypersensitivity (DH) to type II collagen. Surprisingly, the incidence and severity of collagen arthritis, induced in the presence of MDP to increase incidence of the disease, are neither correlated with type II collagen antibody nor DH to type II collagen. However, tarsometatarsal bone erosion is significantly correlated with paw edema. Further studies will be necessary to elucidate the role of both humoral and cellular immune responses in the development of type II collagen arthritis in the rat.
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PMID:Humoral and cellular immunologic responses in collagen-induced arthritis in rats: their correlation with severity of arthritis. 652 9

Defatted joint fluid pellets from 4 patients with the "Milwaukee shoulder" syndrome, an aspirate of milky fluid from subcutaneous tissue of a girl with dermatomyositis/calcinosis, and 2 rabbit synovial membranes calcified by calciphylaxis were studied by Fourier transform infrared analysis. This method permits sequential electronic subtraction ("stripping") of known patterns of highly characterized reference compounds from an unknown sample pattern. Collagen and hydroxyapatite, with carbonate partially (1-3%) substituted for phosphate, and to a lesser extent hydroxyl, were found in all samples. Octacalcium phosphate (OCP) was found in all samples except that from a patient with synovial chondromatosis which contained tricalcium phosphate (TCP). Sulfate was found in 2 of the shoulder joint fluid specimens. An unidentified organic phase was present in all samples. This study confirms recent observations by others that pathologic calcifications contain several mineral phases. These data raise the possibility that hydroxyapatite nucleation may be controlled by hydrolytic alteration of precursor calcium phosphate phases such as OCP or TCP. Studies of the biologic effects of synthetic calcium phosphate crystals must take into account the existence of several crystalline phases in natural pathologic calcifications.
Arthritis Rheum 1983 Oct
PMID:Crystal populations in human synovial fluid. Identification of apatite, octacalcium phosphate, and tricalcium phosphate. 662 80


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