Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nervous system collects information from the outer world by specific senses and from the interior milieu by somatic senses. This information is processed and stored in memory and affects various bodily functions through the efferent arm of the nervous system. The efferent chemical neuropeptide message is transported intra-axonally to the site of action, which imparts site-specificity to the peripheral, paracrine neuropeptide effects. In the present study, immunohistochemistry using the immunoperoxidase method with nickel amplification was applied to visualize the topographical distribution of articular nerve fibres and nerve endings using the markers PGP 9.5 and synaptophysin, respectively. Furthermore, to get a comprehensive idea of the sensory innervation of the articular and para-articular tissue, antisera to calcitonin gene-related peptide (CGRP) and substance P were employed. Samples were collected after fixation by perfusion followed by immersion in fixative and decalcification by a special method, which also allows studies of the bone innervation. PGP 9.5- and synaptophysin-immunoreactive type IVa and IVb nerve fibres and endings were found in the synovial lining and sublining tissue and in the vascularized peripheral parts of the menisci. Furthermore, periosteum, bone marrow and the epiphyseal growth plates were also innervated, whereas innervation of the diaphyseal and metaphyseal bone was more sparse. PGP 9.5- and synaptophysin-immunoreactive nerves were also characterized by their CRGP, and to some extent, substance P content. Because of their distribution, the peripheral peptide-containing type IVa and IVb nerve fibres and nerve endings are in a position to participate in the pathogenesis of arthritis, including aspects of nociception, tissue remodelling and neurogenic inflammation.
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PMID:Distribution of nerve endings and sensory neuropeptides in rat synovium, meniscus and bone. 138 67

Mechanical stress causes remodelling of bone, a transformation of bone structure by physical forces through an unknown mechanism. Inflammation also affects bone structure, through altered use and the production of various inflammatory mediators. The peripheral nervous system may play both a sensory and an efferent role in the mechanical and inflammatory influences on bone structure. We studied the occurrence of substance P and calcitonin gene related peptide (CGRP) containing nerves in periosteal tissue, bone marrow, diaphysis and epiphysis of the ankle and knee joints of healthy and adjuvant arthritic rats. In arthritic animals, only ankle joints were affected by the inflammation. The periosteum was richly innervated both in healthy and arthritic animals. In arthritic rats few nerve fibers penetrated the woven, callous bone underlying the periosteum. Also bone marrow contained substance P and CGRP immunoreactive nerves in normal bone, whereas the hypercellular bone marrow of arthritic rats showed a decrease in the density of substance P and CGRP containing fibers. Epiphysis had a dense innervation compared to diaphysis. In contrast to large erosions, small peripheral erosions contained some CGRP immunoreactive fibers, perhaps as a sign of attempts of reactive repair. Our results suggest a local delivery system of potent peptide regulatory factors in bone, a system also affected by the pathophysiology of arthritis.
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PMID:Innervation of bone from healthy and arthritic rats by substance P and calcitonin gene related peptide containing sensory fibers. 138 42

The influence of mechanical stimulation by intermittent compressive force (ICF) of physiologic magnitude on osteoclastic bone resorption was investigated in cultures of fetal mouse cartilaginous long bones. Exposure to ICF resulted in a significant decrease in mineral resorption, as indicated by the decreased release of 45Ca and a decreased number of osteoclasts in the diaphysis. Conditioned medium (CM) from ICF-exposed periosteum-free cultures (ICF-CM), but not from control cultures (Co-CM), inhibited mineral resorption in fresh bones cultured under control conditions. Co-CM increased, but ICF-CM decreased, the number of tartrate-resistant acid phosphatase-positive cells in 7-day bone marrow cultures. Direct exposure of bone marrow cultures to ICF yielded the same results. Thus, osteoclastic bone resorption in cartilaginous long bones is inhibited by ICF in vitro. A soluble factor(s) acting on tartrate-resistant acid phosphatase-positive, osteoclast precursor-like cells seems to play a role in this effect.
Arthritis Rheum 1990 Jan
PMID:Inhibition of osteoclastic bone resorption by mechanical stimulation in vitro. 230 69

The immunohistology of the synovium-cartilage junction was studied in 8 normal human knees, using monoclonal antibodies. In all joints at the junction with synovium, a vascular, wedge-shaped tongue of tissue was found to cover the cartilage surface. This marginal tissue overlying cartilage was in continuity with and was immunohistochemically similar to the adjacent synovial tissue, and contained cells possessing class II HLA antigens and antigens present on macrophages and type B synoviocytes. Periosteal tissue adjacent to the synovium-cartilage junction contained not only macrophages and other class II-positive cells, but also cells and matrix that stained with monoclonal antibodies specific for articular cartilage (keratan sulfate and type II collagen). This study demonstrates the presence of immunocompetent cells in tissue overlying the cartilage surface and adjacent to bone in normal human joints. It is likely that pannus in chronic inflammatory rheumatic disease develops by the recruitment of inflammatory cells augmenting this normal marginal tissue. Furthermore, overgrowth of tissue onto the cartilage surface may not be necessary in the pathogenesis of joint destruction in rheumatoid arthritis. In addition, our findings suggest that cells in the periosteum, rather than those in the marginal synovium, may be involved in attempted "repair" mechanisms, such as osteophyte formation.
Arthritis Rheum 1990 Aug
PMID:The synovium-cartilage junction of the normal human knee. Implications for joint destruction and repair. 239 Jan 22

Roentgenological analysis of the anterior chest wall was performed in twenty six patients with sternocostoclavicular hyperostosis. Initial hyperostotic change was seen at the first costosternal junction with ventral protrusion. Hyperostosis gradually developed around the first ribs, and irregular hyperostotic changes were also seen along the costoclavicular ligaments. Even in the final stage, however, sternoclavicular joint spaces were well preserved. These findings suggest that sternocostoclavicular hyperostosis is a disorder initiated around the costal cartilage including the periosteum and perichondrium, and that arthritis is not a condition stemming from that disorder.
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PMID:[Roentgenological analysis of sternocostoclavicular hyperostosis by computed tomography]. 278 44

The effects of joint inflammation on bone marrow and periarticular bone were studied in mice using antigen-induced arthritis and zymosan-induced arthritis as models for an immune and a non-immune-mediated chronic inflammation. To allow for a comparison of the two types of arthritis care was taken to induce comparable degrees of inflammation as evaluated with 99mTechnetium uptake and histology. The antigen-induced arthritis caused a significant suppression of the mitotic activity in the bone marrow close to the inflammatory focus during the first days of arthritis. The zymosan-induced arthritis did not produce alterations of the bone marrow activity. Both types of arthritis were able to induce long-lasting and irreversible damage to cartilaginous and bony structures. Apposition of bone was observed in both types of arthritis although much earlier in the antigen-induced arthritis. The apposition of bone was found to emerge largely from the periosteum and not from the epiphyseal plates, as shown by 125I-deoxyuridine autoradiography. Qualitative and quantitative differences suggest that joint inflammation which is immunologically mediated, results in more severe (peri)articular tissue damage than a non-immunological arthritis.
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PMID:Effects of experimental joint inflammation on bone marrow and periarticular bone. A study of two types of arthritis, using variable degrees of inflammation. 299 70

The influence of antigen-induced joint inflammation on periarticular structures was studied in mice on histological sections of whole knee joints prepared at various intervals after arthritis induction. The inflammatory process in the synovial membrane and fluid was associated with alterations in periarticular tissues from the very beginning of inflammation. Muscles nearby the joint became intensely infiltrated by (polymorphonuclear) leucocytes by apparent spreading of the infiltrate out of the synovial tissue into the surrounding muscles. An early destructive effect was found in the bony structures adjacent to the joint leading to erosive changes. The fibrous capsule showed fibroblast proliferation resulting in thickening of the capsule, whereas proliferative changes in the periosteum ultimately resulted in new bone formation. Changes in the fibrous capsule as well as in the periosteum were most pronounced at the sites of severe inflammation and at the sites of attachment of the capsule to the bone, suggesting a role of both the inflammatory process and biomechanical forces in the expression of tissue proliferation. These data indicate that arthritis may profoundly influence periarticular tissues. Whether this results in inflammatory, in proliferative or in destructive changes seems to depend on the structure and the location of the involved tissue.
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PMID:Sequential alterations of periarticular structures in antigen-induced arthritis in mice. Histological observations on fibrous capsule, ligaments, bone and muscles, using whole joint sections. 688 78

A synthetic adjuvant, N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP), induced severe polyarthritis in euthymic rnu/+ rats. The rnu/+ rats were the most susceptible to MDP-induced arthritis among various rat strains tested, whereas congenitally athymic nude rats (rnu/rnu), males or females, did not develop the disease. This disease was clinically and histologically indistinguishable from classic adjuvant-induced arthritis in terms of clinical course, clinical signs, and histologic features such as (1) an initial acute exudative reaction observed primarily in stroma of the synovial membrane, periarticular tissue, about the tendons, tendon sheath, along the periosteum, between muscle bundles and in the subcutaneous tissue; (2) hypertrophy of the synovial villi, hyperplasia of the synovial lining cells; (3) the very active periosteal new bone formation; and (4) granulation tissue growth either in the articular tissues or in liver, lymph nodes, and capsule of the spleen. Thus, it is postulated that MDP-induced arthritis is basically the same disease as classic adjuvant-induced arthritis. The thymus may play an important role in promoting the development of the disease, possibly through some immune mechanisms to undetermined antigen(s). We believe that nonimmune mechanisms may also be involved in some part of acute and chronic inflammatory reactions to MDP molecules. This new model of MDP-induced arthritis will be a very useful tool to elucidate the underlying mechanisms of adjuvant-induced arthritis.
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PMID:New model of a synthetic adjuvant, N-acetylmuramyl-L-alanyl-D-isoglutamine- induced arthritis: clinical and histologic studies in athymic nude and euthymic rats. 708 95

In the mouse, arthritis was induced by a single sub-patellar intraarticular injection of bacterial collagenase. This procedure induces also patellar malalignment. A rich innervation of thin varicose calcitonin gene-related peptide (CGRP) and substance P (SP) immunoreactive fibers was found in the joint capsule, in the periosteum of the patella, in the synovial tissues at the lateral border of the patella, in the femoral groove, and in the subchondral bone of the patella and femur. Moreover, fibers were found in plica tissues between the quadriceps and patellar tendon, and the femoral groove. After the collagenase treatment, the general innervation pattern was comparable to that of the controls, but CGRP and SP innervation was no longer detectable with the antibodies in the plica tissues, and was to a lesser extent detectable in the fat pad of the patella, in the lateral borders of the patella and in the proliferated synovial tissues. Signs of degenerated axonal profiles were observed in these locations with a polyclonal antibody to the growth-associated protein GAP-43/B-50. At all the other peripheral locations, such as the muscles, the GAP-43/B-50 distribution was normal.
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PMID:Innervation of the patella. An immunohistochemical study in mice. 751 3

Homozygous mev mice are first identified at the age of 3-4 days by focal depigmentation of the skin, followed by patchy absence of hair and by necrotic lesions on paws, tail and ears. Of particular interest are the inflammatory reactions in the paws of these animals which consist mainly of polymorphonuclear and mononuclear cell infiltration in the subcutaneous tissue extending to the periosteum and joint, resulting in focal destructive arthritis and osteomylitis. These lesions are to some extent reminiscent of an acute form of rheumatoid-like arthritis. Since mev mice are sterile, a limited number of symptomatic offspring can be obtained by cross-breeding their heterozygous siblings which are phenotypically not distinguishable from mice lacking this mutation. In order to produce a sufficient number of diseased animals for performing pharmacological studies, we have established a model by transferring this disease in lethally irradiated, 8- to 10-week-old syngeneic mice which were grafted with mev spleen cells. Such reconstituted recipients develop first inflammatory symptoms of the paws 2 to 3 weeks after cell transfer. The arthritic inflammation finally affects all paws and toes by 30 to 50 days. This procedure increased the number of mev-like mice expressing arthritis, allowing assessment of the effects of standard reference drugs used in the therapy of rheumatoid arthritis (RA). The immunosuppressants cyclosporin and rapamycin and the steroid dexamethasone at therapeutic concentrations exert a strong inhibitory effect on the development of arthritis in this novel model. In contrast, the non-steroidal anti-inflammatory drug phenylbutazone shows only a moderate effect. These results indicate the particular sensitivity of this model for efficacy of potentially new therapeutic but non-cytostatic compounds for clinical use.
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PMID:The viable motheaten (mev) mouse--a new model for arthritis. 784 Aug 51


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