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 capsaicin (3 microM)-evoked release of the immunoreactive calcitonin gene-related peptide (iCGRP) from dorsal-half slices of the rat lumbar spinal cord was substantially reduced in slices from rats which had undergone dorsal rhizotomy. This suggests that the release is elicited mainly from the nerve terminals of primary afferents. The release was significantly increased in slices from adjuvant arthritic rats compared with those from control rats. This suggests that the amount of iCGRP in a capsaicin-sensitive pool of the nerve terminals of primary afferents is elevated by adjuvant arthritis. Since adjuvant arthritis is known to cause an enhancement of biosynthesis and axonal flow of iCGRP in primary sensory neurons, the present results imply an increased release of iCGRP from the central terminals of the primary afferents in the adjuvant arthritic rat.
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PMID:Capsaicin-induced release of calcitonin gene-related peptide from dorsal horn slices is enhanced in adjuvant arthritic rats. 279 8

Up to 60% of patients with symptomatic Paget's disease develop articular symptoms in its course. Effective therapy may depend on accurate localization of all symptoms and many patients will have an overlap of bone and articular symptoms which may prove impossible to separate. Over the past 10 years there have been major advances in drug therapy for Paget's disease but still the ideal agent is not currently available. Analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) remain the basis of treatment for arthritis and there is no evidence yet that calcitonin or the diphosphonates will inhibit its development. Orthopaedic procedures, especially osteotomy for deformity and joint replacement may be indicated in selected cases.
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PMID:The rheumatology of Paget's disease. 297 46

The effect of bradykinin and desArg9-bradykinin on bone was studied in cultures of calvarial bones taken from 6-7-day-old mice. Bradykinin, at and above a 3-nM concentration, caused a dose-dependent stimulation of bone mineral mobilization and matrix degradation. Bradykinin-stimulated resorption was inhibited by calcitonin, an increased concentration of phosphate in the culture medium, hydrocortisone, dexamethasone, indomethacin, meclofenamic acid, naproxen, and 5, 8, 11, 14-eicosatetraenoic acid. The results suggest that bradykinin stimulates osteoclast-mediated bone resorption by a process that is dependent on endogenous prostaglandin production. The stimulatory effect of bradykinin, but not of parathyroid hormone and prostaglandin E2, was potentiated by the angiotensin-converting enzyme inhibitor, BPP5a. Treatment with carboxypeptidase B did not affect the capacity of the peptide to stimulate 45Ca release. DesArg9-bradykinin (1 mumole/liter) stimulated 45Ca release to the same degree as did bradykinin. Bradykinin (3 microM) did not affect the degradation of cartilage proteoglycans, as assessed by the release of 35S-sulfate from prelabeled calf articular cartilage in organ culture. These findings suggest that generation of bradykinin in inflammatory lesions of rheumatoid arthritis and periodontitis may contribute to the bone resorptive process seen in the joints and alveolar bone; however, bradykinin does not directly activate chondrocytes into a catabolic state.
Arthritis Rheum 1987 May
PMID:Bradykinin, a new potential mediator of inflammation-induced bone resorption. Studies of the effects on mouse calvarial bones and articular cartilage in vitro. 359 36

Fifty patients with Paget's disease of bone were reviewed with regard to the basis of their symptoms and the long-term results of treatment. Twenty-four patients (48%) presented with pain localised within bone, while 17 (34%) presented with symptoms of degenerative joint disease. Three patients presented with bone pain and arthritis and the remaining six with fractures, ataxia, or painless deformity. Symptomatic osteoarthritis of the hip (OA) developed in 25 patients (50%) with approximately half developing radiological changes identical to those of idiopathic OA. Among the other patients those with coxa vara tended to show medial (rather than superior) joint space narrowing and severe Paget's disease on both sides of the joint. Arthritic pain, stiffness, and reduced mobility in other joints (knee, ankle, and wrist) were associated clinically with bone deformity adjacent to the affected joint and radiologically with distorted articular surfaces and narrowed joint spaces; sclerosis, subarticular cyst formation, and osteophytosis were usually absent. Fifteen patients were treated with calcitonin for bone pain alone; all claimed long-term 'good to complete' relief. By contrast, none of the 14 with arthritic symptoms responded to calcitonin when assessed retrospectively. Results of surgical and other medical treatment were analysed. Careful clinical evaluation is a prerequisite for optimal treatment in Paget's disease.
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PMID:Bone and joint symptoms in Paget's disease. 624 Sep 66

The mobilization of calcium from the bone to the extracellular fluid proceeds in parallel with the dissolution of bone matrix, and is subject to the same influences. The role of circulating hormones has been discussed, and the importance of the skeleton as a store of calcium, even though skeletal calcium release is a relatively slow process in maturity. The major circulating hormones stimulating the processes are parathyroid hormone, 1,25-dihydroxyvitamin D3, and epidermal growth factor related substances. These represent three different classes of hormone with respect to their initial mechanisms of action. The most potent known hormonal inhibitor of bone resorption is the peptide, calcitonin, which acts directly upon the osteoclasts to inhibit their activity and generation. Local factors are undoubtedly important in the regulation of bone resorption, especially the prostaglandins. Prostaglandin E2 is the most potent bone resorber of the arachidonic acid metabolites, and is much more likely to be important locally than as a circulating factor especially in disease states such as metastatic bone cancer and arthritis. In understanding the ways in which drugs can influence bone mineral release it is important to appreciate how bone cells interact to resorb mineral and matrix. In this review the view is presented that cells of the osteoblast lineage (perhaps at the stage of osteocytes, or 'lining' cells) are the prime target of the resorbing hormones. Once having been acted upon, they initiate events which result in activation of osteoclasts. If this involves the passage of a message from osteoblast/osteocyte to osteoclast, it will be important to define this in further research.
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PMID:Drug and hormone effects on calcium release from bone. 635 42

Postmenopausal osteoporosis has a multifactorial pathogenesis related to decreases in bone mass, calcium intake, and circulating estrogen levels. Therapy with supplemental calcium, estrogen, fluoride, anabolic steroids, and calcitonin is discussed. Corticosteroid-induced osteopenia is in part related to a decrease in intestinal calcium absorption and therapy with supplemental vitamin D and calcium may favorably alter the outcome. The osteopenia of rheumatoid arthritis appears to be a diffuse process, with increased metabolic bone activity at sites that are remote from the areas of active synovitis.
Semin Arthritis Rheum 1984 May
PMID:Osteopenia in rheumatology practice: pathogenesis and therapy. 637 99

Paget's disease of bone is a process of increased bone remodeling resulting in architecturally abnormal bone that may affect any area of the skeleton. Paget's disease may present with a wide variation in the clinical and radiographic picture. When symptoms arise, they depend on the site and the extent of skeletal involvement. The two major therapeutic agents available for medical treatment are calcitonin and diphosphonate. Surgical intervention in Paget's disease is indicated for (1) selected fractures, (2) severe disabling arthritis, and (3) extreme bowing deformities causing malalignment of weight-bearing joints.
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PMID:Current concepts of Paget's disease of bone. 643 66

A battery of drugs with antirheumatic properties was tested for effects on the progress of osteoarthritis induced by a lateral meniscectomy procedure in knee joint cartilage of rabbits. Oral administration of the potent glucocorticoids, paramethasone acetate or triamcinolone, resulted in dramatic inhibition of cartilage degeneration. Significant protection against development of osteoarthritic lesions was also observed in rabbits treated with pirprofen or CGS 5391B but not with 9 other nonsteroidal antiinflammatory drugs. A marked reduction in joint pathology was also observed in rabbits treated with tribenoside (a glucofuranoside derivative) and with tamoxifen (an anti-estrogen). Slightly protective effects of borderline significance were observed with orgotein (a superoxide dismutase), gold sodium thiomalate, and D-penicillamine. Chloroquine and calcitonin were without effect. Therapeutic effectiveness of drugs in this model of osteoarthritis cannot be explained on the basis of their antiinflammatory properties.
Arthritis Rheum 1983 Sep
PMID:A new model of osteoarthritis in rabbits. II. Evaluation of anti-osteoarthritic effects of selected antirheumatic drugs administered systemically. 668 29

The diagnosis of Paget's disease of bone at its earliest osteolytic phase is difficult and requires radiographs of the highest quality. Calcitonin controls the bone resorption of uncomplicated Paget's disease but does not prevent disuse osteoporosis in normal and pagetic bones. Cessation of treatment leads to a recurrence of the osteolytic phase of the disease in some patients. Retreatment with human calcitonin arrests the bone resorption and permits bony consolidation of resorption clefts.
Arthritis Rheum 1980 Oct
PMID:Radiologic observations on bone resorption in Paget's disease. 677 45

A patient with early Paget's disease of bone was treated for 12 months with calcitonin and 10 months with etidronate. During this time the cortex of each diseased bone showed a progressive 2- to 3-fold increase in thickness. Lytic areas regressed and the new bone appeared radiographically very compact. No bowing deformity developed in 3 years of observation. This form of morphologic evolution differs markedly from those previously reported during treatment. For this patient, treatment was instituted very early during the course of the disease and moderately high doses of vitamin D were given during part of the treatment course. Observation of a larger number of patients will be needed to determine whether these factors actually modified the treatment outcome.
Arthritis Rheum 1981 Dec
PMID:An unusual morphologic evolution of Paget's disease of bone. 679 79


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