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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent changes in lifestyle have considerably reduced the loads that joints have to bear through occupational stresses. It is now essentially during leisure time that most people use somewhat intensely their locomotive systems, mostly as sustained bouts of physical exercise. The physician is therefore led to examining critically these sports activities and their consequences. One has to be aware of the fact that some sports may bring about an articular overuse, partly through trauma and partly through microtrauma. Nevertheless, when reviewing recent literature on the implied relation between exercise and degenerative joint disease, one is amazed in observing how contradictory the current opinions are. This article intends to be both a review and a synthesis of the various factors which are commonly accepted as playing a role in the etiology of degenerative joint disease consecutive to exercise. We take into account by the same token the well-known advantages of physical activity such as prevention of cardiovascular disease and atherosclerosis, the enhancement of psychic well-being and the delaying of the onset of ageing. Thus, knowing which sports may promote degenerative joint disease under given conditions, the physician will be able to counsel people with an identified proneness to joint disease into undertaking more healthful physical workouts.
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PMID:[Sports and arthrosis]. 225 85

Pathologic calcification usually is initiated by the biologic membranes of mitochondria or matrix vesicles. Mitochondria frequently initiate intracellular calcification. Matrix vesicles, derived from the outer membrane of cells by budding or cell disruption, initiate extracellular calcification in calcific tendonitis, apatite-deposition osteoarthritis, atherosclerosis, cardiac valvular calcification, tympanosclerosis, and other calcific diseases. Matrix vesicles and mitochondria usually initiate calcification through the interaction of phosphatase enzymes with calcium-binding phospholipids, both of which are membrane-bound. Hydroxyapatite (HA) crystals are formed first within the protective microenvironment of the membrane-enclosed microspace. Once formed and exposed to the extracellular fluid, HA crystals can serve as nuclei or templates, thus supporting progressive, autocatalytic mineral crystal proliferation.
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PMID:Mechanisms of pathologic calcification. 284 91

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.
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PMID:A comparative study of platelet reactivity in arthritis. 694 59

A multidisciplinary team examined an Aleutian mummy from the collection of the Peabody Museum of Archeology and Ethnology of Harvard University, Cambridge, Mass. The mummy, dating from the early 18th century, was of a middle-aged woman who had suffered from pulmonary and ear infections, atherosclerosis, pediculosis, and degenerative joint disease. Another finding was anthracosis, common in ancient bodies and related to indoor heating and cooking fires. Skeletal lead was not found, in contrast with the high levels seen in modern persons. No neoplasms were identified, again consistent with the results of previous studies of ancient human remains. Such comparisons of ancient and modern morbidity and mortality provide a historical perspective on the evolution and cause of human disease.
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PMID:The paleopathology of an Aleutian mummy. 703 Feb 68

The objective of the present study was to determine if naturally occurring osteoarthritis of the knee joints that is similar to the condition in humans develops in cynomolgus macaques. Knee joints from 58 young adult (mean age, 7.4 years) female cynomolgus macaques were studied with x-ray densitometry, high-detail radiography, and histology. The animals studied were subjects in a triad designed to examine the effects of the administration of sex steroids on atherosclerosis; except for a control group, the monkeys had been either ovariectomized or treated with sex steroids for 2 years. Therefore, the data were analyzed to determine if these treatments, both of which can influence bone density, affected the severity of osteoarthritis. There was a high prevalence of osteoarthritic lesions, morphologically similar to those seen in humans. Bone changes were more common and severe than cartilage changes and morphologically appeared to precede the cartilage changes. Treatment with testosterone resulted in increased body weight, body mass index, and bone mineral content in the femur and tibia but did not affect the severity of osteoarthritis. These data indicate that naturally occurring osteoarthritis developed in the knee joints of cynomolgus macaques; these animals may be a useful model for the study of osteoarthritis in humans.
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PMID:Osteoarthritis in cynomolgus macaques: a primate model of naturally occurring disease. 820 86

Psychological status, including depressive symptoms, anxiety, and mastery, was measured in a community-based sample of 3,076 persons aged 55 to 85 with various chronic diseases. Strong, linear associations were found between the number of chronic diseases and depressive symptoms and anxiety, indicating that psychological distress among elderly people is more apparent in the presence of (more) diseases. Furthermore, in contrast to general assumptions that mastery is a relatively stable state, our results indicate that mastery is affected by having chronic diseases. The 8 groups of chronically ill patients (with cardiac disease, peripheral atherosclerosis, stroke, diabetes, lung disease, osteoarthritis, rheumatoid arthritis, or cancer) did differ in their associations with psychological distress. Psychological distress is most frequently experienced by patients with osteoarthritis, rheumatoid arthritis, and stroke, whereas diabetic and cardiac patients appear to be the least psychologically distressed. Differences in disease characteristics, such as functional incapacitation and illness controllability, may partly explain these observed psychological differences across diseases.
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PMID:Psychological status among elderly people with chronic diseases: does type of disease play a part? 880 61

Heparan sulfate proteoglycans produced by vascular endothelium may function physiologically to restrain the migration, multiplication, and phenotypic transition of vascular smooth-muscle cells, and to maintain an anticoagulant luminal surface by bonding and activating antithrombin III. Thus, ample production of heparan sulfate proteoglycans may act to prevent atherosclerosis and its thrombotic complications. The ability of exogenous heparin to stimulate synthesis of heparan sulfate proteoglycans by vascular endothelium may be largely responsible for the positive outcomes of most controlled evaluations of low-dose heparin as a long-term therapy for coronary disease. Glucosamine, a biosynthetic precursor of mucopolysaccharides, can substantially enhance mucopolysaccharide production when added to cultured fibroblasts or chondrocytes; the clinical utility of oral glucosamine in osteoarthritis may reflect increased synthesis of cartilage proteoglycans. It is reasonable to speculate that exogenous glucosamine will likewise enhance heparan sulfate proteoglycans production by vascular endothelial cells, and, when administered orally in regimens comparable to those effective in osteoarthritis, will thereby act to retard atherogenesis.
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PMID:Glucosamine may retard atherogenesis by promoting endothelial production of heparan sulfate proteoglycans. 914 Aug 89

Recent research has shown that inserting a gene for the protein component of telomerase into senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then display all the other identifiable characteristics of young, healthy cells. This advance not only suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechanism can be reset, extending the replicative life span of such cells and resulting in markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of malignant transformation. It is now possible to explore the fundamental cellular mechanisms underlying human aging, clarifying the role played by replicative senescence. By implication, we may soon be able to determine the extent to which the major causes of death and disability in aging populations in developed countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia--are attributable to such fundamental mechanisms. If they are amenable to prevention or treatment by alteration of cellular senescence, the clinical implications have few historic precedents.
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PMID:Telomerase and the aging cell: implications for human health. 962 27

Obesity is associated with increased morbidity and mortality. The condition, and central obesity in particular, is linked to a number of disorders including glucose intolerance, insulin resistance, hyperinsulinaemia, hypertension, dyslipidaemia, impaired fibrinolysis, atherosclerosis, gall bladder disease, some cancers and osteoarthritis. Weight loss therefore benefits the individual by reducing health risks and improving the quality of life. A body mass index (BMI) of around 22 kg/m2 is related to a minimal risk of mortality compared with higher BMI values. An extensive review of clinical studies has shown the clear benefits of moderate weight loss (5-10% of baseline body weight). Thus in obese individuals for whom a substantial weight loss is not feasible, moderate weight loss should be encouraged.
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PMID:What are the benefits of moderate weight loss? 979 75

Bone diseases such as osteoporosis and osteoarthritis are regarded as age-associated diseases, and occur in a significantly increasing number of patients, but the underlying mechanisms of these age-associated bone diseases are not yet clear. We have established a transgenic mouse line by an insertion mutation. These mice exhibit many features related to precocious aging. Homozygote mutant mice, which lack expression of the newly identified targeted gene,klotho (kl), exhibit atherosclerosis, emphysema, hypogonadism and calcification of soft tissues, and die within 3-4 months. We describe here the radiological and histological characteristics of the skeletal abnormalities in the bones of the mice with a mutation in the kl gene locus. In heterozygous mice (+/kl), the skeletal patterns and structures remain normal and most features are similar to those in the wild-type, whereas histological examinations of homozygous mice (kl/kl) show abnormal elongation of the trabecular bone(s) in the epiphyses of long bones. As with their long bones, on radiographic examination the mid parts of the vertebral bones of these mice show less radiopacity compared with the wild-type, again resembling human vertebrae of osteoporotic patients. The elongation of the trabecular bones results in high radiopacity on both ends of each of the vertebrae, and in the epiphyses of the long bones. Cancellous bone volume in the epiphyses of the homozygote mice is three times that of the wild-type mice. The kl/kl mice are smaller than the wild-type litter mates and hence the size of their long bones is less than that of the wild-type litter mates. These observations, and the osteopenia in the vertebrae and long bones in these mice, suggest the presence of abnormality in bone metabolism, the elongation of the trabecular bone apparently resulting from the relatively low levels of bone resorption. Therefore, thekl/kl mutant mice could serve as an interesting tool to study the effects of the lack of the product of the new gene,klotho, on bone metabolism.
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PMID:Elongation of the epiphyseal trabecular bone in transgenic mice carrying a klotho gene locus mutation that leads to a syndrome resembling aging. 979 35


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