Effects of lesion size and location on equine articular cartilage repair.
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The mechanisms and completeness of equine articular cartilage repair were studied in ten horses over a nine month period. Large (15 mm square) and small (5 mm square) full-thickness lesions were made in weight bearing and nonweight bearing areas of the radiocarpal, middle carpal and femoropatellar joints. The horses were euthanized in groups of two 1, 2.5, 4, 5 and 9 months later. Gross pathology, microradiography, and histopathology were used to evaluate qualitative aspects of articular repair. Computer assisted microdensitometry of safranin-O stained cartilage sections was used to quantitate cartilage matrix proteoglycan levels. Structural repair had occurred in most small defects at the end of nine months by a combination of matrix flow and extrinsic repair mechanisms. Elaboration of matrix proteoglycans was not complete at this time. Statistically better healing occurred in small weight bearing lesions, compared to large or nonweight bearing lesions. Synovial and perichondrial pannus interfered with healing of osteochondral defects that were adjacent to the cranial rim of the third carpal bone. Clinical and experimental experience suggests that these lesions are unlikely to heal, whereas similar lesions in the radiocarpal and femoropatellar joints had satisfactory outcomes. Observations made in this study support the use of early postoperative ambulation, passive flexion of operated joints, and recuperative periods of up to a year for large cartilage defects. (+info)
Microvascular studies in non-specific inflammatory bowel disease.
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The microvasculature was investigated in the normal bowel and in ulcerative colitis and Crohn's disease. Tissue samples from postoperative colectomy specimens in which the microvasculature had been perfused with barium sulphate suspension were examined. Microradiography was used to study intramural vascular pattern which was abnormal in both disease states. A recently described radiograph fluorescence system was used to estimate barium concentration and hence microvascular volume in tissue samples. Highly significant negative correlations were demonstrated between barium concentration and age in normal bowel (n = 44; r = -0.669; p less than 0.001) and in segmental Crohn's disease (n = 11; r = -0.698; p = 0.017). Barium concentration was significantly reduced (p less than 0.05) in segmental Crohn's disease (n = 11) but remained normal in diffuse Crohn's disease of the colon (n = 6) and ulcerative colitis (n = 7). It is postulated that ischaemia may be a factor in the pathogenesis of segmental Crohn's disease in older patients. (+info)
Microfocal radiography, producing x5 magnified images of the wrist and hands with a high spacial resolution (25 microns) in the film, permitted direct measurement of erosion area and joint space width in patients with rheumatoid arthritis. The magnitude of errors relating to direct measurement, repositioning the wrist and hand on successive x ray visits, repeated identification of erosions and their area calculation were assessed. The coefficients of variation for length and area measurements were 3.7% and 13% respectively, while the change in joint space width and erosion area in five patients over 18 months had average coefficients of variation of 12.7% and 42.0% respectively. The combined errors correspond approximately to the fifth percentile level for the total changes in size of these x ray features. The remaining alterations were due to the disease, which was markedly greater that that attributable to errors of measurement. (+info)
Remodelling of bone and bones: effects of altered mechanical stress on caudal vertebrae.
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Sprague-Dawley rats weighing 50 g were divided into two groups: (i) control, (ii) rats with tails bent in situ incorporating 7, 5 and 3 caudal vertebrae in the loop. Tails were radiographed weekly up to six weeks and a microradiographic and histological study undertaken on selected specimens. Results showed that the bones in the apex of the loop of the bent tail moved through their investing soft tissues towards the outer side of the bend, the joints became V-shaped and in tails bent acutely the epiphyses and metaphyses tilted. By six weeks the bones appeared bent with a thinner straight to convex shaft on the outer side and a thicker, more concave one on the inner side. The changes observed can be explained by taking into account (i) strain within the bone, (ii) altered growth and (iii) the translation of bones through their investing soft tissues. The results are consistent with the supposition that, on application of a continuous moderate stress, tension induces formation and pressure resorption of bone. (+info)
25-Hydroxycholecalciferol. A comparative study in deficiency rickets and different types of resistant rickets.
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The effects of 25-hydroxycholecalciferol were studied in 4 children with deficiency rickets and 22 children with D-resistant rickets, including patients with hereditary hypophosphatemic D-resistant rickets, "pseudo-deficiency" rickets, and rickets secondary to cystinosis or to tyrosinosis. Three protocols were used. (a) 8 days after a single oral dose of 16,000 IU of 25-hydroxycholecalciferol, normalization of all biological parameters was observed in all cases of deficiency rickets. A complete lack of response was observed in the different types of resistant rickets. (b) Under prolonged administration of 2,640 IU/day for 2 months, clinical-biological symptoms and X-ray lesions disappeared, and a catch-up growth pattern was observed in deficiency rickets; no relapse of rickets occurred up to 5 months after therapy was stopped. The same dose had no significant effect in 10 patients with hereditary hypophosphatemic D-resistant rickets. A bone biopsy performed in one case showed the persistence of characteristic lesions. (c) With increasing doses of 25-hydroxycholecalciferol varying from 6,000 to 30,000 IU/day and a follow-up of 6 months up to 2 yr duration, clinical-biological-radiologic recovery and catch-up growht was obtained in all cases of "pseudo-deficiency" rickets. In hypophosphatemic hereditary D-resistant rickets, 5 out of 13 patients' serum concentration of phosphorus reached at least 30 mg/liter, but a catch-up growth pattern was not observed. These results indicate that (a) 25-hydroxycholecalciferol is highly active in deficiency rickets; (b) a defect in the conversion of vitamin D(3) to its active 25-hydroxy metabolite is probably not the metabolic defect in any of the different types of vitamin D-resistant rickets studied. (+info)
Short- and long-term effects of estrogen and synthetic anabolic hormone in postmenopausal osteoporosis.
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In 29 women with postmenopausal osteoporosis, the proportion of total bone surface undergoing resorption or formation was evaluated by microradiography of iliac crest biopsy samples before and after short-term (2(1/2)-4 months) and long-term (26-42 months for estrogen and 9-15 months for anabolic hormone) treatment. After estrogen administration, values for bone-resorbing surfaces decreased, although less prominently after long-term than after short-term therapy. The magnitude of this decrease was positively correlated with the pretreatment value for bone-resorbing surfaces (P < 0.001). When the pretreatment value for bone-resorbing surfaces was used as a covariable, estrogen and anabolic hormone appeared to be equally effective. For bone-forming surfaces, short-term therapy with either hormone had no effect but long-term therapy significantly decreased the values. Serum immunoreactive parathyroid hormone (IPTH) increased significantly after estrogen therapy; the change in IPTH was inversely related to the change in serum calcium (P < 0.001, sign test). We conclude that the primary effect of sex hormones in postmenopausal osteoporosis is to decrease the increased level of bone resorption, perhaps by decreasing the responsiveness of bone to endogenous parathyroid hormone. However, this favorable effect, at least in part, is negated after long-term treatment by a secondary decrease in bone formation. Our data are consistent with the concept that the maximal benefit that can be derived from sex hormone therapy in postmenopausal osteoporosis is arrest or slowing of the progession of bone loss. (+info)
Autofluorescence of bone tissues.
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The phenomenen of autofluorescence of bone is due primarily to the collagen itself rather than to incidental substances adsorbed on to it. Fluorescent microscopy is a convenient method of dating the different microanatomical components of bone, and in this respect the same conclusions can be reached from the study of microradiographs or autofluorescent photographs, which is proof of the intimate relation between the development of matrix and the progression of mineralization. (+info)
Effect of sex hormones on bone in primary osteoporosis.
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The effect of sex hormones on bone tissue was studied in 12 osteoporotic patients. Surfaces of bone undergoing formation and resorption were determined by quantitative microradiography of iliac crest biopsy samples before and after treatment with estrogens in 11 postmenopausal women and with testosterone in one gonadally competent man. Before treatment, bone resorption was greater than normal in all but one patient and bone formation was normal. After treatment, bone resorption decreased to within the normal range in all patients, and bone formation did not change significantly. Biochemical studies showed significant decreases in serum calcium, phosphorus, and alkaline phosphatase levels and in urinary excretion of calcium and hydroxyproline. These changes are believed to be the consequence of the effect of the hormones on bone. The data indicate that the major effect of sex hormones in osteoporosis is an inhibition of bone resorption. (+info)