Radiofrequency Energy on Cortical Bone and Soft Tissue: A Pilot Study

Background  

Radiofrequency-generating energy devices have been used clinically in musculoskeletal procedures to provide hemostasis and capsular shrinkage (thermal capsulorrhaphy). However, the dose-effects are not well known.     

Ultrastructural Evaluation of the Effects of Calcitonin on Bone in Thyroparathyroidectomized Rats Administered Vitamin D

Synthetic salmon calcitonin produced ultrastructural alterations in osteoclasts of thyroparathyroidectomized rats administered vitamin D. Osteoclasts in calcitonin-treated rats lacked brush borders and transitional zones, had a uniform peripheral distribution of mitochondria and vesicles and frequently were separated from the bone surface by a layer of osteoblasts. These changes were associated with a significant decrease in serum calcium and phosphorus. Electron microscopic changes were not detected in osteoblasts and osteocytes of rats receiving calcitonin. These findings were interpreted to suggest that the site of action of calcitonin in bone may be principally on osteoclasts.     

The ultrastructural effect of estrogens on bone cells in thyroparathyroidectomized rats.

To determine the direct effect of estrogen on bone cells, female rats were thyroparathyroidectomized and given either 200 microng of estradiol cypionate or placebo treatment for 4 to 30 days. After 8 days, an osteosclerosis of the tibial metaphysis developed in rats treated with estrogens. Osteoblasts in estrogen-treated rats were interpreted ultrastructurally to be less active in bone formation than controls. Osteocytes in estrogen-treated rats were inactive compared to osteocytes in control rats which were continuing the process of bone formation. Osteoclasts were decreased in numbers in rats treated with estrogen; however, the electron microscopic characteristics of osteoclasts did not differ from controls. These cellular changes were associated with a severe hypocalcemia in both estrogen-treated and control rats. Serum phosphorus and urinary hydroxyproline were lowered significantly by the administration of estrogen. It is concluded that metaphyseal osteosclerosis develops in estrogen-treated rats independent of parathyroid hormone and calcitonin. The osteoclerosis is due to an effect of estrogens to reduce osteoclast-numbers and a lesser inhibitory effect on the bone-forming activity of osteoblasts and osteocytes. (Am J Pathol 87:311-322, 1977).     

Ultrastructural development of hyperosteoidosis in 1,25(OH)2D3-treated rats fed high levels of dietary calcium

To evaluate the sequential ultrastructural pathogenesis of the increase in osseous tissue and hyperosteoidosis previously demonstrated in rats administered supraphysiologic doses of 1,25(OH)2D3 and fed high levels of dietary calcium, young adult female rats were placed on a 2.5% calcium and 0.3% phosphorus diet, administered ethanol or 135 ng (5 units) 1,25(OH)2D3 IP daily, and killed after 2, 4, 6, 8, and 10 days. Metaphyseal trabeculae from 1,25(OH)2D3 and placebo-treated rats were examined. Osteoblast hypertrophy characterized by increased cytoplasmic area, abundant rough endoplasmic reticulum, and prominent Golgi apparatus was evident in 1,25(OH)2D3-treated rats at Day 4. These osteoblasts were interpreted to be active in matrix synthesis. Widened osteoid seams were present at Day 6. Osteoblast hypertrophy and widened osteoid seams persisted through Day 10 in 1,25(OH)2D3-treated rats. The unmineralized bone matrix in 1,25(OH)2D3-treated rats contained more numerous cytoplasmic processes from adjacent osteoblasts than did control animals and loosely arranged collagen fibrils, which failed to aggregate in regions adjacent to the osteoid-mineralized bone interface as in placebo-treated rats. Osteoid seams in 1,25(OH)2D3-treated rats contained irregular electron-dense foci, which were often concentrated around embedded cytoplasmic processes. Osteocytic hypertrophy characterized by increased cytoplasmic area, developed rough endoplasmic reticulum, and increased numbers of mitochondria was evident at Day 2 and was sustained through Day 10 in 1,25(OH)2D3-treated rats. Variable-sized aggregates of electron-dense deposits similar to those concentrated around osteoblast cytoplasmic processes were observed in the pericellular space and on and immediately adjacent to the plasma membranes of osteocytes and embedding osteoblasts in 1,25(OH)2D3-treated rats as early as Day 4.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial infarction size and scar dimensions: the influence of activity.

OBJECTIVE: The purpose of this study was to determine myocardial infarct size and scar dimensions in experimentally infarcted rats that were randomly assigned to a moderate, mild, or no exercise condition after infarction. DESIGN: Pretest-posttest control group design (experimental). SUBJECTS: 57 male Harlan Sprague Dawley rats between 62 to 64 days of age and weighing 220 to 290 gm at the onset of the study. OUTCOME MEASURES: Infarction size, scar thickness, thinnest portion of scar. INTERVENTION: Mild exercise versus moderate exercise versus no exercise. RESULTS: No differences were found in infarct size, scar thickness, or thinnest portion of scar among the three groups. CONCLUSION: This study establishes that treadmill exercise, begun after an appropriate period of recovery, does not necessarily increase infarct size or scar thinning in the rat model. Further, animal and human studies are needed to fully explore the benefits and hazards of cardiac rehabilitation or exercise testing before or soon after discharge.     

31P-nuclear magnetic resonance studies of chronic myocardial ischemia in the Yucatan micropig.

In this work, an x-irradiation/high fat/high cholesterol diet-induced atherogenic model was invoked to examine the effects of severe diffuse atherosclerosis on myocardial metabolism in the in vivo porcine heart. This model was studied using spatially localized 31P-nuclear magnetic resonance (NMR) to monitor pH and the levels of inorganic phosphate, phosphomonoesters, creatine phosphate, and adenosine triphosphate as a function of workload transmurally in control swine and in animals suffering from chronic ischemic heart disease. These preliminary studies revealed that the development of severe atherosclerosis and the accompanying chronically diseased state produce changes in high energy phosphates and that increases in rate pressure products result in demonstrable signs of ischemia in the myocardium which span the entire left ventricular wall. Ischemic changes include a global increase in inorganic phosphate and corresponding decreases in creatine phosphate, ATP, and pH. Importantly, changes in intracellular pH are noted with even the slightest increase in workload suggesting that these diseased hearts display elevated glycolytic activity. By challenging these animals with increased cardiac workload, we directly visualize how the chronically compromised heart responds to severe oxygen challenges in a clinically relevant model of this situation.     

Phenotypic changes in T cell populations during the reactivation of tuberculosis in mice

The phenotypic changes of T lymphocytes during the reactivation of latent Mycobacterium tuberculosis infection by activation of the hypothalamic–pituitary–adrenal (HPA) axis was monitored using flow cytometric analysis. Subsets of CD4⁺ and CD8⁺ lymphocyte populations from the lung, spleen and draining lymph nodes of infected mice were identified based on their differential expression of the cell surface antigens CD44 and CD45RB. Latent infection was characterized by an accumulation of both naive, activated and memory CD4 and CD8 T lymphocytes in the lung and mediastinal lymph nodes. No changes were observed in the spleen of mice with latent infection when compared with uninfected mice. Immediately following the activation of the HPA axis, a reduction in all CD4⁺ and CD8⁺ T cells in the lung and mediastinal lymph nodes was observed. This correlated with the reactivation of mycobacterial growth. The decrease was transient for memory and naive CD4 and CD8 T lymphocyte populations in the lung. However, the number of naive CD4 and CD8 T lymphocyte populations in the mediastinal lymph node following reactivation was less than that found in mice with latent infection. These data provide the first characterization of T lymphocyte populations which may be functionally involved in the immunological response to HPA axis-induced reactivation of M. tuberculosis infection.     

Variable hepatocellular vacuolization associated with glycogen in rabbits

Marked variation in hepatocellular vacuolization was present in New Zealand white rabbits used as controls in 28-day and 91-day percutaneous studies conducted at 5 different laboratories. Vacuoles in hepatocytes of alcohol-fixed and formalin-fixed livers contained periodic acid-Schiff (PAS)-positive material which was removed with diastase digestion, indicating the presence of glycogen. The magnitude of hepatocyte vacuolization was subjectively assessed by light microscopy using 5 histologic grades. Quantitative measurements of hepatocyte perimeter and lobule radius for representative liver sections of each histologic grade corroborated the different grades used. Factors associated significantly with the degree of vacuolization were sex (females were affected more severely than males), body weight, relative liver weight, and the laboratory conducting the study. Also apparent were variations in mean severity of hepatocyte vacuolization between studies conducted at the same laboratory, and variation in severity of vacuolization within individual studies. Duration of the study and season had no significant association with the degree of vacuolization. Marked variation of hepatocellular vacuolization due to glycogen accumulation must be recognized when evaluating results of toxicity testing in rabbits.