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Biomedical subjects

C C Capen

Publications and source records attributed to C C Capen.

At least 163 records · Page 9Linked to original sources
PubMed1976

Nutritional osteodystrophy in captive green iguanas (Iguana iguana).

Captive lizards fed a variety of vegetarian and carnivorous diets frequently develop severe nutritional osteodystrophy. Five hatchling iguanas which were captive for 5 months and fed a diet low in calcium and phosphorus developed clinical signs and lesions typical of nutritional osteodystrophy in captive lizards. They had tetany with severe osteoporosis, pathologic fractures, and cartilaginous diaphyseal enlargements of long bones which either were associated with fractures or with intact bones. Hatchling and juvenile iguanas fed a similar diet low in calcium (0.1%) and phosphorus (0.2%) under experimental conditions developed hypocalcemia, tetany, osteoporosis with but adequate in phosphorus (1.1%) developed progressive hypocalcemia and severe osteopososis with pathologic fractures. Control iguanas fed a diet with adequate calcium (2.7%) and phosphours (1.1%) had well mineralized bones with wide cortices and thick metaphyseal trabeculae. Iguanas fed low calcium experimental diets whether low or adequate in phosphorus developed hypocalcemia with compensatory secondary hyperparathyroidism resulting in severe osteodystrophy similar to that reported in captive lizards.

Animal Nutritional Physiological Phenomena↗
PubMed1976

Fine structural changes of bone cells in experimental nutritional osteodystrophy of green iguanas.

Lizards, especially iguanids and varanids, frequently develop nutritional osteodystrophy in captivity, but its pathogenesis is incompletely understood. Green iguanas fed an experimental diet low in calcium (0.2%) and adequate in phosphorus (1.1%) developed severe osteoporosis characterized by flattened inactive osteoblasts, marked resorption of endosteal bone by large multinucleated osteoclasts, and pronounced resorption of cortical bone by osteocytic osteolysis. Iguanas fed an experimental diet low in both calcium (0.1%) and phosphorus (0.2%) developed osteoporosis with osteomalacia characterized by large active osteoblasts overlying wide osteoid seams, marked osteoclastic resorption of endosteal bone, and large osteocytic lacunae which had a prominent layer of osteoid. Osteocytes in iguanas fed the low calcium diets were small in relation to the size of their lacuanae and contained abundant microtubules, microfilaments and mitochondria but a paucity of rough endoplasmic reticulum. Mean ash content of tibias from iguanas fed the low calcium diets was lower, particularly in iguanas that developed severe oseomalacia, than in iguanas fed the control diet (2.7% calcium, 1.1% phosphorus). The ultrastructural evidence suggesting active bone formation, osteoclastic resorption, and osteocytic osteolysis seen in control iguanas was consistent with that of a young growing animal. The results of this investigation demonstrated that experimental iguanas fed diets low in calcium developed hypocalcemia and compensatory hyperparathyroidism resulting in progressive osteoporosis due to osteoclastic and osteocytic osteolysis.

Animals↗
PubMed1976

Model for skeletal resistance to vitamin D in renal failure.

Chronic renal disease in man and animals is associated with disturbances in calcium homeostasis which are resistant to vitamin D-therapy. Partially nephrectomized and intact rats were used to evaluate the effect of uremia on the response of bone to vitamin D. Serum calcium, serum phosphorus and blood urea nitrogen levels were higher in uremic rats than in intact rats, both given vitamin D. Metaphyseal bone in uremic rats was resistant to vitamin D-induced bone resorption; osteoblasts and osteocytes appeared less active ultrastructurally and osteoclass were infrequent. Calcitonin synthesis and release evaluated electron microscopically was greater in uremic rats. It is suggested that the altered response of bone to vitamin D in uremic rats was due in part to elevated serum phosphorus and increased calcitonin release. The present model does not refute experimental and clinical data that metabolism of vitamin D is altered in renal disease. It does, however, emphasize that in chronic renal failure other parameters (phosphorus levels, calcitonin release, uremia) are operating which may influence end organ response to pharmacologic doses of vitamin D. The partially nephrectomized rat may be a useful model for evaluating end-organ resistance to vitamin D in uremia.

Animals↗
PubMed1976

Experimental parturient hypocalcemia in cows following prepartal chemical inhibition of bone resportion.

Cows fed a balanced diet with the required amounts of calcium and phosphorus developed acute hypocalcemia and hypophosphatemia shortly after parturition, even in the presence of the a responsive parathyroid gland, when bone resorption was selectively inhibited by the prepartal administration of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP). When serum total and ionized calcium levels declined below 6.0 and 1.0 mg/100 ml, respectively, cows developed clinical signs similar to naturally occurring parturient paresis. The plasma immunoreactive parathroid hormone levels were similar prepartum, at parturition, and 1 day postpartum in cows administered EHDP as in control cows. Parathyroid chief cells were predominately in the actively synthesizing phase of the secretory cycle with a prominent Golgi apparatus and lamellar arrays of rough endoplasmic reticulum. Many chief cells were degranulated of mature secretory gransules. Calcitonin activity in thyroid extracts, determined by bioassay, and the numbers of secretory granules in thyroid C-cells were similar in both groups of cows. EDTA infusion after 60 days of the experiment demonstrated that the immediately available calcium reserves were reduced in EHDP-treated cows. The serum calcium remained significantly lower and did not return to preinfusion levels by 24 hours. Serum calcium in control cows returned to within the normal range by 6 hours after EDTA infusion. The urinary excretion of hydroxyproline was consistently reduced prepartum and following EDTA infusion in cows receiving EHDP. The experimental induction of parturient of parturient hypocalcemia by the prepartal administration of EHDP provides a valuable model for studies to investigate the mechanisms in bone responsible for the development of severe hypocalcemia that occurs in response to the increased calcium demand imposed by parturition and the initiation of lactation.

Animals↗
PubMed1976

Ultrastructural evaluation of the interaction of glucocorticoids and vitamin D on bone cells in thyroparathyroidectomized rats.

To determine the direct effects of cortisol on bone, rats were thyroparathyroidectomized (T(X)PT(X)), fed a low-calcium diet, and given high (50 mg/kg) or low (8 mg/kg) pharmacologic levels of cortisol with or without excess vitamin D3 (15,000 IU). Rats given vitamin D had osteoblasts and osteocytes interpreted ultrastructurally to be actively engaged in matrix synthesis, mineralization of matrix, and in calcium mobilization. Osteoclasts were numerous on metaphyseal trabeculae and in vascular channels of cortical bone. In T(X)PT(X) rats not given vitamin D, osteoblasts and osteocytes were interpreted to have reduced metabolic activity with minimal evidence of participation in bone formation or resorption. Cortisol at both dose levels failed to alter the electron microscopic appearance of osteoblasts, osteocytes, and osteoclasts with or without vitamin D. Bone turnover indicated by urinary hydroxyproline excretion was unaffected by cortisol treatment. These findings suggest that glucocorticoids have little direct action on bone cells and that their effects on calcium metabolism are probably mediated by an interference in intestinal calcium transport and by secondary hyperparathyroidism.

Animals↗
PubMed1975

Electron microscopic evaluation of bone cells in pigs with experimentally induced Bordetella rhinitis (turbinate osteoporosis).

The development of osseous lesions in the nasal turbinates of pigs with experimentally induced Bordetella rhinitis, occurring 2 to 6 weeks after inoculation with Bordetella bronchiseptica strain B, was evaluated ultrastructurally, and comparisons were made with controls. Progressive degenerative changes were seen in osteoblasts and osteocytes of diseased pigs. These changes included swollen mitochondria, distention of cisternae of endoplasmic reticulum, and lysis of some cells. Bacterial organisms, believed to be B bronchiseptica, were observed in the cytoplasm of osteoblasts and inclose proximity to bone surfaces in diseased pigs. Although osteoclasts occasionally had degenerative changes in the brush border, most osteoclasts wer similar to those of control pigs. Resorption of bone adjacent to degenerative osteoblasts and osteocytes may have contributed to the development of turbinate osteoporosis when combined with the normal cellular resorptive processes. Thes ultrastructural changes were similar to those previously reported in bone cells of the nasal turbinates of pigs with experimentally induced and naturally occurring atrophic rhinitis.

Animals↗
PubMed1974

Effects of parathyroid hormone on bone of thyroparathyroidectomized rats: an ultrastructural and enzymatic study.

Osteoblasts and osteocytes in adult thyroparathyroidectomized (T(x)PT(x)) rats fed a low calcium vitamin D-free diet and given parathyroid (PTH) had ultrastructural evidence of increased activity compared to controls. Osteoblasts in PTH-treated rats had prominent rough endoplasmic reticulum and Golgi apparatuses and large mitochondria. The plasma membranes were extensively convoluted and associated with initial loci of mineralization in osteoid. Osteocytes contained increased rough endoplasmic reticulum, well-developed Golgi apparatuses and large mitochondria. Lacunar walls were roughened, but osteocytic osteolysis was not observed. Osteoclasts were encountered more frequently in PTH-treated rats, but their ultrastructural features were similar to those of controls. Osteoblasts and osteocytes in controls appeared to be inactive cells lining quiescent mineral surfaces. Parathyroid hormone treatment increased serum calcium levels and urinary hydroxyproline excretion, indicating enhanced resorption of bone mineral and matrix. Bone alkaline phosphatase and calcium-adenosine triphosphatase activities were elevated after PTH treatment and may be related to increased calcium transport by bone cells. These findings were interpreted to suggest that PTH mobilizes bone mineral by osteoclasis and increases metabolic activity of the osteocyte-osteoblast pump.

Adenosine Triphosphatases↗
PubMed1974

Ultrastructural evaluation of the effects of vitamin D and uremia on bone in the rat.

Pharmacologic doses of vitamin D given to uremic rats significantly elevated serum calcium levels and produced dramatic ultrastructural changes in osteoblasts and osteocytes compared to placebo-treated uremic rats. Osteocytes in uremic rats given vitamin D were interpreted to have increased metabolic activity, with greater amounts of rough endoplasmic reticulum, and they contained finely granular mineral in pericellular sheaths. Osteoblasts appeared to have reduced activity with lesser amounts of rough endoplasmic reticulum, increased ribosomes and amorphous mineral frequently deposited along plasma membranes compared to uremic rats given placebo treatment. Osteoclasts were seen more frequently in uremic rats given vitamin D. Bone cell response in sham-operated rats administered vitamin D was distinctly different. Osteocytes and osteoblasts appeared to have greater metabolic activity compared to vitamin D-treated uremic rats. Osteocytes in sham-operated rats had increased amounts of rough endoplasmic reticulum and lysosomes. Osteoblasts were larger, with moderate amounts of rough endoplasmic reticulum, and had no mineral deposits along the plasma membranes. Osteoclasts were more numerous in sham-operated rats administered vitamin D. The altered response of bone cells in uremic rats given vitamin D was postulated to be due to the elevated serum phosphorus and greater release of calcitonin from thyroid C cells.

Adenosine Triphosphatases↗
PubMed1974

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.

Animals↗