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Biomedical subjects

I Gera

Publications and source records attributed to I Gera.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Importance of periodic follow up of periodontal diseases for the maintenance of periodontal health and the longevity of dental restoration].

The major objective of the author's investigation was to determine if the progression of attachment loss, the recurrence of active phase of periodontitis and development of new carious lesions can be controlled and prevented in individuals with prior history of aggressive periodontitis provided full mouth reconstruction and maintained at a proper level of oral hygiene. The results of a group on regular periodontal recall program were compared with the five years dental and periodontal findings on a matched group of patients having not been on regular maintenance program. The well maintained group of patients' annual recall data did not vary markedly. In five years basically the same amount of attachment apparatus was maintained. The reexamination of the non recall group at the end of the fifth year shoved a total deterioration of dentition due to the progression of periodontal disease and attachment loss. Especially those of rapidly progressing periodontitis cases shoved 70 to 100% attachment loss. This comparative study attempted to outline the insufficiency of our former dental philosophy of patient management and follow up. Authors emphasize the importance of the follow up, and maintenance of a very high level.

Adult↗
PubMed1990

[The significance of the styloid process syndrome in the differential diagnosis of temporomandibular dysfunction].

Two cases are reported on, both patients came to the clinic on the suspicion of temporo mandibular joint disfunction. Their complaints was caused by overdeveloped processus styloideus. After surgical removal of the processus styloideus the complaints ceased. In cases of seemingly temporo mandibular joint disfunction not improving on conventional treatment the possibility of the processus styloideus syndroma has to be considered.

Adult↗
PubMed1988

1,25 dihydroxyvitamin D3 alone or in combination with parathyroid hormone does not increase bone mass in young rats.

Parathyroid hormone (PTH) alone is known to increase bone mass, but clinical studies of osteoporotic men suggest that when 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) is given in combination with PTH, the effect on bone growth is enhanced. To determine if 1,25(OH)2D3 alone would stimulate bone growth, young male rats were given daily subcutaneous injections of either vehicle or 2.5, 5, 10, or 20 ng 1,25(OH)2D3 per 100 g body weight for 30 days. To determine if 1,25(OH)2D3 would augment the PTH anabolic response, rats were given daily subcutaneous injections of either vehicle for 12 days; or 4 micrograms/100 g hPTH alone or in combination with 5 ng/100 g 1,25(OH)2D3; or 8 micrograms/100 g hPTH alone or in combination with 5 ng/100 g 1,25(OH)2D3. Calcium (Ca), dry weight (DW), and hydroxyproline (Hyp) of the distal femur; the rate of mineralization in the metaphysis of the proximal tibia; and serum calcium and phosphate were measured. Low normocalcemic doses of 1,25(OH)2D3 did not significantly stimulate bone growth. 1,25(OH)2D3 did not augment the PTH-stimulated anabolic effect in young male rats. Low doses (2.5 and 5 ng) of 1,25(OH)2D3 were not hypercalcemic, and there was no increase in total bone calcium or dry weight although the 5 ng dose increased trabecular bone calcium. 1,25(OH)2D3 at 10 and 20 ng increased trabecular bone DW and Hyp, but mineralization was impaired and rats were hypercalcemic. 1,25(OH)2D3 in combination with PTH did not augment the PTH stimulation of bone growth as trabecular and cortical bone Ca, DW, and HYP were not increased in rats given both hPTH and 1,25(OH)2D3 compared with values for rats treated with hPTH alone.

Animals↗
PubMed1988

Human parathyroid hormone-(1-34) increases bone mass in ovariectomized and orchidectomized rats.

In intact growing rats, intermittent administration of low doses of PTH increases bone mass. As gonadal hormones are considered to be essential for normal bone growth, the anabolic effect of PTH may be mediated or modified by these hormones. The objective of this research was to determine if the anabolic effect of PTH would be altered in female ovariectomized (OVX) and male orchidectomized (ORCHX) rats. Two weeks after ovariectomy, orchidectomy, or sham operations, 5-week-old rats (eight per group) were given daily sc injections of human PTH (1-34) (8 micrograms/100 g) or vehicle. After 12 days of treatment, all rats were killed; castration was confirmed, and sera, femurs, tibias, and kidneys were collected. Calcium (Ca) and dry weight (DW) of trabecular and cortical bone of distal half-femurs were measured. Female OVX rats were osteopenic compared to their sham-operated controls, as the bone mass of distal femurs decreased while body weight increased. In PTH-treated females, total bone Ca and DW per 100 g BW increased significantly by 16% and 21%, respectively, in sham-operated rats and by 21% and 25%, respectively, in OVX rats compared to the appropriate control values. ORCHX rats were also osteopenic, as the bone mass of distal femurs was significantly decreased compared to that in sham-operated males. However, as body weight also decreased, the bone mass per unit BW was not altered. In PTH-treated males, total bone Ca and DW per 100 g BW increased significantly by 34% and 25%, respectively, in sham-operated rats by 32% and 29%, respectively, in ORCHX rats compared to their appropriate control values. Serum Ca, creatinine, and alkaline phosphatase levels were normal and comparable in all rats. We conclude that PTH increased bone mass in control, OVX, and ORCHX rats, and the anabolic response to PTH is not dependent on gonadal hormones.

Alkaline Phosphatase↗
PubMed1987

Indomethacin does not inhibit the anabolic effect of parathyroid hormone on the long bones of rats.

Chronic administration of parathyroid hormone, hPTH 1-34, increased bone mass in normocalcemic, young rats. Since PTH can stimulate prostaglandin E2 (PGE2) production in bone in vitro, and since PGE2 can stimulate bone formation, the anabolic effect of PTH could be mediated by PGE2. To test this hypothesis, experiments were done to determine if indomethacin, which blocks endogenous PG production, would inhibit the anabolic response of bone to PTH. In the first experiment, male Sprague-Dawley rats, 70-100 g, in groups of five, were treated for 12 days with either hPTH 1-34, 8 micrograms/100g/day; PTH vehicle; indomethacin, 2 mg/kg/day; or a combination of PTH and indomethacin. In the second experiment, groups of 6 rats each were given vehicle or hPTH 1-34, 8 micrograms/100g/day, in combination with indomethacin, 0, 1, 2, or 4 mg/kg/day. Subcutaneous injections of PTH wee given once daily and indomethacin was given orally in divided doses, twice a day. Rats were killed on day 12 in both experiments; their sera were analyzed and the trabecular and cortical bone of distal femurs processed to determine calcium (Ca) and hydroxyproline content and dry weight. PTH and indomethacin had no significant effect on serum Ca, phosphate, alkaline phosphatase, urea nitrogen and creatinine, or systemic and long-bone linear growth. In rats treated with PTH alone or in combination with indomethacin, bone Ca of distal femurs increased by 28-44%; dry weight by 29-41%, and hydroxyproline by 17-45%. Indomethacin alone had no effect on bone growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Human parathyroid hormone (1-34) and salmon calcitonin do not reverse impaired mineralization produced by high doses of 1,25 dihydroxyvitamin D3.

We have reported recently that pharmacologic doses of 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) stimulated bone matrix formation but impaired mineralization. The objective of this study was to determine if parathyroid hormone (hPTH 1-34) or calcitonin (sCT) would mineralize the osteoid induced by 1,25(OH)2D3 in rat long bones. In one experiment, male Sprague-Dawley rats were given daily subcutaneous injections of vehicle: 8 micrograms hPTH(1-34); 125 ng 1,25(OH)2D3; or both 8 micrograms hPTH and 125 ng 1,25(OH)2D3 per 100 g body weight for 12 days. In a second experiment, rats received daily injections of vehicle: 2 U sCT; 125 ng 1,25(OH)2D3; or both 2 U sCT and 125 ng 1,25(OH)2D3 per 100 g body weight for 18 days. Calcium (Ca), hydroxyproline (Hyp), and dry weight (DW) of the distal femur and serum calcium, phosphate, and serum bone Gla protein (BGP) were measured. In rats given both 1,25(OH)2D3 and hPTH, total bone DW and Hyp increased (P less than .01) without a corresponding increase in bone Ca so that Ca/Hyp decreased 47% (P less than .01) from control and remained comparable to values for rats treated with 1,25(OH)2D3 alone. In rats treated with both 1,25(OH)2D3 and sCT, total bone DW and Hyp increased while Ca decreased so that Ca/Hyp decreased 38% from control (P less than .05), and remained comparable to values for rats treated with 1,25(OH)2D3 alone. These results indicate that hPTH or sCT, given by intermittent injection to rats for 12 or 18 days respectively, failed to mineralize the osteoid induced by high doses of 1,25(OH)2D3.

Animals↗