Biomedical subjects
Publications and source records attributed to D G Gardner.
The occurrence of acinic cell tumors in the minor salivary glands of the oral cavity has, until recently, been considered exceptional. However, three recent papers have documented the details of fifty-two such cases. The purpose of the present article is to record the clinical information and histologic findings in six additional, previously unreported, examples of this tumor in the minor salivary glands.
Three different but probably related central lesions of the jaws have been referred to previously as odontogenic fibromas. They are (1) hyperplastic dental follicles, (2) a fibrous neoplasm having a histologic appearance similar to that of a dental follicle, and (3) a more complicated lesion, illustrated in a WHO publication, consisting of fibrous connective tissue with varying amounts of odontogenic epithelium, dentin, and/or material resembling cementum. The terms simple odontogenic fibroma and odontogenic fibroma (WHO type) are proposed, respectively, for lesions 2 and 3 above. Some examples of lesion 3 may be confused histologically with the calcifying epithelial odontogenic tumor. More information is required on the biologic behavior of both 1 and 2. A central fibroma of the jaws should be considered a desmoplastic fibroma if it does not appear to have arisen from the odontogenic apparatus and is not a neurofibroma.
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To investigate further the mechanism of dopamine (DA)-stimulated and parathyroid hormone (PTH) secretion, we have identified and studied DA-sensitive adenylate cyclase in a particulate preparation of osmotically lysed dispersed bovine parathyroid cells. Adenylate cyclase was responsive to DA at concentrations as low as 0.3 microM, and the maximal stimulation in the presence of GTP was 2- to 4-fold that of activity with GTP alone. (-)Propranolol (1 microM) abolished the stimulation by (-)isoproterenol but did not inhibit the DA-stimulated adenylate cyclase, whereas alpha-flupenthixol (1 microM) inhibited DA stimulation but not that of (-)isoproterenol. The dopaminergic agonists epinine and 6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene were nearly as effective as DA in stimulating the enzyme, while apomorphine displayed partial agonist activity. The dopaminergic antagonists chlorpromazine, fluphenazine, and haloperidol inhibited the DA-stimulated adenylate cyclase. There was a close correspondence between the Ka values for DA and the Ki values of the dopaminergic antagonists for particulate adenylate cyclase activity, cellular cAMP accumulation, and PTH release. These results indicate that DA-stimulated cAMP accumulation and PTH release are mediated through specific activation of a DA receptor linked to adenylate cyclase.
We investigated cAMP metabolism during and after a 15-min infusion of parathyroid hormone (PTH) in 7 normals, 13 patients with typical primary hyperparathyroidism (1HPT), and 6 patients with familial hypocalciuric hypercalcemia (FHH). Nephrogenous urinary cAMP excretion rate reached a peak during the first or second 30 min urine collection interval after the start of the PTH infusion in all subjects. cAMP concentration in plasma reached a peak within 5--20 min of the start of the infusion and then decreased with an initial half-time of 15 min. The peak value of nephrogenous urinary cAMP excretion rate was lower in the group with 1HPT than in the group with FHH or in normals (119 vs, 275 vs. 204 nmol/100 ml glomerular filtrate; P less than 0.0 5 for both comparisons). Similarly, the peak value of plasma cAMP concentration was less in 1HPT subjects than in FHH patients or in normals (11.1 vs. 17.1 vs. 16.6 nmol/100 ml, respectively; P less than 0.05 for both comparisons). For purposes of diagnostic classification, the two hypercalcemia groups could be more completely separated by the values of either the renal calcium to creatinine clearance ratio or the plasma PTH concentration than by the values of inidices of cAMP response to PTH. The differences in cAMP response to PTH between FHH and 1HPT patients could be secondary to differences in circulating PTH concentrations (these are lower in subjects with FHH) or could reflect a renal lesion more closely related to the underlying etiology of FHH.
Freshly dispersed cells were employed to study the effects of various prostaglandins (PGs) on cAMP accumulation and parathyroid hormone release in abnormal human parathyroid tissue. PGE1 and PGE2 effected dramatic increases in intracellular cAMP accumulation over a concentration range of 10(-6)-10(-4) M; the relative effectiveness of these agents varied among different preparations. PGF2 alpha caused a smaller stimulation of cAMP accumulation, and PGF1 alpha was generally without effect. In contrast with the effect previously described in the bovine parathyroid cell system, PGF2 alpha did not suppress agonist-stimulated cAMP accumulation. Both PGE1 and PGE2 enhanced cellular release of parathyroid hormone, with dose-response characteristics similar to those seen with cAMP. In addition, both agents led to a significant stimulation of adenylate cyclase activity in a cellular homogenate preparation. Neither indomethacin (10(-5) M) nor naproxen (10(-4) M) altered the calcium suppressibility of the cells, suggesting that endogenous PG production does not play a major role in the calcium-mediated regulation of parathyroid hormone release.
Of 67 patients referred after unsuccessful surgery for presumed primary hyperparathyroidism, six were shown to be members of kindreds with familial hypocalciuric hypercalcemia. This diagnosis had not been recognized in any of the six previosuly. Most of the remaining 61 cases had proven or probable typical primary hyperparathyroidism, and a subgroup of four had hypercalcemia with suppression of the parathyroid glands. Urine calcium excretion expressed as the calcium:creatinine clearance ratio provided an easily measurable and effective index to separate the groups with familial hypocalciuric hypercalcemia, typical primary hyperparathyroidism, and suppressed parathyroids. Thus, at least 9% of patients referred after unsuccessful parathyroidectomy had familial hypocalciuric hypercalcemia. The assessment of urine calcium excretion by indices such as the calcium:creatinine clearance ratio should facilitate recognition of this condition, which responds poorly to standard subtotal parathyroidectomy.
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A series of odontomas was studied by light microscopy, with special emphasis on abnormal enamel in these lesions. The findings were compared to those in amelogenesis imperfecta and in other conditions in which abnormal enamel is found. It was concluded that dysplastic enamel exhibits a number of appearances which are described in this article. A strongly basophilic laminated material was also found, often covering prismatic enamel, but it did not itself appear to be a form of enamel; its identity is not clear. Odontomas, being readily available, offer a good opportunity to study dysplastic enamel.
Dental casts of fourteen cases of Rubinstein-Taybi syndrome (RTS) were studied. Two exhibited talon cusps, a dental anomaly which is rare in the normal population. Three others exhibited prominent cingula, which were interpreted as representing a tendency toward talon cusp formation. While additional cases should be examined for this anomaly to determine its frequency in RTS, the presence of talon cusps in a suspected case supports that diagnosis. Teeth exhibiting talon cusps are especially prone to caries and often require early treatment if they are to be retained.
Considerable effort has been made in the past to describe the morphologic changes in dentin which characterize various developmental disturbances of teeth. However, there appears to be no previous attempt to describe the spectrum of changes which may be exhibited by abnormal dentin. This paper presents a classification of dysplastic forms of dentin with definitions and illustrations of each abnormality. The classification was derived from reviewing the literature and from a study of 82 odontomas, examples of specific developmental disorders of dentin, regional odontodysplasia, and systemic conditions affecting dentin.
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Sodium nitroprusside effected a significant reduction in intracellular cAMP accumulation and parathyroid hormone release in dispersed bovine parathyroid cells. The inhibition was apparent at 3 x 10-4 M and maximal at 10-2 M nitroprusside. The effect was rapid and reversible and could be demonstrated in both the presence and absence of stimulating agonists [i.e. (-)isoproterenol, dopamine, and cholera toxin]. The inhibition was additive with that previously described for alpha-adrenergic agonists and prostaglandin F2 alpha and was not affected by phentolamine, suggesting that nitroprusside does not act through the inhibitory receptors previously described in this system. The nitroprusside effect on cAMP accumulation and parathyroid hormone release was present at virtually all concentrations of extracellular calcium tested; 2mM EGTA failed to prevent the inhibition. While extracellular calcium may play some role in this inhibition, it is not required for demonstration of the effect.
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