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Biomedical subjects

D G Gardner

Publications and source records attributed to D G Gardner.

At least 19 recordsLinked to original sources
PubMed1979

Ameloblastic change.

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Abnormalities, Multiple↗
PubMed1979

Dysplastic enamel in odontomas.

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 Enamel↗
PubMed1979

Talon cusps: a dental anomaly in the Rubinstein-Taybi syndrome.

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.

Abnormalities, Multiple↗
PubMed1979

A classification of dysplastic forms of dentin.

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.

Dentin↗
PubMed1979

Inhibition of adenosine 3',5'-monophosphate accumulation and parathyroid hormone release by sodium nitroprusside.

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.

Animals↗
PubMed1978

The concept of hamartomas: its relevance to the pathogenesis of odontogenic lesions.

The term hamartoma should be applied only to tumorlike lesions which arise during development of the organ or tissue in question and which are apparently not neoplastic; it should not be used instead of benign tumor. A hamartoma is composed on an abnormal mixture of tissues native to the part, with an excess of one or more of these tissues. The relevance of the concept of hamartomas in the pathogenesis of odontogenic lesions is discussed briefly.

Hamartoma↗
PubMed1978

Effect of gastrointestinal hormones on isolated bovine parathyroid cells.

The effects of gastrointestinal hormones on cAMP accumulation and parathyroid hormone (PTH) release were investigated in dispersed bovine parathyroid cells. Secretin (10 (-7) M) caused a 4- to 6-fold increase in cAMP accumulation, while glucagon, vasoactive intestinal peptide, and gastrin caused little if any stimulation. Cholecystokinin caused a 2- to 3-fold increase in cAMP accumulation at 10(-6) M, but this effect may be related to contamination with endogenous secretin since synthetic cholecystokinin octapeptide had no effect. Maximal intracellular cAMP accumulation due to 10(-7) M secretin was reached within 5 min and returned to control over the next 30-60 min, concomitant with a progressive rise in extracellular cyclic nucleotide. cAMP accumulation was half-maximally stimulated by 5 x 10(-9) to 1 x 10(-8) M secretin and was unaffected by alpha- or beta-adrenergic or dopaminergic blockers. Parallel effects were noted on PTH release : 10(-8) M secretin caused a 20-50% increment in PTH release at 15 min which persisted for up to 2 h; PTH release was stimulated half-maximally by approximately 6--8 x 10(-9) m secretin. The specificity of the observed results for secretin and the lack of effect of adrenergic antagonists suggest the presence of a receptor for secretin on dispersed bovine parathyroid cells. These results also suggest the possibility that secretin may modulate parathyroid function in vivo in the cow.

Animals↗