Human parathyroid autografts: comparison of function in vivo and in vitro.
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Biomedical subjects
Publications and source records attributed to D G Gardner.
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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.
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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.
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Three indices of circulating parathyroid hormone (PTH) activity were compared between two groups: the first a group of 23 patients from three large kindreds with autosomal dominant hypercalcemia without hypercalciuria [familial hypocalciuric hypercalcemia (FHH)] and the second a group of 64 patients with typical primary hyperparathyroidism (1HPT) manifesting comparable hypercalcemia. The group with 1HPT differed from normal with respect to plasma PTH 1HPT concentration (normal, less 0.2 ng/ml), urinary cAMP excretion per 100 ml glomerular filtrate (U cAMP/GF) (normal, 2.3 x/divided by 0.6 nmol/100 ml glomerular filtrate; mean, x/divided 1 SD), and renal tubular maximum of phosphate transport corrected for glomerular filtration rate (TMP/GFR; normal, 3.4 +/- 0.4 mg/dl; mean, +/- 1 SD). The group with 1HPT also diverged significantly from the group with FHH for all three indices: for PTH, 0.37 x/divided by .48 vs. 0.25 x/divided .46 (P less than 0.05); for UcAMP/GF, 4.3 x/divided by .53 vs. 2.6 x/divided .60 (P less than 0.0005); and for TMP/GFR, 2.0 +/- 0.6 vs. 2.6 +/- 0.7 (P less than 0.01). The between-group differences for all three indices were also significant after adjustment for their variation with serum calcium. However, only the difference in TMP/GFR remained significant after adjustment for covariance attributable to serum calcium concentration, age, and creatinine clearance. The group with FHH differed from normal for TMP/GFR but not for UcAMP/GF. However, analysis of changes in UcAMP/GF and serum calcium concentration around the time of parathyroidectomy in three patients with FHH suggested that the parathyroid glands contributed to the abnormalities of mineral homeostasis in at least one. It was concluded that higher serum concentrations of PTH do not account for the lower renal clearance of calcium and magnesium in FHH calcium concentration, the group with FHH showed indices suggesting lower circulating PTH activity than the group with 1HPT.
Typical features of hereditary vitamin D-dependent (pseudovitamin D-deficient) rickets were observed beginning at ages 20 and 5 months in a brother and sister. Both had calcium malabsorption correctable with high doses of 25-hydroxyvitamin D. During periods of hypocalcemia they both manifested secondary hyperparathyroidism with hypophosphatemia and high serum concentrations of endogenously produced 1,25-dihydroxyvitamin D. In each, normalization of serum calcium concentration and resolution of osteomalacia were obtained with continuous administration of high doses of ergocalciferol or high doses of 1,25-dihydroxycholecalciferol. Chemical features of vitamin D deficiency were corrected in the presence of high circulating concentrations of 1,25-dihydroxyvitamin D2, produced endogenously, or of 1,25-dihydroxyvitamin D3, administered by mouth. Serum concentrations of 25-hydroxyvitamin D2, 25-hydroxyvitamin D3, 24,25-dihydroxyvitamin D, and 1,25-dihydroxyvitamin D were normal in five first degree relatives. We conclude that in these five first degree relatives. We conclude that in these siblings, rickets and osteomalacia resulted from a hereditary decreased sensitivity to 1,25-dihydroxyvitamin D at the intestine and perhaps other vitamin D target tissues.
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The peripheral ameloblastoma and the basal cell carcinoma of the gingiva are probably the same lesion. This article describes the clinical features, natural history, and histopathology of nine acceptable cases published as peripheral ameloblastoma, five lesions published as basal cell carcinoma of the gingiva, and seven unpublished cases of peripheral ameloblastoma. Tissue sections were studied from seven of the cases published as peripheral ameloblastoma, three of the cases published as basal carcinoma, and all the unpublished cases. The peripheral ameloblastoma may exhibit several of the various histologic patterns found in the intraosseous ameloblastoma but has a marked tendency to be acanthomatous. These lesions appear to arise from either remnants of the dental lamina within the gingiva or from the surface epithelium. They are relatively innocuous lesions lacking the persistent invasiveness of intraosseous ameloblastoma. Peripheral ameloblastomas should be excised with a small margin of normal tissue and the surgical site re-examined periodically.
This article describes a patient who exhibited taurodontism, relatively short roots, external resorption of the roots of the anterior teeth, and a marked tendency toward microcephalic dwarfism. This case is similar to that reported previously by Sauk and Delaney.
The amorphous areas, which are gray in sections stained with hematoxylin and eosin and which are a prominent feature in the coronal dentin of the more severely affected cases of regional odontodysplasia, were studied ultrastructurally and with an electron probe and a Vickers microhardnesss tester. The ultrastructural findings confirmed previous histochemical evidence that the amorphous material consists of glycosaminoglycans and represents collagen-free dentinal matrix, that is, ground substance. Phosphoproteins may also present. The ultrastructural examination of nondecalcified material and electron-probe and microhardness tests supported previous microradiographic evidence that the amorphous areas are more heavily mineralized than normal dentin. The boundaries of the amorphous areas were found on ultrastructural examination to be distinct but very irregular.
The calcifications associated with the epithelium of the calcifying odontogenic cyst and odontoma were studied ultrastructurally and found to be of three types: (1) spherical calcifications which form on ghost cells and which therefore are dystrophic, (2) spherical calcifications which appear to be dysplastic enamel, and (3) irregularly shaped, diffuse calcifications which form on a collagenous matrix and appear to by dysplastic dentin or cementum.
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