PubMed · 365896
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R A Stockwell. 1978. Chondrocytes.. https://pubmed.ncbi.nlm.nih.gov/365896/
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Recent work by a number of investigators has demonstrated that the process of bone matrix formation and mineralization is under the influence of growth factors and cytokines present in the local environment. Utilizing primary and established osteoblast cell culture systems, these studies have examined the regulation of bone matrix protein synthesis and deposition into the extracellular matrix (ECM) and subsequent mineralization. In previous studies, we have utilized the human osteoblastic cell line, HOS TE85, to study the effects of Tumor Necrosis Factor-alpha (TNF-alpha) on the regulation of matrix proteins and proteolytic function in monolayer cultures as well as during the development and calcification of ECM formed by HOS TE85 cells during extended culture. Our studies demonstrate that TNF-alpha inhibited formation and mineralization of nodules. In the study reported here, we evaluated the ultrastructural morphology of the cell-matrix complex formed by HOS TE85 cells in the presence and absence of TNF-alpha at selected time points during the matrix development process utilizing both transmission electron microscopy and light microscopy. In the presence of TNF-alpha, the cell-matrix complex does not develop normally, with a lack of organization and mineralization, when compared to untreated cells. The lack of mineralization appears to result from the lack of normal collagen fibril deposition and formation of an appropriate ECM essential for the mineralization process. These results support our previous observations that TNF-alpha inhibits HOS TE85 cells from forming a mineralizing ECM by inhibiting incorporation of collagen into the ECM and inducing the synthesis of proteolytic enzymes capable of degrading collagen in the ECM.
Acidic phospholipids, complexed with calcium and inorganic phosphate, are components of extracellular matrix vesicles. Both the complexed acidic phospholipids and matrix vesicles have previously been shown to serve as hydroxyapatite (HA) nucleators in solution and when implanted in a muscle pouch. The present study supplies evidence that complexed acidic phospholipids can persist in mineralizing tissues both because of their affinity for HA and because of their resistance to hydrolysis by phospholipase A2. Calcium-phosphatidylserine-phosphate complex (CPLX-PS) synthesized with 14C-labeled phosphatidylserine (PS) was used to measure CPLX-PS affinity for HA using a Langmuir adsorption isotherm model. The affinity was shown to be higher and more specific than that of PS itself (K = 8.66 ml/mumol; N, the number of binding sites = 20.4 mumol/m2 as compared with previously reported values for PS of K = 3.33 ml/mumol, and N = 4.87 mumol/m2). Incorporated into synthetic liposomes and incubated in a calcium phosphate solution in which mineralization is induced by an ionophore, CPLX-PS showed behavior distinct from free PS. As previously reported, PS in these liposomes totally blocked HA formation. On the other hand, CPLX-PS in similar concentrations had a varied response, having no effect, slightly inhibiting, or actually promoting HA formation. CPLX-PS was also shown to be a poorer substrate for phospholipase A2 than PS, with Km = 4.63 mM for CPLX-PS and Km = 0.27 mM for PS; and Vmax = 0.029 ml/minute for CPLX-PS and Vmax = 0.066 ml/minute for PS. These data explain how complexed acidic phospholipids may persist in the growth plate and facilitate initial mineral deposition.
Calcified concretions including typical laminated psammoma bodies can be detected on routine hematoxylin-eosin (H&E) examination of fetal and neonatal anterior pituitary glands. This finding has seldom been reported in the literature and, to the authors' knowledge, no ultrastructural examinations of fetal or neonatal pituitary calcifications have been reported to date. In this study, histological sections of anterior pituitary glands from 200 fetuses and infants ranging in age from 15 weeks of gestation to 1 year of life revealed calcified concretions in all the cases up to 1 month of life. They decreased in incidence postnatally and were not found after 6 months of age. Most were round to ovoid, basophilic or eosinophilic, often laminated, and measured between 5 and 30 microm in diameter. Immunohistochemical stains showed that the calcifications followed no particular pattern of distribution among the most prevalent pituitary cell types. Ultrastructural examination revealed small single or multiple intracellular calcified deposits, and larger, sometimes laminated, extracellular calcifications, suggesting an intracellular origin for the concretions with cell death occurring concomitant with their formation. This phenomenon, which to some extent resembles the formation of psammoma bodies in certain tumors, seems to represent a distinctive morphological type of developmental cell death. Apoptosis, a more common form of developmental cell death, was also found in some of the sections. Pathologists should be aware of the fact that calcified concretions represent a normal finding in the anterior pituitary gland of fetuses and young infants. Their mere presence in cases of fetal or perinatal demise with no other pertinent findings should not be attributed to intrauterine viral infections or ischemic-anoxic events.