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At least 19 recordsLinked to original sources
PubMed1976

The influence of immobilization on osteocyte morphology: osteocyte differential count and electron microscopical studies.

Differential counts and electron microscopical studies of osteocytes were performed on rats immobilized by spinal cord severing, plaster cast and ischiatic nerve dissection. In undecalcified ground sections of tibia and femur (100 micron) stained with basic fuchsin, osteocytes were differentiated into small (metabolically inactive) osteocy es enlarged (metabolically activated) osteocytes and empty lacunae. In rats (immobilizedfor' three weeks) with functioning parathyroid glands, but not after parathyroidectomy, the number of activated cells is markedly increased, whereas the number of small osteocytes is reduced. In animals with spinal cord severing the number of empty lacunae is also increased. Electron microscopical studies of undecalcified tibiae taken from rats immobilized for ten days showed a periosteocytic osteolysis with destruction of the lacunar wall, fragmentation of collagen fibres and loss of mineral crystals. The cytoplasmic seams of osteocytes were broadened, mitochondria were enlarged, and the cytoplasma showed vacuoles containing amorphous material which could be found in the pericellular space. Deep invaginations of the cytoplasma and an increase of the cell processes were typical findings. The results of the investigation point to an activation of osteocyte metabolism by immobilization. The osteocytes thus play an important part at the onset of immobilization osteoporosis. Periosteocytic osteolysis can be inhibited by parathyroidectomy. Therefore, the response of osteocytes to endogenous parathyroid hormone must be altered under conditions of immobilization.

Animals↗
PubMed1979

An electron microscopic investigation of human familial bone dysplasia. Inhibition of osteocytic osteolysis and induction of osteocytic formation of elastic fibers following calcitonin treatment.

Familial bone dysplasia with hyperphosphatasemia is characterized by excessive bone resorption early in life with resulting severe skeletal deformity. The disease can be ameliorated by treatment with human calcitonin. We have the studied the ultrastructure of bone from diseased patients before treatment and at intervals during 1 year of treatment with calcitonin. Pretreatment osteoblasts, osteoclasts, and osteocytes exhibited mitochondria which contained vast amounts of dense microcrystal deposits. Osteocytes were also distinguished by minimal organellar development. Osteoclasts were rare. Calcitonin treatment included a progressive development of a more normal bone structure. Intramitochondrial crystal deposits were absent in mitochondria of osteocytes and osteoclasts but were still present in mitochondria of osteoblasts. Surprisingly, the developing bony matrix during calcitonin treatment exhibited large numbers of elastic fibers. These appeared to develop normally in alignment with the surface membrane of osteocytes. Calcitonin treatment caused a proliferation of osteocyte organellar development. It is concluded that familial bone dysplasia is primarily a disease of osteocytes and that osteocytic activity is influenced by calcitonin.

Bone Diseases, Developmental↗
PubMed2026

Genome-wide CRISPR interference screen identifies Clip2 as a novel regulator of osteocyte maturation and morphology.

Osteocytes play critical roles in bone, making them attractive targets for therapeutics aimed at improving bone mass and strength. The genes driving osteocyte maturation and function are not fully understood. Here, we aimed to identify novel genes responsible for osteocyte differentiation and dendrite development by performing a genome-wide CRISPR-interference (CRISPRi) screen in the Ocy454 osteocyte-like cell line. We identify CD61 (integrin β3) as a marker of osteocyte maturation: surface CD61 expression increases during osteocyte maturation, and CD61high cells express higher levels of osteocyte marker genes. We then developed a flow cytometry-based assay to quantify surface CD61 protein levels as a phenotypic endpoint for functional genomic screening. In a genome-wide screen, we identified Clip2, which encodes a microtubule-binding protein, as one of dozens of genes necessary for CD61 expression. Clip2 inhibition decreased surface CD61 expression, reduced expression of osteocyte-specific genes Dmp1 and Sost, and impaired dendrite morphology in vitro. Together, these results highlight the utility of surface CD61 as a marker of osteocyte maturity and identify the role of the microtubule cytoskeleton for osteocyte differentiation, form, and function.

Osteocytes↗
PubMed1979

Studies on the biology of fish bone. III. Ultrastructure of osteogenesis and resorption in osteocytic (cellular) and anosteocytic (acellular) bones.

The comparative ultrastructure of fish bone osteogenesis and resorption induced by scale removal was described in the osteocytic (cellular-boned) Carassius auratus and the anosteocytic (acellular-boned) Tilapia macrocephala. Osteocytes, present in osteocytic bone, were lacking in anosteocytic bone. In osteocytic bone the osteoblast secreted a collagenous preosseous matrix in which it became enmeshed and then was termed a preosteocyte. When the preosseous matrix mineralized, the preosteocyte was termed an osteocyte and was completely surrounded by bone. In anosteocytic bone the osteoblasts receded from the mineralizing front and never became trapped as osteocytes. During resorption, types A and B resorptive cells, present in both bone types, invaded the matrix and demineralized the osseous zone. These cells were characterized by large amounts of granular endoplasmic reticulum and intracellular inclusions containing crystal-like material. Although functionally similar to mammalian osteoclasts, these cells lacked a characteristic ruffled border and were not multinucleated. The osteocytes of cellular bone did not appear to be involved during demineralization.

Animals↗
PubMed1976

Correlation between the structure of the wall of the bone lacuna and the localization of the osteocyte within this lacuna. Electron-microscopic studies.

A correlation between the structure of the wall of the bone lacuna and the localization of the osteocyte within this lacuna was the object of investigation under light and electron microscopes. On the basis of the structural divergences detected, the author distinguished zones A and B in the osteocyte situated in the lacuna. Zone B is characterized by a parallel, compact system of collagen fibrils which form a characteristic ridge in the lacunar wall, a continuous demarcating line bordering this wall, the osteocyte cytoplasm in this part lying far from the lacuna wall and surrounding the nucleus with a narrow band, and the pericellular space which is wide here and containing a large number of mucopolysaccharides. This picture may correspond to the area of temporary non-reactivity of the osteocyte. Zone A is characterized by a loosened and disordered system of collagen fibrils forming the lacunar wall. These fibrils being exposed in this place by nature, the demarcating line bordering the lacunar wall is broken in some places, the osteocyte cytoplasm is considerably concentrated around the nucleus and contains a large number of organelles. It also lies closer to the lacunar wall, which results in a decreased width of the pericellular space and a diminished mucopolysaccharide content in this part of the lacuna. Structural variations in the lacuna wall and its space (zones A and B) observed in the images obtained with a normal bone in the light and electron microscopes show their immediate dependence on the position of the osteocyte in the lacuna, which may be associated with the osteocyte activity. On the other hand, the occurrence of significant changes in a definite zone (zone A) of the lacuna only points to the oriented character of this activity.

Animals↗
PubMed1977

Osteocyte ultrastructure in renal osteodystrophy.

The ultrastructure of the osteocyte has been studied in 80 needle biopsies from the iliac crest of uremic subjects with renal osteodystrophy. Different types of osteocytes were present in the osseous trabeculae. Those recognizable in completely uncalcified osteoid tissue looked like normal osteocytes, even though the matrix was not mineralized. Those present in hypomineralized areas showed enlarged and irregular lacunae when examined under the light microscope; under the electron microscope these osteolytic-like changes were not evident and were found to have been produced by defective calcification of the perilacunar matrix. Osteocytes placed in matrix whose mineralization was normal were often surrounded by a border of crystals protruding side-to-side from the bone matrix into the lacunar space. Other osteocytes were placed in unusually wide lacunae. They showed evidence of osteolytic activity, chiefly consisting of irregularity of the lacunar wall, presence of flocculent, granular and filamentous material in the pericellular space, and calcification of mitochondria. Degenerating and degenerate osteocytes were also recognizable.

Adolescent↗
PubMed1977

The cellular basis of bone turnover and bone loss: a rebuttal of the osteocytic resorption--bone flow theory.

There is now sufficient evidence to conclude that the osteocytic resorption--bone flow theory of bone turnove is untenable. According to this theory bone is resorbed not from the surface by osteoclasts but from within by osteocytes, towards which bone flows through tissue space away from bone forming surfaces. The need to invoke resorption by osteocytes stems from the belief that too few osteoclasts are present to account for normal bone resoption, a belief which reflects unawareness of the enormous capacity of the osteoclast and the rapidity of its advance. The belief that osteocytes resorb substantial amounts of bone rests on invalid conclusions from indirect techniques, various artifacts of specimen processing and unawareness of the microscopic characteristics of woven bone. Osteocytes enlarge their lacunae by resorbing bone only as a prelude to resorption from the surface, the osteocyte and osteoclast working together as a resorbing unit. The belief that bone can flow is incompatible both with the physical properties of bone and with a substantial body of evidence relating to Haversian remodelling; the experimental data purporting to demonstrate such flow can all be explained by conventional concepts of bone turnover.

Animals↗
PubMed1978

Phagocytosis of osteocytes by osteoclasts in femora of two week-old rabbits.

The osteoclast-osteocyte relationship at the endosteal surface of femora of two-week old rabbits was studied. Light microscopic observations suggest that during physiological resorption phagocytosis by osteoclasts of osteocytes takes place. Serial sections confirm that the cells are totally engulfed within the cytoplasm of the osteoclasts. Ultrastructural studies support these findings and indicate that the initial stage of phagocytosis of the osteocytes consists of the insinuation of an extnesion of the ruffled border into the osteocyte lacuna. These extensions are seen to make close contact with the osteocytes prior to their engulfment by the osteoclasts and their final digestion within phagosomes.

Animals↗
PubMed2026

Myeloma engraftment suppresses osteocytic ossification signatures rescued by loading in mice and reveals predictors of patient outcome.

Multiple myeloma (MM) is a malignant plasma cell disease inducing osteolytic lesions by disrupting bone homeostasis, fostering catabolic and suppressing anabolic functions. While the impact on osteoblast generation and function is well documented, alterations of osteocyte function and extracellular matrix (ECM) are not yet fully understood. Thus, using a syngeneic mouse model of MM by injecting MOPC315.BM cells intratibially into BALB/c mice (n = 95), we performed transcriptomic profiling of an osteocyte-enriched population and identified a mechanosensitive matrisomal gene signature, which was disrupted by tumor engraftment. Non-invasive tibial loading restored the expression of 94 ECM-associated genes, including collagens, fibronectin, and aggrecan. Cross-species integration with RNA-seq data from 387 MM patients revealed eight ECM-related genes whose expression correlated with overall survival (VEGFA, BCAN, FGF13, TNFSF8, SDC1, LAMC1, SEMA3A, and CCL2). Four of these genes (Vegfa, Sdc1, Sema3a, Ccl2) were also load-responsive in a murine osteocyte (IDG-SW3 cells) bioreactor model. Our findings indicate that an existing mechanosensitive osteocytic repair program is suppressed by MM cells, which can be reinvigorated via a brief single loading session. It suggests that exercise-based interventions may be beneficial to restore bone mass through endochondral ossification programs in patients with MM.

Bone disease↗
PubMed1978

Effect of PTH on osteocyte ultrastructure.

Osteocyte ultrastructure was studied in the cortical bone of the tibia of rats after acute or chronic administration of supraphysiological doses of PTH. Confirming previous reports, an increase in the width of the cytoplasm with the appearance of numerous thin cytoplasmic processes, an increase in rough ergastoplasmic reticulum and Golgi apparatus, an increase in lacunar width and lysis of the lacunar wall ("brush border" after Bonucci) were observed. Particularly striking was the appearance of numerous microfilaments and microtubules in the cytoplasm of activated osteocytes. The appearance of microfilaments, often densely packed in cytoplasmic processes or running parallel to the plasma membrane, points to a role of the cytoskeleton in mediating the effects of PTH on conformational changes of the plasma membrane (and possible on cell motility); microtubules were particularly prominent in the Golgi field and are presumably involved in the exocytosis of lysosomes. Another striking feature was the non-random distribution of periosteocytic osteolysis along the lacunar perimeter. Osteolysis was particularly pronounced at the cell pole opposite to the cell nucleus. After chronic administration of PTH, autolysis of osteocytes, associated with signs of excessive periosteocytic osteolysis, was frequently encountered.

Animals↗
PubMed1978

Effects of hormones on osteocyte function and perilacunar wall structure.

Microradiographical and ultrastructural aspects of periosteocytic lacunae are determined by osteocytic activity, lacunar modeling and perilacunar miniremodeling in particular. The miniremodeling activity is constituted by two alternating processes: osteolysis and osteoplasis. Modifications of lacunar shape and size and of perilacunar wall ultrastructure, caused by a direct or indirect effect of certain hormones on osteocytic activity, were observed. The lacunar modeling alterations, particularly in cases of VDH or PTH deficiency, result in an irreversible impaired calcification of the lacunar walls and consequently, mottled lacunae. The alterations of periosteocytic osteolysis are characterized by an increase in number of enlarged lacunae and/or by increased magnitude of this lacunar enlargement. Usually observed as an effect of PTH and VDH, these alterations can also be induced by GC, T4, PG. On the other hand, CT causes a decrease in periosteocytic osteolysis. Periosteocytic osteoplasis is characterized by perilacunar bone formation of various aspects and is known to be stimulated by CT. The osteocytic response to hormones is a function of concentration and not of time; it is transient and not integrative. It can be concluded that none of the perilacunar wall modifications observed is characteristic of any particular hormonal effect or metabolic bone disease.

Calcitonin↗
PubMedDate not supplied

Chondrocyte-to-osteocyte transformation in grafts of perichondrium-free epiphyseal cartilage.

When perichondrium-free pieces of embryonic quail epiphyseal cartilage are incubated on the chorioallantoic membranes of chick embryos, 2 developmental changes are observed. First, most grafts develop a periosteum in which the osteoblasts and osteocytes are of donor, i.e., chondrocytic origin. No such periosteum is observed around explants of demineralized, inductive bone matrix. Second, the matrix surrounding some chondrocytes within the original graft became more bone-like with respect to staining pattern, birefringence and collagen morphology. We conclude that, under some conditions, the avian chondrocyte may in situ or subsequent to release from the cartilage lacuna synthesize a bone-like matrix and, in this sense, be thought to have undergone a "transformation" into an osteocytic or osteoblastic type of cell.

Allantois↗
PubMed1977

Histochemical reactions for mucopolysaccharides in the dinosaur bone. Studies on Epon- and methacrylate-embedded semithin sections as well as on isolated osteocytes and ground sections of bone.

The dinosaur bone was examined with the aim to detect in it the presence of mucopolysaccharides. The methacrylate- and Epon-embedded semithin sections of the studied bone were found to contain substances giving positive reaction on application of histochemical procedures used for identification of mucopolysaccharides (mucosubstances). These substances were also shown to be localized in the perivascular space, within the vascular canal, and around the osteocytes. The distribution of mucopolysaccharides in the dinosaur bone turned out to be comparable with their distribution in the bones of contemporary animals.

Animals↗
PubMed1977

Osteocytic osteolysis in a cretaceous reptile.

Bone resorption through osteocytic activity already recognized in all classes of Vertebrates, has been demonstrated in fragments of long bones from a non-identified reptile found in an Upper Cretaceous rock formation in Dinosaur National Park, Patricia, Alberta.

Animals↗
PubMedDate not supplied

A laboratory model demonstrating osteocyte-osteoblast control of plasma calcium concentrations. Table model for plasma calcium control.

This report describes a laboratory model designed to illustrate a newer concept for the control of plasma calcium concentrations. This postulate suggests that plasma calcium levels are the result of a balance or imbalance in opposing calcium ion fluxes between plasma and bone fluid compartments existing around osteocyte-lining cells (osteoblasts) units in bone. The metabolic control of these fluxes is postulated to reside within the lining cells on the surface of bone. These cells serve as a cellular interface between the two fluid compartments. The model described in this report illustrates these principles by using the height of columns of water in cylinders to represent calcium ion concentrations. A water pump, representing the calcium transcellular transport system in the lining cells, maintains a higher level of water in the cylinder representing plasma than in that representing bone fluid. This is accomplished by continuous pumping of water from the bone fluid cylinder to the plasma cylinder. Water is returned to the bone fluid cylinder as long as a differential in the height of water in the two cylinders exists. A constant height of water in the plasma cylinder is maintained when the two fluxes are in equilibrium. A constant height of water in the cylinder representing bone fluid is maintained by the level of water in a much larger cylinder representing calcium equilibrium between the solid and liquid phases of bone. The primary hormone controlling the rate of calcium transfer from bone fluid to blood, or in the model regulating the speed of water pump, is parathyroid hormone.

Adult↗