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At least 253 records · Page 14Linked to original sources
PubMed1984

Cartilage calcification: normal and aberrant.

Hydroxyapatite crystal deposition occurs physiologically in cartilage as a prelude to bone formation via endochondral ossification. Both extracellular molecules and organelles, and the chondrocytes themselves control the initial formation of hydroxyapatite, as well as the growth and orientation of the hydroxyapatite crystals. In this study pathologic calcium containing deposits from 48 patients (27 hydroxyapatite and 21 calcium pyrophosphate dihydrate) were subjected to crystallographic, histologic (light microscopy, scanning electron microscopy, transmission electron microscopy) and chemical analyses and compared to normal controls. It is suggested that both hydroxyapatite and calcium pyrophosphate dihydrate deposition involve elevations in ionic concentrations, exposure of mineral nucleators, and removal of mineral inhibitors. Peculiar to the matrices of pathologic deposits of hydroxyapatite are elevated concentrations of calcium acidic phospholipid phosphate complexes and lower concentrations of hexosamine while collagen (hydroxyprolin) and total lipid contents are not altered. Matrices of deposits of calcium pyrophosphate dihydrate were similar biochemically except that calcium acidic phospholipid phosphate complexes concentrations were not elevated.

Calcification, Physiologic↗
PubMed1990

Deviatoric and hydrostatic mode interaction in hard and soft tissue.

It has been established that many hard and soft tissues have anisotropic material symmetry. It is noted here that the deviatoric and hydrostatic modes interact with each other in a general anisotropic elastic material. In the special case of isotropic, linear elastic, materials these modes are non-interactive. As a consequence of the interaction of these modes encountered in anisotropic materials, the decomposition into hydrostatic and deviatoric modes, and deviatoric mode concepts such as the von Mises effective stress are not appropriate for anisotropic materials in general. The implications of this observation for the presentation of computationally generated stress contours for hard and soft tissues are discussed. It is also pointed out that the mode coupling and mode interaction raise the question of whether anisotropic living tissues respond directly to stress or to some other physical quantity such as strain or strain energy, in view of the recent hypothesis concerning the proliferation and ossification of cartilage.

Adaptation, Physiological↗
PubMed1988

Age related changes in the concentration of serum keratan sulphate in children.

Serum was obtained from 155 children at the time of admission to hospital for elective surgery. The concentration of serum keratan sulphate was determined by an ELISA which uses an antibody specific for keratan sulphate, a molecule found predominantly in cartilage. Concentrations of keratan sulphate rise progressively during the first four years of life (0-2: mean = 357 micrograms/l; 2-4: mean = 422 micrograms/l) and then remain high until 12 years of age (mean = approx. 500 micrograms/l). At this time, concentrations drop markedly (13-year olds: mean = 377 micrograms/l; 14-year olds: mean = 318 micrograms/l). After age 15, concentrations continue to fall toward the concentrations found in normal adults. Serum concentrations did not show significant differences with respect to disease category, sex or race but were found to vary, sometimes markedly, from child to child at any one age. The results suggest human cartilage undergoes significant changes in metabolic activities during maturation. Measurements of keratan sulphate concentration in serum may prove useful in studying the biochemical and physiological bases of these changes and in monitoring growth or endochondral ossification during maturation.

Adolescent↗
PubMed1994

Immunolocalization of complement C1s and matrix metalloproteinase 9 (92kDa gelatinase/type IV collagenase) in the primary ossification center of the human femur.

The first component of complement C1s has been shown to degrade type I and type II collagens (Yamaguchi et al. 1990), the latter of which is a major constituent of the cartilage matrix. In order to understand the physiological roles of C1s in cartilage resorption, the expression of C1s was examined by immunohistochemistry in the primary ossification center where the matrix is removed and replaced by bone marrow. Hypertrophic chondrocytes, endothelium and hematogenous elements in the capillary buds were intensely stained by a monoclonal antibody against C1s. Matrix metalloproteinase 9 (MMP-9, 92kDa gelatinase/type IV collagenase) was also immunolocalized in hypertrophic chondrocytes, mesenchymal cells in the primitive bone marrow and the cartilage matrix adjacent to the marrow. In addition, C1s was found to activate the zymogen of MMP-9. These observations suggest that C1s and MMP-9 coordinately participate in matrix degradation in cartilage.

Antibodies, Monoclonal↗
PubMedDate not supplied

Connective tissue growth factor: what's in a name?

Connective tissue growth factor (CTGF) is a member of the recently described CCN gene family which contains CTGF itself, cyr61, nov, elm1, Cop1, and WISP-3. CTGF is transcriptionally activated by several factors although its stimulation by transforming growth factor beta (TGF-beta) has attracted considerable attention. CTGF acts to promote fibroblast proliferation, migration, adhesion, and extracellular matrix formation, and its overproduction is proposed to play a major role in pathways that lead to fibrosis, especially those that are TGF-beta-dependent. This includes fibrosis of major organs, fibroproliferative diseases, and scarring. CTGF also appears to play a role in the extracellular matrix remodeling that occurs in normal physiological processes such as embryogenesis, implantation, and wound healing. However, recent advances have shown that CTGF is involved in diverse autocrine or paracrine actions in several other cell types such as vascular endothelial cells, epithelial cells, neuronal cells, vascular smooth muscle cells, and cells of supportive skeletal tissues. Moreover, in some circumstances CTGF has negative effects on cell growth in that it can be antimitotic and apoptotic. In light of these discoveries, CTGF has been implicated in a diverse variety of processes that include neovascularization, transdifferentiation, neuronal scarring, atherosclerosis, cartilage differentiation, and endochondral ossification. CTGF has thus emerged as a potential important effector molecule in both physiological and pathological processes and has provided a new target for therapeutic intervention in fibrotic diseases.

Amino Acid Sequence↗
PubMed2003

Physiology and pathophysiology of the growth plate.

Longitudinal growth of the skeleton is a result of endochondral ossification that occurs at the growth plate. Through a sequential process of cell proliferation, extracellular matrix synthesis, cellular hypertrophy, matrix mineralization, vascular invasion, and eventually apoptosis, the cartilage model is continually replaced by bone as length increases. The regulation of longitudinal growth at the growth plate occurs generally through the intimate interaction of circulating systemic hormones and locally produced peptide growth factors, the net result of which is to trigger changes in gene expression by growth plate chondrocytes. This review highlights recent advances in genetics and cell biology that are illuminating the important regulatory mechanisms governing the structure and biology of the growth plate, and provides selected examples of how studies of human mutations have yielded a wealth of new knowledge regarding the normal biology and pathophysiology of growth plate cartilage.

Animals↗
PubMed1977

Cleft palate following prenatal food restriction in mice: association with elevated maternal corticosteroids.

Following food restriction of pregnant CD-1 mice, the maternal serum corticosteroid levels and incidence of skeletal and visceral abnormalities of the progeny were determined. Dams from the groups receiving restricted food on gestation days 6 to 15 had increased resorptions, and the progeny had delayed ossification of the skeleton with cleft palate accompanied by delayed ossification of the presphenoid bone. The incidence and intensity of these changes was correlated with the level of food restriction. The incidence of cleft palate for progeny from dams receiving 4.0 to 2.5 g of feed per day ranged from 6.3% to 100.0%, respectively. Serum corticosteroid levels of pregnant control and food restricted dams were similar on gestation day 10, but the levels of food restricted dams were 6 to 10 times greater than controls on gestation day 15. Thus cleft palate, delayed skeletal ossification, and increased resorptions are predictably produced by food restriction of CD-1 mice and were highly correlated with the elevated endogenous serum corticosteroid levels.

Adrenal Cortex Hormones↗