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At least 1,711 records · Page 95Linked to original sources
PubMed2001

Incomplete ossification of the humeral condyle in two Labrador retrievers.

Incomplete ossification of the humeral condyle (IOHC) was identified in two Labrador retrievers using computed tomography. Both dogs were non-weightbearing on the affected forelimbs. The dogs were treated by means of a bone screw placed across the humeral condyle. IOHC was originally reported in spaniel and chondrodystrophic breeds. The pathogenesis of the condition remains unknown, but may be related to impaired antebrachial bone growth, similarly to the pathogeneses of elbow dysplasia and radius curvus.

Animals↗
PubMed2000

The ALX4 homeobox gene is mutated in patients with ossification defects of the skull (foramina parietalia permagna, OMIM 168500).

Foramina parietalia permagna (FPP) (OMIM 168500) is caused by ossification defects in the parietal bones. Recently, it was shown that loss of function mutations in the MSX2 homeobox gene on chromosome 5 are responsible for the presence of these lesions in some FPP patients. However, the absence of MSX2 mutations in some of the FPP patients analysed and the presence of FPP associated with chromosome 11p deletions in DEFECT 11 (OMIM 601224) patients or associated with Saethre-Chotzen syndrome suggests genetic heterogeneity for this disorder. Starting from a BAC/P1/cosmid contig of the DEFECT 11 region on chromosome 11, we have now isolated the ALX4 gene, a previously unidentified member of the ALX homeobox gene family in humans. Mutation analysis of the ALX4 gene in three unrelated FPP families without the MSX2 mutation identified mutations in two families, indicating that mutations in ALX4 could be responsible for these skull defects and suggesting further genetic heterogeneity of FPP.

Amino Acid Sequence↗
PubMed1976

New standards of ossification of the newborn.

Physical and neurological examinations of American and Swedish populations confirm that epiphyseal ossification of the newborn in the shoulder, knee, and foot is related to gestational age. The causes of accelerated, retarded, and dysharmonic osseous maturation of the neonate are reviewed.

Bone Diseases, Developmental↗
PubMed1980

The vanishing epiphyseal ossification center: a sequel to septic arthritis of childhood.

Radiographic disappearance of a previously ossified epiphyseal center may occur during the acute episode of septic arthritis, or during the healing phase after adequate treatment. The fact that the cartilage remains normal suggests that reparative revascularization, rather than enzymatic dissolution of bone and cartilage by the infecting organism, is responsible for the disappearance of the ossification center.

Arthritis, Infectious↗
PubMed1985

The distal femoral epiphyseal ossification center in the assessment of third-trimester menstrual age: sonographic identification and measurement.

The distal femoral epiphyseal secondary ossification center (DFE), which can be reliably identified and measured sonographically, may assist the sonologist in predicting third-trimester menstrual age. Between 28 and 35 menstrual weeks, the percentage of fetuses with a DFE progressively increases. Although the mean age at DFE appearance is approximately 32-33 menstrual weeks, the DFE may be seen as early as 29 menstrual weeks. Nevertheless, the age of a fetus without an identifiable DFE is most likely less than or equal to 34 menstrual weeks. Measurements of the DFE show that its size increases linearly: the menstrual age of a fetus whose DFE measures greater than or equal to 7mm is most likely greater than or equal to 37 weeks.

Embryonic and Fetal Development↗
PubMed2005

Weight loading young chicks inhibits bone elongation and promotes growth plate ossification and vascularization.

The mechanical stimuli resulting from weight loading play an important role in mature bone remodeling. However, the effect of weight loading on the developmental process in young bones is less well understood. In this work, chicks were loaded with bags weighing 10% of their body weight during their rapid growth phase. The increased load reduced the length and diameter of the long bones. The average width of the bag-loaded group's growth plates was 75 +/- 4% that of the controls, and the plates showed increased mineralization. Northern blot analysis, in situ hybridization, and longitudinal cell counting of mechanically loaded growth plates showed narrowed expression zones of collagen types II and X compared with controls, with no differences between the relative proportions of those areas. An increase in osteopontin (OPN) expression with loading was most pronounced at the bone-cartilage interface. This extended expression overlapped with tartarate-resistant acid phosphatase staining and with the front of the mineralized matrix in the chondro-osseous junction. Moreover, weight loading enhanced the penetration of blood vessels into the growth plates and enhanced the gene expression of the matrix metalloproteinases MMP9 and MMP13 in those growth plates. On the basis of these results, we speculate that the mechanical strain on the chondrocytes in the growth plate causes overexpression of OPN, MMP9, and MMP13. The MMPs enable penetration of the blood vessels, which carry osteoclasts and osteoblasts. OPN recruits the osteoclasts to the cartilage-bone border, thus accelerating cartilage resorption in this zone and subsequent ossification which, in turn, contributes to the observed phenotype of narrower growth plate and shorter bones.

Adaptation, Physiological↗
PubMed1984

The role of cartilage canals in the ossification of the talus.

Interrupted serial sections of the foot region from 14 human fetuses, crown-rump (CR) lengths between 32 and 240 mm, were studied, using HE, PAS, Alcian blue, Gomori's trichrome and von Kossa stains. Cartilage canals carrying vascular connective tissue from the perichondrium entered the talus by 68-mm. The centre of ossification developed in the neck region of the talus cartilage by 240 mm CR length, but early stages of chondrocyte proliferation and hypertrophy were noted by 108-mm CR length. The latter is marked by 170 mm CR length. A number of cartilage canals were observed around the developing centre. Branches from these cartilage canals appeared to supply vascular osteogenic tissue to its marrow spaces.

Cartilage↗
PubMed1990

Ossification of the antler in the Lapland reindeer (Rangifer tarandus tarandus).

A histological and histochemical study of biopsy specimens from the Lapland reindeer antler indicated that the intercellular matrix of the cartilage that forms the partitions of longitudinal channels becomes calcified at virtually the initial stage of formation. The lacunae at the peripheries of the cartilaginous partitions are invaded by osteoblasts in a process comparable to endochondral ossification. The very centres of the partitions evidently become directly converted into bone without the presence of e.g. osteoclasts. The osseous partitions are remodelled by osteoclasts. The antler increases in diameter by periosteal apposition.

Animals↗
PubMed1992

In vitro studies on the regulation of endochondral ossification by vitamin D.

The research described in this article has focused on the complex autocrine, paracrine, and endocrine regulation of endochondral ossification using vitamin D metabolites and TGF-beta as models. By comparing results from a number of laboratories utilizing a diverse array of in vivo and in vitro systems, a coherent picture is beginning to emerge. Vitamin D metabolites influence cell differentiation and maturation and have direct effects on cell function. Differentiation of the mesenchymal cells into chondroblasts is regulated by both 1,25-(OH)2D3 and 24,25-(OH)2D3, as well as by TGF-beta. The resting zone chondrocytes respond primarily to 24,25-(OH)2D3 in terms of matrix synthesis and matrix vesicle biochemistry. They synthesize both metabolites and other factors that stabilize matrix vesicle enzymes like AHSG. In addition to the paracrine role these factors may play in regulating the matrix, it is possible that they may influence the cells in the growth plate itself. Growth zone chondrocytes also synthesize both metabolites, but respond primarily to 1,25-(OH)2D3 for the parameters measured in the studies described. These cells also synthesize TGF-beta which further increases alkaline phosphatase activity, perhaps via an autocrine stimulation of the cell. While cells from the calcified zone have not yet been studied directly in culture, it is likely that they respond to paracrine signals from the avascular cartilage as well as to serum-derived factors. How the signals are transferred among the cells is unknown. Certainly one can postulate information flow in both upward and downward directions. The signal transduction mechanisms for the factors at the cellular level are complex. While it is known that 1,25-(OH)2D3 stimulates gene transcription and stabilization of mRNA for proteins like alkaline phosphatase, its nongenomic effects are only beginning to emerge. Membrane effects of this metabolite have been shown in intestine and kidney in conjunction with studies on Ca flux. It is becoming increasingly evident that other steroid hormones may operate in similar ways. Studies with the rat costochondral chondrocytes are the first to show that there are specific membrane effects for at least two vitamin D metabolites and that membrane enzymes, including those involved in phospholipid metabolism, can be differentially regulated by them. Furthermore, these experiments have provided for the first time a clear hypothesis for how cells can regulate events in the extracellular matrix after the matrix vesicles are produced and incorporated into the matrix.

Animals↗
PubMed1999

Testosterone stimulates insulin-like growth factor-I and insulin-like growth factor-I-receptor gene expression in the mandibular condyle--a model of endochondral ossification.

Puberty is associated with an increase in the plasma concentration of sex steroids, GH, and insulin-like growth factor-I (IGF-I). Gonadal steroid hormones are important for the normal pubertal growth spurt and skeletal growth. The mechanism by which gonadal steroids induce skeletal growth is still not fully understood. To better understand the direct effect sex steroids have on bone growth, we studied an isolated organ culture system of the mandibular condyle, derived from 3.5-5.5-week-old male and female mice. We found that testosterone 10(-6) M, but not estradiol, stimulated thymidine incorporation into the DNA of male-derived condyle. Three days of testosterone treatment doubled the condyle size and increased the chondroprogenitor zone, while maintaining the normal gradient of the developing chondrocytes. Immunohistochemistry and in situ hybridization techniques showed that testosterone stimulated IGF-I and IGF-I-R and their messenger RNAs (mRNAs) mainly in the mature chondrocyte layer. Immunoneutralization of IGF-I in the testosterone-treated condyle caused the disappearance of the chondroblast and young chondrocyte layers, though the progenitor cell layer remained almost unaffected. Overtreatment with testosterone (dose or duration) accelerated condylar ossification. In the presence of testosterone 10(-5) M (high dose), calcification "climbs" up to the chondroprogenitor zone, and most of the condylar chondrocytes are replaced by bone tissue. Similar changes occurred after 7 days of testosterone treatment (long duration) with 10(-6) M. In conclusion, testosterone stimulates growth and local production of IGF-I and IGF-I-R in chondrocyte cell layers of an isolated organ culture of mice mandibular condyle. Part of the effect testosterone has on condylar growth is mediated by IGF-I.

Animals↗
PubMed1996

Mice lacking tartrate-resistant acid phosphatase (Acp 5) have disrupted endochondral ossification and mild osteopetrosis.

Mature osteoclasts specifically express the purple, band 5 isozyme (Acp 5) of tartrate-resistant acid phosphatase, a binuclear metalloenzyme that can generate reactive oxygen species. The function of Acp 5 was investigated by targeted disruption of the gene in mice. Animals homozygous for the null Acp 5 allele had progressive foreshortening and deformity of the long bones and axial skeleton but apparently normal tooth eruption and skull plate development, indicating a rôle for Acp 5 in endochondral ossification. Histomorphometry and mineralization density analysis of backscattered electron imaging revealed widened and disorganized epiphyseal growth plates with delayed mineralization of cartilage in 6- to 8-week-old mutant mice. The membrane bones of the skull showed increased density at all ages examined, indicating defective osteoclastic bone turnover. Increased mineralization density was observed in the long bones of older animals which showed modelling deformities at their extremities: heterozygotes and homozygous Acp 5 mutant mice had tissue that was more mineralized and occupied a greater proportion of the bone in all regions. Thus the findings reflect a mild osteopetrosis due to an intrinsic defect of osteoclastic modelling activity that was confirmed in the resorption pit assay in vitro. We conclude that this bifunctional metalloprotein of the osteoclast is required for normal mineralization of cartilage in developing bones; it also maintains integrity and turnover of the adult skeleton by a critical contribution to bone matrix resorption.

Acid Phosphatase↗
PubMed2003

Defective endochondral ossification in mice with strongly compromised expression of JunB.

Functional analysis in mice has established an absolute requirement of JunB, a member of the AP-1 transcription factor family, during early embryonic development. To investigate the role of JunB during mid and late gestation and postnatally Ubi-junB transgenic mice were used to generate two junB-/- Ubi-junB mutant lines, in which embryonic lethality was rescued but strongly reduced JunB expression in several adult tissues was observed. Mutant mice from both rescue lines were growth retarded and shared significantly reduced longitudinal bone growth. Mutant long bones were characterised by reduced numbers of growth plate chondrocytes and a severe osteoporosis. Decreased JunB levels in epiphysal growth plate chondrocytes and bone lining osteoblasts correlated with deregulated expression of Cyclin A, Cyclin D1 and p16INK4a, key regulators of cell cycle control. Furthermore, junB-/- Ubi-junB bone marrow stromal cells were unable to differentiate into bone forming osteoblasts in vitro. Our data demonstrate that JunB plays a crucial role in endochondral ossification by regulating proliferation and function of chondrocytes and osteoblasts.

Animals↗
PubMed2006

Unusual CT/MR features of putative ligamentum flavum ossification in a North African woman.

To display the unusual spinal CT and MR findings in a 48-year-old North African woman presenting with two adjacent intracanalar mineralized epidural outgrowths exhibiting mature bone organization with "cortical" and "trabecular" areas and pseudoarthritic changes at their interface. An unusual form of ligamentum flavum ossification (LFO) was speculated, of which features are discussed under the light of the available literature.

Female↗
PubMed2005

Gastric adenocarcinoma with ossification in a ferret (Mustela putorius furo).

A 6-year-old female ferret had a firm mass 2 cm in diameter in the pyloric region of the stomach. Histopathologically, the mass was composed of neoplastic proliferation of well-differentiated epithelial cells, showing tubular or glandular growth patterns. Osseous metaplastic foci were often found in the tumor. Tumor cells showed a positive reaction for immunohistochemistry against bone morphogenetic protein-6, an osteogenic factor. A diagnosis of gastric adenocarcinoma with ossification was made.

Adenocarcinoma↗
PubMed1979

Old fibrin coagula and their ossification in simple bone cysts.

Old calcified fibrin coagula are frequently found in simple bone cysts. They provide a scaffold on which new bone is laid down, in a process analogous to endochondral ossification. It is suggested that these coagula are derived in substantial part from the plasma-like contents of the cyst, after the release of plasma-clotting factors as the result of injury. Major haemorrhage is not involved and in many cases there is no antecedent fracture. The phenomenon is not seen in other common cystic conditions of bone and its recognition is thus helpful in the histological diagnosis of simple bone cyst. Cystic bone infarcts and their possible confusion with simple bone cysts are also briefly discussed.

Blood Coagulation↗
PubMed1989

Pseudomalignant heterotopic ossification ("myositis ossificans"). Recurrence after excision with subsequent resorption.

An eight-year-old boy presented with massive pseudomalignant heterotopic ossification around the upper femur. The mass was completely excised because of severe pain, systemic illness and a flexion contracture at the hip. Symptomatic improvement was swift, but two weeks later the mass had recurred and was even more extensive. During the subsequent 18 months of conservative management he has been free of pain and there has been progressive resorption and remodelling of the heterotopic bone. There is now no limitation of physical activity and movement at the hip is full.

Bone Resorption↗
PubMed1992

The ossific nuclei and the cartilage anlage of the talus and calcaneum.

We studied the ossific nuclei on radiographs of the feet of three stillborn infants, two with club feet, relating the size, position and alignment of each nucleus to the cartilaginous talus or calcaneum in which it lay. Anteroposterior projections of the nucleus of the talus show deformity of that bone as well as subtalar malalignment. Lateral projections of the calcaneal nucleus may underestimate the degree of hindfoot equinus.

Calcaneus↗
PubMed2003

Delayed ossification of the proximal capital femoral epiphysis in Legg-Calvé-Perthes' disease.

We studied radiographs of 125 children (105 boys, 20 girls) with unilateral Legg-Calvé-Perthes' disease to examine the epiphyseal development of the femoral head in the contralateral (unaffected) hip. The epiphyseal height (EH) and width (EW) of the unaffected hip were measured on the initial anteroposterior pelvic radiograph. In 109 of the patients (87.2%) the EH was below the mean for normal Japanese children and a significantly small EH (below -2 SDs) was observed in 23 patients (18.4%). By contrast, the EW of most patients (95.2%) lay within +/- 2 SDs of normal values except for six with a significantly small EW. A strong positive linear correlation (R = 0.87) was observed in the EH:EW ratio in the patients. A smaller EH than expected for EW in our series indicated epiphyseal flattening of the femoral head in Legg-Calvé-Perthes' disease. Our findings support the hypothesis that a delay in endochondral ossification in the proximal capital femoral epiphysis may be associated with the onset of Perthes' disease.

Adolescent↗