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PubMed1997

Congenital renal tubular dysplasia and skull ossification defects similar to teratogenic effects of angiotensin converting enzyme (ACE) inhibitors.

An apparently autosomal recessive syndrome of congenital renal tubular dysplasia and skull ossification defects is described in five infants from two separate, consanguineous, Pakistani Muslim kindreds. The clinical, pathological, and radiological features are similar to the phenotype associated with fetal exposure to angiotensin converting enzyme (ACE) inhibitors: intrauterine growth retardation, skull ossification defects, and fetal/ neonatal anuric renal failure associated with renal tubular dysplasia. There was no fetal exposure to ACE inhibitors in the affected infants. Phenotypic similarities between these familial cases and those associated with ACE inhibition suggest an abnormality of the "renin-angiotensin-aldosterone" system (RAS). It is postulated that the molecular pathology in this uncommon autosomal recessive proximal renal tubular dysgenesis could be related to mutations of the gene systems governing the RAS.

Abnormalities, Drug-Induced↗

PubMed1982

Ossification of the thoracic posterior longitudinal ligament in a fixed population. Radiological and neurological manifestations.

Reportedly, ossification of the posterior longitudinal ligament (OPLL) usually involves the cervical spine and often accompanies other ligamentous ossification such as diffuse idiopathic skeletal hyperostosis (DISH). It is considered serious because it sometimes causes severe radiculomyelopathy; however, the present study, based on a fixed population sample, revealed that OPLL of the thoracic spine is nearly always asymptomatic. The prevalence of thoracic OPLL was 0.6%, with three times as many women as men being affected, compared with cervical OPLL which occurs predominantly among men. No marked radiculomyelopathy was observed, nor definite evidence of neurological involvement due to thoracic OPLL. DISH was rare, especially among women.

Adult↗

PubMed1982

Ossification in the caudal attachments of the ligamentum flavum. An anatomic and computed tomographic study.

A review of anatomic specimens and routine computed tomographic (CT) scans of the chest and abdomen demonstrated that ossification in the caudal attachments of the ligamentum flavum is a common anatomic finding, but a much less common CT finding. Its characteristic location should help prevent confusion with other entities. The present study was prompted by a case of thoracic spine trauma, reported here, in which areas of bone density in the spinal canal simulated fracture fragments. The true nature of these bony projections, namely ossification in the ligamentum flavum, was established by computer reconstruction of axial CT images.

Adult↗

PubMed1986

Epiphyseal ossification centers in the assessment of fetal maturity: sonographic correlation with the amniocentesis lung profile.

The epiphyseal ossification centers of the distal femur (DFE) and proximal tibia (PTE) appear and enlarge during the third trimester of pregnancy. Late in the third trimester, the epiphysis of the proximal humerus (PHE) begins to ossify in some fetuses. Using the amniocentesis lung profile to determine the value of sonographic epiphyseal visualization as a predictor of pulmonary maturity, we studied 50 fetuses prospectively and compared the sonographic epiphyseal findings with results from the amniocentesis lung profiles. Nine fetuses with a visible PHE had a mature amniocentesis lung profile (accuracy of positive prediction = 100%), and then fetuses with an immature amniocentesis lung profile had no visible PHE (conegativity = 100%). Fetuses in which the combined DFE and PTE diameters were greater than 11 mm or in which the DFE and the PTE diameters were similar in size (DFE less than or equal to 1 mm larger than PTE) also yielded positive results. Copositivity and accuracy of prediction of an immature amniocentesis lung profile, on the other hand, were low (22%-25%) for the same epiphyseal parameters. These data suggest that antenatal visualization and measurement of the epiphyseal ossification centers of the fetal knee and shoulder may help to identify fetuses that would have a mature amniocentesis lung profile.

Amniocentesis↗

PubMed1991

Variations in acromial ossification simulating infant abuse in victims of sudden infant death syndrome.

A variation in ossification of the acromial process of the scapula is described. Postmortem radiographs, obtained in 78 infants who died of sudden infant death syndrome, showed an ossific opacity adjacent to the acromial process in 10 infants (13%). This finding was noted bilaterally in six patients and unilaterally in four patients. No two ossicles were identical. Histologically, no growth plate cartilage was evident between the bony structure and the acromion proper; therefore, this appeared to represent a "pseudoepiphysis." Superficially, this normal variation may appear similar to an acromial fracture resulting from infant abuse. However, a careful analysis of the findings of this normal variation should help prevent any confusion with inflicted injury.

Acromion↗

PubMed1992

Ossification of the human fetal ilium.

Ossification of the ilium is similar to that of a long bone. It possesses three cartilaginous epiphyses and one cartilaginous process. Moreover, it undergoes peculiar osteoclastic resorption, comparable with that of the cranium bones. Asymmetrical ossification of the ilium, haversian bone remodelling and apposition of chondroid tissue posterosuperiorly to the acetabulum most probably emphasize the importance of mechanical factors in the morphogenesis of the hip bone during fetal life.

Fetus↗

PubMed2002

Potential role of leptin in endochondral ossification.

Leptin, a 16-kD circulating hormone secreted mainly by white adipose tissue, is a product of the obese (ob) gene. Leptin acts on human marrow stromal cells to enhance differentiation into osteoblasts and inhibit differentiation into adipocytes. Leptin also inhibits bone formation through a hypothalamic relay. To obtain a better understanding of the potential role of leptin in bone formation, the localization of leptin in endochondral ossification was examined immunohistochemically. High expression of leptin was identified in hypertrophic chondrocytes in the vicinity of capillary blood vessels invading hypertrophic cartilage and in a number of osteoblasts of the primary spongiosa beneath the growth plate. The hypertrophic chondrocytes far from the blood vessels were negative for leptin. Moreover, we detected the production and secretion of leptin by a mouse osteoblast cell line (MC3T3-E1) and a mouse chondrocyte cell line (MCC-5) by RT-PCR, immunocytochemistry, and Western blotting. Leptin enhanced the proliferation, migration, tube formation, and matrix metalloproteinase-2 (MMP-2) activity of human endothelial cells (HUVECs) in vitro. These findings suggest the possibility that leptin exerts its influence on endochondral ossification by regulating angiogenesis.

Animals↗

PubMed1990

Labyrinthine ossification after meningitis: its implications for cochlear implantation.

Labyrinthine ossification can be found in a high percentage of patients with profound deafness resulting from bacterial meningitis. Radiographic evidence of ossification can be found as early as 2 months after the acute infection, indicating that the intracochlear process probably begins much earlier. If long, intracochlear cochlear implants are to be most successfully used in these patients, an aggressive approach to clinical management following the meningitis should be taken. Illustrative case reports and suggested guidelines for evaluation and treatment are given.

Calcinosis↗

PubMed2005

Runx2 regulates endochondral ossification in condyle during mandibular advancement.

Runx2 is a transcription factor prerequisite for chondrocyte maturation and osteoblast differentiation. We tested the hypothesis that Runx2 is responsible for signaling chondrocyte maturation and endochondral ossification in the condyle during mandibular advancement. Fifty 35-day-old Sprague-Dawley rats were fitted with functional appliances for 3, 7, 14, 21, and 30 days. Experimental animals with 50 matched controls were labeled with bromodeoxyuridine for evaluation of the invasion of chondroclasts and osteoblasts into condylar cartilage. Mandibular advancement elicited Runx2 expression in condylar cartilage, and subsequently led to an expansion of type X collagen domain in the hypertrophic layer. Stronger Runx2 mRNA signals in subchondral bone corresponded with the increase in the recruitment of osteoblasts and chondroclasts, which preceded the increase of new bone formation in the condyle. Thus, Runx2 mediates chondrocyte terminal maturation and endochondral ossification in the mandibular condyle in response to mandibular advancement.

Animals↗

PubMed2006

Effect of early postnatal body weight on femoral head ossification onset and hip osteoarthritis in a canine model of developmental dysplasia of the hip.

Developmental dysplasia of the hip (DDH) is a well-known precipitator of hip osteoarthritis. An increase in body weight during the critical early postnatal growth period may alter joint contact, and thus alter hip development and influence joint health in adulthood. The objective of this study was to determine whether early postnatal body weight affected the course of hip development and the onset of osteoarthritis in a canine model of DDH. A longitudinal study, from birth to skeletal maturity, was conducted. Serial body weight, age at femoral head ossification onset, and femoral head coverage at 4 mo were measured. Presence and severity of degeneration at 8 mo were determined using necropsy and cartilage biochemistry. There was a negative association between birth weight and age at femoral head ossification onset; however, the association was likely due to skeletal maturity level rather than body weight per se. Lower birth weight subjects had greater femoral head coverage at 4 mo. Greater birth weight was associated with greater probability of moderate degenerative changes or macroscopic lesions at 8 mo. These results support the hypothesis that increased birth weight is sufficient to alter the course of hip development and result in measurable degenerative changes at adulthood.

Animals↗

PubMed1994

Induction of growth plate cartilage ossification by basic fibroblast growth factor.

In mammals, longitudinal bone growth results from the precise coupling of chondrogenesis and osteogenesis within the epiphyseal growth plate, a process termed endochondral ossification. The mechanisms coupling chondrogenesis and osteogenesis are unknown. Previous studies have shown that both basic fibroblast growth factor (bFGF) and acidic FGF are expressed by growth plate chondrocytes. Here we show that bFGF, infused directly into the rabbit proximal tibial growth plate, accelerates vascular invasion and ossification of growth plate cartilage. Our results suggest the possibility that bFGF (or a related member of the FGF family) couples osteogenesis to chondrogenesis by attracting vascular and bone cell invasion from the adjacent metaphyseal bone.

Animals↗

PubMed1980

Embryonic development of NMRI mice: relationship between the weight, age and ossification of embryos.

The time and the order of the appearance of the ossification centres were found to be similar in C3H and NMRI mice. Bodyweight comparisons confirmed these results. Location in the right as opposed to the left uterine horn, or in the upper, middle or lower part, was not found to influence the weight of the embryo. Significant differences in the weight of embryos within the same litter were used in investigating the sequence of ossification in embryos. This should prove useful in comparative morphology and teratology.

Animals↗

PubMed1986

Ossification centre of the hyoid bone in DiGeorge syndrome and tetralogy of Fallot.

The incidence of radiographic visibility of the ossification centre of the body of the hyoid bone in radiographs taken during the first month of life was analysed for 34 autopsied infants: 16 with DiGeorge syndrome (DGS), 14 with tetralogy of Fallot (TOF), four with interrupted aortic arch (IAA) and a further 13, surviving infants with non-DGS TOF or non-DGS IAA. The incidence of visible hyoid ossification centre (HOC) was 75.7% in a control series of infants with neither congenital heart disease (CHD) nor DGS. Autopsied patients with DGS, TOF without DGS, and IAA without DGS showed a significantly low incidence of visible HOC. Infants with TOF (and possibly those with IAA) who did not have DGS and who did not die during infancy showed a normal incidence of visible HOC in radiographs taken during the first post-natal month. Radiological visibility of the HOC in the first post-natal month appears useful in the diagnosis of DGS and forms of CHD often seen in association with DGS and in assessing prognosis of neonates with certain types of CHD.

Age Factors↗

PubMed1986

Ossification centre of the hyoid bone in complete transposition of great vessels, Ivemark asplenia syndrome, and Down's syndrome with congenital heart disease: correlation with the humeral capital epiphysis.

The incidence of radiographic visibility of the ossification centres of the body of the hyoid bone and of the humeral capital epiphysis in antero-posterior or lateral chest radiographs taken during the first month of life of 63 autopsied infants were analysed. The group comprised patients with Down's syndrome (DS) with congenital heart disease, 15; complete transposition of the great vessels (TGV), 10; Ivemark asplenia syndrome (IS), 17; and a control group of infants with congenital heart disease (CHD) who had none of the above conditions, nor tetralogy of Fallot, interrupted aortic arch, DiGeorge syndrome or hypoplastic left-heart complex, 31. The incidence of radiographically visible hyoid ossification centre (HOC) in the control group was 71% and of humeral capital epiphysis (HE), 16.1%. Autopsied infants with TGV, IS or DS with CHD showed increased visibility of HOC (100%); the incidence of visible HE was increased in neonates with IS (71.4%) and with TGV (50%). The differences in the incidence of radiographic visibility of HOC and HE in neonates with CHD, in this study and in others in the literature, appear to have diagnostic value.

Age Factors↗

PubMed2004

Possible roles of Runx1 and Sox9 in incipient intramembranous ossification.

UNLABELLED: We evaluated the detailed expression patterns of Runx1 and Sox9 in various types of bone formation, and determined whether Runx1 expression was affected by Runx2 deficiency and Runx2 expression by Runx1 deficiency. Our results indicate that both Runx1 and Sox9 are intensely expressed in the future osteogenic cell compartment and in cartilage. The pattern of Runx1 and Sox9 expression suggests that both genes could potentially be involved in incipient intramembranous bone formation during craniofacial development. INTRODUCTION: Runx1, a gene essential for hematopoiesis, contains RUNX binding sites in its promoter region, suggesting possible cross-regulation with Runx2 and potential regulatory roles in bone development. On the other hand, Sox9 is essential for chondrogenesis, and haploinsufficiency of Sox9 leads to premature ossification of the skeletal system. In this study, we studied the possible roles of Runx1 and Sox9 in bone development. MATERIALS AND METHODS: Runx1, Runx2/Osf2, and Sox9 expression was evaluated by in situ hybridization in the growing craniofacial bones of embryonic day (E)12-16 mice and in the endochondral bone-forming regions of embryonic and postnatal long bones. In addition, we evaluated Runx2/Osf2 expression in the growing face of Runx1 knockout mice at E12.5 and Runx1 expression in Runx2 knockout mice at E14.5. RESULTS: Runx1 and Sox9 were expressed in cartilage, and the regions of expression expanded to the neighboring Runx2-expressing osteogenic regions. Expression of both Runx1 and Sox9 was markedly downregulated on ossification. Runx1 and Sox9 expression was absent in the regions of endochondral bone formation and in actively modeling or remodeling bone tissues in the long bones as well as in ossified craniofacial bones. Runx2 expression was not affected by gene disruption of Runx1, whereas the expression domains of Runx1 were extended in Runx2(-/-) mice compared with wildtype mice. CONCLUSIONS: Runx1 and Sox9 are specifically expressed in the osteogenic cell compartments in the craniofacial bones and the bone collar of long bones, and this expression is downregulated on terminal differentiation of osteoblasts. Our results suggest that Runx1 may play a role in incipient intramembranous bone formation.

Animals↗

PubMed2001

Activation of transforming growth factor beta in chondrocytes undergoing endochondral ossification.

Transforming growth factor beta (TGF-beta) has well-documented roles in chondrocyte maturation and endochondral ossification, but the mechanisms of TGF-beta activation during these processes remain unclear. In this study, we analyzed TGF-beta activation in chick embryo resting, proliferating, and hypertrophic chondrocytes in culture. We found that both levels and activation of TGF-beta increased substantially with maturation. The majority of TGF-beta produced by resting cells over culture time remained latent, but a larger portion produced by proliferating and hypertrophic cells was activated with increasing maturation. Zymography of gelatin gels revealed that matrix metalloprotease 2 (MMP-2) and MMP-9 were expressed by each population and that MMP-13 characterized hypertrophic chondrocytes and to a lesser extent proliferating chondrocytes in late cultures. Treatment with pharmacologic agents revealed that both MMPs and serine proteases are involved in activation. However, because inhibition of MMPs almost completely prevented TGF-beta activation, MMPs appear crucial for activation. During culture, inclusion of the tetracycline-derived, collagenase/gelatinase inhibitor chemically modified nonantimicrobial tetracycline (CMT-8) at concentrations specific for MMP-13 inhibition resulted in complete inhibition of TGF-beta activation by proliferating and hypertrophic chondrocytes. These results show that TGF-beta production, release, and activation are regulated developmentally in chondrocytes. Our findings point to a strict mode of regulation of this potent factor to elicit diverse and highly specific effects during chondrocyte maturation and ossification.

Animals↗

PubMed2002

Annexin VIII is differentially expressed by chondrocytes in the mammalian growth plate during endochondral ossification and in osteoarthritic cartilage.

Endochondral ossification is the developmental process that leads to the formation and coordinated longitudinal growth of the majority of the vertebrate skeleton. Central to this process is chondrocyte differentiation occurring in the growth plate that lies at the junction between the epiphyseal cartilage and the bone. To identify novel factors involved in this differentiation process, suppression subtractive hybridization was performed to amplify preferentially cDNAs uniquely expressed in fetal bovine growth plate chondrocytes as opposed to epiphyseal chondrocytes. The subtracted product was used to screen a fetal bovine chondrocyte cDNA library. One of the cDNA clones identified encoded the bovine orthologue of annexin VIII, a protein not previously described in the growth plate. Northern and Western blotting confirmed that annexin VIII was expressed by growth plate chondrocytes and not by epiphyseal chondrocytes. Immunohistochemistry of the fetal bovine growth plate identified a gradient of increasing annexin VIII protein from the proliferative to the hypertrophic zone. Immunofluorescence localized annexin VIII largely to the chondrocyte cell membrane. In a preliminary study, we examined the distribution of annexin VIII in normal and osteoarthritic (OA) articular cartilage. In OA cartilage, the protein was located in a subset of mid- to deep zone chondrocytes and in the matrix surrounding these cells; no annexin VIII was detected in normal articular cartilage. Thus annexin VIII is a marker for chondrocyte differentiation during normal endochondral ossification and may act as a marker for cells undergoing inappropriate differentiation in OA.

Amino Acid Sequence↗

PubMed2002

A role for the BMP antagonist chordin in endochondral ossification.

Bone morphogenetic proteins (BMPs) are ubiquitous regulators of cellular growth and differentiation. A variety of processes modulate BMP activity, including negative regulation by several distinct binding proteins. One such BMP antagonist chordin has a role in axis determination and neural induction in the early embryo. In this study, a role for chordin during endochondral ossification has been investigated. During limb development, Chordin expression was detected only at the distal ends of the skeletal elements. In cultured embryonic sternal chondrocytes, Chordin expression was related inversely to the stages of maturation. Further, treating cultured chondrocytes with chordin interfered with maturation induced by treatment with BMP-2. These results suggest that chordin may negatively regulate chondrocyte maturation and limb growth in vivo. To address this hypothesis, chordin protein was expressed ectopically in Hamburger-Hamilton (HH) stage 25-27 embryonic chick limbs. The phenotypic changes and alteration of gene expression in treated limbs revealed that overexpression of chordin protein delayed chondrocyte maturation in developing skeletal elements. In summary, these findings strongly support a role for chordin as a negative regulator of endochondral ossification.

Animals↗