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PubMed2004

Intramembranous ossification mechanism for bone bridge formation at the growth plate cartilage injury site.

Salter's type III and type IV growth plate injuries often induce bone bridge formation at the injury site. To understand the cellular mechanisms, this study characterized proximal tibial transphyseal injury in rats. Histologically, bony bridge trabeculae appeared on day 7, increased on day 10, and became well-constructed on day 14 with marrow. Prior to and during bone bridging, there was no cartilage proteoglycan metachromatic staining and no collagen-X immunostaining at the injury site, nor was there any up-regulation of BrdU-labelled chondrocyte proliferation at the adjacent physeal cartilage, suggesting no new cartilage formation at the injury site. However, infiltration of vimentin-immunopositive mesenchymal cells from metaphysis and epiphysis was apparent on day 3, with the mesenchymal population being prominent on days 7 and 10 and subsided on day 14. Among these infiltrates were osteoprogenitor precursors expressing osteoblast differentiation factor (cbf-alpha1) on day 3, along with some cbf-alpha1+ osteoblast-like cells lining bone trabeculae on days 7 and 10. Some mesenchymal cells and trabecula-lining cells were also alkaline phosphatase-immunopositive, further suggesting their osteoblast differentiation. From day 7 onwards, some trabecula-lining cells became osteocalcin-producing mature osteoblasts. These results suggest that bone bridge formation after growth plate injury occurs directly via intramembranous ossification through recruitment of marrow-derived osteoprogenitor cells.

Animals↗
PubMed2004

Endochondral ossification in fracture callus during long bone repair: the localisation of 'cavity-lining cells' within the cartilage.

Successful fracture healing typically involves the production of a cartilaginous callus, which is eventually remodelled into new bone. The blood vessels in the advancing front of endochondral ossification are likely to play an important role in the replacement of cartilage with bone within the callus. This was investigated by histology and immunohistochemistry techniques carried out on rabbit tibial osteotomy tissue. Cavities within the cartilage were identified by histology and in many cases, there appeared to be vascular structures within them, identified by the immunolocalisation of the transmembrane proteins CD31 and CD34. Osteocalcin localisation and Alizarin red histology was carried out to identify 'osteoblastic' cells and mineral localisation within the cartilaginous callus respectively. However, it was the identification of a population of cells lining the cavities within the cartilage that became the main focus of this study. These cells were 'osteoblastic' in nature, (positive localisation of osteocalcin), and were also positive for the adhesion proteins CD31 and CD34. It is thought that these cells play a role in the conversion of cartilage to bone during the fracture healing process.

Animals↗
PubMed2005

Altered hematopoiesis in glypican-3-deficient mice results in decreased osteoclast differentiation and a delay in endochondral ossification.

Loss of function mutations in the gene encoding the heparan sulfate proteoglycan Glypican-3 (GPC3) causes an X-linked disorder in humans known as Simpson-Golabi-Behmel Syndrome (SGBS). This disorder includes both pre- and postnatal overgrowth, a predisposition to certain childhood cancers, and a complex assortment of congenital defects including skeletal abnormalities. In this study, we have identified a previously unrecognized delay in endochondral ossification associated with the loss of Gpc3 function. Gpc3 knockout animals show a marked reduction in calcified trabecular bone, and an abnormal persistence of hypertrophic chondrocytes at embryonic day 16.5 (E16.5). These hypertrophic chondrocytes down-regulate Type X collagen mRNA expression and undergo apoptosis, suggesting a normal progression of hypertrophic chondrocyte cell fate. However, replacement of these cells by mineralized bone is delayed in association with a marked delay in the appearance of osteoclasts in the bone in vivo. This delay in vivo correlates with a significant reduction in the capacity to form osteoclasts from bone marrow macrophage precursors in vitro in response to M-CSF and RANKL, and with a reduction in the numbers of bone-marrow-derived cells expressing the markers CD11b and Gr-1. Together, these results indicate selective impairment in the development of the common hematopoietic lineage from which monocyte/macrophages and PMNs are derived. This is the first report of a requirement for heparan sulfate, and specifically Gpc3, in the lineage-specific differentiation of these cell types in vivo.

Animals↗
PubMed2006

Intramembranous ossification of scleral ossicles in Chelydra serpentina.

Scleral ossicles are present in many reptiles, including turtles and birds. In both groups the sclerotic ring situated in the eye is composed of a number of imbricating scleral ossicles or plates. Despite this gross morphological similarity, Andrews (1996. An endochondral rather than a dermal origin for scleral ossicles in Cryptodiran turtles. J. Herpetol. 30, 257-260) reported that the scleral ossicles of turtles develop endochondrally unlike those in birds, which develop intramembranously after a complex epithelial-mesenchymal inductive event. This study re-explores one of the species examined by Andrews in order to determine the mode of ossification of scleral ossicles in turtles. A growth series of Chelydra serpentina embryos, including the stages examined by Andrews, were examined by staining separately for cartilage and bone. Results clearly contradict Andrews (1996) and show that the scleral ossicles of Chelydra serpentina develop similarly to those in birds. That is, they develop intramembranously without a cartilage precursor and are likely induced by transient scleral papillae. The sequence of scleral papillae development is broadly similar, but the papillae themselves are not as distinct as those seen in chicken embryos. This study has important consequences for understanding the homology of scleral ossicles among tetrapods.

Animals↗
PubMed1996

Accessory ossification centres associated with osteochondral fragments in the extremities of horses.

Fifty-six tarsocrural joints and 94 metatarsophalangeal joints were examined, at necropsy, from horses aged < or = 2 years. Osteochondral fragments at the cranial aspect of the intermediate ridge of the distal part of the tibia were seen in six horses, and at the proximoplantar aspect of the proximal phalanx in seven horses. Defects in the proximoplantar aspect of the proximal phalanx without osteochondral fragments were seen in a further two horses. Inflammatory and degenerative changes were not observed in any of the joints examined. From the incidence and natural course of these fragments, and from the radiological and microscopical findings, accessory ossification centres would seem the most probable cause of the osteochondral fragments at the cranial aspect of the intermediate ridge of the distal part of the tibia and at the proximoplantar aspect of the proximal phalanx.

Animals↗
PubMed1994

A quantitative study on the spatial and temporal ossification patterns of vertebral centra and neural arches and their relationship to the fetal age.

A double-staining technique on 37 human embryos and fetuses (crown-rump length, CRL, between 38 and 116 mm) has been performed to study the ossification patterns of the vertebral column. Different growth sequences for centra and neural arches were observed. The survey of ossified centers suggested it was possible to relate significantly their appearance with the CRL. On the basis of already known data defining the developmental age in relationship to the latter parameter, we suggest their numerical evaluation as a further parameter for the assessment of the fetal age. Therefore, we have worked out a table that may be used either to determine the normal fetal growth, or when other parameters cannot be relied upon (i.e. in morphological diseases) for this aim.

Cervical Vertebrae↗
PubMed2002

Spontaneous differentiating primary chondrocytic tissue culture: a model for endochondral ossification.

Primary cartilage-derived cell cultures tend to undergo dedifferentiation, acquire fibroblastic features, and lose most of the characteristics of mature chondrocytes. This phenomenon is due mainly to the close matrix-cell interrelationship typical of cartilage tissue, which is vital for the preservation of the cartilaginous features. In this study we present a model for spontaneous redifferentiation of primary chondrocytic culture. Mandibular condyles excised from 3-day-old mice, thoroughly cleaned of all soft tissue, were digested with 0.1% collagenase. These mandibular condyle-derived chondrocytes (MCDC) were cultured under chondrogenesis-supporting conditions; that is, 5 x 10(5) cells/mL were incubated in Dulbecco's modified Eagle medium supplemented with 100 microg/mL ascorbic acid, 1 mmol/L calcium chloride, 10 mmol/L beta-glycerophosphate, 10% fetal calf serum, and antibiotics. Development and growth rates of these cartilage-derived cultures were determined by following morphological and functional changes. MCDC proliferated intensively during the first 24-48 h following plating, showing fibroblast-like (long spindle-shaped) morphology and producing mainly type I collagen. The proliferation rate gradually declined, and the cells developed polygonal shapes and started to produce type II collagen. In the 10-14-day-old cultures, cells began to aggregate in cartilaginous nodules and exhibited positive staining for acidic Alcian blue, type X collagen, and von Kossa. Expression of core-binding factor alpha(1) increased between 3 and 5 days and declined gradually thereafter. The condylar-derived tissue culture presented here depicts a spontaneous redifferentiation chondrocytic tissue culture that exhibits features of mature chondrocytes typically found in skeletal growth centers. The present study offers a model for primary chondrocytic tissue culture, which might serve as a model for in vitro endochondral ossification.

Animals↗
PubMed1989

Three cases of inter-sterno-costo-clavicular ossification associated with tonsillar infection.

Three cases of inter-sterno-costo-clavicular ossification (ISCCO) associated with chronic tonsillitis are reported. Two cases had additional symptoms of pustulosis palmaris et plantaris (PPP). All the patients underwent tonsillectomy. The histological changes of the palatine tonsils of case 1 and case 2 were characterized by so-called focal small lacunar ulcers and periarteriolar fibrosis (onion-skin lesion). Some multinucleated giant cells were observed in case 2. Following tonsillectomy, symptoms in the clavicular region and the PPP improved. It is possible to consider that ISCCO is caused by focal tonsillar infection.

Adult↗
PubMed1989

Early ossification within the human fetal otic capsule: morphological and microanalytical findings.

Besides the use of conventional techniques such as light and polarization microscopy, the present paper proposes the combined use of transmission electron microscopy, secondary and backscattered electron imaging, energy dispersive X-ray analysis and computed tomography for the diagnostic evaluation of ear pathology in the human fetus. These methods were used to revisit the primary calcification front of the fetal otic capsule between 16 and 23 weeks gestational age. Ultramicroscopic evaluation demonstrates similar fetal bone formation to that found in other bones of the human fetus. The formation of the endosteal and periosteal layers is a typical example of early intra-membranous ossification. The enchondral layer is made up of fibrillar bone, laid down around the calcified cartilage remnants. Microchemical analysis indicates a significantly higher Ca/P ratio in the endochondral layer with respect to the endosteum and periosteum. The consequences of a lower Ca/P ratio in the endosteal layer are discussed in view of calcium homeostasis and inner ear function.

Ear Cartilage↗
PubMed1998

Is acid phosphatase activity present in bone matrix at sites of endochondral ossification in rabbit fracture callus?

It has been suggested that acid phosphatase activity is present in newly formed bone matrix at sites of endochondral ossification in rabbit fracture calluses. Because acid phosphatases are usually found intracellularly, it was decided to test this possibility more rigorously. Tissue from 10- and 14-day healing rabbit fractures was subjected to a series of critical tests for acid phosphatases with a pH optimum of 5.0. Fluoride, tartrate and molybdate were used as potential inhibitors of acid phosphatase activity. The effects of several counterstaining protocols were also investigated. A fluoride- and tartrate-resistant acid phosphatase is located in osteoclasts and mononuclear phagocytes. Diffuse staining of the bone matrix is seen, but it is dependent upon the length of incubation in the substrate medium and the distance from the acid phosphatase-reacting cells. It is concluded that the coloration of the bone matrix is probably caused by diffusion of the dye and reaction product and is, therefore, artifactual.

Acid Phosphatase↗
PubMed1998

Immunohistochemical study on a macrophage calcium-type lectin in mouse embryos: transient expression in chondroblasts during endochondral ossification.

We investigated expression of mouse macrophage galactose/N-acetylgalactosamine-specific calcium-type lectin (MMGL) in mouse embryos using a rat monoclonal antibody (mAb) LOM-14 that we previously developed. Immunoblot analysis revealed that a significant expression of MMGL was first detected in detergent extracts of whole embryos of 11 days post coitus (dpc) and the level of its expression increased during further fetal development (examined up to 18-dpc embryos). Tissue sections of 12, 14, 16, and 18-dpc embryos, newborn and adult mice were investigated by immunohistochemical staining. In embryos of 12-dpc and later stages, mesenchymal cells (typically distributed in the embryonic skin) exhibited positive signals for MMGL. Interestingly, a conspicuous staining was observed during endochondral ossification in temporary cartilage tissue, in which chondroblasts were transiently positive for MMGL. The staining intensity for the chondroblasts peaked in 14-dpc embryos and then gradually decreased. The staining was diminished while hypertrophy and maturation of chondrocytes proceeded, and was eliminated in areas with calcification. Immunoelectron microscopic study demonstrated the presence of MMGL in rough endoplasmic reticulum in the chondroblasts in the temporary cartilage tissue in 14-dpc embryos. These results provide first evidence showing the expression of MMGL in cells other than macrophages.

Animals↗
PubMed2003

Skeletal dysplasias caused by a disruption of skeletal patterning and endochondral ossification.

Identification of a number of the genes that cause skeletal dysplasias has helped clinicians to provide accurate diagnoses, genetic counseling, and pre-natal diagnosis for this complex group of disorders. This review considers how some of the recent advances in human and murine genetics have led to an increased understanding of normal bone development and, in particular, the processes of skeletal patterning and endochondral ossification.

Animals↗
PubMed2000

Functional haploinsufficiency of the human homeobox gene MSX2 causes defects in skull ossification.

The genetic analysis of congenital skull malformations provides insight into normal mechanisms of calvarial osteogenesis. Enlarged parietal foramina (PFM) are oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month. PFM are usually asymptomatic, but may be associated with headache, scalp defects and structural or vascular malformations of the brain. Inheritance is frequently autosomal dominant, but no causative mutations have been identified in non-syndromic cases. We describe here heterozygous mutations of the homeobox gene MSX2 (located on 5q34-q35) in three unrelated families with PFM. One is a deletion of approximately 206 kb including the entire gene and the others are intragenic mutations of the DNA-binding homeodomain (RK159-160del and R172H) that predict disruption of critical intramolecular and DNA contacts. Mouse Msx2 protein with either of the homeodomain mutations exhibited more than 85% reduction in binding to an optimal Msx2 DNA-binding site. Our findings contrast with the only described MSX2 homeodomain mutation (P148H), associated with craniosynostosis, that binds with enhanced affinity to the same target. This demonstrates that MSX2 dosage is critical for human skull development and suggests that PFM and craniosynostosis result, respectively, from loss and gain of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.

Adult↗
PubMed2001

Haploinsufficiency of the human homeobox gene ALX4 causes skull ossification defects.

Inherited defects of skull ossification often manifest as symmetric parietal foramina (PFM; MIM 168500). We previously identified mutations of MSX2 in non-syndromic PFM and demonstrated genetic heterogeneity. Deletions of 11p11-p12 (proximal 11p deletion syndrome, P11pDS; MIM 601224) are characterized by multiple exostoses, attributable to haploinsufficiency of EXT2 and PFM. Here we identify ALX4, which encodes a paired-related homeodomain transcription factor, as the PFM disease gene in P11pDS.

Animals↗
PubMed1999

Expression of tissue transglutaminase in the developing chicken limb is associated both with apoptosis and endochondral ossification.

The cross-linking enzyme tissue transglutaminase (tTG) participates in a variety of cellular functions. To assess its contribution to extracellular and intracellular processes during development we cloned the cDNA for chicken heart tissue transglutaminase and localized the sites of transglutaminase expression by in situ hybridization and immunohistochemistry. Compared with the chicken red blood cell transglutaminase cDNA, the heart cDNA encodes a transglutaminase with an amino-terminal truncation. The truncated enzyme retains full catalytic activity and is GTP-inhibitable. Tissue transglutaminase expression was observed in developmentally transient structures in embryonic chicken limb at day 7.5 of incubation suggesting that its expression is dynamically regulated during limb morphogenesis. The major morphogenetic events of the limb associated with transglutaminase expression were cartilage maturation during skeletal development, interdigital apoptosis, and differentiation of skeletal muscle. Maturation of the cartilage during endochondral ossification was characterized by intra- and extracellular transglutaminase accumulation in the zone of hypertrophic chondrocytes. Only intracellular enzyme could be detected in mesenchymal cells of the prospective joints, in apoptotic cells of the interdigital web, and in skeletal muscle myoblasts. An apparently constitutive expression of tissue transglutaminase was found in vascular endothelial cells corresponding to the adult expression pattern. The dynamic pattern of transglutaminase expression during morphogenesis suggests that tissue remodeling is a major trigger for transglutaminase induction.

Animals↗
PubMed1998

Complete absence of rib ossification, micrognathia and ear anomalies: extreme expression of cerebro-costo-mandibular syndrome?

We describe a newborn with complete absence of ossification of the ribs, extreme micrognathia, absence of external ear canals and the inner ears, and diminished mobility in the upper extremities. It is suggested that this represents an unusually severe expression of the cerebro-costo-mandibular syndrome. Some developmental genes that may have played a role in the pathogenesis are briefly reviewed.

Abnormalities, Multiple↗
PubMed2000

Radiotherapy as a local treatment option for heterotopic ossifications in patients with spinal cord injury.

OBJECTIVE: Heterotopic ossifications (HO) occur in about 20% of patients with spinal cord injury and may seriously compromise the rehabilitation process. The aim of the present study was to ascertain whether radiotherapy (RT) administered early in the course of the disease prevents the manifestation of HO and whether in patients, whose HO have been resected, recurrence can be avoided. METHODS: Thirty-six patients (46 joints) were irradiated; 33 patients were evaluable. Mean follow up was 23.6 months. In 27 patients RT was performed as primary treatment in the inflammatory phase of soft tissue swelling that precedes manifest HO. Eleven patients were treated after resection of manifest HO, while two had primary and postoperative RT in different joints. The dose was 10 Gy in fractions of 2-2.5 Gy in 25 patients. Four patients were treated with total doses between 7.5 and 20 Gy. Seven patients received single dose irradiation with 8 Gy. RT was performed with 8 MV photons after simulation on the basis of CT scans. RESULTS: The mean duration of follow up was 23.6 months. Thirty of the 36 irradiated patients showed no progression of HO. In three patients reossifications after therapy caused a moderate decrease in joint mobility. No relevant adverse effects were observed. CONCLUSION: These results suggest that RT is a safe and effective local treatment option for spinal cord injury patients with HO.

Adolescent↗
PubMed2003

Angiogenesis in the distal femoral chondroepiphysis of the rabbit during development of the secondary centre of ossification.

In the developing chondroepiphyses of long bones, the avascular cartilaginous anlage is invaded by numerous blood vessels, through the process of angiogenesis. The objective of this study was to investigate the chronology of this vascular invasion with the spontaneous calcification of the cartilaginous epiphysis during development of the secondary ossification centre in the rabbit distal femur. The time-course of chondroepiphyseal vascular invasion was determined histologically and standardized for eight gestational and four postnatal intervals by plotting kit body mass against crown-rump length. Similarly, microcomputed tomography (micro-CT) helped to visualize calcification at those same gestational and postnatal intervals. To confirm the angiogenic nature of the avascular chondroepiphysis, such samples were assayed on the chick chorio-allantoic membrane (CAM). Neovascular outgrowths from the CAM were apparent 48 h following introduction of an 18-day (gestational) chondroepiphyseal sample. Chondroepiphyseal samples were assayed for the potent developmental angiogenic factors bFGF and VEGF, with the mRNA expression for both these mediators being confirmed using RT-PCR. As angiogenesis and calcification during chondroepiphyseal development occur in a defined tissue environment initially devoid of blood vessels and mineral, those processes provided a unique opportunity to study their progression without complication of injury-related inflammation or extant vasculature and mineral. Furthermore, the discovery of angiogenic, angiostatic or mineral-regulating mediators specific to developing connective tissue may prove useful for analysing the regulation of vascular and mineral pathogenesis in articular tissues.

Actins↗