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PubMedDate not supplied

Postnatal development of the human sternum.

Postnatal development and maturation of the human sternum are highly variable. Endochondral ossification centers (sternebrae) form within each cartilaginous segment of the sternum, with each center enveloped by a spherical growth plate. Within a cartilaginous center there may be either one or two ossification centers, those with two centers retaining and reflecting features of their bilateral embryonic origin. Malaligned bifid centers are clearly associated with rib articulation asymmetry as well. Expansion of individual ossification centers progresses within the peripheral cartilaginous domains of the sternum. With respect to the rostrocaudal axis, sternebrae form between the costosternal articulations. Consistent with the biology of endochondral transition, cartilage canals are evident throughout unossified regions of the hyaline matrix. Expanding ossification of adjacent sternebrae results in depletion of the common area of cartilage between the two sternebrae, and eventually in physiologic epiphysiodesis. Fusion of the mesosternebrae reciprocates the initial pattern of sternebral ossification site appearance, proceeding in a caudal-to-cranial direction. Union of adjacent sternebrae, initiated through a central osseous bridge, progresses through anterior, lateral, cephalocaudal, and posterior domains to achieve synostosis. Accessory and bifid centers of ossification within the same intercostal space coalesce prior to adjoining adjacent sternebrae. Manubriosternal fusion is rare due to the presence of a fibrocartilaginous joint restricting ossification. The xiphoid process remains connected to the most caudal mesosternum via a common zone of hyaline cartilage that ossifies by middle to late adulthood. A single pattern of development does not appear fundamental to successful growth of the sternum, as morphological variants were common.

Adolescent↗
PubMed2004

Macrophagic response to human mesenchymal stem cell and poly(epsilon-caprolactone) implantation in nonobese diabetic/severe combined immunodeficient mice.

Nonobese diabetic, severe combined immunodeficient (NOD/SCID) mice are extensively used to assess in vivo potentials for human cellular differentiation, development, and neophysiology. They are not only deficient in T and B cells, but also exhibit macrophage dysfunction and an absence of circulating complement. However, the survival of engrafted human mesenchymal stem cells (hMSCs) is limited and minimal mature bone tissue develops from implanted hMSCs in this model. The aim of the present study was to investigate the response to such implants in NOD/SCID mice. To this end, hMSCs genetically marked with enhanced green fluorescent protein, a biodegradable polymer, poly(epsilon-caprolactone) (PCL), and a bioconstruct incorporating the enhanced green fluorescent protein-labeled hMSCs with PCL after culture together for 3 weeks in vitro, were implanted into NOD/SCID mice and followed for up to 10 weeks. Monocytes/macrophages appeared to be the major invading cell type in all the implants and remained in the materials regardless of whether or not hMSCs were present over the time periods studied. When the hMSCs were implanted without the PCL scaffold, host macrophage invasion was also observed with the majority of hMSCs being eliminated within 2 weeks. Multinuclear giant cells or foreign body giant cells were seen in the cases of PCL implantation. These cells slowly infiltrated into the central core of the materials over a 10-week period of implantation with neutrophils and mast cells also being observed. In conclusion, in NOD/SCID mice, monocytes/macrophages still effectively respond to the implantation of xenografts and biopolymers with functional migration, phagocytosis, adhesion, foreign body recognition and formation of multinuclear giant cells, or foreign body giant cells. Thus, these animals still retain a level of innate immune responsiveness to these implantations and in addition may provoke a physiological environment that is unsuitable for extensive intramembranous ossification by engrafted hMSCs.

Animals↗
PubMed1987

Ultrasonography of the infant hip. Part III: Clinical application.

We report on our results of ultrasonography of the infant hip over 2 years. Twenty-three percent of patients with abnormal sonogram showed no clinical suggestion of hip disorder. Suspicion of dislocation based on mobility, asymmetrical trochanteric distance, click or snapping of the hip and inhibited abduction were the most useful clinical criteria predicting disease in 93%, 19% and 16%, respectively. Breech presentation and family history of hip dysplasia or dislocation were important anamnestic data (21% and 16% predictive value, respectively). The significantly shorter duration of therapy in early detected dislocation or dysplasia makes the need for early diagnosis of these disorders obvious. Special emphasis lies on the physiological maturation of the acetabulum and the femoral ossification center. Normal ranges of important diagnostic criteria and angles depending on chronological age are presented.

Hip↗
PubMed1995

Osteochondroma of the distal tibia. A case study.

Osteochondromas can undergo malignant transformation, and although the incidence is low, it is important to recognize symptoms that might suggest transformation. Complaints of increasing pain or a dramatic increase in the size of the lesion must not be ignored. If the physician is confident that the lesion is benign and chooses not to resect it, the patient should be monitored periodically with serial radiographs in order to identify any potential degenerative changes that might develop. Since osteochondromas are usually associated with the growth plate of a long bone, the potential for progressive growth exists. This growth takes place through the process of enchondral ossification until closure of the physis occurs. After physiologic fusion of the physis, remnants of the cartilaginous cap may remain, possibly explaining the occasional development of peripheral chondrosarcomas later in life.

Adolescent↗
PubMed1997

Bone mineral density in patients with ossification of the posterior longitudinal ligament. Minimal decrease of bone mineral density with aging.

STUDY DESIGN: Bone mineral density of individuals with ossification of the posterior longitudinal ligament and that of normal people was determined by dual-energy x-ray absorptiometry. OBJECTIVES: To determine whether bone mineral density in the people with ossification of the posterior longitudinal ligament is higher than that in normal individuals even in body parts other than the spine, and to evaluate the relation between bone mineral density and age in patients with ossification of the posterior longitudinal ligament. SUMMARY OF BACKGROUND DATA: It is unknown whether the bone mineral density of patients with ossification of the posterior longitudinal ligament is greater in body parts other than the spine. If so, it provides a basis for the theory that certain systemic factors are involved in the pathogenesis of ossification of the posterior longitudinal ligament. Because bone mineral density decreases physiologically after middle age, the influence of age must be considered in evaluating bone mineral density. METHODS: In the rib area and upper and lower limb areas, which are not affected by ossification of the spinal ligament, bone mineral density of 45 men with ossification of the posterior longitudinal ligament of the cervical spine was compared with that of 25 men without ossification of the posterior longitudinal ligament (normal group). RESULTS: Bone mineral density was higher in the group with ossification of the posterior longitudinal ligament in each part and significantly higher in the rib and lower limb areas (rib: P < 0.01, lower limb: P < 0.05). The age-related decrease was significantly less in the group with ossification of the posterior longitudinal ligament (rib: P < 0.01, upper limb: P < 0.05, lower limb: P < 0.01). CONCLUSIONS: Systemic factors that increase bone mineral density appear to be involved in the pathogenesis of ossification of the posterior longitudinal ligament, and these factors may be activated after middle age.

Absorptiometry, Photon↗
PubMed2002

Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18.

Gain of function mutations in fibroblast growth factor (FGF) receptors cause chondrodysplasia and craniosynostosis syndromes. The ligands interacting with FGF receptors (FGFRs) in developing bone have remained elusive, and the mechanisms by which FGF signaling regulates endochondral, periosteal, and intramembranous bone growth are not known. Here we show that Fgf18 is expressed in the perichondrium and that mice homozygous for a targeted disruption of Fgf18 exhibit a growth plate phenotype similar to that observed in mice lacking Fgfr3 and an ossification defect at sites that express Fgfr2. Mice lacking either Fgf18 or Fgfr3 exhibited expanded zones of proliferating and hypertrophic chondrocytes and increased chondrocyte proliferation, differentiation, and Indian hedgehog signaling. These data suggest that FGF18 acts as a physiological ligand for FGFR3. In addition, mice lacking Fgf18 display delayed ossification and decreased expression of osteogenic markers, phenotypes not seen in mice lacking Fgfr3. These data demonstrate that FGF18 signals through another FGFR to regulate osteoblast growth. Signaling to multiple FGFRs positions FGF18 to coordinate chondrogenesis in the growth plate with osteogenesis in cortical and trabecular bone.

Animals↗
PubMed2006

Effectiveness of posterior decompression for patients with ossification of the posterior longitudinal ligament in the thoracic spine: usefulness of the ossification-kyphosis angle on MRI.

STUDY DESIGN: A reliability study was conducted. OBJECTIVE: To report the utility of the ossification- kyphosis angle of a decompression site in the sagittal view of MRI in the preoperative evaluation of the effectiveness of posterior decompression for patients with ossification of the posterior longitudinal ligament in the thoracic spine. SUMMARY OF BACKGROUND DATA: In patients with ossification of the posterior longitudinal ligament, in the thoracic spine, posterior decompression may not always be effective for those with physiologic kyphosis; however, posterior decompression is sometimes useful for patients with multilevel lesions or with ossification of the ligamentum flavum. Therefore, it is necessary to evaluate the indications or limitations of posterior decompression before surgery. METHODS: The indications or limitations of posterior decompression for this disease were reviewed from the findings of intraoperative ultrasonography and various parameters on preoperative imaging in 22 patients with thoracic myelopathy. RESULTS: Thirteen patients had echo-free space and 9 patients had no echo-free space in intraoperative ultrasonography after posterior decompression. In the kyphosis angle of the decompression site and the configuration of the maximal prominent OPLL, there was no significant difference between the group with echo-free space and the group without echo-free space (P = 0.49, P = 0.55). On the other hand, the ossification-kyphosis angle of the decompression site was more than 23 degrees in all patients with no echo-free space (23 degrees -34 degrees , 28.2 degrees +/- 3.6 degrees ), and it was less than 23 degrees in all patients with echo-free space (10 degrees -23 degrees , 17.4 degrees +/- 4.1 degrees ). There was also significant difference between the groups statistically (P < 0.01, P = 1.50789E-06). In addition, in the occupation rate of the greatest prominence of the OPLL, there was statistically significant difference between the groups (P = 0.032). CONCLUSION: The ossification-kyphosis angle in the sagittal view of MRI has potential as an indicator of the effectiveness of posterior decompression in this disease. It is thought that there is a critical point of posterior decompression at nearly 23 degrees of the ossification-kyphosis angle of the decompression site. When the ossification-kyphosis angle is more than 20 degrees , the presence of echo free space should be carefully confirmed in intraoperative ultrasonography.

Adult↗
PubMedDate not supplied

CTGF/Hcs24 as a multifunctional growth factor for fibroblasts, chondrocytes and vascular endothelial cells.

Connective tissue growth factor/hypertrophic chondrocyte-specific gene product 24 (CTGF/Hcs24), a member of the CCN family, is a multifunctional growth factor for fibroblasts, chondrocytes and vascular endothelial cells. Depending on the type of cell with which it interacts, it promotes chemotaxis, migration, adhesion, proliferation, differentiation and/or extracellular matrix formation. Because gene expression of CTGF/Hcs24 is maximal in hypertrophic chondrocytes in the physiological state, a major physiological role for this factor should be the promotion of endochondral ossification. On the other hand, its expression is up-regulated during wound healing, indicating the involvement of this factor in this process as well. When overexpressed, CTGF/Hcs24 may cause pathological states such as fibrotic disorders and angiogenic diseases. This review focuses on the physiological and pathological significances of this novel type of growth factor.

Animals↗
PubMed2005

AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer.

Inhibition of vascular endothelial growth factor-A (VEGF) signaling is a promising therapeutic approach that aims to stabilize the progression of solid malignancies by abrogating tumor-induced angiogenesis. This may be accomplished by inhibiting the kinase activity of VEGF receptor-2 (KDR), which has a key role in mediating VEGF-induced responses. The novel indole-ether quinazoline AZD2171 is a highly potent (IC50 < 1 nmol/L) ATP-competitive inhibitor of recombinant KDR tyrosine kinase in vitro. Concordant with this activity, in human umbilical vein endothelial cells, AZD2171 inhibited VEGF-stimulated proliferation and KDR phosphorylation with IC50 values of 0.4 and 0.5 nmol/L, respectively. In a fibroblast/endothelial cell coculture model of vessel sprouting, AZD2171 also reduced vessel area, length, and branching at subnanomolar concentrations. Once-daily oral administration of AZD2171 ablated experimental (VEGF-induced) angiogenesis in vivo and inhibited endochondral ossification in bone or corpora luteal development in ovary; physiologic processes that are highly dependent upon neovascularization. The growth of established human tumor xenografts (colon, lung, prostate, breast, and ovary) in athymic mice was inhibited dose-dependently by AZD2171, with chronic administration of 1.5 mg per kg per day producing statistically significant inhibition in all models. A histologic analysis of Calu-6 lung tumors treated with AZD2171 revealed a reduction in microvessel density within 52 hours that became progressively greater with the duration of treatment. These changes are indicative of vascular regression within tumors. Collectively, the data obtained with AZD2171 are consistent with potent inhibition of VEGF signaling, angiogenesis, neovascular survival, and tumor growth. AZD2171 is being developed clinically as a once-daily oral therapy for the treatment of cancer.

Administration, Oral↗