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PubMed2004

The balance between concurrent activation of ERs and PPARs determines daidzein-induced osteogenesis and adipogenesis.

UNLABELLED: The soy phytoestrogen daidzein has biphasic dose responses, but the underlying mechanisms are not yet clear. Transcriptional and biochemical data show that PPARs, in addition to ERs, are molecular targets of daidzein, which divergently regulates osteogenesis and adipogenesis. Dose responses are the result of a balance among PPARs and between ERs and PPARs. INTRODUCTION: Soy phytoestrogens have been used for the purposes of treatment and prevention of osteoporosis. Biphasic dose responses of daidzein, one of the main soy phytoestrogens, have long been recognized, but the underlying molecular mechanisms of action are not yet clear. MATERIALS AND METHODS: Mouse bone marrow cells and mouse osteoprogenitor KS483 cells that concurrently differentiate into osteoblasts and adipocytes were cultured. Biochemical measurement of alkaline phosphatase (ALP) activity, RT-PCR, and gene reporter assays were used in this study. RESULTS: Daidzein, one of the major soy phytoestrogens, had biphasic effects on osteogenesis and adipogenesis. Daidzein stimulated osteogenesis (ALP activity and nodule formation) and decreased adipogenesis (the number of adipocytes) at concentrations below 20 microM, whereas it inhibited osteogenesis and stimulated adipogenesis at concentrations higher than 30 microM. When estrogen receptors (ERs) were blocked by ICI182,780, daidzein-induced effects were not biphasic. A decrease in osteogenesis and an increase in adipogenesis were observed at the concentrations higher than 20 and 10 microM, respectively. In addition to ERs, daidzein transactivated not only peroxisome proliferator-activate receptor gamma (PPARgamma), but also PPARalpha and PPARdelta at micromolar concentrations. Activation of PPARalpha had no direct effects on osteogenesis and adipogenesis. In contrast, activation of PPARdelta stimulated osteogenesis but had no effects on adipogenesis, whereas PPARgamma inhibited osteogenesis and stimulated adipogenesis. Transfection experiments show that an activation of PPARalpha or PPARgamma by daidzein downregulated its estrogenic transcriptional activity, whereas activation of PPARdelta upregulated its estrogenic transcriptional activity. Activation of ERalpha or ERbeta by daidzein downregulated PPARgamma transcriptional activity but had no influence on PPARalpha or PPARdelta transcriptional activity. CONCLUSIONS: Daidzein at micromolar concentrations concurrently activates different amounts of ERs and PPARs, and the balance of the divergent actions of ERs and PPARs determines daidzein-induced osteogenesis and adipogenesis.

Adipocytes↗

PubMed1993

Heterotopic induction of osteogenesis in the course of neural injury.

Encountered in orthopedics cases of accelerated bone union and abundant formation of the callus in patients after craniocerebral injuries as well as cases of extraskeletal ossification in neural diseases give rise to a question whether neural damage affects in any way the course of osteogenesis. The present study was carried out in an attempt to answer this question in an animal model. The study included 120 inbred WAG rats in which heterotopic induction of osteogenesis was performed by intramuscular placement of decalcified and lyophilized implants of rat cortical bones. By producing various neural damages their effect on the course of osteogenesis was evaluated. The rats were divided into four groups of 30 subjects each. In group I cerebral cortical damage was induced by intracortical injection of kainic acid solution, in group II paraplegia was produced by transverse dissection of the spinal cord on the level of Th 10-11, in group III denervation of the hind limb was performed by dissection of all supplying peripheral nerves, group IV consisted of controls. An attempt was made to evaluate changes in the course of osteogenesis while observing advancing with the passage of time changes in histological patterns of the preparations obtained from the site of bone implantation at 3, 5, 10, 20 and 40 days after the operation. While analyzing the histological pattern I paid attention to features characteristic for the process of osteogenesis such as: formation of granulation around bone grafts, penetration of mesenchymal cells into transplants, differentiation of mesenchymal cells into osteogenic cells, formation of bone tissue and development of bone marrow. The rate of development of these features in the consecutive preparations reflected the dynamics of induced osteogenesis. Analysis of the results showed that experimentally induced neural damage affects the course of osteogenesis. In case of cerebral cortical injury and peripheral neurotomy the formation of granulation around bone grafts was very abundant, whereas penetration of mesenchymal cells into the implants and differentiation of mesenchymal cells into chondroblasts occurred more rapidly than in other animal groups. In contrast, spinal cord injury resulted in a markedly decreased dynamics of osteogenesis which was manifested by weaker cell reaction around the implants and delayed differentiation of mesenchymal cells into chondroblasts. The effect was seen on the 20th day. In the final stage of the study--at 40 days--the effect of neural damage on the course of osteogenesis was reduced and the histological pattern was similar in all animal groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Regulation of osteogenesis by fetuin.

Osteoporosis is a common problem of aging and results from a failure of homeostatic mechanisms to regulate osteogenesis and mineralization. Bovine and human forms of fetuin glycoprotein bind to the transforming growth factor (TGF)-beta/BMP (bone morphogenic protein) cytokines and block their osteogenic activity in cell culture assays (Demetriou, M., Binkert, C., Sukhu, B., Tenenbaum, H. C., and Dennis, J. W. (1996) J. Biol. Chem. 271, 12755-12761). Fetuin is a prominent serum glycoprotein and a major noncollagenous component of mineralized bone in mammals. In this study, we show that recombinant fetuin and native serum protein have similar potency as inhibitors of osteogenesis in dexamethasone-treated rat bone marrow cell cultures (dex-RBMC). Recombinant bovine fetuin also bound to TGF-beta1 and BMP-2 in vitro with kinetics similar to native fetuin. Although TGF-beta1 is required for osteogenesis in dex-RBMC, the cytokine also inhibited osteogenesis at concentrations >/=10 pM. Titration of fetuin or anti-TGF-beta1 antibodies into the bone marrow cultures in the presence of 10 pM TGF-beta1 restored osteogenesis, whereas titrations of the same reagents into cultures with 0.3 pM added TGF-beta1 were inhibitory, confirming the biphasic nature of the TGF-beta1 response. Suppression of osteogenesis by both TGF-beta1 and the antagonist proteins required their presence within the first 6 days of culture, well before mineralization at 10-12 days. Northern analysis showed that both fetuin and high dose TGF-beta1 suppressed expression of the bone-associated transcripts alkaline phosphatase, osteopontin, collagen type I, and bone sialoprotein. The suppression of osteogenesis by fetuin and by high dose TGF-beta1 was accompanied by the differentiation of an alternate cell lineage with adipocyte characteristics. In summary, the biphasic osteogenic response to TGF-beta1 suggests that overlapping gradients of TGF-beta/BMP cytokines and fetuin regulate osteogenesis in remodeling bone.

Amino Acid Sequence↗

PubMed2006

Temporomandibular joint bony ankylosis: comparison of treatment with transport distraction osteogenesis or the matthews device arthroplasty.

Temporomandibular joint (TMJ) bony ankylosis with micrognathia is a rare congenital condition that is difficult to treat and may result in recurrence. In a series of affected patients, we compared two new methods of treatment: transport distraction osteogenesis and Matthews Device arthroplasty. All patients had computed tomography scan documented bilateral TMJ bony ankylosis. Group I (transport distraction osteogenesis) underwent distraction advancement of the mandible (for micrognathia) followed by resection of the condyles, recontouring of the glenoid fossas with interposition temporoparietal-fascial flaps, and transport distraction osteogenesis of mandibular rami segments. Group II (Matthews Device arthroplasty) underwent all of the above procedures except for transport distraction osteogenesis. Instead, the Matthews Devices were anchored to the temporal bone and mandibular rami. Hinged arms allowed for motion at the reconstructed TMJ. In both groups, patients underwent extensive postoperative therapy. Preoperative, postoperative, and follow-up lateral cephalograms were obtained, and incisor opening distances were recorded. All patients but one had severe micrognathia (n = 9). For group I (transport distraction osteogenesis), mean age was 6.8 years. and mean advancement was 28.5 mm. For group II (Matthews Device arthroplasty) mean age was 8.2 years, and mean advancement was 23.5 mm. In group I (transport distraction osteogenesis), mean incisor opening was 1 mm preoperatively and 27.5 mm postoperatively; however, it relapsed to 14.3 mm by 12.5 months follow-up (48% relapse). Mean incisor opening in group II (Matthews Device arthroplasty) was 3.9 mm preoperatively and 33.4 mm postoperatively and remained at 30.6 mm after 11.1 months follow-up (8% relapse). One patient in group I (transport distraction osteogenesis) underwent surgical revision because of relapse. Our data showed that for congenital TMJ bony ankylosis both transport distraction osteogenesis and Matthews Device arthroplasty techniques were successful initially; however, the Matthews Device arthroplasty avoided long-term relapse.

Adolescent↗

PubMed2000

Potential of gene therapy for treating osteogenesis imperfecta.

Osteogenesis imperfecta is a heterogeneous group of genetic disorders that affect connective tissue integrity, with bone fragility being the major clinical feature. Most forms of osteogenesis imperfecta are the result of mutations in the genes that encode the pro alpha1 and pro alpha2 polypeptide chains of Type I collagen. Because osteogenesis imperfecta is an incurable genetic disease, cell therapy and gene therapy are being investigated as potential treatments. Gene therapy for osteogenesis imperfecta however is a major challenge; because most of the mutations in osteogenesis imperfecta are dominant negative, supplying the normal gene without silencing the abnormal gene may not be beneficial. Null mutations in which an allele is not expressed or absent may be amenable to gene therapy or alternatively after silencing a mutant allele, a normal gene could be supplied. In addition, overexpression of the normal collagen gene in cells expressing mutant collagen polypeptide chains potentially could lead to synthesis of a sufficient percentage of normal molecules to normalize clinical status. The authors currently are examining the possibility of developing gene therapy for treating a mouse model of human osteogenesis imperfecta (oim) using bone marrow stromal cells as vehicles for delivering normal collagen genes to bone. In the current study, the potential of gene therapy for treating osteogenesis imperfecta is discussed in the context of the complexity of the mutations in Type I collagen genes that lead to different osteogenesis imperfecta phenotypes.

Animals↗

PubMed1998

Rat mandibular distraction osteogenesis: Part I. Histologic and radiographic analysis.

The application of distraction osteogenesis to craniofacial surgery has altered the approach and treatment of congenital and acquired craniofacial defects. Although the histologic and ultrastructural changes associated with distraction osteogenesis have been described extensively, relatively little is known about the molecular regulation of this process. The elucidation of the molecular mechanisms of distraction osteogenesis has important clinical implications because it may facilitate the use of recombinant proteins or gene therapy to accelerate bone regeneration. Molecular analysis of distraction osteogenesis has been hindered by the use of large animal models in which only limited genetic information is available. In this study, a rat model of mandibular distraction osteogenesis is described. This report includes a pilot study (n = 50) to develop an appropriate distraction device and to determine the optimal placement of the osteotomy. The study subsequently included 80 animals, 35 of which were distracted at a rate of 0.25 mm per day for 6 days (1.5 mm total) and 35 that were distracted at a rate of 0.25 mm twice per day (3.0 mm total). These animals were killed at various time points (after latency and during the distraction and consolidation periods) and displayed histologic and radiographic findings of membranous bone distraction osteogenesis that were consistent with those in large ,animal and clinical models. In addition, five animals each were acutely lengthened 1.5 mm and 3.0 mm and demonstrated a fibrous nonunion. Furthermore, the utility of this model is demonstrated in the analysis of the molecular mechanisms of distraction osteogenesis by applying the polymerase chain reaction to total cellular RNA isolated from normal and distracted rat mandibles. In conclusion, it is believed that the rat model of distraction osteogenesis has significant advantages over traditional models, including decreased costs and facilitation of molecular analysis.

Animals↗

PubMed1999

Spinal deformity, pulmonary compromise, and quality of life in osteogenesis imperfecta.

STUDY DESIGN: A cross-sectional radiologic and clinical study of patients with osteogenesis imperfecta. OBJECTIVES: To determine whether pulmonary compromise is more closely correlated with scoliosis, kyphosis, or chest wall deformity in the population with osteogenesis imperfecta, and to assess the impact of spinal deformity, chest wall deformity, and pulmonary function on quality of life. SUMMARY OF BACKGROUND DATA: The incidence of scoliosis in osteogenesis imperfecta is between 39% and 80%. Up to 60% of patients with osteogenesis imperfecta have significant chest wall deformities. Pulmonary compromise is the leading cause of death in adults with osteogenesis imperfecta. METHODS: Fifteen patients with osteogenesis imperfecta between the ages of 20 and 45 were evaluated with sitting or standing anteroposterior and lateral radiographs of the entire spine, pulmonary function testing, and a validated health self-assessment questionnaire (Short Form-36). Radiographs were evaluated for thoracic scoliosis, thoracic kyphosis, and chest wall deformity. Correlation analysis was performed. RESULTS: Thoracic scoliosis was strongly correlated with decreased predicted vital capacity (r = -0.76). Significant diminution in vital capacity below 50% occurred at a curve magnitude of 60 degrees. Kyphosis and chest wall deformity were not predictive of decreased pulmonary function. Physical health (PCS) was closely correlated with predicted vital capacity (r = 0.65; P < 0.01) and with scoliosis (r = -0.52; P < 0.05). CONCLUSIONS: Thoracic scoliosis of more than 60 degrees has severe adverse effects on pulmonary function in those with osteogenesis imperfecta. This finding may partly explain the increased pulmonary morbidity noted in adult patients with osteogenesis imperfecta and scoliosis compared with that in the general population.

Adult↗

PubMed2003

Focal adhesion kinase expression during mandibular distraction osteogenesis: evidence for mechanotransduction.

Distraction osteogenesis is an established treatment strategy in the reconstruction of the craniofacial skeleton. The underlying mechanisms that drive bone formation during this process are largely unknown, but a regulatory role for mechanical force is believed to be critical. The integrin-mediated signal transduction cascade is a primary pathway by which signal transduction of mechanical stimuli (i.e., mechanotransduction) occurs. Focal adhesion kinase (FAK) is a significant regulator in this pathway. The authors hypothesize that mechanical forces created during distraction osteogenesis are responsible for the osteogenic response that takes place, and that these changes arise through integrin-dependent mechanotransduction. Using a rat model of distraction osteogenesis, the authors examined the expression of FAK in critical size defects (n = 15), subcritical size defects (n = 15), and mandibles undergoing distraction osteogenesis (n = 15). Their findings demonstrated FAK immunolocalization in mandibles undergoing distraction osteogenesis, but not in the critical size defects or in subcritical size defects, despite varying degrees of bone formation in the latter two groups. Furthermore, bone sialoprotein mRNA in situ hybridization patterns were found to mirror FAK immunolocalization patterns in mandibles undergoing distraction osteogenesis, demonstrating an association of FAK expression with the osteogenic process specific to distraction osteogenesis. These findings suggest that the bone formation in distraction osteogenesis is regulated by mechanical force by means of integrin-dependent mechanotransduction pathways.

Animals↗

PubMed1993

Serum concentrations of procollagen I C-terminal propeptide, osteocalcin and insulin-like growth factor-I in patients with non-lethal osteogenesis imperfecta.

Serum concentrations of procollagen I C-terminal propeptide (PICP) were studied in 74 patients with various forms of non-lethal osteogenesis imperfecta and 27 unaffected family members. Using the standard deviation (SD) score, PICP concentrations were found to be > or = -1 SD in 16%, between -1 and -2 SD in 26% and < or = -2 SD in 58% of the patients with osteogenesis imperfecta compared to healthy controls. PICP values were lowest in osteogenesis imperfecta type I (-2.4 +/- 0.4 SD, n = 37) followed by type III (-1.9 +/- 0.5 SD, n = 13) and type IV (-1.3 +/- 0.7 SD, n = 20). Four patients with osteogenesis imperfecta with an atypical clinical course had normal or even elevated levels which may indicate heterogeneity in the underlying primary defects. In osteogenesis imperfecta type I, PICP concentrations proved to be a helpful serum marker for pedigree screening. Osteocalcin was high in 25 of 28 patients with osteogenesis imperfecta in the first decade but only in 1 of 18 older patients. Insulin-like growth factor-I was within the normal range in 53 cases of osteogenesis imperfecta, decreased in 2 and elevated in 3 patients. We conclude that PICP concentration is a useful parameter in the clinical management of osteogenesis imperfecta, including the assessment of future therapeutic interventions.

Adolescent↗

PubMed1995

Characterization of inhibitory effects of suspected periodontopathogens on osteogenesis in vitro.

By using an in vitro bone-forming culture system, the chick periosteal osteogenesis (CPO) model, the direct effects on osteogenesis of sonicated extracts derived from oral bacteria were examined. Both extracts from bacterial species having strong associations with periodontal diseases (Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Prevotella intermedia, hereinafter referred to as suspected periodontopathogens) and extracts from species not correlated with periodontal disease (Streptococcus sanguis, Veillonella atypica, and Prevotella denticola, hereinafter referred to as nonpathogenic bacteria) were tested. All bacterial cultures were grown under standard anaerobic culture conditions. Sonicated bacterial extracts were prepared from the bacterial pellet. These were added in various proportions to the CPO cultures. Parameters of osteogenesis, including alkaline phosphatase activity, calcium and P(i) accumulation, and collagen synthesis, were measured in 6-day-old cultures. Compared with controls grown in the absence of bacterial products, osteogenesis was inhibited significantly in cultures treated with extracts derived from the suspected periodontopathogens. No osteogenic inhibition was observed in cultures treated with extracts from the nonpathogenic bacteria. These results suggest that the ability to inhibit osteogenesis in vitro may be a pathogenic property shared by a limited group of species. Further characterization of the P. gingivalis extracts revealed that both proteinaceous and nonproteinaceous products, including lipopolysaccharide, were able to inhibit osteogenesis. P. gingivalis extract-mediated inhibition of osteogenesis in CPO cultures was blocked by indomethacin, implicating prostaglandins in the regulation of the bacterial effects. The bacterial extracts had either reversible or irreversible inhibitory effects on osteogenesis when added after differentiation or before/during differentiation of bone cells, respectively.

Animals↗

PubMed1999

Anthropometry of patients with osteogenesis imperfecta.

Standing height, sitting height, armspan, subischial leg length, head circumference, and growth hormone-insulin-like growth factor I (IGF-I) axis were determined in 86 patients with osteogenesis imperfecta. The aim of this study was to determine standing height and body proportions and their variability among osteogenesis imperfecta types and collagen defects. Mean standing height was reduced in all groups of patients, to the greatest extent and variability in osteogenesis imperfecta type III/IV and in those with qualitative collagen defects. The mean standing height of patients with osteogenesis imperfecta was lower than that of their unaffected first degree family members. Truncal height of patients with osteogenesis imperfecta was reduced; head size was increased, and this was more pronounced in patients with osteogenesis imperfecta type III/IV and qualitative collagen defects than in patients with osteogenesis imperfecta type I and quantitative collagen defects. Mean concentrations of IGF-I and IGF binding protein 3 (IGFBP-3) were low, but most values were within age specific reference values. The reduction of standing height appears to correlate with osteogenesis imperfecta type and the type of collagen defect. A relatively short trunk is typical and head circumference and body length are disproportionate.

Adolescent↗

PubMed2005

Angiogenesis is required for successful bone induction during distraction osteogenesis.

UNLABELLED: The role of angiogenesis during mechanically induced bone formation is incompletely understood. The relationship between the mechanical environment, angiogenesis, and bone formation was determined in a rat distraction osteogenesis model. Disruption of either the mechanical environment or endothelial cell proliferation blocked angiogenesis and bone formation. This study further defines the role of the mechanical environment and angiogenesis during distraction osteogenesis. INTRODUCTION: Whereas successful fracture repair requires a coordinated and complex transcriptional program that integrates mechanotransductive signaling, angiogenesis, and osteogenesis, the interdependence of these processes is not fully understood. In this study, we use a system of bony regeneration known as mandibular distraction osteogenesis (DO) in which a controlled mechanical stimulus promotes bone induction after an osteotomy and gradual separation of the osteotomy edges to examine the relationship between the mechanical environment, angiogenesis, and osteogenesis. MATERIALS AND METHODS: Adult Sprague-Dawley rats were treated with gradual distraction, gradual distraction plus the angiogenic inhibitor TNP-470, or acute distraction (a model of failed bony regeneration). Animals were killed at the end of distraction (day 13) or at the end of consolidation (day 41) and examined with muCT, histology, and immunohistochemistry for angiogenesis and bone formation (n = 4 per time-point per group). An additional group of animals (n = 6 per time-point per group) was processed for microarray analysis at days 5, 9, 13, 21, and 41. RESULTS AND CONCLUSIONS: Either TNP-470 administration or disruption of the mechanical environment prevented normal osteogenesis and resulted in a fibrous nonunion. Subsequent analysis of the regenerate showed an absence of angiogenesis by gross histology and immunohistochemical localization of platelet endothelial cell adhesion molecule in the groups that failed to heal. Microarray analysis revealed distinct patterns of expression of genes associated with osteogenesis, angiogenesis, and hypoxia in each of the three groups. Our findings confirm the interdependence of the mechanical environment, angiogenesis, and osteogenesis during DO, and suggest that induction of proangiogenic genes and the proper mechanical environment are both necessary to support new vasculature for bone induction in DO.

Angiogenesis Inhibitors↗

PubMed2006

Changes in nasorespiratory function in association with maxillary distraction osteogenesis in subjects with cleft lip and palate.

OBJECTIVE: The current study aimed to determine how nasorespiratory function changes in association with maxillary distraction osteogenesis (DO). Furthermore, with regard to impaired nasorespiratory function, the possibility of a relationship between the cleft side and laterality and any effect of maxillary distraction osteogenesis was investigated. DESIGN: In this descriptive, prospective clinical report, subjective and objective data regarding nasorespiratory function before and after maxillary distraction osteogenesis were compared. SUBJECTS: Data from 13 subjects with cleft lip and palate were used. Subjects had a severe maxillary deficiency and underwent distraction osteogenesis using a rigid external device system. OUTCOME MEASURES: The subjective measure was the score on a questionnaire regarding nasorespiratory function using a visual analog scale. The objective measure was nasal resistance. RESULTS: The visual analog scale score for two items significantly decreased just after distraction osteogenesis. Nasal resistance also significantly decreased 1 year after distraction osteogenesis. Moreover, nasal resistance on the cleft side was significantly greater than that on the noncleft side just before and 1 year after distraction osteogenesis. There was a significant positive correlation between changes in the visual analog scale score and nasal resistance. CONCLUSIONS: These results suggest that nasorespiratory function changes in association with maxillary distraction osteogenesis in subjects with cleft lip and palate. Moreover, it appears that nasal obstruction on the cleft side does not change in subjects with unilateral cleft lip and palate.

Adolescent↗

PubMed2002

The molecular biology of distraction osteogenesis.

Distraction osteogenesis has become a mainstay in bone tissue engineering and has significantly improved our armamentarium for reconstructive craniomaxillofacial procedures. However, although the biomechanical, histological, and ultrastructural changes associated with distraction osteogenesis have been widely described, the molecular mechanisms governing the formation of new bone in the interfragmental gap of gradually distracted bone segments remain largely unclear. Recently, a rat model of mandibular distraction was described that provides an excellent environment for deciphering the molecular mechanisms that mediate distraction osteogenesis. This article presents the hypotheses and current research that have furthered knowledge of the molecular mechanisms that govern distraction osteogenesis. Recent studies have implicated a growing number of cytokines that are intimately involved in the regulation of bone synthesis and turnover. The gene regulation of numerous cytokines (transforming growth factor-beta1, -beta2, -beta3, bone morphogenetic proteins, insulin-like growth factor-1, fibroblast growth factor-2) and extracellular matrix proteins (osteonectin, osteopontin) during distraction osteogenesis have been best characterized and are discussed in this article. It is believed that understanding the biomolecular mechanisms that mediate membranous distraction osteogenesis may guide the development of targeted strategies designed to improve distraction osteogenesis and accelerate bone healing.

Animals↗

PubMed1998

Post-traumatic hormonal disturbances: prolactin as a link between head injury and enhanced osteogenesis.

Traumatic brain injury (TBI) combined with fractures of long bones or large joints is often associated with enhanced osteogenesis (early fracture healing accompanied by hypertrophic callus formation and/or heterotopic ossifications). Humoral factors that cause enhanced osteogenesis in patients with TBI are not yet identified. The aim of this study was to reveal if post-traumatic change(s) of hormone levels in patients with TBI and bone fractures could be associated with the phenomenon of enhanced osteogenesis. The blood values of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH), parathyroid hormone (PTH) and prolactin (PRL) were studied weekly over a period of three months after injury in patients with bone fractures only, those with TBI only or combined bone fractures and TBI (patients exerting enhanced osteogenesis). Stress-hormones, ACTH and cortisol, or the hormones related to the bone growth (GH and PTH) did not show any particular post-traumatic changes in the blood of patients with combined injury that could be associated with the enhanced osteogenesis. On the other hand, patients with combined bone fractures and TBI accompanied by enhanced osteogenesis had significantly elevated PRL levels in blood during the 5th week of the post-traumatic period. Thus, the maximal PRL values were measured at the time when in this group of patients fractures were in consolidation and hypertrophic callus or heterotopic ossifications were developing (as verified by x-ray imaging). Hence, PRL does not only influence physiology of the bone metabolism but also seems to be one of the humoral factors involved in the phenomenon of enhanced osteogenesis in patients with TBI.

Adrenocorticotropic Hormone↗

PubMed2001

Distraction osteogenesis of the craniofacial skeleton.

In summary, distraction osteogenesis is a safe and effective means of achieving bone lengthening. These techniques were originally applied to the long bones of the extremities; over the past 10 years they have been effectively applied to the bones of the craniofacial skeleton. The new bone regenerate that is observed after distraction osteogenesis is stable, and relapse rates after skeletal advancement are believed to be lower than with conventional osteotomy and bone graft techniques. There is considerable variability in distraction protocols employed in clinical practice, including differences in the types of devices used and in the rate, rhythm, latency, and period of consolidation for distraction osteogenesis. The greatest application for distraction osteogenesis in the craniofacial skeleton has been with mandible lengthening, for which there is presently a 10-year clinical experience. Midfacial advancement is a newer application of distraction osteogenesis, for which clinical experience has been accrued over the past 5 years. This latter experience indicates that distraction osteogenesis is a viable treatment option for lengthening of the hypoplastic mandible and midface. These techniques have advantages over conventional means of bone graft and rigid fixation because of the quality of the bone regenerate, the decrease in the long-term relapse rate of the advanced bone segments in both the mandible and the midface, and the simultaneous soft-tissue elongation that accompanies the distraction process. Distraction osteogenesis is particularly applicable to the correction of severe deformities of the mandible and midface in children with developmental hypoplasia and syndromic craniosynostosis. However, growth is an added variable in this patient population. The amount of overcorrection in lengthening of the hypoplastic bone required to compensate for continued growth discrepancy of the adjacent facial bones is difficult to predict. Therefore, the families of these patients should be informed that many children will require repeated operations at a later age as they reach skeletal maturity.

Child↗

PubMed2007

Reconstruction of juxta-articular huge defects of distal femur with vascularized fibular bone graft and Ilizarov's distraction osteogenesis.

BACKGROUND: We evaluate the effect of reconstructing huge defects (mean, 15.8 cm) of the distal femur with Ilizarov's distraction osteogenesis and free twin-barreled vascularized fibular bone graft (TVFG). METHODS: We retrospectively reviewed a consecutive series of five patients who had cases of distal femoral fractures with huge defects and infection that were treated by the Ilizarov's distraction osteogenesis. After radical debridement, two of the five cases had free TVFG and monolocal distraction osteogenesis, and another two cases had multilocal distraction osteogenesis with knee fusion because of loss of the joint congruity. The other case with floating knee injury had bilocal distraction osteogenesis and a preserved knee joint. The mean defect of distal femur was 15.8 cm (range, 14-18 cm) in length. RESULTS: The mean length of distraction osteogenesis by Ilizarov's apparatus was 8.2 cm. The mean length of TVFG was 8 cm. The average duration from application of Ilizarov's apparatus to achievement of bony union was 10.2 months (range, 8-13 months). At the end of the follow-up, ranges of motion of three knees were 0 to 45 degrees, 0 to 60 degrees, and 0 to 90 degrees. Two cases had knee arthrodesis with bony fusion because of loss of the joint congruity. There were no leg length discrepancies in all five patients. In addition, three patients had pin tract infections and one case had a 10 degree varus deformity of the femur. CONCLUSIONS: Juxta-articular huge defect (>10 cm) of distal femur remains a challenge to orthopedic surgeons. Ilizarov's technique provides the capability to maintain stability, eradicate infection, restore leg length, and to perform adjuvant reconstructive procedure easily. In this study, we found that combining Ilizarov's distraction osteogenesis with TVFG results in improved patient outcome for patients with injuries such as supracondylar or intercondylar infected fractures or nonunion of distal femur with huge bone defect.

Adolescent↗

PubMed1996

Causes of death in osteogenesis imperfecta.

AIMS: To determine the causes of death in patients with osteogenesis imperfecta, excluding infants with the perinatal lethal form (type II). METHODS: Seventy nine patients with known osteogenesis imperfecta were identified, 37 of whom had been seen clinically in life. Causes of death were identified from death certificates, postmortem reports, medical records, hospital consultants, relatives, and the Brittle Bone Society's records. RESULTS: Patients with the milder types of osteogenesis imperfecta, I and IV, often had a normal lifespan and died of unrelated illnesses such as myocardial infarction and malignancy. In some of these patients and in many patients with the more severe type III disease, it was clear that osteogenesis imperfecta contributed significantly to death, almost certainly to many of the respiratory deaths and to deaths from cardiac failure due to kyphoscoliosis. Osteogenesis imperfecta also caused six deaths, directly or indirectly, due to basilar invagination of the skull. Osteogenesis imperfecta may have contributed to deaths from intracranial bleeding. Apparently minor traumatic incidents may have disastrous consequences in patients with this disorder. CONCLUSIONS: Prompt care for respiratory infections and prevention of trauma in patients with osteogenesis imperfecta is essential.

Adolescent↗