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PubMed1993

Surface adhesion and attachment factors in bone morphogenetic protein-induced chondrogenesis in vitro.

Bone morphogenetic protein (BMP) induces cartilage and bone development in embryonic and post-fetal life. Bone morphogenetic protein-induced chondrogenesis in outgrowths of muscle connective tissues on various furrowed and unfurrowed fibronectin-coated substrata was observed by biochemical and histologic methods. The substrata consisted of cellulose acetate membranes, atelocollagen, denatured autoclaved demineralized bone matrix, bone matrix deactivated by extraction of BMP with guanidine hydrochloride (GuHCl), and aggregates of insoluble BMP and associated noncollagenous proteins (BMP/NCP) prepared from bovine bone. The furrows, which were mechanically cut into the substrata, were intended to increase surface area and provide extra spaces for cell proliferation under compression. The extent to which extracellular attachments were required for induced cartilage development was reflected in the quantity of cartilage formed when BMP/NCP, either in insoluble or in water-soluble form, was introduced was greatest on GuHCl-extracted bone matrix. On cellulose acetate and atelocollagen, BMP-induced cartilage development was relatively scanty. A substratum of bone matrix, denatured by autoclaving at a minimum of 125 degrees, permitted cell-to-cell adhesion but not cell-to-substratum attachments; the end product was loose fibrous connective tissue only. In contrast, cartilage development occurred on surfaces of undissolved particles of BMP/NCP. Water-soluble human BMP induced development of masses of amorphous cartilage. Even after it was extracted with GuHCl, rat bone matrix may have retained trace amounts of endogenous BMP. Thus, when the requirements of cells for cell-to-cell adhesion and cell-to-substratum attachment, including mechanical factors such as furrows to enlarge surface area, were met, cartilage development was a manifestation of temporal, spatial, and BMP distribution patterns. In situ hybridization and immunofluorescent microscopy with the aid of antirecombinant BMP antibiotics may provide new information about morphogenesis.

Animals↗

PubMed1999

Novel findings about 24,25-dihydroxyvitamin D: an active metabolite?

The physiological role of 24,25-dihydroxyvitamin D remains controversial. Recent results suggest that 24,25-dihydroxyvitamin D is essential for fracture healing, and binding sites for 24,25-dihydroxyvitamin D have been identified in fracture callus tissue. Mice deficient in the 25-hydroxyvitamin D-24-hydroxylase enzyme provide novel genetic tools in which to study the role of 24,25-dihydroxyvitamin D in bone development and fracture repair.

24,25-Dihydroxyvitamin D 3↗

PubMed1980

[Effect of participation in certain types of sports on the hand bones of adolescents and youth].

The effect of such sports training as boxing, basket-ball and football on the hand skeleton was studied. Roentgenograms of hands in 80 young sportsmen 15--17 years old were examined. Synostosis in the hand bones, in distal portion of the forearm and mineral saturation of the metacarpal bones were studied by the standard method of roentgenodensitometry. It was stated that specific loading on the hand bones as a result of sports training (boxing, basket-ball) produces certain adaptive-compensatory changes in the hand bones development and structure. These changes are manifested as: decreasing rate of synostosis in the distal epiphysis of the forearm and hand bones in young boxers; certain time changes in sinostosis of definite parts of basket-ballers' hand skeleton. Their structural changes are seen as increased mineral saturation in the hand bones (more in boxers and less in basket-ballers) that correspondingly results in their increasing resistivity.

Absorptiometry, Photon↗

PubMedDate not supplied

Bone loss and the evolving role of bisphosphonate therapy in prostate cancer.

Androgen deprivation therapy (ADT) can result in significant loss of bone mineral density (BMD) but to date, there are no prospective studies that document the true severity of bone loss and resulting fracture rates. In the general population, however, the incidence of low BMD is increasing in elderly men. Men suffer more morbidity and mortality from fractures associated with low BMD than women. Problems of underdiagnosis and undertreatment in men can be addressed with enhanced awareness of the risk factors for bone loss in men and the available treatment options. Guidelines for diagnosis of low BMD in women can probably be applied to men. Treatment options have not been studied as extensively in men. For men treated with ADT for prostate cancer, however, use of intravenous zoledronic acid at the initiation of ADT has been shown to prevent and even reverse bone loss. Although the routine use of bisphosphonates to prevent bone loss is not yet recommended, zoledronic acid is a logical choice of therapy in men who have low BMD at baseline or who develop bone loss during the course of therapy. In addition to its effects on BMD, zoledronic acid has also been shown to decrease skeletal morbidity in men with metastatic hormone-refractory prostate cancer. Whether zoledronic acid or other bisphosphonates might actually prevent or delay the development of bone metastases remains to be studied in randomized clinical trials.

Age Factors↗

PubMed1992

Rat prostate adenocarcinoma cells disseminate to bone and adhere preferentially to bone marrow-derived endothelial cells.

Approximately 70% of patients with prostatic cancer develop bone metastases. Metastatic prostate adenocarcinomas are associated with high mortality rates and represent a leading cause of cancer-related deaths among males. To study the host-tumor interactions underlying the predilection of prostate cancer cells for skeletal bone, an experimental model was developed using rat Dunning carcinoma Mat-LyLu cells. Inoculations of these cells into the left ventricle of the heart led to the development of spinal metastases in 100% of inoculated animals. A subline of Mat-LyLu (Mat-LyLu-B5) was subsequently selected through the sequential inoculation of bone marrow-derived carcinoma cells into the left ventricle and was found to have an increased metastatic potential compared to the parental line. The possible role of tumor cell adhesion to host cells in the process of bone marrow colonization was then investigated in vitro using the metastatic line and primary cultures of rat bone marrow-derived stromal cells. It was found that the adhesion of the metastatic Mat-LyLu cells to a bone marrow stromal cell culture highly enriched for endothelial cells was significantly higher than the adhesion to other bone-derived cells, including nonendothelial bone marrow stromal cells (3.5x) and osteoblasts (1.7x). It was also significantly higher than the adhesion to rat fibroblasts (7x) and to hepatic endothelial cells (7.5x). The results suggest that the adhesion of prostate carcinoma cells to the bone marrow endothelium may play a role in their metastasis to bone.

Adenocarcinoma↗

PubMed2002

Differentiation and growth of kype skeletal tissues in anadromous male Atlantic salmon (Salmo salar).

The re-initiation of bone development in adult starving Atlantic salmon (Salmo salar) during their energetically expensive upstream migration is remarkable and deserves closer examination. Dramatic alterations of the skull bones and teeth, most prominently, the development of a kype in males, are widely known but little studied or understood. We describe the microstructure and the cellular processes involved in the formation of the skeletal tissues of the kype. Fresh bone material, obtained from animals migrating upstream was subjected to radiological, histological or histochemical analysis. We show that the kype is, in part, composed of rapidly growing skeletal needles arising at the tip of the dentary. Proximally, the needles anastomose into a spongiosa-like meshwork which retains connective tissue inside bone marrow spaces. Ventrally, the needles blend into Sharpey fiber bone. Skeletal needles and Sharpey fiber bone can be distinguished from the compact bone of the dentary by radiography. Rapid formation of the skeleton of the kype is demonstrated by the presence of numerous osteoblasts, a broad distal osteoid zone, and the appearance of proteoglycans at the growth zone. The mode of bone formation in anadromous males can be described as 'making bone as fast as possible and with as little material as possible'. Unlike the normal compact bone of the dentary, the new skeletal tissue contains chondrocytes and cartilaginous extracellular matrix. Formation of the skeleton of the kype resembles antler development in deer (a form of regeneration), or hyperostotic bone formation in other teleost fishes, rather than periosteal bone growth. The type of boneformation may be understandable in the light of the animals' starvation and the energetic costs of upstream migration. However, the structured and regulated mode of bone formation suggests that the skeleton of the kype has functional relevance and is not a by-product of hormonal alterations or change of habitat.

Animals↗

PubMedDate not supplied

[Computerized tomography aspects of tibial distraction regeneration].

Computer tomography (CT) potentialities in examinations of patients over the course of distraction osteosynthesis and in assessment of the bone regenerate structure of different sites in various periods of its formation and 'maturation' were studied in 25 patients (22 men and 3 women aged 14 to 54, mean age 31.7) in periods from 24 days to 5 years. CT permitted a visual and densitometric assessment of the developing bone regenerate surrounded by metal constructions. The distraction osteogenesis involves the development of bone regenerate copying the anatomical shape and structure of the regenerated tubular bone at the site of its osteotomy. CT helps follow up all the periods of bone regenerate formation and maturation and permits the detection of deviations in this process, if any. This method permits analysis of the bone regenerate ossification time course, that is important for the assessment of the distraction rate and of the time of removing the external fixation apparatus.

Adolescent↗

PubMed1983

Changes in tissue concentration of prostaglandins during endochondral bone differentiation.

Prostaglandins are known to be involved in bone metabolism as evidenced by the ability of PGE2 to induce bone resorption. It was, therefore, of interest to determine if there was an association of specific prostaglandin metabolites with the various stages of developing bone by utilizing the matrix-induced endochondral bone formation system. During mesenchymal cell proliferation a peak of endogenous thromboxane B2 was detected. In the subsequent stages of chondrogenesis and chondrolysis PGF2 alpha was in high concentration, whereas during bone formation PGE2, 6-Keto-PGF1 alpha and thromboxane B2 were elevated. These changes in the peak levels of the various prostaglandin metabolites may reflect differences in the cell populations and function associated with various stages of endochondral bone formation.

6-Ketoprostaglandin F1 alpha↗

PubMed2005

Hypoxia and HIF-1 alpha in chondrogenesis.

In endochondral bone development chondrocytes undergo well-ordered and controlled phases of proliferation, hypertrophic differentiation, mineralization of the surrounding matrix, death, blood vessel invasion, and finally replacement of cartilage with bone. The chondrocytic growth plate is a unique mesenchymal tissue, as it is avascular but it requires blood vessel invasion, i.e. the angiogenic switch, in order to be replaced by bone. We have recently provided evidence that the growth plate is hypoxic during fetal development. Adaptation to hypoxia is a critical event in numerous pathological settings, such as tumor progression and survival of tissues in which blood flow has been suddenly interrupted. One of the hallmarks of the response to hypoxia is activation of the transcription factor HIF-1alpha. The von Hippel Lindau tumor suppressor protein VHL is a component of a ubiquitin ligase promoting proteolysis of HIF-1alpha. By using a genetic approach, we have demonstrated the essential role of the hypoxia/VHL/HIF-1alpha pathway in endochondral bone development. Hypoxia-dependent up regulation of HIF-1alpha transcriptional activity is critical for survival of hypoxic chondrocyte, and it shapes up the fetal growth plate by inhibiting chondrocyte proliferation, increasing matrix accumulation and probably modulating cell size. The findings overall highlight the usefulness of studying fetal growth plate development as a model to address issues such as adaptation of normal tissues to hypoxia, survival of hypoxic cells, and regulation of the angiogenic switch. They also demonstrate a crucial role of hypoxia and HIF-1alpha in development and differentiation.

Animals↗

PubMed1992

[Effects of zinc deficiency and vitamin D deficiency on bone calcification and development of rats].

Zinc deficiency rat model was made by feeding zinc deficiency diet. The level of bone calcium of the zinc deficiency rats was significantly lower than that of the control rats. Their bone cortex was thinner and bone density decreased. The counts of their cartilage cells and hypertrophic cells of epiphyseal plate were less frequent, and the diameter of their hypertrophic cells was smaller than that of the controls. It suggested that zinc deficiency caused defective bone calcification which was similar to that in vitamin D deficiency. Zinc deficiency seemed to hinder the linear growth of long bone and might be the cause of dwarf.

Animals↗

PubMed1981

Osteopetrosis of the temporal bone.

Osteopetrosis is a rare hereditary disorder of bone development. We examined the right temporal bone of a 17-year-old boy with recessive osteopetrosis and a conductive hearing loss and describe the histopathologic characteristics. The conductive deafness in this case was caused primarily by recurrent otitis media.

Adolescent↗

PubMed2006

Who's afraid of the big bad Wolff?: "Wolff's law" and bone functional adaptation.

"Wolff's law" is a concept that has sometimes been misrepresented, and frequently misunderstood, in the anthropological literature. Although it was originally formulated in a strict mathematical sense that has since been discredited, the more general concept of "bone functional adaptation" to mechanical loading (a designation that should probably replace "Wolff's law") is supported by much experimental and observational data. Objections raised to earlier studies of bone functional adaptation have largely been addressed by more recent and better-controlled studies. While the bone morphological response to mechanical strains is reduced in adults relative to juveniles, claims that adult morphology reflects only juvenile loadings are greatly exaggerated. Similarly, while there are important genetic influences on bone development and on the nature of bone's response to mechanical loading, variations in loadings themselves are equally if not more important in determining variations in morphology, especially in comparisons between closely related individuals or species. The correspondence between bone strain patterns and bone structure is variable, depending on skeletal location and the general mechanical environment (e.g., distal vs. proximal limb elements, cursorial vs. noncursorial animals), so that mechanical/behavioral inferences based on structure alone should be limited to corresponding skeletal regions and animals with similar basic mechanical designs. Within such comparisons, traditional geometric parameters (such as second moments of area and section moduli) still give the best available estimates of in vivo mechanical competence. Thus, when employed with appropriate caution, these features may be used to reconstruct mechanical loadings and behavioral differences within and between past populations.

Adaptation, Physiological↗

PubMed2006

Osteoclastogenesis in the nonadherent cell population of human bone marrow is inhibited by rhBMP-2 alone or together with rhVEGF.

During bone development and repair, angiogenesis, osteogenesis, and bone remodeling are closely associated processes that share some common mediators. In the present study nonadherent human bone marrow mononuclear cells under the induction of sRANKL and M-CSF, differentiated into osteoclasts with TRAP-positive staining, VNR expression, and Ca-P resorptive activity. The effects of various combinations of rhBMP-2 (0, 3, 30, and 300 ng/mL) and rhVEGF (0 and 25 ng/mL) on osteoclastogenesis potentials were examined in this experimental system. The percentages of TRAP-positive multiple nucleated cells represent osteoclast differentiation potential, and the percentages of resorptive areas in the Ca-P coated plates resemble osteoclast resorption capability. The presence of rhBMP-2 at 30 and 300 ng/mL showed inhibitory effects on osteoclast differentiation and their resorptive capability in the human osteoclast culture system. rhVEGF (25 ng/mL) enhanced the resorptive function of osteoclast whenever it was used alone or combined with 3 ng/mL rhBMP-2. However, rhVEGF-induced resorptive function was inhibited by 30 ng/mL and 300 ng/mL rhBMP-2 in a dose-dependent manner. Statistical analysis demonstrated that an interactive effect exists between rhBMP-2 and rhVEGF on human osteoclastogenesis. These findings suggested that an interactive regulation may exist between BMPs and VEGF signaling pathways during osteoclastogenesis; exact mechanisms are yet to be elucidated.

Acid Phosphatase↗

PubMed1999

Ectopic Msx2 overexpression inhibits and Msx2 antisense stimulates calvarial osteoblast differentiation.

Msx2 is believed to play a role in regulating bone development, particularly in sutures of cranial bone. In this study we investigated the effects of retroviral-mediated overexpression of Msx2 mRNA, in both sense and antisense orientations, on primary cultured chick calvarial osteoblasts. Unregulated overexpression of sense mRNA produced high levels of Msx2 protein throughout the culture period, preventing the expected fall as the cells differentiate. The continued high expression of Msx2 prevented osteoblastic differentiation and mineralization of the extracellular matrix. In contrast, expression of antisense Msx2 RNA decreased proliferation and accelerated differentiation. In other studies, we showed that the Msx2 promoter was widely expressed during the proliferative phase of mouse calvarial osteoblast cultures but was preferentially downregulated in osteoblastic nodules. These results support a model in which Msx2 prevents differentiation and stimulates proliferation of cells at the extreme ends of the osteogenic fronts of the calvariae, facilitating expansion of the skull and closure of the suture.

Animals↗

PubMed1986

The role of bone scintigraphy in osteogenic sarcoma.

Hospital records of 27 children with osteogenic sarcoma were reviewed in an effort to define the usefulness of skeletal scintigraphy in the initial evaluation and follow-up of their disease. Serial bone scans as well as plain radiographs, linear tomograms, and computed tomograms were evaluated for evidence of bone or lung metastases. Eighteen patients developed lung metastases and three developed bone metastases. Seven patients demonstrated uptake of tracer in lung metastases, however, the lesions were all easily identifiable by radiographic means. All bone metastases were detected by scintigraphy, in one instance prior to radiographic abnormality. In no cases were bone metastases known to occur in the absence of lung metastases. None of the bone scans performed for routine follow-up purposes resulted in altered therapy for the patient. We propose that skeletal scintigraphy is useful in the initial metastatic work up of osteogenic sarcoma, and may be helpful in some patients with specific indications during their follow-up, but is less valuable when there is no clinical suspicion for bone metastases.

Adolescent↗

PubMed1996

Cranio-facial fibro-osseous dysplasia. A case report and overview of the management of the condition.

Fibro-osseous dysplasia is a developmental non familial, benign anomaly of bone development occurring in single or multiple bones, characterised by the replacement of normal bone by fibro-osseous tissue. We describe the case of a fourteen year old boy, which illustrates many of the difficulties confronting surgeons dealing with this uncommon condition. Complete surgical excision was required, before a definitive histological diagnosis could be established. We report the clinical, radiological and pathological features of this unusual case. We review the pathology of the condition and discuss the approaches to surgical management.

Adolescent↗

PubMed1998

Evaluation of filling materials in membrane--protected bone defects. A comparative histomorphometric study in the mandible of miniature pigs.

In recent years, bone grafts and bone substitutes have been increasingly utilized underneath barrier membranes to optimize the treatment outcome of bone reconstructive therapy for defects in the alveolar process. In the present study, 4 different filling materials were evaluated in bone defects of similar dimensions in the mandible of miniature pigs. Blood clots and autografts were used as controls. The defects were covered with barrier membranes and allowed to heal for 4, 12 or 24 weeks. Histologic examination demonstrated that bone repair progressed through a programmed sequence of maturation steps closely resembling the pattern of bone development and growth regardless of whether bone grafts or substitutes were present or not. Histomorphometric analysis showed that autologous bone grafts (autografts) had the best osteoconductive properties during the initial healing period, with 39% of newly formed bone inside the membrane-covered defects at 4 weeks of healing. In addition, 87% of the graft surfaces were already covered by bone at this time. Both values were significantly higher for autografts than for the 4 alternative bone fillers (P < or = 0.05). At 12 weeks, these differences were no longer apparent, with all 5 filling materials showing similar values. Among the tested bone substitutes, tricalcium phosphate (TCP) showed a significantly higher percentage of bone fill at 24 weeks of healing. It can be concluded that sites filled with autografts clearly demonstrated the best results underneath barrier membranes in the early phase of healing. As far as degradation and substitution are concerned, TCP showed the most promising results. This filler, however, needs to be tested further in a more demanding animal model. Less favorable results were obtained for coral-derived hydroxyapatite granules and for demineralized freeze-dried bone allografts.

Alveolar Bone Loss↗

PubMed2000

Mutations in the thrombopoietin receptor, Mpl, in children with congenital amegakaryocytic thrombocytopenia.

Congenital amegakaryocytic thrombocytopenia (CAMT) is a rare disorder of undefined aetiology. The disease presents with severe thrombocytopenia and absence of megakaryocytes in the bone marrow. Furthermore, CAMT patients may develop bone marrow aplasia. To obtain more insight into the mechanism underlying CAMT, five children were analysed. All patients had increased plasma thrombopoietin (Tpo) levels, indicating a platelet production defect. Bone marrow-derived CD34+ stem cells from three patients were cultured in an in vitro liquid culture system to study megakaryocytopoiesis. CD34+ cells from two of the three patients failed to differentiate into megakaryocytes. The lack of megakaryocyte formation could imply that a defect in the c-mpl gene, encoding the Tpo receptor, exists. Sequencing of c-mpl revealed mutations in four of five patients. Three patients had point mutations and/or a deletion in the coding regions of c-mpl. All point mutations led to an amino acid substitution or to a premature stop codon. In one patient, a homozygous mutation in the last base of intron 10 was found that resulted in loss of a splice site. This study showed that mutations in c-mpl could be the cause of thrombocytopenia in CAMT in the majority of patients. Furthermore, Tpo has been shown to have an anti-apoptotic effect on stem cells. Therefore, mutations in c-mpl might not only affect megakaryocyte formation but may also impair stem cell survival, which could explain the occurrence of bone marrow failure as final outcome in patients with CAMT.

Amino Acid Substitution↗