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PubMed1996

Effects of spaceflight and recovery on rat humeri and vertebrae: histological and cell culture studies.

Skeletal changes associated with spaceflight in the rat have been well documented, but few data are available on bone tissue and bone cell metabolism after subsequent on-Earth recovery. We therefore investigated the effects of microgravity and subsequent recovery on trabecular bone morphology and cellular activities in rat humeri and thoracic vertebrae and compared histomorphometric parameters in caudal vertebrae with the behavior of vertebral osteoblastic cells in culture. We report here that humeral weight showed normal growth during the experiment but was unaffected by spaceflight or recovery from spaceflight. However, the 14-day spaceflight resulted in inhibition of static indexes of bone formation in humeral proximal metaphyses and thoracic vertebral bodies. This was associated with a decrease in bone volume in humeral metaphyses. After 14 days of on-Earth recovery, osteoblastic and osteoid surfaces returned toward normal and bone volume was normalized in humeri, whereas the static bone formation parameters were not restored in thoracic vertebrae. In addition, histological indexes of bone formation and osteoblastic cell growth in vitro were not affected by spaceflight in caudal vertebrae. This study shows that rat humeri and thoracic and caudal vertebrae exhibit different patterns of response to spaceflight and subsequent on-Earth recovery, which could be due, at least in part, to the different loading pattern of these bones, and also to differences in bone turnover rate.

Alkaline Phosphatase↗
PubMed1998

Response to long-term hGH therapy in two children with Schwachman-Diamond syndrome associated with GH deficiency.

Schwachman-Diamond syndrome is a rare congenital disorder characterized by pancreatic insufficiency, metaphyseal anomalies, recurrent infections, hematologic abnormalities, and growth retardation. Slow growth in these patients has been attributed to nutritional deficits, recurrent infections, and skeletal anomalies. Two cases of Schwachman-Diamond syndrome associated with growth hormone deficiency have been previously reported. We report here on 2 additional cases with this unusual association. Therefore, growth failure in Schwachman-Diamond syndrome should not be assumed to be due to chronic illness or recurrent infections; other etiologies for growth failure should be sought. However, the presence of metaphyseal disorders probably interferes with the long-term efficacy of growth hormone substitutive therapy.

Adolescent↗
PubMed2001

Delusions in first-admitted patients: gender, themes and diagnoses.

Whether there is a specific link between certain delusional symptoms and particular etiologies has not yet been completely clarified. In this study, 639 first ever admitted deluded patients were investigated in order to find out whether age and gender are associated with certain delusional contents, whether age at first admission may be linked to certain etiologies and whether it is possible to detect indicators particularly related to basic dysfunctions. At first admission, delusional female patients were older than men with a significant predomination of delusions of persecution, while men presented significantly more frequently delusions of jealousy and grandiosity. Within delusions of persecution, of religious or metaphysical content and of grandiosity, women were even significantly older than men. Religious or metaphysical and grandiosity contents occurred significantly more frequently in ICD-8 schizophrenia, indicating that these themes seem to be particularly linked to ICD-8 schizophrenia. Additionally, some target symptoms not included in the delusional symptomatology were investigated to test the relationship between delusions and schizophrenia. Overall, the results of the present investigation indicate that delusions are not specific for schizophrenia, and therefore, other symptomatological criteria should be applied for the nosographic attribution.

Adolescent↗
PubMed2002

IMAGe association: additional clinical features and evidence for recessive autosomal inheritance.

Congenital adrenal hypoplasia (CAH) normally occurs in the neonatal period, with patients presenting with more or less severe salt-wasting syndrome. X-linked CAH has been associated with mutations in the DAX-1 gene, and boys have also been shown to have hypogonadotrophic hypogonadism. Recently, in three unrelated boys, CAH was associated with intrauterine growth retardation (IUGR), metaphyseal dysplasia and genital abnormalities, defining a new association called IMAGe. We now report four additional patients with this association, including the first living female. The four patients belong to two unrelated families (one brother and one sister from each family). These patients have the main clinical characteristics of IMAGe association: IUGR, facial dysmorphy (frontal bossing, broad nasal bridge, low-set ears), short limbs due to metaphyseal dysplasia, and adrenal insufficiency. As these patients are older than the initial three patients, we can also describe additional features: short adult height, normal puberty in boys as well as in the living girl. The boys have hypospadias associated with micropenis. The living girl came to clinical attention at the age of 5 years as a result of a familial survey, and careful questioning revealed that she had been suffering from mild adrenal insufficiency since early childhood. At least one boy has congenital hypotonia due to muscular dystrophy. In conclusion, these four new cases display familial transmission, strongly suggesting Mendelian autosomal recessive inheritance. Adrenal insufficiency may be mild. Hypotonia, described in all the patients, might be related to paucisymptomatic muscular dystrophy, as this condition is clearly heterogeneous varying with regard to severity, associated manifestations and outcome. If this symptom is part of the syndrome, which we cannot assume, it could help to localize the candidate gene.

Adolescent↗
PubMed2003

Isoflavone consumption does not increase the bone mass in osteopenic obese female zucker rats.

Some controversy exists in the literature concerning the effects of leptin on bone metabolism. Thus we have compared femoral bone density and biochemical markers of bone metabolism in male and female fatty (leptin-resistant) Zucker rats and their lean homozygous controls at 3 and 6 months of age. At 3 months, no differences concerning total, diaphyseal (cortical bone), and distal metaphyseal (trabecular bone) femoral bone densities, plasma osteocalcin concentrations, and urinary deoxypyridinoline excretion were observed between fatty and lean rats. On the opposite, at 6 months of age, in both males and females, total, diaphyseal, and distal metaphyseal femoral bone densities and plasma osteocalcin concentrations were lower in Zucker than in lean rats. Soybean isoflavone consumption (40 microg/g body weight/day for 90 days, a dose which prevents osteopenia following ovariectomy both in lean Zucker homozygous controls and in Wistar rats) by obese female Zucker rats had no significant effect upon their bone mass.

Aging↗
PubMedDate not supplied

Percutaneous fixation of comminuted fractures of the femur and tibia. Preliminary study.

OBJECTIVE: To present initial experience of treating patients with comminuted fractures of the diaphyseal and metaphyseal areas of the femur and tibia. SUBJECTS AND METHODS: Sixteen patients were involved in the study. All the 16 patients (11 males and 5 females, average age 34 years) with closed, comminuted fractures of femur (n = 9) and tibia (n = 7) were operated on using the principle of minimal access surgery and biological fixation that maximally preserved the soft tissues and fracture hematoma. RESULTS: All the fractures united, operated limbs had good function, and no complications occurred. CONCLUSION: Our findings indicate that minimal access surgery is a useful fixation method in the treatment of comminuted diaphyseal and metaphyseal fractures of the femur and tibia.

Adolescent↗
PubMed1991

Tibial dimensions before and during the recovery phase in the osteopetrotic mutant mouse.

Osteopetrosis is a genetic bone disease characterized by excessive bone mass and 'clubbing' of long bones. In the osteopetrotic (op) mouse, remission of the disease begins at 45 days of age. This study attempted to describe changes in the op tibia before and during remission. Osteopetrotic and normal littermates were killed at intervals from 10 to 120 days of age. Left tibiae were processed for transmission electron microscopy. Microradiographs of right tibiae were projected and drawn. Bone dimensions were compared between mutants and controls by ANOVA and bones were viewed in a scanning electron microscope. Differences between mutants and controls were: at all ages mutant tibiae were shorter than those of controls; 10-day distal shafts of mutant tibiae were significantly narrower; 30-day proximal shafts of mutant tibiae were wider, distal shafts were narrower, and there was no bone resorption along the external proximal metaphysis. At 48 days, resorption was seen along the proximal metaphyses of the mutant tibiae and by 60 days, extensive resorption areas were evident. However, proximal shafts of mutant tibiae were still significantly wider than those of controls. These results indicated that before remission there was an unequal deposition of bone on the mutant tibia. After remission, resorption occurred along the external proximal shaft, but was not enough to remove significant amounts of bone from the proximal metaphyses of mutant tibiae by 120 days of age.

Analysis of Variance↗
PubMed1993

Bone marrow-derived osteoclast-like cells from a patient with craniometaphyseal dysplasia lack expression of osteoclast-reactive vacuolar proton pump.

Craniometaphyseal dysplasia (CMD) is a rare craniotubular bone dysplasia transmitted in autosomal dominant or recessive form. This disease is characterized by cranial bone hyperostosis and deformity of the metaphyses of the long bones. Using osteoclast-like cells formed from patient bone marrow cells, we investigated the pathophysiology of CMD in a 3-yr-old patient. Untreated bone marrow cells from the patient differentiated into osteoclast-like cells in vitro. These cells were shown to have vitronectin beta-receptors using a specific monoclonal antibody, i.e., 23C6 (CD51), which reacts with osteoclasts in human bone biopsy samples. However, the number of these osteoclast-like cells formed from the patient's bone marrow was only 40% of the normal controls. 1,25-dihydroxyvitamin-D3, bovine 1-34 parathyroid hormone, recombinant human interleukin-1 beta, recombinant human interleukin-6, or recombinant human macrophage colony-stimulating factor significantly increased, while salmon calcitonin significantly inhibited, the number of osteoclast-like cells. However, these cells could not resorb sperm whale dentin slices and lacked the osteoclast-reactive vacuolar proton pump as evidenced by a monoclonal antibody (E11). Western blot analysis using a monoclonal antibody to pp60c-src (327) revealed that protooncogene c-src expression by the platelets of the CMD patient was comparable to the normal control. These data suggest that: (a) the hyperostosis and the metaphyseal long bone deformity in the present CMD patient might be explained by osteoclast dysfunction due to impaired expression of the osteoclast-reactive vacuolar proton pump; and (b) a protooncogene c-src was not associated with the pathogenesis of the present CMD patient.

Blood Platelets↗
PubMed2004

Soluble VEGF isoforms are essential for establishing epiphyseal vascularization and regulating chondrocyte development and survival.

VEGF is crucial for metaphyseal bone vascularization. In contrast, the angiogenic factors required for vascularization of epiphyseal cartilage are unknown, although this represents a developmentally and clinically important aspect of bone growth. The VEGF gene is alternatively transcribed into VEGF(120), VEGF(164), and VEGF(188) isoforms that differ in matrix association and receptor binding. Their role in bone development was studied in mice expressing single isoforms. Here we report that expression of only VEGF(164) or only VEGF(188) (in VEGF(188/188) mice) was sufficient for metaphyseal development. VEGF(188/188) mice, however, showed dwarfism, disrupted development of growth plates and secondary ossification centers, and knee joint dysplasia. This phenotype was at least partly due to impaired vascularization surrounding the epiphysis, resulting in ectopically increased hypoxia and massive chondrocyte apoptosis in the interior of the epiphyseal cartilage. In addition to the vascular defect, we provide in vitro evidence that the VEGF(188) isoform alone is also insufficient to regulate chondrocyte proliferation and survival responses to hypoxia. Consistent herewith, chondrocytes in or close to the hypoxic zone in VEGF(188/188) mice showed increased proliferation and decreased differentiation. These findings indicate that the insoluble VEGF(188) isoform is insufficient for establishing epiphyseal vascularization and regulating cartilage development during endochondral bone formation.

Angiography↗
PubMed2000

Bone morphogenetic protein (BMP) localization in developing human and rat growth plate, metaphysis, epiphysis, and articular cartilage.

We assessed the distribution and relative staining intensity of bone morphogenetic protein (BMP)-1-7 by immunohistochemistry in tibial growth plates, epiphyses, metaphyses, and articular cartilage in one 21-week and one 22-week human fetus and in five 10-week-old Sprague-Dawley rats. In the rats, articular cartilage was also examined. BMP proteins were mostly cytoplasmic, with negligible matrix staining. Highest BMP levels were seen in (a) hypertrophic and calcifying zone chondrocytes of growth plate (BMP-1-7), (b) osteoblasts and/or osteoprogenitor fibroblasts and vascular cells of the metaphyseal cortex and medulla (BMP-1-6), (c) osteoclasts of the metaphysis and epiphysis (BMP-1,-4,-5, and -6), and (d) mid to deep zone articular chondrocytes of weanling rats (BMP-1-7). BMP staining in osteoclasts, an unexpected finding, was consistently strong with BMP-4, -5, and -6 but was variable and dependent on osteoclast location with BMP-2,-3, and -7. BMP-1-7 were moderately to intensely stained in vascular canals of human fetal epiphyseal cartilage by endothelial cells and pericytes. BMP-1,-3,-5,-6, and -7 were localized in hypertrophic chondrocytes adjacent to cartilage canals. We conclude that BMP expression is associated with maturing chondrocytes of growth plate and articular cartilage, and may play a role in chondrocyte differentiation and/or apoptosis. BMP appears to be expressed by osteoclasts and might be involved in the intercellular "cross-talk" between osteoclasts and neighboring osteoprogenitor cells at sites of bone remodeling.

Animals↗
PubMed1984

Radiography of healing dialysis osteodystrophy.

Characteristic skeletal changes of dialysis bone disease associated with multiple fractures were found in ten patients on prolonged regular (high aluminium) haemodialysis. A subsequent prospective investigation with serial radiography demonstrated healing approximately twelve months after a changed treatment regime. The treatment used was deionized or reverse osmosis water dialysis and renal transplantation. The typical osteomalacic and osteosclerotic changes and particularly metaphyseal sclerosis were found to be associated with more rapid clinical healing, whereas secondary hyperparathyroidism indicated delayed healing. It is suggested that plasma aluminium imbalance may lead to disturbance of bone formation with fractures, while healing is associated with normal serum aluminium levels and is manifested radiologically by osteosclerosis, particularly in the metaphyses.

Adult↗
PubMed1982

Canine hypertrophic osteodystrophy, a study of the spontaneous disease in littermates.

All members of a weimaraner litter had clinical and radiographic signs of hypertrophic osteodystrophy shortly after weaning. Three dogs were necropsied. Radiographic metaphyseal densities, which are used to make a clinical diagnosis of hypertrophic osteodystrophy, were found to result from elongation of the calcified cartilage lattice of the primary spongiosa. Intertrabecular acute inflammation was associated with necrosis, failure to deposit osseous tissue on the calcified-cartilage lattice, and trabecular microfractures. This process led to metaphyseal infraction and separation of the epiphysis. Defective bone formation (osteodystrophy) was considered a secondary process resulting from inflammation of osteochondral complexes, marrow, and periosteum. Enamel hypoplasia also was found to be associated with inflammation of the dental crypt, and abnormal enamel matrix was observed in the developing teeth. The histopathology of the bones and teeth was different from alterations which occur in infantile scurvy or congenital syphilis, although these diseases of man have radiographic similarities to canine hypertrophic osteodystrophy. Because the radiologic lesion is nonspecific, a clinical diagnosis of hypertrophic osteodystrophy is not necessarily diagnostic of a specific disease due to a single etiologic agent. Liver levels of ascorbic acid were within the normal range. Although an infectious agent could not be identified, the conditions may have an infectious origin with systemic manifestations.

Animals↗
PubMed1990

Congenital spinal stenosis in beef calves in western Canada.

Nineteen calves with a clinical history of posterior weakness or ataxia were examined at necropsy. Dorsoventral narrowing of the vertebral canal and myelopathy were found in the thoracic and lumbar areas of the spinal cord; vertebral metaphyseal growth plates had focal areas of premature closure. Malformation of the cranial base and hydrocephalus were also observed. Shortening of long bones and malformation of long bone epiphyses were prominent findings and were associated with focal premature closure of metaphyseal growth plates. The cause of these lesions is unknown; possible causes, including a maternal deficiency of manganese, are discussed.

Animals↗
PubMed1994

Avian tibial dyschondroplasia: a morphological and biochemical review of the growth plate lesion and its causes.

Avian tibial dyschondroplasia is a disease found in fast growing strains of chickens, ducks, and turkeys worldwide in which growth plate cartilage accumulates in the metaphyseal region of the tibiotarsus; it is similar to mammalian osteochondrosis. Several biochemical and pathologic studies have shown that the growth plate chondrocytes do not reach their expected size in the hypertrophic zone and necroses prematurely. The chondrocytes also produce decreased amounts of extracellular proteins, such as collagen X and fibroblast growth factor-beta, that are necessary for cartilage maturation. This immature cartilage becomes highly cross-linked in the collagen molecules and apparently resistant to resorption and vascularization by the metaphyseal vessels. The dyschondroplastic cartilage remains in the metaphysis for several weeks. Not until the growth rate of the birds slows down is the cartilage able to be resorbed and replaced by trabecular bone. Many conditions have been found to induce tibial dyschondroplasia, including copper deficiency; fusarochromanone, thiram, and antabuse intoxication; excessive dietary levels of cysteine and homocysteine; metabolic acidosis; and bird rearing environment. However, the mechanism(s) by which these various methods induce tibial dyschondroplasia is presently not known. Current research is focusing on understanding the development of the disease and whether or not all these methods work by the same physiological chain of events. Recent biochemical evidence suggests that a copper deficiency might be caused by a different mechanism than genetically and thiram-induced tibial dyschondroplasia.

Animals↗
PubMed1997

Osteochondrodysplasia occurring in transgenic mice expressing interferon-gamma.

In addition to various biological activities, interferon-gamma (IFN-gamma) inhibits bone resorption and collagen synthesis. We produced a transgenic mouse line expressing the murine IFN-gamma gene and protein in the bone marrow and thymus. Forty-five transgenic FVB/NCr mice, 23 days-9 months of age, were studied for anomalies in the skeletal system. The transgenic mice had short, wide, and deformed long bones. Young transgenic mice had epiphyseal plates severely thickened with zones of hypertrophy and degeneration with irregular metaphyseal borders. Cartilagenous masses were also observed in the metadiaphyseal marrow cavities. These lesions were primarily seen in long bones and ribs. Adult transgenic mice had residues of degenerated cartilagenous masses in the diaphyses. Many osteoclasts with well-developed ruffled borders were present on the metaphyseal cartilagenous masses in young transgenic mice. Adult transgenic mice had less prominent primary spongiosa with fewer osteoclasts at the metaphysis as compared with nontransgenic controls. The cortical bones of the transgenic mice were thinner and more immature compared with controls. Transgenic mice also had fractures, disruption of the epiphyseal plate, and degeneration of articular cartilage. Thus, the IFN-gamma transgenic mice developed a complex chondro-osseous lesion that was diagnosed as osteochondrodysplasia. The lesions may originate from primarily decreased matrix synthesis in bone and cartilage and also possible osteoclast-related changes caused by IFN-gamma overexpression in the bone marrow. Our IFN-gamma transgenic mouse will be a useful model to investigate the role of IFN-gamma in bone metabolism.

Acid Phosphatase↗
PubMedDate not supplied

Pull-out strength of suture anchors for rotator cuff and Bankart lesion repairs.

Surgical reconstructions of anterior-inferior shoulder instabilities and rotator cuff injuries require secure fixation of soft tissue to bone. Sutures are inserted directly through transosseous tunnels in current techniques, which are surgically complex and not always adequate for fixation strength. Using fresh-frozen cadaveric human specimens, our objectives were 1) to compare immediate pull-out strength of two versions of polyacetal suture anchors (wedge and rod) with conventional suture-only attachment techniques in Bankart lesion and rotator cuff repairs, and 2) to compare pull-out strength of the two polyacetal suture anchors with a metallic suture anchor. Our results indicate no significant differences in fixation strength of Bankart lesions or rotator cuff repairs using sutures only, or using wedge or rod polyacetal suture anchors (P = 0.70). Pull-out force did not differ significantly (P = 0.37) between the two polyacetal anchors. Polyacetal anchors exhibited higher pull-out forces than metallic anchors when inserted into metaphyseal regions of the tibia and significantly higher pull-out forces (P < 0.001) when inserted into metaphyseal regions with thicker cortical walls. Our results indicate that both polyacetal suture anchors provide adequate immediate fixation for soft tissue repairs in the human shoulder.

Acetals↗
PubMed2005

Excerpt from Medicinische Psychologie oder Physiologie der Seele by Dr Rudolph Hermann Lotze.

Hermann Lotze (1817-81) is a neglected figure in the history of psychiatry although it has been claimed that his early views were influential, for example, on the young Griesinger. Trained as a physician, psychologist and philosopher he saw better than many the impending epistemological crisis that was to affect disciplines such as psychology and medical psychology as they were being taken over by the natural sciences. The problem he endeavoured to resolve was double-headed. On the one hand, Lotze believed that the mechanisms proposed by physiology and other relevant natural sciences were essential to the explanation of human behaviour provided that its meaning and context were respected; on the other, he wanted to do away with the mysterious (metaphysical) explanations such as 'vital force' which in his time were still popular in biology. The solutions he eventually offered can understandably be seen as a weak compromise and one which statisfied no one. Materialists à outrance such as Vogt, Büchner, Lange and Ribot though he was too 'metaphysical'; spiritualist philosophers believed that he had surrendered too much to biology. It is likely that Lotze remained, in fact, a metaphysician as can be ascertained by studying his concept of Seele (soul, mind) into which he packed enough furniture to make many believe that he was an idealist thinker. This paper discusses some of these issues and justifies the choice of classic text, namely, Lotze's illuminating Introduction to his book Medicinische Psychologie oder Physiologie der Seele.

Germany↗
PubMed1998

Is all bone the same? Distinctive distributions and properties of non-collagenous matrix proteins in lamellar vs. woven bone imply the existence of different underlying osteogenic mechanisms.

The purpose of this review is to summarize recent functional and structural findings regarding non-collagenous matrix proteins in bone and teeth, to compare gene locations for bone and tooth matrix proteins with loci for hereditary skeletal diseases, and to present several provocative hypotheses which integrate this new information into a physiological context. Hypothesis I proposes that the molecular composition of rapidly deposited and mineralized woven bone, as well as the responsiveness of cells synthesizing woven bone to stimuli, is different from that for more slowly synthesized lamellar bone, implying the existence of distinctive osteogenic mechanisms. This review of recent research strongly supports this proposal. Briefly, the protein composition of woven bone matrix is enriched in acidic phosphoproteins BAG-75 and BSP, which are not expressed in lamellar bone, which is itself enriched in osteocalcin. De novo deposition and mineralization of woven bone occurs faster than in lamellar bone by means of a matrix-vesicle-assisted mechanism. Deposition of woven bone occurs at sites experiencing biomechanical strains higher than those experienced by lamellar bone. In addition, woven bone in metaphyseal regions is more susceptible to osteoclastic resorption after space flight, ovariectomy, and loss of weightbearing than is lamellar bone. Finally, osteoprogenitor cells responsive to parathyroid hormone reside in the metaphyseal region of long bones. Taken together, these findings suggest that Hypothesis I represents a useful paradigm for future studies. Specific functions mediated by most individual bone and tooth matrix proteins remain uncertain. A review of current literature suggests that the functionality of skeletal matrix proteins is expressed through specific binding sites composed of particular species-conserved structural motifs (Hypothesis 2). Examples include the previously recognized Asp-Ser-Ser motif of dentin phosphophoryns and the gamma-carboxyglutamic acid motif of matrix GLA protein and osteocalcin. A new polyacidic amino acid motif composed of consecutive Asp and Glu residues (n > 7) was defined in extracellular matrix components osteopontin, bone sialoprotein, and bone acidic glycoprotein-75 on the basis of strong functional analogies with similar polyacidic stretches in divalent metal storage proteins of the endoplasmic reticulum and sarcoplasmic reticulum. These structural motifs represent prime targets for future structure-function studies in vivo and in vitro.

1-Carboxyglutamic Acid↗