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The following study consisted of an anatomical description of the bony segments of the splanchnocranium of older animals, focused on horses (Equus caballus) and cattle (Bos taurus). The skull constitutes the bony skeleton of the head, housing the brain and sense organs; thus, it gives structural support to the face and contains the initial sections of the respiratory and gastrointestinal systems. It comprises a series of bones articulated with each other, allowing us to distinguish bone segments that limit the face (splanchnocranium). However, although the vast literature on their anatomy in these species is one of the contents in anatomy subject programs for students of the veterinary area, there are very few texts that generate a comparative differentiation in parallel to the time to study these structures. For this reason, we sought to create an article that allows a comparative start to be made to the head of larger animals, focused on cattle and horses, specifically at the level of the bones of the face or splanchnocranium. It was possible to distinguish a series of structural differences and dimensions between the bone segments of both species. [ABSTRACT FROM AUTHOR]

Osteoporosis is a major global health problem. The increase in the incidence of osteoporosis in the elderly poses a challenge to treat and also results in an economic burden for the nation. Osteoporosis has been given more importance in females, and there is an urgent need to address this disease in males. Various drugs, such as nitrogen-containing phosphonates, RANK ligand inhibitors, parathormones, and alendronate, have been used for effective treatment of osteoporosis. Alendronate (alendronic acid), a nitrogen-containing bisphosphonate that inhibits bone resorption by osteoclasts, was synthesized during the 1970s. In the present review, we discuss the pharmacokinetics, mechanism of action, adverse effects, contraindications, and toxicity monitoring of alendronate. The drug may be effectively used for the treatment of male osteoporosis in order to increase bone mineral density and prevent fractures., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Abstract Objective: to determine the incidence of falls among the elderly population of the city of Barbacena in the state of Minas Gerais, together with causal factors, circumstances and major consequences. Methods: a cross-sectional study was performed through questionnaires applied to 206 patients over the age of 60, from November 2014 to February 2015 in the city of Barbacena, in the state of Minas Gerais. Risk factors related to falls were analyzed, as well as the incidence of falls and the consequences for the lives of elderly persons. The existence of a relationship between the reporting of falls and possible risk factors was determined by the Chi-squared and Fischer's exact tests as indicated. Results: an incidence of falls of 36.41% was observed among the elderly, 45.95% of which occurred outside the home. A total of 85.71% of respondents had previously suffered strokes and 39.78% were taking medication. Among elderly persons who have fallen and suffered fractures (18.67%), 50% had suffered strokes, 50% were suffering from chronic kidney disease, and 61.54% could not perform their activities of daily living after the fall. Conclusion: it was concluded that the incidence of falls among the elderly was 36.41%, while the most correlated factors were drug use, stroke victims and people with chronic kidney disease. Among those who suffered fractures, 61.54% failed to perform activities of daily living. Preventing falls is a public health concern, and simple changes can reduce its prevalence.

Alveolar ridge deformities can be caused by several factors. Managing alveolar deformities prior to implant placement is essential to increase bone width, height or both. Several techniques and materials are now available to perform ridge augmentation procedures. The postoperative exposure of the membrane is the most frequent postoperative complications of ridge augmentation procedures. The present case describes the horizontal ridge augmentation procedure and the outcome of surgical attempt to manage post-operative membrane exposure, and shows the unpredictability of managing postoperative membrane exposure surgically.

Slipped capital femoral epiphysis (SCFE) mainly affects overweight prepubertal children. It is usually idiopathic, but endocrinological diseases are proposed as the main cause. SCFE occurs before the closing of the femoral physis, which generally occurs at 18 years in males and 16 years in females, therefore it is considered a children’s disease. However, there have been several reports of adults with SCFE and some familial cases. We present a case of bilateral SCFE in a 47 years old female with possible relationship with inhaled corticosteroids, and for the first time we collect and analyze all published cases in adults.

Highlights: [•] PTH/PKA/AP1 pathway may play an important role in bone damage of fluorine. [•] It was first found that arsenic may indirectly influence bone damage of fluorine. [•] It has the important theoretical significance and practical value for the study of mechanism on syndrome of endemic arsenism and fluorosis. [ABSTRACT FROM AUTHOR]

We studied the effect of metal mixture (MM), comprising As, Cd, and Pb, in developing female rat skeleton from gestation day 5 until postnatal day 60 (P-60). MM resulted in synergistic inhibition in viability and differentiation of osteoblasts in vitro, likely induced by reactive oxygen species. MM, administered at their most frequently occurring concentrations present in the groundwater of India, i.e., As: 0.38 ppm, Pb: 0.22 ppm, and Cd: 0.098 ppm or 10× of the ratio to developing rats, exhibited a synergistic decrease in ex vivo mineralization of bone marrow stromal (osteoprogenitor) cells. MM group showed a dose-dependent attenuation in weight and axial lengths and shortening of tibias at P-60. Furthermore, the growth plate was shortened, which was associated with shorter proliferative and hypertrophic zones, decreased parathyroid hormone–related protein and Indian hedgehog expression in the chondrocytes, reduced primary and secondary spongiosa, and hypomineralized osteoids—a major characteristic of osteomalacia. In addition, compared with the control, MM-treated rats were clearly osteopenic based on bone mineral density, microarchitecture, biomechanical strength, and particularly the biochemical profile, that suggested high turnover bone loss. Finally, in comparison to the control, the fracture-healing ability of MM group was delayed and accompanied by inferior quality of the healed bone. Together, these data demonstrated that the mixture of As, Cd, and Pb induced synergistic toxicity to developing skeleton, thereby diminishing modeling-directed bone accrual, inducing osteopenia and dampening fracture healing. [ABSTRACT FROM AUTHOR]

Bone disorders such as osteopenia, osteoporosis. and osteonecrosis have been reported in patients infected with the human immunodeficiency virus (HIV), but the etiology and mechanism of these disorders arc unknown. The prevalence estimates vary widely among studies and may be influenced by the presence or absence of antiretroviral therapy and lipodystrophy, severity of HIV disease, and overlapping bone loss risk factors. Addressing potential underlying hone disease risk factors (e.g., smoking and alcohol intake), evaluating calcium and vitamin D intake, and performing dual x-ray absorptiometry in patients with IIIV who have risks [or bone disease are important strategies in preventing osteopenia and osteoporosis in HIV- infected patients. Management of osteopenia and Osteoporosis is still being evaluated. Administration of bisphosphonates (e.g., alendronate), with calcium and vitamin D supplementation, may he reasonable in treating osteoporosis; however, surgical intervention is the only method for treating symptomatic osteonecrosis. [ABSTRACT FROM AUTHOR]

Mucopolysaccharidosis type VI (MPS VI) is a genetically inherited lysosomal storage disorder. Severely affected children exhibit a range of skeletal abnormalities including short stature, facial dysmorphia, and dysostosis multiplex. Naturally occurring and transgenic animal models of MPS VI are also found which exhibit pathology similar to the human disorder. In this paper we have characterized the formation of trabecular bone from growth plate cartilage in a feline model of MPS VI. Tibial trabecular bone was shown to be osteopenic in MPS VI animals with a bone mineral volume (BV/TV) of 4.51% compared with a BV/TV of 15.64% in normal animals. In addition to osteopenia, a rearrangement of trabecular bone architecture was also observed in MPS VI tibiae, with fewer, thinner trabeculae noted; bone formation rate was also decreased. These observations support those previously made in the L5 vertebrae of MPS VI animals. When the sequential formation of growth plate cartilage structural elements, their transition into primary bone spongiosa, and remodeling into secondary bone spongiosa was characterized, no difference between normal and MPS VI could be detected in the number of cartilage septae and their arrangement in the proliferative and hypertrophic regions of the growth plate or trabecular elements in the primary spongiosa. However, a deviation from normal was observed in the resting zone of the growth plate and in the secondary spongiosa of bone. Thus, the osteopenia observed in MPS VI bone appears to arise primarily from a defect in bone production within the metaphysis and diaphysis rather than the creation of an abnormal template in the preceding growth plate cartilage. [ABSTRACT FROM AUTHOR]

We measured bone mineral density (BMD in g/cm(2)) of the spine (L2-L4) and femur (four regions) in 1472 and 1487 cases, respectively, of ambulatory white women ages 20-79 years in the USA. A DPX densitometer was used in a mobile setting. The BMD values for women up to 69 years corresponded closely with published values for the USA, the UK, and northern Europe; our values were somewhat lower than those from other studies only in women over 70 years. The USA data were combined with data from Europe to give reference curves on about 12,000 subjects. Decreases of BMD with age in women below 50 years were much smaller than in older women (0.2% versus 0.6-1.0% per year). Femoral bone decreased from the neck region, but not the trochanter with age; the decrease of total femur BMD with age was due to loss from the former region. Loss of bone mineral content (BMC in g) from the femur neck and total femur region did not accelerate until after age 50 years, much like the spine. The apparent decrease of BMD in these regions that begins about age 40 actually is due to an increase of bone area. About 20% of USA women aged 50-79 years had BMD levels for the lumbar spine, or for the femur neck, more than -2.5 SD below the average values in young adult women 20-39 years old. Body weight had several times more impact on BMD than height, and in fact, a change of 1 kg in postmenopausal women was commensurate with the effect of a 1-year change in age. Subjects in the lowest quartile of body weight had T-scores that were 1 SD below those in the highest quartile. [ABSTRACT FROM AUTHOR]

Heterotopic bone and cartilage formation was studied in a bone induction model in abdominal muscles of guinea pigs using demineradized allogenic dentin as inductive material. The light microscopic study showed high activity of acid phosphatase (AcP) and leucine aminopeptidase (LAP) in young matrix-producing cells. The highest activity was seen in cells surrounded by unmineralized matrix. In the surrounding matrix there was strong staining of AcP, especially in matrix with high glycosaminoglycan content. Electron microscopic studies of AcP in sections from unfixed frozen tissue showed intracellular activity mainly located in lysosomes. Extracellular AcP activity was found in matrix vesicles in the newly formed hard tissue. It was most pronounced in areas of cartilaginous differentiation. By means of energy dispersive X-ray microanalysis in a scanning transmission electron microscope, the deposits were confirmed to contain lead precipitates. With the exception of some lysosomal staining, prefixation with formaldehyde prevented demonstration of the enzyme activity. Both AcP and LAP may be involved in degradation of organic components of the matrix which enable the matrix to mineralize. [ABSTRACT FROM AUTHOR]

The carbonate and phosphate vibrational modes of different synthetic and biological carbonated apatites were investigated by Raman microspectroscopy, and compared with those of hydroxyapatite. The nu1 phosphate band at 960 cm-1 shifts slightly due to carbonate substitution in both A and B sites. The spectrum of type A carbonated apatite exhibits two nu1 PO43- bands at 947 and 957 cm-1. No significant change was observed in the nu2 and nu4 phosphate mode regions in any carbonated samples. The nu3 PO43- region seems to be more affected by carbonation: two main bands were observed, as in the hydroxyapatite spectrum, but at lower wave numbers. The phosphate spectra of all biominerals apatite were consistent with type AB carbonated apatite. In the enamel spectrum, bands were observed at 3513 and at 3573 cm-1 presumably due to two different hydroxyl environments. Two different bands due to the carbonate nu1 mode were identified depending on the carbonate substitution site A or B, at 1107 and 1070 cm-1, respectively. Our results, compared with the infrared data already reported, suggest that even low levels of carbonate substitution induce modifications of the hydroxyapatite spectrum. Increasing substitution ratios, however, do not bring about any further alteration. The spectra of dentine and bone showed a strong similarity at a micrometric level. This study demonstrates the existence of acidic phosphate, observable by Raman microspectrometry, in mature biominerals. The HPO42- and CO32- contents increase from enamel to dentine and bone, however, these two phenomena do not seem to be correlated. [ABSTRACT FROM AUTHOR]

The present study was undertaken to clarify the receptor distribution and the pharmacokinetics of 3H-1alpha(OH)D3, and 3H-1alpha,25(OH)2D3 for comparison. Receptor autoradiography was used after intravenous injection to 3-day-old neonatal rats and radioassay-HPLC after oral application to young adult rats. Corresponding results were obtained from both receptor autoradiography and radioassay. After 3H-1alpha(OH)D3 administration, uptake was delayed but sustained over a long period of time and the concentration of silver grains (autoradiography) or recovered 3H-1alpha,25(OH)2D3 (radioassay) peaked at a lower level. After 3H-1alpha,25(OH)2D3 administration, osteoblast nuclear, whole bone uptake and retention of radiolabeled compound were relatively rapid and short in duration. Nuclear uptake in osteoblasts after administration of 3H-1alpha(OH)D3 was abolished in competition studies with 10-fold unlabeled 1alpha,25(OH)2D3. These results indicate that 1alpha(OH)D3 continuously supplies osteoblasts with converted 1alpha,25(OH)2D3 and would not spread to the cells because of the low binding affinity of the receptor. Accordingly, 1alpha(OH)D3 appears to have some therapeutic properties different from 1alpha,25(OH)2D3 because of a relatively slow and sustained accumulation of the receptor and less Cmax (pharmacokinetics) compared with 1alpha,25(OH)2D3. [ABSTRACT FROM AUTHOR]

Insulin-like growth factors (IGF)-I and IGF-II are produced by osteoblasts and are important paracrine/autocrine regulators of osteoblast proliferation and differentiation. Estrogen has been reported to increase gene expression of IGF-I in rodent osteoblasts. However, because species differences have been demonstrated in expression of various aspects of the IGF system in bone cells, it is not known whether this action also occurs in human osteoblasts. Thus, we assessed the effects of estrogen treatment on IGF-I and IGF-II gene expression in vitro in a recently developed human fetal osteoblast cell line that has high levels of estrogen receptors. As assessed by a quantitative reverse transcriptase-polymerase chain reaction method, treatment of hFOB/ER9 cells with 17β-estradiol (E2) increased steady state levels of IGF-I mRNA in a time- and dose- dependent fashion with a maximal increase of 319% ± 33% ( P < 0.01) of control occurring after treatment with 10−7 M E2 for 48 hours. In contrast, E2 did not alter steady state levels of IGF-II mRNA. The pure (type 2) antiestrogens ICI 182,780 (10−7 M) and ICI 164,384 (10−6 M) blocked the E2- induced increase in IGF-I mRNA levels. Interestingly, 4-hydroxytamoxifen (10−7 M), a documented pure antiestrogen in reproductive tissues, also increased IGF-I mRNA to levels similar to those observed in E2-treated cells. Since E2 was shown to mediate its effects on some target genes through a cAMP-dependent pathway, we studied the interaction between E2 and agents that are known to increase intracellular cAMP. Forskolin (10−8 M) and dibutyryl cAMP (10−3 M) increased IGF-I mRNA levels sixfold, and cotreatment with E2 did not affect these changes, consistent with a possible mediation of the estrogen effect on IGF-I gene expression by cAMP. We conclude that in human osteoblastic cells, the IGF-I gene is a target for estrogen action, suggesting that IGF-I may mediate part of the effects of estrogen in human bone. [ABSTRACT FROM AUTHOR]

Presents a case report of pregnancy-associated cancer with multiple metastases in a 32-year-old woman. Clinical presentation of the disease; Medical background of the patient; Diagnosis and treatment.

Non-steroidal anti-inflammatory drugs (NSAIDs), including cyclooxygenase-2 (COX-2)-selective NSAIDs, are associated with adverse effects on bone tissue. These drugs are frequently the treatment of choice but are the least studied with respect to their repercussion on bone. The objective of this study was to determine the effects of celecoxib on cultured human osteoblasts. Human osteoblasts obtained by primary culture from bone samples were treated with celecoxib at doses of 0.75, 2, or 5μM for 24 h. The MTT technique was used to determine the effect on proliferation; flow cytometry to establish the effect on cell cycle, cell viability, and antigenic profile; and real-time polymerase chain reaction to measure the effect on gene expressions of the differentiation markers RUNX2, alkaline phosphatase (ALP), osteocalcin (OSC), and osterix (OSX). Therapeutic doses of celecoxib had no effect on osteoblast cell growth or antigen expression but had a negative impact on the gene expression of RUNX2 and OSC, although there was no significant change in the expression of ALP and OSX. Celecoxib at therapeutic doses has no apparent adverse effects on cultured human osteoblasts and only inhibits the expression of some differentiation markers. These characteristics may place this drug in a preferential position among NSAIDs used for analgesic and anti-inflammatory therapy during bone tissue repair., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Alveolar ridge deformities can be caused by several factors. Managing alveolar deformities prior to implant placement is essential to increase bone width, height or both. Several techniques and materials are now available to perform ridge augmentation procedures. The postoperative exposure of the membrane is the most frequent postoperative complications of ridge augmentation procedures. The present case describes the horizontal ridge augmentation procedure and the outcome of surgical attempt to manage post-operative membrane exposure, and shows the unpredictability of managing postoperative membrane exposure surgically., Competing Interests: No competing interests were disclosed.

Bone marrow mesenchymal stem cells (MSCs) can differentiate into multiple cell types including osteoblasts. How this differentiation process is controlled, however, is not completely understood. Here we show that activating transcription factor 4 (ATF4) plays a critical role in promoting bone marrow MSC differentiation towards the osteoblast lineage. Ablation of the Atf4 gene blocked the formation of osteoprogenitors and inhibited osteoblast differentiation without affecting the expansion and formation of MSCs in bone marrow cultures. Loss of ATF4 dramatically reduced the level of β-catenin protein in MSCs in vitro and in osteoblasts/osteoprogenitors located on trabecular and calvarial surfaces. Loss of ATF4 did not decrease the expression of major canonical Wnt/β-catenin signaling components such as Wnt3a, Wnt7b, Wnt10b, Lrp5, and Lrp6 in MSCs. Furthermore, shRNA knockdown of ATF4 expression decreased the level of β-catenin protein in MC-4 preosteoblasts. In contrast, overexpression of ATF4 increased β-catenin protein levels in MC-4 cells. Finally, ATF4 and β-catenin formed a protein-protein complex in COS-7 cells coexpressing both factors or in MC-4 preosteoblastic cells. This study establishes a new role of ATF4 in controlling the β-catenin protein levels and MSC differentiation towards the osteoblast lineage.

Osteoporosis and low bone mineral density affect millions of Americans. The majority of adults in North America have insufficient intake of vitamin D and calcium along with inadequate exercise. Physicians are aware that vitamin D, calcium and exercise are essential for maintenance of bone health. Physicians are less likely to be aware that dietary insufficiencies of magnesium, silicon, Vitamin K, and boron are also widely prevalent, and each of these essential nutrients is an important contributor to bone health. In addition, specific nutritional factors may improve calcium metabolism and bone formation. It is the authors' opinion that nutritional supplements should attempt to provide ample, but not excessive, amounts of factors that are frequently insufficient in the typical American diet.In contrast to dietary insufficiencies, several nutrients that support bone health are readily available in the average American diet. These include zinc, manganese, and copper which may have adverse effects at higher levels of intake. Some multivitamins and bone support products provide additional quantities of nutrients that may be unnecessary or potentially harmful.The purpose of this paper is to identify specific nutritional components of bone health, the effects on bone, the level of availability in the average American diet, and the implications of supplementation for each nutritional component. A summary of recommended dietary supplementation is included.

Objectives: Peptide-15 (P-15) is an analogue of the cell binding domain of collagen. P-15 has been shown to facilitate physiological to process in a way similar to collagen, to serve as anchorage for cells, and to promote the binding, migration and differentiation of cells. However, how P-15 alters osteoblast activity to promote bone formation is poorly understood. To study the osteoinductive properties of peptide P-15, we analyzed the expression levels of bone related genes in human mesenchymal stem cells treated with this biomaterial., Material and Methods: Using real time Reverse Transcription-Polymerase Chain Reaction the quantitative expression of specific genes, like transcriptional factors (RUNX2 and SP7), bone related genes (SPP1, COL1A1, COL3A1, BGLAP, ALPL, and FOSL1) and mesenchymal stem cells marker (ENG) were examined., Results: P-15 causes a considerable induction of osteoblast transcriptional factor like osterix (SP7) and of the bone related genes osteopontin (SPP1) and osteocalcin (BGLAP). In contrast the expression of endoglin (ENG) was markedly decreased in stem cells treated with P-15 respect to untreated cells, indicating the differentiation effect of this biomaterial on stem cells., Conclusions: The present study shows the effect of P-15 on mesenchymal stem cells in the early differentiation stages: P-15 is an inducer of osteogenesis on human stem cells as indicated by the activation of bone related markers SP7, SPP1 and BGLAP.The results may allow a better understanding of the molecular mechanism of bone regeneration and as a model for comparing other materials with similar clinical effects.