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Bone Sections (bone + section)
Selected AbstractsThe Effect of In Vivo Mechanical Loading on Estrogen Receptor , Expression in Rat Ulnar Osteocytes,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2002P. J. Ehrlich Abstract The presence of estrogen receptor , (ER,) in osteocytes was identified immunocytochemically in transverse sections from 560 to 860 ,m distal to the midshaft of normal neonatal and adult male and female rat ulnas (n = 3 of each) and from adult male rat ulnas that had been exposed to 10 days of in vivo daily 10-minute periods of cyclic loading producing peak strains of either ,3000 (n = 3) or ,4000 microstrain (n = 5). Each animal ambulated normally between loading periods, and its contralateral ulna was used as a control. In animals in which limbs were subject to normal locomotor loading alone, 14 ±1.2% SEM of all osteocytes in each bone section were ER, positive. There was no influence of either gender (p = 0.725) or age (p = 0.577) and no interaction between them (p = 0.658). In bones in which normal locomotion was supplemented by short periods of artificial loading, fewer osteocytes expressed ER, (7.5 ± 0.91% SEM) than in contralateral control limbs, which received locomotor loading alone (14 ± 1.68% SEM; p = 0.01; median difference, 6.43; 95% CI, 2.60, 10.25). The distribution of osteocytes expressing ER, was uniform across all sections and thus did not reflect local peak strain magnitude. This suggests that osteocytes respond to strain as a population, rather than as individual strain-responsive cells. These data are consistent with the hypothesis that ER, is involved in bone cells' responses to mechanical strain. High strains appear to decrease ER, expression. In osteoporotic bone, the high strains assumed to accompany postmenopausal bone loss may reduce ER, levels and therefore impair the capacity for appropriate adaptive remodeling. [source] Investigation of bone and cartilage by synchrotron scanning-SAXS and -WAXD with micrometer spatial resolutionJOURNAL OF APPLIED CRYSTALLOGRAPHY, Issue 3-1 2000Biological materials such as bone or wood are hierarchically structured to optimize mechanical and other properties. Several methods and experimental techniques are usually needed to study these materials on different length scales. We developed a device for small angle X-ray scattering (SAXS) and wide-angle X-ray diffraction (WAXD), optimized for position resolved investigations of bone sections using synchrotron radiation. Thin samples can be scanned with 20 µm steps, acquiring two-dimensional SAXS or WAXD patterns at every point. The system was tested by performing one-dimensional scans across bone cartilage interfaces, revealing information about size, shape and orientation of nanometer sized mineral particles as well as about crystal type and texture of these particles. [source] Perspective: Quantifying Osteoblast and Osteocyte Apoptosis: Challenges and Rewards,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2007Robert L Jilka Abstract Since the initial demonstration of the phenomenon in murine and human bone sections ,10 yr ago, appreciation of the biologic significance of osteoblast apoptosis has contributed greatly not only to understanding the regulation of osteoblast number during physiologic bone remodeling, but also the pathogenesis of metabolic bone diseases and the pharmacology of some of the drugs used for their treatment. It is now appreciated that all major regulators of bone metabolism including bone morphogenetic proteins (BMPs), Wnts, other growth factors and cytokines, integrins, estrogens, androgens, glucocorticoids, PTH and PTH-related protein (PTHrP), immobilization, and the oxidative stress associated with aging contribute to the regulation of osteoblast and osteocyte life span by modulating apoptosis. Moreover, osteocyte apoptosis has emerged as an important regulator of remodeling on the bone surface and a critical determinant of bone strength, independently of bone mass. The detection of apoptotic osteoblasts in bone sections remains challenging because apoptosis represents only a tiny fraction of the life span of osteoblasts, not unlike a 6-mo -long terminal illness in the life of a 75-yr -old human. Importantly, the phenomenon is 50 times less common in human bone biopsies because human osteoblasts live longer and are fewer in number. Be that as it may, well-controlled assays of apoptosis can yield accurate and reproducible estimates of the prevalence of the event, particularly in rodents where there is an abundance of osteoblasts for inspection. In this perspective, we focus on the biological significance of the phenomenon for understanding basic bone biology and the pathogenesis and treatment of metabolic bone diseases and discuss limitations of existing techniques for quantifying osteoblast apoptosis in human biopsies and their methodologic pitfalls. [source] Bone resorption activity of osteolytic metastatic lung and breast cancersJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 6 2004Lih-Yuann Shih Abstract Production of bone resorption mediators and bone resorption activity were compared among osteolytic metastatic cancers, normal bone tissues, and soft tissue metastatic cancers to search for the possible factors leading to cancer-induced bone resorption. Twenty-five patients with untreated osteolytic metastatic breast or non-small cell lung cancers consisted of the study group. Normal bone tissues obtained from the same patient were used as internal controls; and tumor tissues from patients with soft tissue metastasis were used as external controls. Serum and urinary bone turnover markers were measured. Tissues harvested during surgery were subjected to tissue culture. The levels of prostaglandin E2 (PGE2), tumor necrosis factor-, (TNF-,), and interleukin-6 (IL-6) in the supernatant after 72 h of culture were measured. Bone resorption activity was measured by calcium release from cultured calvarias, and bone volume as well as osteoclast number in bone sections. Patients with osteolytic metastatic cancers showed significantly decreased serum osteocalcin, increased serum alkaline phosphatase, and urinary deoxypyridinoline levels. Osteolytic metastatic cancers produced significantly more PGE2 than both controls. Conditioned medium from osteolytic metastatic tumors showed significantly enhanced bone resorption activity, and indomethacin significantly reduced this activity. Levels of PGE2, and bone resorption activity increased in osteolytic tumor tissues than soft tissue metastatic tissues in the same patient indicated that the same tumor cells might respond differently to different microenvironments. Our observation showed that PGE2 was produced by osteolytic metastatic cancers and stimulated bone resorption in mice calvarias. PGE2 inhibitor may be applicable in reducing bone resorption by osteolytic metastatic cancers. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Bone Remodeling in Maxilla, Mandible, and Femur of Young DogsTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2008Sarandeep S. Huja Abstract Bone remodeling in the jaw is essential for metabolic needs, mechanical demands and for growth of the skeleton. Currently, there is no information on remodeling in the jaw of young dogs. Four ,5-month-old male dogs were given a pair of calcein bone labels. After killing, bone sections were obtained from the maxilla, mandible, and femur. The jaw specimens were obtained from regions associated with erupting permanent teeth. Undecalcified specimens were prepared for examination by histomorphometric methods to evaluate mineral apposition rate (,m/d), mineralizing surface/bone surface (%), and bone formation rate (BFR, %/yr) in the bone supporting erupting teeth and in the femurs. Only intracortical secondary osteonal remodeling units were measured. There were significant (P < 0.05) differences in the BFR for the three sites examined, with the highest BFR (72%/yr) being in the femur. The mandible had a BFR twofold greater than the maxilla (51%/yr vs. 25.5%/yr). The rate of turnover in the jaw and femur of young dogs is distinct from a similar comparison between the jaw and appendicular skeleton of adult (,1 yr old) dogs. Although BFR decreases with age in the femur, it remains elevated in the jaws. Anat Rec, 291:1,5, 2007. © 2007 Wiley-Liss, Inc. [source] Glucocorticoid-induced bone loss in mice can be reversed by the actions of parathyroid hormone and risedronate on different pathways for bone formation and mineralizationARTHRITIS & RHEUMATISM, Issue 11 2008Wei Yao Objective Glucocorticoid excess decreases bone mineralization and microarchitecture and leads to reduced bone strength. Both anabolic (parathyroid hormone [PTH]) and antiresorptive agents are used to prevent and treat glucocorticoid-induced bone loss, yet these bone-active agents alter bone turnover by very different mechanisms. This study was undertaken to determine how PTH and risedronate alter bone quality following glucocorticoid excess. Methods Five-month-old male Swiss-Webster mice were treated with the glucocorticoid prednisolone (5 mg/kg in a 60-day slow-release pellet) or placebo. From day 28 to day 56, 2 groups of glucocorticoid-treated animals received either PTH (5 ,g/kg) or risedronate (5 ,g/kg) 5 times per week. Bone quality and quantity were measured using x-ray tomography for the degree of bone mineralization, microfocal computed tomography for bone microarchitecture, compression testing for trabecular bone strength, and biochemistry and histomorphometry for bone turnover. In addition, real-time polymerase chain reaction (PCR) and immunohistochemistry were performed to monitor the expression of several key genes regulating Wnt signaling (bone formation) and mineralization. Results Compared with placebo, glucocorticoid treatment decreased trabecular bone volume (bone volume/total volume [BV/TV]) and serum osteocalcin, but increased serum CTX and osteoclast surface, with a peak at day 28. Glucocorticoids plus PTH increased BV/TV, and glucocorticoids plus risedronate restored BV/TV to placebo levels after 28 days. The average degree of bone mineralization was decreased after glucocorticoid treatment (,27%), but was restored to placebo levels after treatment with glucocorticoids plus risedronate or glucocorticoids plus PTH. On day 56, RT-PCR revealed that expression of genes that inhibit bone mineralization (Dmp1 and Phex) was increased by continuous exposure to glucocorticoids and glucocorticoids plus PTH and decreased by glucocorticoids plus risedronate, compared with placebo. Wnt signaling antagonists Dkk-1, Sost, and Wif1 were up-regulated by glucocorticoid treatment but down-regulated after glucocorticoid plus PTH treatment. Immunohistochemistry of bone sections showed that glucocorticoids increased N-terminal Dmp-1 staining while PTH treatment increased both N- and C-terminal Dmp-1 staining around osteocytes. Conclusion Our findings indicate that both PTH and risedronate improve bone mass, degree of bone mineralization, and bone strength in glucocorticoid-treated mice, and that PTH increases bone formation while risedronate reverses the deterioration of bone mineralization. [source] | |||||||||||||