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1. |
Workshop introduction |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 449-449
Joan McGowan,
Maryann Redford,
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ISSN:0884-0431
DOI:10.1002/jbmr.5650081302
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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2. |
Acknowledgments |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 450-450
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ISSN:0884-0431
DOI:10.1002/jbmr.5650081303
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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3. |
Executive summary and research recommendations |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 451-453
Maryann Redford,
Joan McGowan,
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ISSN:0884-0431
DOI:10.1002/jbmr.5650081304
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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4. |
Plenary Session |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 455-455
Claude Arnaud,
Michael A. Parfitt,
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ISSN:0884-0431
DOI:10.1002/jbmr.5650081305
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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5. |
Bone cell biology: New approaches and unanswered questions |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 457-465
Lawrence G. Raisz,
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摘要:
AbstractIn an effort to define the major unanswered questions in bone cell biology and suggest new approaches to answering these questions, I have outlined the bone remodeling cycle and briefly described the major local and systemic factors that regulate bone cell function. These factors include calcium‐regulating and systemic hormones as well as locally produced prostaglandins, cytokines, and growth factors. To understand the individual roles of this large number of regulators, it will be necessary to develop new approaches to measure their production and activity in bone under physiologic and pathologic conditions. Quantitative methods in molecular and cellular biology have been developed that should make this identification possibl
ISSN:0884-0431
DOI:10.1002/jbmr.5650081306
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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6. |
Bone loss in the oral cavity |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 467-473
Marjorie K. Jeffcoat,
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摘要:
AbstractBone loss in the oral cavity may occur due to many causes, including infection, systemic or local alterations in the host response, or multifactorial causes. The purpose of this article is to review our present understanding of the major causes of oral bone loss in adults, with special emphasis on two major oral diseases: periodontitis and residual ridge resorption. Periodontitis is characterized by resorption of the alveolar bone as well as loss of the soft tissue attachment to the tooth. Progressive periodontitis will result in continued alveolar bone loss and may result in tooth mobility, abscesses, and ultimately tooth loss. Although the reported prevalence may vary according to the epidemiologic study design, the 1985 National Survey of Oral Health of United States Adults indicated that 94% of female senior citizens examined demonstrated at least one site with at least 2 mm loss of attachment. Resorption of alveolar bone that occurs following tooth extraction is termed residual ridge resorption. In many cases, the denture will loosen because of the inability of the resorbed ridge to stabilize the prosthesis. In the most severe cases, the denture may impinge on the exposed mandibular nerve, resulting in pain or total inability to tolerate the prostheses. Although clear statistics on the prevalence of residual ridge resorption are not available, this boss loss may result in the need for new dentures to replace ill‐fitting prosthese
ISSN:0884-0431
DOI:10.1002/jbmr.5650081307
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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7. |
Skeletal osteoporosis |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 475-480
Claus Christiansen,
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摘要:
AbstractOsteoporosis is characterized by decreased bone mass and increased susceptibility to fractures. The clinical consequences of osteoporosis are fracture, most commonly seen at the wrist, the spine, and the hip. The prevalence of osteoporotic fracture is extremely high with 30%–40% of 70‐year‐old women having had at least one osteoporotic fracture. The prevalence in men is lower but may constitute a larger problem than expected. Osteoporotic fracture is, therefore, a significant cause of morbidity and mortality and represents a major problem of health care. Bone is the site of substantial metabolic exchanges, with bone resorption and formation continuing throughout life. The turnover processes are carried out by osteoclasts and osteoblasts in specialized cellular units. After cessation of growth, the skeleton probably consolidates to reach the peak bone mass at the age of 35–40 years. The relatively slow subsequent age‐related bone loss occurs in both men and women, but women are additionally exposed to accelerated bone losses after the menopause. Estrogen deficiency is the dominating pathogenetic factor for osteoporosis in women. The role of disturbances in the calcium‐regulating hormones and vitamin D deficiency is less sure. The pathophysiologic mechanisms of osteoporosis in men are not well investigated. Those who are endowed with a low peak bone mass and/or are exposed to a large bone loss are at particular risk of developing symptomatic osteoporosis. Several risk factors have been recognized but are insufficiently sensitive and specific to predict an individual's overall risk of developing o
ISSN:0884-0431
DOI:10.1002/jbmr.5650081308
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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8. |
Session II: Basic bone biology and structure |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 481-481
Arnold Kahn,
William T. Butler,
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ISSN:0884-0431
DOI:10.1002/jbmr.5650081309
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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9. |
Structure and molecular regulation of bone matrix proteins |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 483-487
Pamela Gehron Robey,
Neal S. Fedarko,
Theresa E. Hefferan,
Paolo Bianco,
Ulrich K. Vetter,
Wojciech Grzesik,
Alexander Friedenstein,
Gabri van der Pluijm,
Keith P. Mintz,
Marian F. Young,
Janet M. Kerr,
Kyomi Ibaraki,
Anne‐Marie Heegaard,
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摘要:
AbstractThe organic matrix of bone contains several protein families, including collagens, proteoglycans, and glycoproteins, all of which may be extensively modified by posttranslational events, such as phosphorylation and sulfation. Many of the glycoproteins contain Arg‐Gly‐Asp (RGD), the integrin‐binding sequence, within their structure, whereas other constituent proteins contain gamma‐carboxyglutamic acid. The deposition of bone matrix by cells in the osteoblastic lineage is regulated by extrinsic factors, such as systemic and local growth factors and physical forces, and factors that are intrinsic to the cell, such as position in the cell cycle, maturational stage, and developmental age of the donor. Recent studies of several bone matrix gene promoters have identifiedcis‐ andtrans‐acting elements that are responsible for gene activity, although the precise sequence of regulatory events is not known. Development of in vitro assays, coupled with studies of the appearance of these proteins during development in vivo, provides insight into the functions of these proteins during the various stages of bone metabolism. Potential roles for these proteins include proliferation and maturation of stem cells, formation of matrix scaffolding elaborated by bone‐forming cells, modeling, and remodeling. Changes in the functional properties of the extracellular matrix may be involved in a variety of disease processes, including osteoporosis and o
ISSN:0884-0431
DOI:10.1002/jbmr.5650081310
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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10. |
Mutations in Type 1 Procollagen That Cause Osteogenesis Imperfecta: Effects of the Mutations on the Assembly of Collagen into Fibrils, the Basis of Phenotypic Variations, and Potential Antisense Therapies |
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Journal of Bone and Mineral Research,
Volume 8,
Issue S2,
1993,
Page 489-492
Darwin J. Prockop,
Alain Colige,
Heikki Helminen,
J.S. Khillan,
Ruth Pereira,
Philipp Vandenberg,
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摘要:
AbstractWork by a large number of investigators over the last decade has established that over 90% of patients with osteogenesis imperfecta have mutations in one of the two genes for type I procollagen, that most unrelated probands have different mutations in the genes, and that the mutations found in most of the serious variants of the disease cause synthesis of abnormal proα chains of the protein. The results have demonstrated that synthesis of structurally abnormal but partially functional proα chains can interfere with folding of the central region of the protein into a triple‐helical conformation, prevent processing of the N‐terminal propeptides of procollagen, or produce subtle alterations in conformation that interfere with the self‐assembly of the protein into collagen fibrils. One of the unsolved mysteries about the disease is why some mutations produce severe phenotypes, whereas very similar mutations produce mild phenotypes. Recent studies in transgenic mice suggest that nongenetic factors, such as stochastic events during development, may determine the severity of the disease phenotype produced by a specific mutation. Also, recent results raised the possibility that strategies of antisense gene therapy may be effective in treating the disease some time in the future. Specific inhibition of expression of a mutated collagen gene has been obtained with antisense oligonucleotides in cell culture experiments. However, there is no means of selective delivery of antisense oligonucleotides to the appropriate
ISSN:0884-0431
DOI:10.1002/jbmr.5650081311
出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)
年代:1993
数据来源: WILEY
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