Last edited by Akiramar
Thursday, February 6, 2020 | History

8 edition of The Genetics of Osteoporosis and Metabolic Bone Disease found in the catalog.

The Genetics of Osteoporosis and Metabolic Bone Disease

  • 295 Want to read
  • 4 Currently reading

Published by Humana Press .
Written in English

    Subjects:
  • Diseases & disorders,
  • Endocrinology,
  • Medical genetics,
  • Orthopaedics & fractures,
  • Musculoskeletal Diseases,
  • Molecular Genetics,
  • Medical / Nursing,
  • Medical,
  • MED,
  • MED005000,
  • MED073000,
  • Orthopedics,
  • Endocrinology & Metabolism,
  • Genetics,
  • Medical / Endocrinology & Metabolism,
  • Anatomy,
  • Physical Medicine & Rehabilitation

  • The Physical Object
    FormatHardcover
    Number of Pages462
    ID Numbers
    Open LibraryOL8253684M
    ISBN 100896037029
    ISBN 109780896037021

    Genetic factors in determining bone mass. Spine 27 19E—E Fibrodysplasia Ossificans Progressiva, Eileen M. Authoritative and state-of-the-art, The Genetics of Osteoporosis and Metabolic Bone Disease offers today's endocrinologists, rheumatologists, and geneticists a gold-standard compendium of current knowledge and thinking about the genetic disorders of bone and mineral metabolism, and a sound basis for the powerful new genetic therapies.

    Science ;— Eisman JA. Bone mass is low in relatives of osteoporotic patients. Given the complex biology of the skeleton it is likely that bone mass is under the control of a large number of genes, many of which exert relatively small effects on BMD minor genes whereas a few contribute substantially to variation in this trait major genes.

    No meta-analysis of ER association studies is available so far. Free shipping for individuals worldwide Usually dispatched within 3 to 5 business days. Singer and Robin J. At the same time the age-related estrogen deficiency may induce the increase of pro-inflammatory cytokines IL1, IL6 and TNF that enhances the expression of adhesion molecules on leukocytes and endothelial cells favoring the progression of atherosclerosis plaques. Genetic and environmental contributions to the association between quantitative ultrasound and bone mineral density measurements: A twin study. Strength of linkage disequilibrium between two vitamin D receptor markers in five ethnic groups: Implications for association studies.


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The Genetics of Osteoporosis and Metabolic Bone Disease book

Backache and crystal deposition arthropathies Gout and pseudogout are rarely associated with backache. Estrogens have vasodilatatory, antiinflammatory and antiproliferative effects on the cardiovascular system and they have been reported to provide protection against CAD in postmenopausal women [ 58 ].

ER seems to have a role in mediating estrogen effect on bone growth and bone size but not on BMD [ 54 ]. A meta-analysis by Ioannidis et al. April 23, Genetics of Bone Density A new study linked 32 novel genetic regions to bone mineral density.

Arthritis Rheum ;— You'll find comprehensive coverage of specific rheumatic conditions, including osteoarticular and extraarticular findings. Animal, clinical and epidemiological studies suggest that high blood pressure is associated with abnormalities of calcium metabolism, leading to increased calcium loss, increased movement of calcium from bone and long-term risk of bone demineralization and osteoporosis [ 24 — 26 ].

Mol Endocrinol ;— There are known genetic factors which influence the onset of osteoporosis, mostly related to oestrogen function. More than 40 million people nationwide either have osteoporosis or are at increased risk for broken bones because of low bone mineral density osteopenia.

The publishers should be commended for the good quality of X-rays. Effects of heredity, age, weight, puberty, activity, and calcium intake on bone mineral density in children. Pollak et al. The genetics of vertebral fractures from other metabolic bone diseases The most common lysosomal storage disease, Gaucher disease, is due to a genetic deficiency in lysosomal glucocerebrosidase.

Bilezikian, Editor-in-Chief, is the Dorothy L. The presence of a polymorphism at the translation initiation site of the vitamin D receptor gene is associated with low bone mineral density in postmenopausal Mexican-American women. The disease process in RA affects the lumbar spine causing symptomatic backache of at least three months in one-third of patients [61].

Genetic Determinants of Osteoporosis: Common Bases to Cardiovascular Diseases?

Calcium absorption on high and low calcium intake in relation to vitamin D receptor genotype. The development of anti-citrullinated cyclic peptide anti-CCP antibodies in patients with RA can help distinguish early RA from other arthropathic processes, and also identifies those patients most likely to develop joint erosions.

Osteoporosis International 17, — Erdogan et al. A COL1A1 Sp1 binding site polymorphism predisposes to osteoporotic fracture by affecting bone density and quality.

Osteopetrosis

Shore, John G. References 1. Bones are made of a mineral and protein scaffold filled with bone cells. A concise, well illustrated and easy readable text. Vitamin D and estrogen receptor allelic variants in postmenopausal women: Evidence of multiple gene contribution on bone mineral density.

Download preview PDF. Most studies have focused on the repeat microsatellite in the promoter region and on the PvuII and XbaI single nucleotide polymorphisms SNPs in the intron 1 of the gene. However, these studies generated conflicting results, suggesting the needing of large-scale investigations and analysis standardization.

The influence of family history of hip fracture on the risk of vertebral deformity in men and women: The European Vertebral Osteoporosis Study. Genetic factors in determining bone mass. The risk of developing SLE is known to be greatly increased in homozygotes for complement deficiencies of C1q, C3 and C4 [68].

Linkage of a gene causing high bone mass to human chromosome 11 11ql2— Estimates suggest that about half of all women older than 50, and up to one in four men, will break a bone because of osteoporosis.Osteoporosis (OP) is the most prevalent metabolic bone disease among developed countries and it is defined as a systemic skeletal disease characterized by low bone mass and microarchitectural.

Osteoporosis is by far the most common bone disease. Osteoporosis is “a skeletal disorder characterized by compromised bone strength, predisposing to an increased risk of fracture” (Osteoporosis ).

The composition of the mineral and matrix, the fine structure of the trabecular bone, the porosity of the cortical bone, and the presence of. We are specialists collaborating to provide the best possible care, discover better treatments, and train tomorrow’s health care experts.

Lorenzo Botto, MD, is a professor of Pediatrics at the University of Utah School of Medicine. He trained in Europe and the United States in Pediatrics, Pediatri. The Center for Osteoporosis and Metabolic Bone Diseases of the University of Arkansas for Medical Sciences (UAMS) is a unique academic research facility, dedicated to the study of osteoporosis and its treatment.

It is one of the largest research units of its kind in the United States, and is nationally. Mar 30,  · Osteoporosis is a progressive bone disease in which the bone density reduces over years that affects many people, with the number of patients increasing annually.

The patient suffering from this bone disease becomes prone to bone fractures. Women, especially postmenopausal women, have greater risk of showing symptoms of this disease.

Osteoporosis causes bones to become weak and brittle — so brittle that a fall or even mild stresses such as bending over or coughing can cause a fracture.

Osteoporosis-related fractures most commonly occur in the hip, wrist or spine. Bone is living tissue that is constantly being broken down and replaced.