By Fayez F. Safadi, Mary F. Barbe, Samir M. Abdelmagid, Mario C. Rico (auth.), Jasvir S. Khurana (eds.)
Bone Pathology is the second one version of the publication, A Compendium of Skeletal Pathology that released 10 years in the past. just like the previous version, this ebook enhances general pathology texts and blends new yet quite validated info at the molecular biology of the bone. Serving as a bench-side significant other to the surgical pathologist, this re-creation displays new advances in our knowing of the molecular biology of bone. New chapters on soft-tissue sarcomas and soft-tissue tumors were additional in addition to numerous extra chapters akin to Soft-tissue pathology and Biomechanics. the amount is written by means of specialists who're demonstrated within the box of musculoskeletal illnesses. Bone Pathology is a mixed attempt from authors of other specialties together with surgeons, pathologists, radiologists and simple scientists all of whom have in universal an curiosity in bone illnesses. will probably be of significant price to surgical pathology citizens in addition to training pathologists, skeletal radiologists, orthopedic surgeons and scientific students.
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Additional info for Bone Pathology
Collagenases and several other enzymes, such as cathepsin B, are capable of degrading collagen and have been implicated in the pathogenesis of collagen-vascular diseases. Urinary excretion of hydroxyproline (found exclusively in collagen) and other products of collagen degradation (cross-linked products such as pyridinoline and deoxypyridinoline), act as markers of collagen breakdown. The level of collagen degradation byproducts in urine or serum reflect the amounts of bone turnover (see section on the laboratory in orthopaedic practice).
In situ hybridization and immunohistochemical analyses demonstrated that CTGF mRNA and protein are localized in osteoblasts lining metaphyseal trabeculae. Examination of CTGF expression in the fracture callus of a fracture repair model demonstrated that CTGF was primarily localized mesenchymal cells and in osteoblasts lining active, osteogenic surfaces. In primary osteoblast cultures, CTGF mRNA levels demonstrated a bimodal pattern of expression, being high during the peak of the proliferative period, abating as the cells became confluent, and increasing to peak levels and remaining high during mineralization (205).
Examples include Ehlers-Danlos syndrome (loose joints, characterized by a Gly to Serine change) or Osteogenesis imperfecta (brittle bones, characterized by a Gly to Cystine change). Osteogenesis imperfecta (see section on metabolic diseases) is a heritable disorder of Type I collagen. It is due to a variety of point mutations in either the pro-a1 or pro-a2 collagen chains. Over 100 point mutations have been found in probands with osteogenesis imperfecta. In a few cases, the mutations cause a decrease in the synthesis of pro-a1 and pro-a2 chains.
Bone Pathology by Fayez F. Safadi, Mary F. Barbe, Samir M. Abdelmagid, Mario C. Rico (auth.), Jasvir S. Khurana (eds.)