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Related Concept Videos

Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Compact Bone01:27

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Most bones contain compact and spongy osseous tissue, but their distribution and concentration vary based on the bone's overall function.
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Bone Formation by Endochondral Ossification01:24

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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Creating Rigidly Stabilized Fractures for Assessing Intramembranous Ossification, Distraction Osteogenesis, or Healing of Critical Sized Defects
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Osteogenesis imperfecta.

Antonella Forlino1, Joan C Marini2

  • 1Department of Molecular Medicine, Biochemistry Unit, University of Pavia, Pavia, Italy.

Lancet (London, England)
|November 7, 2015
PubMed
Summary
This summary is machine-generated.

Osteogenesis imperfecta, a group of inherited disorders, causes brittle bones due to defects in collagen and other proteins. Recent discoveries reveal diverse genetic causes, improving understanding and potential treatments for bone fragility.

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Area of Science:

  • Genetics
  • Biochemistry
  • Orthopedics

Background:

  • Osteogenesis imperfecta (OI) is a heterogeneous inherited connective tissue disorder.
  • Characterized by skeletal abnormalities, bone fragility, and deformity.
  • Previously linked primarily to Type I collagen defects, recent discoveries show broader genetic causes.

Purpose of the Study:

  • To review the defects causing osteogenesis imperfecta.
  • To explore their mechanisms, interrelations, and classification.
  • To discuss diagnosis, management, and treatment strategies.

Main Methods:

  • Literature review of recent discoveries in OI genetics.
  • Analysis of causative genes and protein functions.
  • Classification of OI based on compromised metabolic pathways.

Main Results:

  • Identified diverse causative genes beyond Type I collagen, including those for structural, enzymatic, transport, and chaperone proteins.
  • Supported a predominantly collagen-related pathophysiology with broader implications.
  • Advanced understanding of normal bone development through studying OI defects.

Conclusions:

  • Knowledge of specific molecular bases is crucial for advancing clinical diagnosis and targeted therapies for OI.
  • Classification into five groups based on metabolic pathways aids understanding.
  • Holistic approach to OI management, diagnosis, and treatment is essential.