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Related Concept Videos

Bone Formation by Intramembranous Ossification01:29

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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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Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
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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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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
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All bones comprise an outer layer of compact bone, and an interior made up of spongy bone tissue, also called cancellous or trabecular bone. In long bones, spongy bone tissue is mainly found in the interior of the epiphyses (broad ends of the bone).
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Related Experiment Video

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Direct Mouse Trauma/Burn Model of Heterotopic Ossification
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The traumatic bone: trauma-induced heterotopic ossification.

Devaveena Dey1, Benjamin M Wheatley2, David Cholok3

  • 1Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Md.

Translational Research : the Journal of Laboratory and Clinical Medicine
|July 3, 2017
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Summary

Heterotopic ossification (HO), abnormal bone growth after trauma, involves complex molecular pathways. Understanding these mechanisms aids in developing new diagnostic and treatment strategies for this condition.

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Area of Science:

  • Orthopedics
  • Regenerative Medicine
  • Trauma Surgery

Background:

  • Heterotopic ossification (HO) frequently occurs after significant trauma, including surgeries, brain/spinal cord injuries, burns, and combat wounds.
  • HO involves endochondral ossification through a cartilaginous matrix, often requiring surgical excision with risks of complications and recurrence.
  • Trauma-induced HO results from aberrant wound healing, immune activation, infection, vascularization, and innervation, triggering stem cell activation.

Purpose of the Study:

  • To review recent advancements in understanding the molecular basis of trauma-induced HO.
  • To summarize updated diagnostic modalities and emerging treatment strategies for HO.
  • To highlight the role of animal models in mechanistic studies and therapeutic development.

Main Methods:

  • Review of current literature on trauma-induced heterotopic ossification.
  • Analysis of molecular pathways, immune responses, and cellular mechanisms involved in HO.
  • Evaluation of diagnostic technologies (e.g., micro- and nano-CT) and therapeutic interventions.

Main Results:

  • Trauma-induced HO is a complex process driven by aberrant wound healing and immune system activation.
  • Advanced imaging techniques show promise for early HO detection and intervention.
  • Animal models are crucial for elucidating HO pathogenesis and testing novel small molecule therapies.

Conclusions:

  • Significant progress has been made in understanding the molecular underpinnings of trauma-induced HO.
  • Refined diagnostics and targeted molecular therapies offer improved management options.
  • Continued research using advanced models is essential for combating HO effectively.