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Скачать или смотреть Endochondral Ossification of Bone - Animated

  • MedicoVisual - Visual Medical Lectures
  • 2025-02-04
  • 1718
Endochondral Ossification of Bone - Animated
endochondral ossificationbone developmenthistologybone formationosteoblastsosteoclastssecondary ossification centerbone remodelingoxygen depletionhistology lectureskeletal developmentcartilage ossificationbone marrowbone histologymedical educationanatomy and physiologybone growthskeletal systemmedical histologybone structurecartilage transformationbone formation processendochondral bone growthosteogenesisbone development lecture
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Описание к видео Endochondral Ossification of Bone - Animated

Ossification of Bone Playlist:    • Ossification of Bone - Visual Lecture Series  

Endochondral Ossification steps:

Mesenchyme (the Starting Material)
Embryonic mesenchymal cells in a gelatinous ground substance form the foundation for bone development.

Condensation of Mesenchyme
Mesenchymal cells cluster together, forming a dense shape resembling the future bone.

Formation of the Hyaline Cartilage Model

Mesenchymal cells differentiate into chondroblasts, which produce hyaline cartilage, creating a cartilaginous “template” for the bone.
The surrounding mesenchyme forms the perichondrium.
Cartilage, being avascular (except the perichondrium), relies on diffusion for nutrients.

Cartilage Enlargement: Appositional and Interstitial Growth

Appositional Growth: Chondroblasts on the outer surface add new layers of cartilage, increasing thickness.
Interstitial Growth: Chondrocytes within the cartilage divide and secrete matrix, lengthening the cartilage.

Bone Collar Formation

Chondrogenic cells transform into osteogenic cells.
Around the diaphysis (shaft), a bone collar forms under the perichondrium, now called the periosteum, via intramembranous ossification.
This bone collar limits nutrient diffusion to deeper cartilage.

Chondrocyte Hypertrophy and Matrix Calcification

Reduced oxygen and nutrients cause chondrocytes to enlarge (hypertrophy).
Sodium accumulation inside cells draws water in, causing swelling.
Hypertrophic chondrocytes secrete enzymes and factors that calcify the matrix, further reducing diffusion.
Chondrocytes die, leaving empty lacunae or primary areolae.

Blood Vessel Invasion and Primary Ossification Center

Chemicals from dying chondrocytes attract blood vessels to the diaphysis.
Blood vessels bring mesenchymal cells (perivascular collar), forming osteoblasts and hematopoietic stem cells (HSCs).
HSCs, initially from the liver, produce monocytes circulating in blood.
Monocytes unite to form chondroclasts, which dissolve the calcified cartilaginous matrix, creating secondary areolae.
Osteoblasts build spongy woven bone in the primary ossification center.
The outer bone collar becomes compact bone and periosteum.
Woven bone is remodeled into mature lamellar bone, with osteoclasts forming the marrow cavity filled by bone marrow–forming mesenchymal cells.

Secondary Ossification Centers (After Birth)

These form in the epiphyses postnatally, following chondrocyte hypertrophy, calcification, vascular invasion, and new bone formation.
No bone collar forms in the epiphyses, which lack periosteum.

Important Points:

Growth Plate and Articular Cartilage

The growth plate (epiphyseal cartilage) remains between the epiphysis and diaphysis, enabling bone lengthening until ossification in adolescence.
Articular cartilage reduces friction at joints.

Oxygen Depletion Hypothesis vs. Genetic Programming

Oxygen depletion from the bone collar is often cited as causing chondrocyte death.
However, secondary ossification centers form without a bone collar, suggesting an inherent genetic program.
The oxygen depletion idea remains a useful mnemonic.

Endochondral Ossification as Modified Intramembranous Ossification

Endochondral ossification is intramembranous ossification within a cartilage template.
The cartilage is replaced and remodeled into the final bony structure.

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