Endochondral ossification

Endochondral ossification[1][2] is one of the two

Endochondral ossification
essential processes during fetal development of the
mammalian skeletal system by which bone tissue is
created. Unlike intramembranous ossification, which is
the other process by which bone tissue is created,
cartilage is present during endochondral ossification.
Endochondral ossification is also an essential process
during the rudimentary formation of long bones,[3] the
growth of the length of long bones,[4] and the natural
healing of bone fractures.[5]

Contents
Growth of the cartilage model
Primary center of ossification
Secondary center of ossification
Appositional bone growth
Histology
Fracture healing
Additional images
See also Light micrograph of undecalcified epiphyseal
plate showing endochondral ossification:
References
healthy chondrocytes (top) become
degenerating ones (bottom), characteristically
Growth of the cartilage model displaying a calcified extracellular matrix.
Anatomical terminology
The cartilage model will grow in length by continuous
cell division of chondrocytes, which is accompanied by further secretion of extracellular matrix. This is
called interstitial growth.
The process of appositional growth occurs when the cartilage model also grows in
thickness due to the addition of more extracellular matrix on the peripheral cartilage surface, which is
accompanied by new chondroblasts that develop from the perichondrium.

Primary center of ossification

The first site of ossification occurs in the primary center of ossification, which is in the middle of diaphysis
(shaft). Then:

1. Formation of periosteum

The perichondrium becomes the periosteum. The periosteum contains a layer of

undifferentiated cells (osteoprogenitor cells) which later become osteoblasts.
 2. Formation of bone
collar

The osteoblasts
secrete osteoid
against the shaft
of the cartilage
model
(Appositional
Growth). This
serves as support
for the new bone.

3. Calcification of matrix

Chondrocytes in
the primary center
of ossification begin to grow (hypertrophy). They stop secreting collagen and other
proteoglycans and begin secreting alkaline phosphatase, an enzyme essential for
mineral deposition. Then calcification of the matrix occurs and osteoprogenitor cells
that entered the cavity via the periosteal bud, use the calcified matrix as a scaffold and
begin to secrete osteoid, which forms the bone trabecula. Osteoclasts, formed from
macrophages, break down spongy bone to form the medullary (bone marrow) cavity.

Secondary center of ossification

About the time of birth in mammals, a secondary ossification center appears in each end (epiphysis) of long
bones. Periosteal buds carry mesenchyme and blood vessels in and the process is similar to that occurring in
a primary ossification center. The cartilage between the primary and secondary ossification centers is called
the epiphyseal plate, and it continues to form new cartilage, which is replaced by bone, a process that
results in an increase in length of the bone. Growth continues until the individual is about 20 years old or
until the cartilage in the plate is replaced by bone. The point of union of the primary and secondary
ossification centers is called the epiphyseal line.

Appositional bone growth

The growth in diameter of bones around the diaphysis occurs by deposition of bone beneath the
periosteum. Osteoclasts in the interior cavity continue to resorb bone until its ultimate thickness is achieved,
at which point the rate of formation on the outside and degradation from the inside is constant.

Histology
During endochondral ossification, five distinct zones can be seen at the light-microscope level.
 Name Definition
Zone of
resting This zone contains normal, resting hyaline cartilage.
cartilage
Zone of
proliferation In this zone, chondrocytes undergo rapid mitosis,
/ cell forming distinctive looking stacks.
columns
In this zone, the chondrocytes undergo hypertrophy
Zone of
(become enlarged). Chondrocytes contain large
maturation /
amounts of glycogen and begin to secrete alkaline
hypertrophy
phosphatase.
In this zone, chondrocytes are either dying or dead,
leaving cavities that will later become invaded by bone-
Zone of forming cells. Chondrocytes here die when they can no
calcification longer receive nutrients or eliminate wastes via
diffusion. This is because the calcified matrix is much
less hydrated than hyaline cartilage.
Osteoprogenitor cells invade the area and differentiate
into osteoblasts, which elaborate matrix that becomes
Zone of
calcified on the surface of calcified cartilage. This is
ossification
followed by resorption of the calcified cartilage/calcified
bone complex.

Fracture healing
Drawing of part of a longitudinal
During fracture healing, cartilage is often formed and is called section of the developing femur of a
rabbit. a. Flattened cartilage cells. b.
callus. This cartilage ultimately develops into new bone tissue
Enlarged cartilage cells. c, d. Newly
through the process of endochondral ossification. Recently it has
formed bone. e. Osteoblasts. f. Giant
been shown that biomimetic bone like apatite inhibits formation of
cells or osteoclasts. g, h. Shrunken
bone through endochondral ossification pathway via
cartilage cells. (From “Atlas of
hyperstimulation of extracellular calcium sensing receptor
Histology,” Klein and Noble Smith.)
(CaSR).[6]

Additional images


Masson Goldner Section of fetal bone

trichrome stain of of cat. ir. Irruption of
growth plate in a the subperiosteal
rabbit tibia. tissue. p. Fibrous
layer of the
periosteum. o. Layer
of osteoblasts. im.
Subperiosteal bony
deposit. (From
Quain’s “Anatomy,”
E. A. Schäfer.)

See also
Intramembranous ossification
Ossification

References
1. Etymology from Greek: ἔνδον/endon, "within", and χόνδρος/chondros, "cartilage"
2. "Etymology of the English word endochondral" (http://www.myetymology.com/english/endoc
hondral.html). myEtymology. Retrieved December 2009. {{cite web}}: Check date
values in: |access-date= (help)
3. Netter, Frank H. (1987), Musculoskeletal system: anatomy, physiology, and metabolic
disorders. Summit, New Jersey: Ciba-Geigy Corporation ISBN 0-914168-88-6, p. 130: One
exception is the clavicle.
4. Brighton, Carl T., Yoichi Sugioka, and Robert M. Hunt (1973), "Cytoplasmic structures of
epiphyseal plate chondrocytes; quantitative evaluation using electron micrographs of rat
costochondral junctions with specific reference to the fate of hypertrophic cells", Journal of
Bone and Joint Surgery, 55-A: 771-784
5. Brighton, Carl T. and Robert M. Hunt (1986): "Histochemical localization of calcium in the
fracture callus with potassium pyroantimonate: possible role of chondrocyte mitochondrial
calcium in callus calcification", Journal of Bone and Joint Surgery, 68-A (5): 703-715
6. Sarem, Melika; Heizmann, Miriam; Barbero, Andrea; Martin, Ivan; Shastri, V. Prasad (2018-
07-03). "Hyperstimulation of CaSR in human MSCs by biomimetic apatite inhibits
endochondral ossification via temporal down-regulation of PTH1R" (https://www.ncbi.nlm.ni
h.gov/pmc/articles/PMC6142224). Proceedings of the National Academy of Sciences. 115
(27): E6135–E6144. doi:10.1073/pnas.1805159115 (https://doi.org/10.1073%2Fpnas.18051
59115). ISSN 0027-8424 (https://www.worldcat.org/issn/0027-8424). PMC 6142224 (https://
 www.ncbi.nlm.nih.gov/pmc/articles/PMC6142224). PMID 29915064 (https://pubmed.ncbi.nl
m.nih.gov/29915064).

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