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ch. 6 (b)
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formation of the bony skeleton
-ossification (osteogenesis) is the proceas of bone tissue formation
-formation of bony skeleton begins in month 2 of fetal development
-postnatal bone growth occurs in early childhood and continues through adolescence
-growth in length & height (of long bones) is finite and ends between 18 and 21 years of age
-growth in width & thickness (appositional growth) is ongoing throughout adult life
-bone remodeling and repair are lifelong
Formation of the bony skeleton (From week 2 up to about week 8,fibrous membranes and hyaline cartilage of fetal skeleton are replaced with bone tissue through two distinct modes of ossification
Endochondral ossification: Bone forms by replacing hyaline cartilage; bones are called cartilage (endochondral) bones; form most of skeleton
Intramembranous ossification: Bone develops from fibrous membrane; bones are called memrane bones
Formation of the bony skeleton- Endochondral ossification
-forms essentially all bones inferior to base of skull, except clavicles
-begins late in month 2 of development
-uses previously formed hyaline cartilage models
-begins at primary ossification center in center of shaft
*blood vessels infiltrate perichondrium, converting it to periosteum
*mesenchymal cells specialize into osteoblasts
Fomration of the bony skeleton- 5 main steps in endochondral ossification
bone collar forms around diaphysis of cartilage model
central cartilage in diaphysis calcifies, then develops cavities
periosteal bud invades cavities, leading to formation of spongy bone (bud is made up of blood vessels, osteogenic cells, and osteoclasts)
diaphysis elongates, and medullary cavity forms
secondary ossification centers appear in epiphyses *epiphyses ossify: hyaline cartilage remains only in epiphyseal plates and articular cartilages
formation of the bony skeleton
intramembranous ossification: begins within fibrous connective tissue membranes formed by mesenchymal cells
-forms frontal, parietal, occipital, temporal, and clavicle bones
four major steps involved in intramembranous ossification
ossification centers are formed when mesenchymal cells cluster and become osteoblasts
osteoid is secreted, then calcified
immature (woven) bone is formed when osteoid is laid down around blood vessels, resulting in trabeculae *outer layer of woven bone forms periosteum
compact bone replaces immature bone, and red marrow appears
postnatal bone growth
-long bones grow lengthwise by interstitial (longitudinal) growth of epiphyseal plate
-bones increase thickness through appositional growth
-long bones stop growing during adolescence (some facial bones continue to grow slowly through life)
growth in length of long bones
-endochondral ossification continues in epiphyseal plates of long bones as they grow in length (interstitial growth)
-interstitial growth requires presence of epiphyseal cartilage in the epiphyseal plate
-epiphyseal plate maintains constant thickness (rate of cartilage growth on one side balanced by bone replacement on other)
growth in length of long bones
-near end of adolescence, chondroblasts divide less often
-epiphyseal plate thins, then is replaced by bone
-epiphyseal plate closure occurs when epiphysis and diaphysis fuse
bone lenghtening ceases
females: around 18 years of age
males: 21 years of age
epiphyseal line- remnant of growth plate seen in adults
bone growth in width
-as bones increase in length, they also expand in width through appositional growth
-bone widening can occur throughout life (bones thicken in response to increased stress from muscle activity or added weight)
-usually more building up than breaking down which leads to thicker, stronger bone that is not too heavy
osteoblasts
beneath periosteum secrete bone matrix on external bone
osteoclasts
remove bone on endosteal surface
hormonal regulation of bone growth (can be afffected by several diff. hormones)
-growth hormone: most important hormone in stimulatinf epiphyseal plate activity in infancy and childhood
-thyroid hormone: modulates activity of growth hormone, ensuring proper proportions
-testosterone and estrogens at puberty: promotes adolescent growth spurts
-excesses or deficits of any hormones cause abnormal skeletal growth
control of blood calcium levels- Hormonal control of blood calcium involves PTH and calcitonin
-parathyroid hormone (PTH): produced by parathyroid glands in response to low blood calcium levels
-main hormone in blood calcium regulation
-stimulates osteoclasts to resorb bone
-calcium is released into blood, raising levels
-PTH secretion stops when homeostatic calcium levels are reached
control of blood calcium levels- Hormonal control of blood calcium involves PTH and calcitonin
-calcitonin: produced by parafollicular cells of thyroid gland in response to high levels of blood calcium levels
-effects are negligible, but at high pharmacological doses it can lower blood calcium levels temporarily
Bone fracture
-fractures are breaks in the bone
-during youth, most fractures result from trauma
-in old age, most result from weakness of bone due to bone thinning
Fracture classification- can also be described by location of fracture, external appearance, and nature of break
three either/or fracture classifications
-position of bone ends after fracture, non displaced: ends retain normal position; displaced: ends are out of normal alignment
completeness of break
-complete: broken all the way through; incomplete: not broken all the way through
whether skin is penetrated
-open (compound): skin is penetrated; closed (simple): skin is not penetrated
Fracture healing stages
hematoma formation: bleeding and inflammation
fibrocartilaginous callus formation: chondroblasts form cartilage
bony callus formation: osteoblasts synthesize bone matrix
bone remodeling: bone regains normal shape
osteoporosis
-a group of diseases in which bone resorption exceeds deposit
-matrix remains normal, but bone mass declines
-spongy bone of spine and neck of femur most susceptible
-vertebral and hip fractures common