A&P unit 2 - bones

compact bone

-”dense cortical bone”

-hard bone

-on outside of bones

-80% of bone mass

spongy bone

-”trabecular bone”

-soft/spongy

-inside of compact bone

-20% of bone mass

hyaline cartilage

-most common cart.

-growth plates, precursor to bone

-on ends of bones

→ ribs to sternum, nose, throat

fibrocartilage

-support & absorb shock

→ in between vertebrae, btwn knee

compare ligaments vs tendons

-both are dense regular connective tissue

ligaments = bone to bone

tendons = bone to muscle

functions of bone

-support, protection

-levers for movement

-storage of calcium and phosphate

-hemopoiesis = produce blood cells

4 bone types

long bone, short bone, flat bone, irregular bone

long bone

-longer than they are wide

-bigger on ends

→ femur, humerus

short bone

-long as they are wide

-support, not movement

→ tarsals, carpals

flat bone

-flat

-for protection

→ skull

irregular bone

-doesn’t fit into the other bone types

→ vertebrae

red bone marrow vs yellow bone marrow

yellow = fat storage

red = hemopoiesis → make blood cells from stem cells

where is red bone marrow found children vs adults

children = in spongy bone and medullary cavity of long bones

adults = axial skeleton only

what kind of tissue is bone

connective tissue

osteogenic/osteoprogenitor cells

-stem cells

-hemopoiesis

-in periosteum and endosteum

-matures to become osteoblast

osteoblast

-bone matrix, hard bone

-from osteogenic cells

-synthesize osteoid

-differentiate into ostecytes

osteocyte

-maintain bone tissue

-mature bone cell derived from osteoblasts

-detect stress on bone & trigger new bone formation

osteoclast

-break down & reabsorb bone

-phagocytic → ruffled border = large surface area, more efficient

-derived from fused bone marrow cells

-make reabsorption lacuna in depression of bone surface

organic parts of bone

-make bone bendy

-osteoblast secrete osteoid

-osteoid = collagen & glycoprotein

→ it will calcify

inorganic parts of bone

-make bone rigid

-salts, calcium, phosphate

-form hydroxyapatite crystals that deposit around osteoblast collagen fibers

bone formation brief overview

1) osteoblast secretes osteoid layer

2) osteoid layer calcifies & hardens

3) deposition of inorganic hydroxyapatite crystal

what materials are needed for basic bone formation

- vitamin D = help calcium absorption in gut

- vitamin C = needed to make collagen

- calcium and phosphate = needed for calcification

osteon

circular portion. total “system” of bone microscopic anatomy

**IN COMPACT BONE

central canal

in center of each osteon

allows blood vessel and nerve

concentric lamellae

the circle layers in each osteon

made of calcified matrix, and organic collagen

lacunae

pits where osteocytes are located

osteocytes (in osteon function)

located in a lacuna

maintain bone matrix

→ bone strength

canaliculi

small canals reaching from each lacuna

for intercellular communication and nutrient passageway

draw a long bone and identify

-diaphysis

-epiphysis

-medullary cavity

-periosteum

-endosteum

2 layers of periosteum

-fibrous layer → outer. made of collagen. for support and connection

-osteogenic layer → inner, closer to endosteum. house osteoblasts

what is bone remodeling and why is it important?

remove mineralized bone followed by formation of new bone

-calcium & phosphorus homeostasis

-maintain skeleton integrity w/o adding weight

-adds strength to stress lines

2 steps of bone remodeling

1) Resorption of old mineralized bone → osteoclasts

2) build new bone → osteoblasts secrete osteoid

Resorption process

-osteoclasts adhere to bone and create seal via integrin proteins, form resorptive pit

-then secrete acid to dissolve calcium phosphate, and protease to dissolve organic osteod

-uses RANK, RANKL, OPG

-negative feedback, maintained by calcium levels

osteoclast picture

(need to know CAM/integrin, H-pump, lysosome, protease, RANK, RANKL, OPG)

osteopetrosis vs osteoporosis

osteopetrosis =overly dense bones. caused by too much OPG, or too little RANK

osteoporosis = too thin bones. caused by not enough OPG, or too much RANK

RANK and RANKL function

RANK = receptor protein

RANKL = receptor ligand. binds RANK. secreted by osteocytes

-stimulates osteoclast activation to break down bone

—> resorption & decrease bone mass

OPG function

OPG = osteoprotegin. decoy receptor for RANKL, stops breakdown of bone

-no osteoclasts activated so bone is not destroyed. osteoblast action

—> build new bone & increase bone mass

RANK, RANKL, OPG feedback loop (image)

basic multicellular unit (BMU)

title for osteoclast and blast ‘team’

-regulated by paracrine and endocrine communication

-located on surface of spongy bone, and in osteons (in cortical bone)

-5 steps = activation, resorption, reversal, formation, termination

non-targeted remodeling vs targeted remodeling

non-targeted = happens everywhere in body. initiated by systemic hormone

targeted = specific regions. initiated by osteocytes

how does an osteocyte detect stress in bone?

-osteocyte is floating in plasma by bone

-stress causes plasma to move

-plasma moves cilia on osteocyte → detection

-osteocyte will activate B catenin → this will increase OPG and decrease RANKL to build bone

increasing OPG and decreasing RANKL leads to

more building of bone (osteoblast)

decreasing OPG and increasing RANKL leads to

more resorption of bone (osteoclast)

non-targeted resorption

-parathyroid glands release PTH

-PTH bind to GPCR pathway in osteoblast/cyte

-activate cAMP and DAG/IP3 pathway

-cell increase RANKL and decrease OPG → more resorption

what happens to your bones if there is no weight-bearing activity

bones will weaken

-osteocytes not activated → stop releasing OPG

-now there is nothing to stop RANKL so increased resorption

compare the 4 types of bone fractures

-stress fracture = thin break caused by phys activity

-pathologic fracture = occurs in bone weakened by disease

-simple fracture = bone break but does not penetrate skin

-compound fracture = bone break penetrates skin

step 1 of bone fracture repair

hematoma forms from fracture → blood clot

-BV torn within periosteum

step 2 of bone fracture repair

form soft callus

-fibroblasts produce collagen

-hematoma is reorganized into connective tissue procallus

-chondroblasts form dense regular CT

-procallus becomes soft callus

step 3 of bone fracture repair

form hard (bony) callus

-osteoblasts near soft callus produce trabeculae → replace soft callus

-form hard callus

-then callus continues to grow and thicken

step 4 of bone fracture repair

bone is remodeled

-osteoclasts remove excess material

-compact bone replaces primary bone

-usually leaves slight thickening of bone

what are the 2 types of bone growth?

interstitial growth = get longer

appositional growth = get wider

interstitial growth depends on ______

the epiphysial plate (5 zones)

zone 1 of epiphysial plate (interstitial growth)

zone of resting cartilage

-closest to epiphysis

-small chondrocytes → make cartilage

-secures epiphysis to epiphyseal plate

zone 2 of epiphysial plate (interstitial growth)

zone of proliferation

-chon. do mitosis

-then form columns → flattened lacunae

-columns are parallel to diaphysis of bone

zone 3 of epiphysial plate (interstitial growth)

zone of hypertrophic cartilage

-chon. stop dividing

-do hypertrophy → the chon. get bigger

-walls of lacunae thin

zone 4 of epiphysial plate (interstitial growth)

zone of calcification

-only 2-3 layers of chon.

-mineral deposition

-minerals destroy chondrocytes

zone 5 of epiphysial plate (interstitial growth)

ossified bone

-walls of lacunae break down

-space invaded by osteoprogenitor cells

-new bone forms on top of calcified matrix

appositional growth process

-in periosteum

-bone matrix deposited within layers parallel to surface

-osteoclasts resorb inner/old bone to keep bone light

what is calcium required for?

-initiation of muscle contraction

-exocytosis

-blood clotting

-stimulation of heart by pacemaker cells

-calcium is part of mineral structure in bones

vitamin D production and activation (photo)

what does calcitriol do?

provides Ca2+ absorption in small intestine

→ binds vit D receptor in epithelial cell in SI → initiates creation of proteins that help transport Ca2+

Calcitriol protein channels

1) TRPV6 - Ca channel (facilitated)

2) PMCA1 - Ca pump into blood (primary active transport)

3) NCX - Ca pump into blood (secondary active transport) (sodium moves Ca against gradient into blood)

synergistic effect between PTH and vit D

they act together to increase concentration of calcium in blood

how does PTH affect kidney function related to calcium?

it stimulates kidney to excrete less Ca in urine → you hold onto more calcium, increase Ca lvl in blood

(opposite of calcitonin)

calcitonin

hormone produced by thyroid gland

-regulated blood calcium lvls by inhibiting Ca absorption

how does calcitonin affect kidney function related to calcium?

stimulate kidneys to excrete more Ca in urine → you lose more, meaning it decreases Ca blood lvls

(opposite of PTH)

How does aging affect bone?

lose tensile strength

-make less osteoblasts/collagen and more minerals → ↓ organic, ↑ inorganic = bones more brittle

-osteopenia = insufficient ossification. precursor to osteoporosis

-menopause means ↓ estrogen, which helps with OPG. ↓ OPG means nothing to stop RANKL binding

pituitary gland posterior vs anterior

PP - neural tissue → part of nervous system

AP - epithelial tissue → part of endocrine system

regulatory hormones

-hormones secreted by hypothalamus that go into AP gland

-releasing hormone = stimulate AP to release a hormone into blood (→ GHRH)

-inhibiting hormone = stimulate AP to stop releasing hormones into blood (→ GIH)

what are the hormones of the anterior pituitary gland?

TSH - Thyroid stimulating hormone

PRL - Prolactin

FSH - Follicle-Stimulating hormone

LH - Luteinizing Hormone

ACTH - Adrenocorticotropic hormone

GH - Growth hormone

**TP-FLAG acronym

Thyroid stimulating hormone

-TSH

-secreted by AP

-thyroid → control metabolism

Prolactin

-PRL

-secreted by AP

-females = breast dev. and milk production

*NOT a tropic hormone

Follicle-Stimulating hormone

-FSH

-secreted by AP

-females = ovary follicle growth, & estrogen prod.

-males = sperm prod.

Luteinizing Hormone

-LH

-secreted by AP

-females = ovulation

-males = testosterone secretion

Adrenocorticotropic hormone

-ACTH

-secreted by AP

-adrenal cortex → secrete cortisol

Growth hormone

-GH

-secreted by AP

-body growth

tropic hormones

hormones that tell another endocrine gland to secrete its own hormones

-most hormones from AP are tropic hormones

Posterior pituitary hormones

-PP does NOT make own hormones, instead 2 hormones from hypothalamus are stored there

-ADH/vasopressin = tell kidneys to store water, don’t pee

-oxytocin = uterine contraction during birth, milk ejection during breastfeeding

How do the hypothalamus and PP work together to release hormones?

-the hormones ADH/vasopressin and oxytocin are made in the hypothalamus

-they travel down axon to be stored in neural terminals in PP

-when neuron gets excited, the hormones are released from the terminals into BV for distribution thru the body

what does growth hormone release?

Insulin-like growth factor IGF from liver

-hepatocytes in liver secrete IGF

-IGF is like GH but has longer half-life

what kinds of cells do GH and IGF bind to?

ALL CELLS have receptors for GH, IGF, or both

→ when bound it stimulates growth

how do GH and IGF stimulate growth?

2 ways

-increase protein synthesis

-increase division/mitosis of cells

what are 3 results of GH?

-hyperplasia of chondrocytes → more mitosis

-linear growth @ epiphysis → bones grow

-increase amino acid uptake from muscle fibers

glycogenolysis

break glycogen into glucose (for energy)

→ stimulated by GH and IGF

gluconeogenesis

convert nutrients into glucose (storage)

→ inhibited by GH and IGF

glycogenesis

make glycogen (storage)

→ inhibited by GH and IGF

lipolysis

break down triglycerides (for energy)

→ stimulated by GH and IGF

lipogenesis

form triglycerides (storage)

→ inhibited by GH and IGF

Pituitary Dwarfism/GH deficiency

-present @ birth, but not seen until age 1

-decreased GH production

-short stature, low blood sugar

-Rx = GH injection over years

Pituitary Gigantism

-oversecretion of GH in childhood

-extremely tall, large organs, large tongue

-short life span, diabetes/hyperglycemia

Acromegaly

-excessive GH in adults

-no growth in height → epiphyseal plate closes in adolescence

-growth in appositional → face, jaw, hands, feet

-Rx = take synthetic form of GIH

hypothalamus/pituitary feedback loop (photo)