Le Histology Ii

Front 1

Describe Periosteum

Back 1

Dense irregular connective tissue full of type I collagen,
Anchored to the bone with Sharpey's fibers
A medium for MM attachment to B
Break your bone and it's gonna hurt b/c periosteum is highly innervated

Front 2

Bone and cartilage sometimes look alike in a stained section, what is a good way to tell them apart?
What does this mean as far as growth?

Back 2

Bone has cells in lacunae, but just ONE, no isogenous groups.
Bone only undergoes appositional growth, (no interstitial)

Front 3

What is endosteum?

Back 3

a simple layer of bone-lining stem cells

Front 4

Describe how endosteum controls bone resporption and repair.

Back 4

No need for sharpey's fibers, Bone liniing cells cover every surface of all the trabecular bone. If they retract it exposes
bone mineral and osteoclasts are formed. This directs the resorption of bone. Has Stem cells for bone repair.

Front 5

Two classifications of bones

Back 5

1: Woven then lamellar
2: cortical and trabecular

Front 6

What is the difference in woven or llamellar bone (what is the basis of the first classification?

Back 6

The basis is how the collagen is laid down.
Woven: first to form in fetal development and bone repair
Irregular bundles of collagen, less calcified, replaced
Lamellar: Replaces woven, Orderly arrnagement of collage into lamellae, More calcified= stronger

Front 7

What is the difference in the Trabecular or Compact bone (what is the basis of the second classification?)

Back 7

2nd is a macroscopic classification of bone
Trabecular: cancellous, spongy bone
Compact: Dense/cortical bone

Front 8

What is the distribution of compact and lamellar bone?

Back 8

Trabecular is prominent at epipyses at ends of bone. Trabeculae directed down into the cortical bone in directions to distribute the force uniformly

Front 9

What is the basic structural unit and organization of compact bone?

Back 9

Osteon
Central canal (haversion) lined by endosteum
Lamellae
Lacunae (w/cells)
Canaliculi that connect central canal to lacunae
The whole thing is wrapped up by a nice cement line

Front 10

What canals run parallel with the bone shaft? Perpendicular?

Back 10

Parallel: central canals
Perp: Volkman's (travel from the inside out

Front 11

How can you tell the difference between Osteoblasts, osteocytes, and Osteoclasts in a slide?

Back 11

Osteocytes are IN the bone, easy
Osteoblasts are lining the bone and have ONE nucleus
Osteoclasts are lining the bone and have MULTIPLE Nuclei

Front 12

Where are osteoprogenitor stem cells located?

Back 12

Found in periosteum and endosteum

Front 13

What is measured in blood to evaluate bone formation?

Back 13

Osteocalcin and Alkaline Phosphatase

Front 14

Osteoblasts talk to eachother via__? Addition of calcium phosphate around the Osteoblasts they will become?

Back 14

Talk with gap junctions
Adding CaPO4 + surround themselves with bone ECM to become osteocytes

Front 15

What is the nature of osteocytes?

Back 15

They are amitotic b/c can't go anywhere/ Communicate via canaliculi, they maintain the ECM and can mobilize Ca

Front 16

What is the purpose of the canaliculi?

Back 16

Source of gap junction and diffusion. In lecture she added that blood vessel in central canal out through this system of canaliculi. NEVER contain BVs

Front 17

What is a disorder of Type I collagen?

Back 17

Osteogenesis imperfecta, Affects all bones in the body.
Demineralized bones because type I collagen and its arrangement contributes to the minearlization of bone.

Front 18

What do Matrix vessicles contain, from where do they come, what do they do?

Back 18

Matrix vessicles contain Alkaline phosphatase, Ca++ and PO4. THey are in the osteoblast, Vessicles act as seeding areas that promotes a nice set-down of mineral that will thoroughly mineralize collagen.

Front 19

Osteoblasts lay down _____ which in time will become ____.

Back 19

Osteoid,
Mineralized bone after mineralization guided by Matrix vessicles.

Front 20

Child vs adult Vitamin D Deficiency

Back 20

CHild: larger osteoid seam, rickets, greater lag time, not enough Ca++ to mineralize the osteoid
Adult: Osteomalacia

Front 21

Osteoclasts are derived from?

Back 21

bone marrow precursor cells Granulocyte/Monocyte progenitors (not osteoprogenitor cellsd) of myeloid lineage, they fuze into a big blob.

Front 22

As osteoclasts eat through bone it forms what is called """ or """

Back 22

Ruffled border,
Howship's lacuna

Front 23

How does Osteoclast resorb bone?

Back 23

Golgi pumps out tons of immiture lysosomes, which bind to membrane and cause it to rufffle, it also causes subosteoclast compartment to be acidic.
There is an actin plaque filament donut that seals off the ruffled border.
Bone resorbs and sends ot nearby capillary
. Note: no capillary, no resorption, defective actin= defective osteoclast

Front 24

What are the three things Osteoblasts secrete to affect Osteoclasts.?
Whats another effector not from Osteoblasts (2)?

Back 24

M-CSF
RANKL
OPG
(PTH from parathyroid)
RANKL from T lymphocytes

Front 25

What does M-CSF do, where is its source?

Back 25

from Osteoblasts
1-stimulates precursor osteoclast formation and
2-induces them to make RANK and then express at their surface.

Front 26

What does RANKL do, where is its source?

Back 26

from Osteoblasts
1- binds to RANK receptor on Osteoclasts inducing further differentiation into Osteoclasts
such as fusing with other precursors, etc.

Front 27

Essentially what's the difference in M-CSF and RankL?

Back 27

MCSF- increase in cell numbers with receptors
Rank L- increase activated cells/cell activation

Front 28

What is PTH's effect on Osteoclast cells? How?

Back 28

PTH from chief cells of the parathyroid. Acts on osteoBLasts to increase MCSF and RANKL
secretion to lead to osteoclast differentiation. it "activates the cascade"

Front 29

Explain how inflammation can increase bone resorption

Back 29

Activated t lymphocytes during inflammation secrete RANKL and increased osteoclast activity to increase bone resorption (increased Ca++ demand on the body)

Front 30

What is OPGs effect on Osteoclast activity? How?

Back 30

from osteoblast
Osteoprotegerin acts as a
decoy receptor for RANKL ; so
less RANKL available to bind to real RANK on osteoclast precursor cells,
OPG inhibits cascade
Both RANKL and OPG from osteoblasts

Front 31

WHat does Calcitonin do to Osteoclast activity?
From where does it come?

Back 31

Shuts down by binding to calcitonin receptors.
from C Cells.
THis is the FASTER response to shut down osteoclasts

Front 32

What happens when normal bone remodeling pattern becomes uncoupled?

Back 32

Bone remodeling: osteoclast and osteoblast reformation of bone.
Decreased bone density

Front 33

What is the primary form of osteoporosis?

Back 33

Osteoclasts work perfectly normal but osteoblasts don't make enough bone.

Front 34

What are secondary forms of osteoporosis?

Back 34

Hyperparathyroidism and
Steroids

Front 35

What are the three elements needed for fracture healing?

Back 35

Approximation of fractured segments
Limited movement of bone fragments through stabilization and immobilization
and Most importantly Intact periosteum and endosteum

Front 36

What is a risk in fragment stabilization and immobilization?

Back 36

Too much stabilization vs weakening of supporting tissues

Front 37

Why is Intact periosteum/endosteum the most important requirement for fracture repair?

Back 37

it is the source of stem cells and blood supply.
IF no periosteum available due to nature of fracture may cause healing problems.
Endosteal side will heal quicker b/c of availability of regeneration factors

Front 38

Stem cells in the periosteum/endosteum can become three different "blasts" depending on oxygen levels. What are they?

Back 38

Low O2= fibroblast
Mid O2= Chondroblast
High O2= Osteoblast
Blood= O2 nutrtition, hormones, GFs, etc= better stem cell attraction and
differentiation.

Front 39

Explain what happens at initial fracture of the bone

Back 39

Bleeding=clot
BVs shut down on either side of fracture = more death
"Tissue dies in either side of the fracture as a result of the fracture itself. Area of
damaged tissue is greater than just the actual site of damage.
Endosteum is usually less affected.

Front 40

After break what is the order of tissue as vasculature improves?

Back 40

Fibroblasts- granulation tissue in really low O2 environ
Chondroblasts as Medium O2 levels.
Cartilage replaced with bone as vascularity continues to improve.

Front 41

What are the four major parts of the long bone?

Back 41

Epiphyses- ends
Diaphysis- includes everything other than the epiphysis
Epiphyseal plates- located between the epiphysis and the metaphyses
Metaphyses- where it flares out.

Front 42

Where is the bone marrow cavity?

Back 42

in the diaphysis between the trabecular bone ends, surrounded by cortical bone.

Front 43

Explain blood supply to Epiphysis and metaphysis in child vs adult.

Back 43

As long as there is cartilage between epi and metaphysis there is very little anastamoses
that occur. Yound individuals will NOT have anastamoses. Adults may, depends.

Front 44

What is intramembranous ossification?

Back 44

Bone formed directly by stem cells, no cartilage structure first.
Plates of skull formed this way.
Directly from mesenchyme in a highly vascular environment
NOTE: Fracture repair can have a component of intramembranous ossification

Front 45

In limb bud formation all of the vasculaature originates in the periphery of the limb, this promotes what growth in the center? Then what?

Back 45

This promotes chondroblast formation- a cartilage bone model.
Then, as vasculature becomes increasingly dense a Perichondrium forms around the cartilage model
Around the same time central chondroblasts calcify the matrix (not bone, just calcified chondroblasts CaCO3 crystals) and die.

Front 46

After the CaCO3 skeleton of part of a bone's cartilage model what happens?

Back 46

Perichondrium now changes name to periosteum (8th week) and primary ossification centers have begun to grow.

Front 47

What are required to say that a bone has "growth plates"?

Back 47

you must have a primary and secondary center of ossification

Front 48

identify the arrows

Back 48

Secondary centers of ossification

Front 49

Identify the bony structure

Back 49

Bony collar

Front 50

Identify the center of the structure

Back 50

CaCO3 chondrocyte skeleton ready for primary growth to occur

Front 51

Arrows are pointing to what type of tissue?

Back 51

Endosteum

Front 52

What are the arrows pointing to?

Back 52

Front 53

What is identified here?

Back 53

Fractures at the epiphyseal plates cause bony bridges Ostosis and uneven growth of long bones

Front 54

What is shown in this image?

Back 54

Osteoclasts and Howship's lacunae

Front 55

type of bone formation?

Back 55

Intramembranous ossification

Front 56

What cells are these?

Back 56

Osteoblasts

Front 57

Identify these cells

Back 57

Osteoblasts
Osteocytes
Osteoclasts (multinucleated

Front 58

Identify these cells

Back 58

Osteoclasts with ruffle border

Front 59

What is this?

Back 59

Osteocyte with cannaliculi

Front 60

What is this diagnosis?

Back 60

Osteogenesis imperfecta

Front 61

Label these

Back 61

Front 62

Diagnosis

Back 62

Osteoporosis

Front 63

Identify

Back 63

Primary center of ossification

Front 64

These arrows are pointing at what?

Back 64

Inside= trabecular
outside= compact or cortical

Front 65

identify types of bone

Back 65

Cortical or compact
trabecular

Front 66

Identify red and blue

Back 66

Red= volkmans in and out
Blue= central canal up and down