S&F Exam 2

Osteoid tissue

Bone tissue before it’s been hardened by the ECM

Location of the two types of bone

Compact bone - on the outside of all bones

Spongy bone - in the epiphyses

Middle - medullary cavity

Epiphysis

Ends of the bone; home of the epiphyseal plates (growth plates)

Growth only occurs here!!!

Diaphysis

The middle of the bone; medullary cavity is here

Medullary cavity

Hollow center of bone; houses bone marrow

Endosteum

Lines the inside of bones

Periosteum

Covers the outer surface of bones

What cells are in the periosteum and endosteum?

Osteogenic cells (stem cells!)

Organic components of bone ECM and effects

Collagen; causes brittle bones

Inorganic components of bone ECM and effects

Minerals (phosphate and calcium); bones cannot resist compression (bendy bones)

osteons

structural units of compact bone

lamella

thin sheets of bone matrix that make up osteons.

canaliculi

small channels that connect osteocytes to the artery, vein and nerve, and each other

arteries

deliver O2 and nutrients

veins

remove waste away from bone tissue

central canal

a channel located in the center of osteons that contains blood vessels and nerves, supplying nutrients and signaling to the surrounding bone tissue.

red bone marrow

found in the medullary cavities of kids but only in the axial skeleton of adults. Produces red, white, and platelets for the blood.

osteogenic cells

bone stem cells; found in the periosteum and endosteum that differentiate into other bone cells

osteoblasts

bone builders; responsible for bone deposition

osteocytes

mature bone cells that maintain bone tissue and communicate with other bone cells through canaliculi. (strain sensors)

osteoclasts

break down bones for minerals; responsible for bone resorption

intramembraneous ossification

• embryonic bone formation

• bone is deposited onto mesenchyme

• forms bone in skull, clavicle, and mandible

bone ECM

1/3 organic - including collagen and proteoglycans

2/3 inorganic - minerals such as calcium and phosphate

endochondral ossification

• forms every other bone

• bone is deposited on cartilage

steps of endochondral ossification

1. There is a cartilage model that is based on the bone it will become

2. Primary ossification center: osteoblasts deposit bones and chondrocytes die. Bone collar is formed

3. Growth continues toward epiphyses. Middle hollows out and medullary cavity forms

4. Secondary ossification centers: in the epiphyses; growth plates are formed

5. The only cartilage left is the articular cartilage (joints), and at the epiphyseal (growth) plates

interstitial bone growth

growth in length (only occurs in growth plates)

appositional growth

growth in width, only kind that can occur in adults!

how do bones continue to grow after birth?

New chondrocytes (near epiphyses) continue to divide, pushing the epiphyses away from the diaphysis, resulting in interstitial growth. Osteoclasts remove old chondrocytes.

What happens when the growth plates close?

Chondrocytes stop dividing, and everything is replaced by bone through osteoblasts, and osteoblasts remove old chondrocytes.

Difference between adult bones and child bones?

Children have epiphyseal lines; cartilage between bones for growth

brittle bone disease

A genetic disorder characterized by fragile bones that break easily due to a deficiency in collagen production, affecting the strength and structure of the bones.

rickets

a bone disease caused by vitamin D deficiency/lack of minerals, leading to weakened and softened bones in children.

Vitamin D deficiency is due to an inability to absorb dietary calcium

achondroplastic dwarfism

A genetic disorder resulting in abnormal bone growth, specifically affecting the growth plates, leading to short stature and disproportionate limb length.

Growth plates close too soon because osteoblasts deposit too quickly.

Wolff’s law of bone

architecture of bone is determined by stress; bone adapts to stress

gigantism

A condition caused by excessive growth hormone, resulting in abnormal increase in height and size, typically due to a pituitary tumor.

acromegaly

bones in skull, hands, and feet grow thicker due to excess GH and maybe pituitary tumor

hyperparathyroidism

A condition characterized by excessive secretion of parathyroid hormone, leading to elevated calcium levels in the blood and potential bone loss.

hypoparathyroidism

A condition marked by insufficient secretion of parathyroid hormone, resulting in low calcium levels in the blood and potential muscle cramps or spasms.

hypercalcemia

• high BCa2+ levels

• lower NM excitability

• muscle weakness

• impaired reflexes

• cardiac arrest

hypocalcemia

• low BCa2+ levels

• increased NM excitability

• muscle cramps or spasms

• potential tetany and suffocation

calcitonin

• produced by thyroid

• lowers BCa2+

• treates hypercalcemia

• too much = hypocalcemia

• stimulates osteoblasts, inhibits osteoclasts

PTH

• produced by parathyroid glands

• increases BCa2+

• treats hypocalcemia

• too much = hypercalcemia

• stimulates osteoclasts, inhibits osteoblasts

calcitriol (Vit. D)

• Raises BCa2+ by stimulating absorption of dietary Ca2+

stress fracture

abnormal trauma to bone

pathological fracture

a fracture caused by disease

non-displaced fracture

A type of fracture where the bone cracks but maintains its proper alignment and position.

displaced fracture

A type of fracture where the bone breaks and the ends are not in alignment, often requiring realignment.

comminuted fracture

A type of fracture where the bone is broken into several smaller pieces or fragments

greenstick fracture

A type of fracture that occurs when a bone bends and cracks on one side without breaking completely through, typically seen in children.

steps of fracture healing

• Osteoblasts and clasts form granulation tissue

• Fibroblasts deposit collagen

• Osteoblasts form hard callus

• New bone gets deposited over 3-4 mos.

osteoporosis

A condition characterized by weak and brittle bones due to loss of bone density. It increases the risk of fractures. Osteoclasts invade spongy bone

bone remodeling

• bone deposition and resorption

• 10% of skeleton a year on areas that need it most

• Reshapes bone in response to use/disuse

ectopic ossification

bone is deposited on soft tissue

characteristics of muscles

• excitability - can be stimulated

• conductivity - ability to transmit electrical impulses

• contractility - can shorten

• extensibility - can lengthen; 3x contracted length

• elasticity - can return to original length

muscle organization

muscle = bundle of fascicles

fasicle = bundle of muscle fibers

fibers = myofibers

myofibers = myofilaments

myofilaments = sarcomeres

epimysium

surrounds whole muscle

perimysium

surrounds fascicles within a muscle

endomysium

surrounds individual muscle fibers

significance of connective tissue wrappings in a muscle

each one comes out to form a tendon and attach to bone

sarcomeres

smallest unit of a muscle that can contract; runs down the whole length of the fiber

why is skeletal muscle striated?

the arrangement of actin and myosin

what happens in a muscle contraction?

the z line of a sarcomere moves toward the center, actin slides over the myosin, and myosin does not move

what is good for bones?

insulin, GH, estrogen, testosterone, thyroid hormone, Vit. A and Vit. C (collagen)

bad for bones?

cortisol; inhibits deposition and stimulates resorption

I-band

only actin

H-band

region between the actin filaments in a sarcomere that contains only myosin.

A band

dark band in a sarcomere that contains both actin and myosin filaments.

What bands shorten?

I band - actin pulls z-line

H band - actin accordions the H band

Why doesn’t the A band shorten?

Myosin doesn’t move

troponin

binds Ca2+ when released from sarcoplasmic reticulum; allows myosin to bind to actin.

tropomyosin

covers the binding sites for myosin heads when muscle is relaxed

how does muscle contraction with tropomyosin and troponin work?

Calcium is released from SR, binds to troponin, tropomyosin moves away to expose myosin head binding sites, allowing cross-bridge formation and contraction.

sarcolemma

The plasma membrane of a muscle cell, responsible for initiating action potentials and coordinating muscle contractions.

sarcoplasmic reticulum

stores calcium while muscle is relaxed, releases it during contraction

glycogen

carbs stored by liver and skeletal muscle

energy reserve for muscle contraction

glycocemia

blood sugar regulation in skeletal muscle

myoglobin

a protein that binds oxygen in muscle cells, aiding in oxygen storage and transport during muscle contraction.

myosin

A motor protein found in muscle cells has a head to grab actin to cause muscle contraction.

Neuromuscular junction (NMJ)

Synapse between a somatic motor neuron and a skeletal muscle cell

Excitation-Contraction Coupling (EC)

Events linking AP on somati motor neuron to AP on sarcolemma and to activation of myofilaments

steps of EC (11)

1. action potential (AP) travels down to the axon terminal

2. AP reaches the terminal and Ca++ channels open

3. Ca++ moving in causes synaptic vesicles containing Ach to move to the end of the terminal

4. Exocytosis of Ach occurs into synaptic cleft

5. Ach diffuses across synaptic cleft and binds to NM (nicotinic receptor) on sarcolemma

6. Binding Ach causes opening of Na+ channels, and AP begins on sarcolemma

7. AP travels along the sarcolemma and down the T-tubules

8. AP in T-tubules causes Ca++ in sarcoplasmic reticulum to open

9. Ca++ binds to troponin, and tropomyosin moves away from actin's binding sites

10. Cross bridges form - myosin heads attach

11. Power stroke occurs - myosin heads pull actin filaments toward the center of the sarcomere, shortening the muscle.

What role does ATP play in muscle contraction and relaxation?

ATP breaks cross-bridges

1. becomes ADP + P through hydrolysis - enough energy to straigten myosin heads

2. ADP + P are released, power stroke occurs

requirements for muscle relaxation

1. AP in somatic motor neuron must stop

2. Ach must stop production

3. AchE must eat leftover AchE

4. Ca++ transported back to SR

5. ATP breaks cross bridges

result of AchE inhibition

muscles can’t relax

spastic paralysis

inhibited movement due to muscle contraction and inability to relax.

flaccid paralysis

inhibited movement due to inability to contract muscles

effects of botox on muscles

inhibits exocytosis of Ach - leads to flaccid spasticity

effects of neuromuscular blockers on muscles

binds to nicotinic receptor to stop Ach from binding - leads to flaccid paralysis

effects of myasthenia gravis on muscles

the immune system attacks nicotinic receptors - flaccid paralysis

effects of pesticides/nerve agents on muscles

inhibits AchE - spastic paralysis

rigor mortis

• raised Ca++ in muscles - spastic

• No ATP to break cross bridges

motor unit

somatic motor neuron and all the fibers it innervate

fine vs. coarse control

fine motor units

smaller; require precise control, such as in fingers or eyes.

large motor units

larger; innervate many fibers, providing less precise but more powerful muscle contractions, such as in the legs or back.

recruitment

the process of activating more motor units to increase muscle force during contraction.

The brain recruits more motor units as needed to produce greater muscle strength.