Skeletal System - Bone Tissue (235 #6)

Question 1

Skeletal System Functions

Answer 1

1) Support - soft tissue and attachments for muscles
2) Protection - internal organs
3) Assistance in Movement - with muscles
4) Mineral Homeostasis - storage & release
5) Blood Cell Production - red bone marrow = homeopoiesis
6) Triglyceride Storage - yellow bone marrow

Question 2

Diaphysis

Answer 2

the bone’s shaft or body

Question 3

Epiphyses

Answer 3

the proximal and distal ends of the bone

Question 4

Metaphyses

Answer 4

the regions between the diaphysis and epiphyses. Contains Epiphyseal Growth Plate = hyaline cartilage that allows the diaphysis of the bone to grow in length. Replaced by Epiphyseal Line = bone.

Question 5

Articular Cartilage

Answer 5

thin layer of hyaline cartilage covering part of epiphyses where bone forms articulation (joint) with other bone. Reduces friction and absorbs shock. repair is limited due to lack of perichondrium.

Question 6

Periosteum

Answer 6

tough connective tissue sheath, associated blood supply surrounds bone where there is no articular cartilage. Outer fibrous layer is dense irregular connective tissue, inner osteogenic layer is cells for growing in thickness. Nourishes, protects, repairs, attachment point. Connected to bone by perforating (Sharpey’s) fibres - collagen bundles extending into bone ECM.

Question 7

Medullary/Marrow Cavity

Answer 7

hollow cylindrical space in diaphysis that contains fatty yellow blood marrow and numerous blood vessels. Reduces weight of bone.

Question 8

Endosteum

Answer 8

thin membrane that lines the medullary cavity. Small amount of connective tissue plus a single layer of bone-forming cells.

Question 9

Osseous Tissue / Bone

Answer 9

abundant ECM with widely-separated cells. ECM is 15% water, 30% collagen and 55% crystallized mineral salts - calcium phosphate, calcium hydroxide, hydroxyapatite, CaCO3, Fl, Mg, K, S. Undergo CALCIFICATION, initiated by osteoblasts, requires presence of collagen.
hardness = mineral salts
flexibility = collagen

Question 10

Cells in Bone

Answer 10

1) osteogenic cells
2) osteoblasts
3) osteocytes
4) osteoclasts

Question 11

osteogenic cells

Answer 11

unspecialized bone stem cells derived from mesenchyme - only bone cells to undergo cell division, resulting in osteoblasts. Found along inner surface of periosteum, the endosteum and the canals within bones that contain blood vessels.

Question 12

osteoblasts

Answer 12

bone-building cells. Synthesize and secrete collagen and other stuff for ECM. As they are surrounded by ECM, they become osteocytes.

Question 13

osteocytes

Answer 13

mature cone cells - the main cells in bone tissue and maintain metabolism, waste removal, etc.

Question 14

osteoclasts

Answer 14

huge cells derived from the fusion of up to 50 monocytes (WBC) concentrated in the endosteum. Facing bone surface, cell has ruffly border and releases lysosomal enzymes/acids to break down ECM - RESORPTION. Minerals enter osteoclasts by endocytosis, then exit on the other side by exocytosis and into the interstitial fluid, then blood capillaries. In response to hormones, they help regulate blood Ca2+ levels and are target cells for osteoporosis drug therapy.

Question 15

COMPACT bone

Answer 15

1) few spaces
2) strongest form of bone tissue
3) beneath periosteum of all bones
4) bulk of diaphyses of long bones
5) protection, support, resists stresses
6) 80% of skeleton

Question 16

COMPACT tissue histology

Answer 16

made of repeating osteons (haversian systems) with little space btwn them:

1) central (haversian) canal - blood vessels, nerves, lymphatics
2) concentric lamellae - mineralized ECM
3) lacunae - btwn CL, contain osteocytes
4) canaliculi - tiny channels radiate from lacunae with ECF and fingerlike processes of osteocytes, which talk using gap junctions.
5) interstitial lamellae - btwn neighbouring osteons, actually older partially-destroyed osteons
6) perforating (Volkmann’s) canals penetrate compact bone and bring blood vessels, nerves, lymphatic vessels from periosteum.
7) circumferential lamellae - around entire inner & outer circumference of long bone from initial bone formation. Outer is attached to periosteum by perforating (Sharpey’s) fibers. Inner lines medullary cavity.

Question 17

SPONGY BONE (trabecular/cancellous)

Answer 17

1) no osteons
2) located in interior of bone
3) lamellae in irregular pattern called trabeculae.
4) spaces are filled with red bone marrow in RBC-producing bones, or yellow bone marrow (adipose tissue) in others.
5) many small blood vessels that nourish osteocytes.
6) short, flat, sesamoid and irregular bones.
7) core of the epiphyses and narrow rim of medullary cavity in long bones

Question 18

SPONGY tissue histology

Answer 18

1) concentric lamellae - mineralized ECM
3) lacunae - btwn CL, contain osteocytes
4) canaliculi - tiny channels radiate from lacunae with ECF and fingerlike processes of osteocytes, which talk using gap junctions.

Question 19

SPONGY vs. COMPACT

Answer 19

1) spongy is lighter
2) spongy supports and protects red bone marrow
3) spongy trabeculae are arranged along lines of stress. Typically found where stresses are low or from many directions
4) compact bone osteons are parallel to diaphysis.
5) compact bone is thickest where stress is applied in relatively few directions.

Question 20

Blood & Nerve Supply

Answer 20

1) periosteal arteries & veins - small vessels + nerves make periosteum VERY sensitive to tearing or tension.
2) nutrient arteries & veins (large) - centre of diaphysis, through nutrient foramen, divides into proximal and distal inside medullary cavity.
3) metaphyseal arteries & veins - enter the metaphyses and supply RBM and bone tissue.
4) epiphyseal arteries & veins

Question 21

Intramembranous Ossification

Answer 21

Simpler method - bone forms directly in mesenchyme.
1) Dvlp Ossification Centre - chemical changes cause mesenchymal cells to cluster and differentiate into osteogenic cells and then osteoblasts - secrete ECM.
2) Calcification - ECM secretion stops, osteocytes in lacunae. In days, Ca2+ and other mineral salts are deposited and ECM hardens
3) formation of trabeculae - bone ECM develops into trabeculae that fuse together to form spongy bone. Connective tissue associated with RB vessels differentiates into RBM
4) Dvlp Periosteum - mesenchyme condenses at bone periphery and turns into periosteum. Thin layer of compact bone replaces spongy bone.
Much of newly formed bone is remodeled as bone is transformed into adult size/shape.

Question 22

Endochondral Ossification

Answer 22

1) Dvlp Cartilage Model - chemical changes => mesenchymal cells to cluster and differentiate into chondroblasts - secrete ECM, producing cartilage model of hyaline plus covering called perichondrium.
2) Growth of Model - chondroblasts are buried in ECM, now called chondrocytes - undergo cell division and more ECM secretion to grow the model - INTERSTITIAL & APOSITIONAL growth. Chondrocytes in the mid-region hypertrophy and the ECM calcifies. Others die due to lack of nutrients in calcified ECM, forming lacunae
3) Dvlp Primary Ossification Centre - inward from external surface of bone. Mid-region of cartilage model, nutrient artery penetrates the perichondrium, goes through a nutrient foramen. Osteogenic cells in perichondrium are stimulated to differentiate into osteoblasts as a result. Perichondrium develops into periosteum once it starts to form bone. Osteoblasts deposit bone ECM over calcified cartilage, forms spongy bone. Ossification spreads toward ends of model
4) Dvlp Medullary Cabity - osteoclasts break down some of new spongy, leaving a cavity.
5) Dvlp Secondary Ossification Centre - epiphyseal arteries enter epiphyses, secondary OC starts. No Medullary cavities form in epiphyses. Proceeds OUTWARD from centre of epiphyses.
6) Dvlp Articular Cartilage and Epiphyseal Growth Plate - hyaline over epiphyses becomes articular. Hyaline remains btwn diaphysis and epiphyses.

Question 23

Epiphyseal Growth Plate

Answer 23

later of hyaline cartilage in the metaphysis of a growing bone - 4 zones:

1) resting cartilage - nearest epiphysis, small scattered chondrocytes. anchor plate to epiphysis, don’t take part in growth.
2) proliferating cartilage - slightly larger chondrocytes stacked like coins, divide and secrete ECM, replacing dead chondrocytes at diaphyseal side.
3) hypertrophic cartilage - large maturing chondrocytes in columns
4) calicified cartilage - few cells thick, dead chondrocytes with calcified ECM. Osteoclasts dissolve calcified cartilage and osteoblasts replace with bone ECM -> endochondral ossification (replacement of cartilage with bone). Becomes new diaphysis!

If a bone fracture damages EGP, bone may be shorter than normal in adult size, since damage to cartilage (avascular) accelerates closure of EGP due to cessation of chondrocyte division.

Question 24

Epiphyseal Line

Answer 24

in adults, EGP closes due to cartilage cells no longer dividing. EGP fades, leaving bony structure called Epiphyseal LINE.

Question 25

Interstitial Growth

Answer 25

1) interstitial growth of cartilage on the epiphyseal side of the EGP
2) replacement of cartilage on the diaphyseal side of the EGP with bone by endochondral ossification.

Question 26

Apositional Growth

Answer 26

1) periosteal cells at bone surface differentiate into osteoblasts -> secrete bone ECM. Develop into osteocytes, forming bone ridges on either side of a periosteal blood vessel. Ridges enlarge and create a groove for the vessel.
2) ridges fold together and fuse. Former periosteum becomes endosteum lining tunnel.
3) osteoblasts secrete bone ECM, creating concentric lamellae -> new osteon.
4) osteoblasts under periosteum deposit new circumferential lamellae.

Question 27

Bone Remodeling

Answer 27

ongoing replacement of old bone by new.
1) bone resorption = removal of minerals and collagen fibres by osteoclasts
2) bone deposition = addition of minerals and collage fibres by osteoblasts
At any time, 5% of bone in body is being remodeled. Different rates for different parts of the body - compact ~ 4% per year, spongy ~ 20% per year.

Question 28

Benefits of Remodeling

Answer 28

1) renews old bone
2) removes injured bone
3) increases tolerance to stressors placed on newly formed bones (will be thicker)
4) shape of bone can be altered due to changes in stressors
5) new bone is more resistant to fracture than old bone

Question 29

Factors affecting Remodeling

Answer 29

1) minerals - Ca, Mg, F, Mn
2) vitamins - Vit A stimulates activity of osteoblasts. Vit C needed for collagen synthesis. Vit D helps increase absorption of Ca from foods. Vit K & B12 also needed for bone protein synthesis.
3) hormones - insulinlike growth factors (IGF) during childhood to stimulate osteoblasts, T3 and T4 thyroid hormones stimulate osteoblasts. Insulin helps bone protein synthesis.

Androgens & estrogens -> osteoblast activity in teenage years. Estrogens promote changes in skeleton typical of females, also responsible for closing EGPs. In adults, slow down resorption and promote deposition of new bone - estrogen promotes apoptosis of osteoclasts.

Question 30

fracture

Answer 30

any break in a bone

Question 31

stress fracture

Answer 31

a series of microscopic fissures in bone that forms without any evidence of injury to other tissues. usually from repeated strenuous activities. 25% involve the tibia! Cannot see in x-rays, only bone scans.

Question 32

open (compound) fracture

Answer 32

broken ends of the bone protrude through the skin

Question 33

closed (simple) fracture

Answer 33

broken ends of bone do not penetrate the skin

Question 34

comminuted fracture

Answer 34

the bone is splintered, crushed at the site

Question 35

greenstick fracture

Answer 35

partial fracture - one side of bone is broken and other side bends

Question 36

impacted fracture

Answer 36

one end of the fractured bone is forcefully driven into the interior of the other.

Question 37

Pott fracture

Answer 37

fracture of the distal end of the fibula with serious injury of the distal tibial articulation

Question 38

Colles’ fracture

Answer 38

fracture of the distal end of the radius in which the distal fragment is displaced posteriorly.

Question 39

reduction

Answer 39

setting a fracture - the ends are brought into alignment by manual manipulation.

Question 40

Repair of Fracture

Answer 40

1) formation of hematoma - blood clot forms, swelling and inflammation occur in response to dead bone cells. Phagocytes and osteoclasts remove dead/damaged tissue (several weeks)
2) fibrocartilaginous callus formation - fibroblasts from periosteum invade site and produce collagen. mass of repair tissue of collagen and cartilage (3 weeks)
3) bony callus fomation - fibrocartilage is converted to spongy bone, trabeculae connect living and dead portions of original bone fragments
4) bone remodeling (of the callus) - compact replaces spongy, osteoclasts eat old dead portions.

Question 41

Calcium Homeostasis

Answer 41

Stores 99% of total Ca - blood plasma level is regulated at 9-11mg/100mL.
INCREASE:
1) parathyroid hormone (PTH) secreted by parathyroid glands - increases blood Ca2+ level. Negative feedback -> Ca2+ drops, increase cAMP in gland cells, gene in cell detect and speeds up PTH synthesis.
2) PTH increases, oseoclast activity and number increase, bone resorption is stepped up, Ca2+ increases.
3) PTH also tells kidneys to stop releasing Ca2+ in urine.
4) PTH stimulates formulation of calcitriol (active form of vit D) to promote absorption of Ca from foods.
DECREASE:
1) Calcitonin (CT) - parafollicular cells in thyroid produce it when Ca2+ is too high.
2) CT inhibits osteoclast activity, speeds uptake of Ca2+ by bone and accelerates Ca2+ deposition into bone.

Question 42

osteoporosis

Answer 42

bone resorption takes place more quickly than bone deposition. Decrease in sex hormones (after menopause esp in females) causes loss of bone mass.

Question 43

Aging

Answer 43

1) loss of bone mass - demineralization, reduced osteoblast activity (problem with osteoporosis)
2) brittleness - decreased rate of protein synthesis -> less collagen -> deformity, pain, loss of height, loss of teeth, susceptibility to fractures.