EXAM2_HE10_11_Cartilage_Bone Flashcards
Hyaline Cartilage 7 Locations and Function
Resists compression
- Articular cartilage
- Trachea, bronchi
- Embryonic skeleton
- Growth plate
- Larynx
- Nose
- Costal Cartilage
Elastic Cartilage 4 Locations and Function
Elastic support
- Pinna
- External auditory meatus
- Larynx
- Auditory tube
Fibrocartilage 3 locations and function
Resist tension & compression
- Articular & Intervertebral disks
- Labra, menisci
- Tendon insertions
Perichondrium two layers? What cells within? what is it a mixture of?
Outer- DiRCT
Inner- Chondrogenic cells (stem cells) that can turn into cartilage cells.
-Contains Fibroblast cells
-Type I Collagen CT associated with Cartilage
If cartilage is avascular- what cells support/nourish cartilage?
Cartilage is Avascular and depends on Diffusion from Perichondrium for its blood supply/nourishment
Perichondritis or Perichondrium hematoma what is it? Where? repair? associated abnormalities?
Blood between perichondrium and cartilage tissues.
Ct repaired by fibroblasts laying down type 3 and replacing with type 1
Fibrosis of type 1–>cauliflower ear
Chondrocyte Function. Replication?
Regulate ECM Synthesis by using MGP’s to mechanically sense any changes in ECM. and it then adjusts the gene expression for SECRETION
-multiply mitotically- form isogenous groups (clusters of recently divided chondrocytes)
What are isogenous groups? What happens when it develops?
- clusters of recently divided chondrocytes.
- Clusters will separate and push each other away when they start secreting their own ECM
- mitotic-stim by mechano sensation of mgp’s
Where are chondrocytes derived?
Mesoderm- mesenchymal stem cells- chondrogenic cell- chondrocyte
What is the 3 components of ECM of hyaline cartilage?
2 Functions? How do they stain?
-Type 2 Collagen
-Proteoglycan Agregates
-MGP’s
1. Resists compression
2. Diffusion of nutrients/waste (sponge)
collagen pink (acidophilic)
PG’s blue/purple (basophilic)
What are the two types of cartilage growth?
- Appositional growth- on surface (surface is under perichondrium)– chondrogenic cells make chondrocytes that secrete ECM onto cartilage surface
- Interstitial growth- from within- Chondrocytes divide & secrete ECM within cartilage
What is the limitation of cartilage growth? What happens if it gets too thick?
Cartilage is Avascular so it’s growth is limited by the ability of diffusion of nutrients/waste
ie: it can get too big in the perichondrium that the blood can’t diffuse down into the cartilage and the tissue will start to die
An Orcein stain displays_____(color) for _____ fibers and H&E/Orcein stain shows___color for _____fibers.
What is differs Hyaline from Elastic cartilage?
Black for elastic fibers
Blue for elastic fibers/cartilage
Elastic cartilage has elastic fibers in ECM
How does hyaline cartilage differ from Fibrocartilage?
Fibrocartilage has Type 1 and 2 collagen fibers in ECM
-NO PERICHONDRIUM
(but has fibroblasts, isogenous groups,
What is an example of hyaline cartilage that does NOT have a perichondrium?
Articular cartilage because CT can’t resist the compression of an articulating joint (it would get crushed).
where does articular cartilage get its nutrient if it is avascular and it doesn’t have a perichondrium? What is a side effect of this?
Fluid in the joints- degenerates without scarring (no perichondrium, Ct, fibroblasts, thus no fibrosis)
Damage is Irreversible and can damage bone if bad enough
What are two crystal induced arthropathies? (crystal types)
Gout (monosodium urate crystals)- too much uric acid
Pseudo-gout (calcium pyrophosphate dihydrate CPPD)
Lysosomal enzymes released during inflammatory response destroy tissue
What is mechanically/physical trauma induce degeneration of cartilage?
Osteoarthritis (OA)
What is RA (rheumatoid arthritis) what caused by? what is an indication of RA?
Inflammation - autoimmune disease- no known cause-
RF- rheumatoid factor (antibody) may or may not be increased
3 terms for the lattice looking type of bone. Where found? Function?
-Trabecular*, spongy, cancellous.
-Epiphysis & medullary cavity.
-Stores Bone Marrow
Forms internal structure- Stores calcium
ION EXCHANGE between bone & blood
Compact (cortical) bone- where? composition? Function?
- Diaphyses & on external surfaces of bone
- Lamellae (sheets) concentric rings of bone (looks like lines)
- Has bv canals
- Supports, forms external bone surfaces
Osteon- 3 Structure details, function?
Cylinders of bone, bv central/haversian canal, concentric lamellar rings
- abundant in adults- increase w/ age
- formed during bone remodeling/repairs
what canals link the central canals?
Perforating canals- Volkmann’s canals- important nutrient exchange
Perforating fibers (sharpy’s fibers)- structure- function-
Type 1 Collagen fibers in the bone periosteum that are embedded in the bone ECM.
-Attach muscle tendons & ligaments to bone
Endosteum- structure- function- 3 cell types found there?
THIN- Monolayer of cells lining all the inner surfaces of the bone (all the trabeculae/spongy bone “medullary surfaces”)
- protect/monitor surface of bone
1. osteoprogenitor cells
2. osteoblasts
3. bone-lining cells
Osteoclasts- structure-function-derivation
Big multi-nucleated cells;
- Resorb Bone
- derived from granulocyte/macrophage progenitor cells in bone marrow
- All osteoclast cells fuse together to form one big multi-nucleated cell
RANKL and OPG
RANKL- stimulates formation of osteoclasts (Bone resorption)
OPG- inhibits RANKL (inhibits osteoclast activity/resorption)
Clear zone-structure/ function
- Adherence site of osteoclast to bone
- seals cavity so lysosomal contents don’t leak out into the cell.
Ruffled border- structure and function
osteoclast folded plasma membrane increases surface area to increase amount of proton pumps so it can breakdown minerals and elevate serum calcium levels
- increase level of secretion for lysosomal enzymes (like secretory vesicles)
- ca transcellular transport through osteoclast, exocytosed into ECM into blood
What elevates serum CTX?
Lysosomes inside osteoclasts secrete lysosomal enzymes that are exocytosed into the resorptive bay where they break down collagen which then gets reabsorbed into the osteoclast and exocytosed back into the blood.
this collagen breakdown elevates CTX
indicates how much resorption occurred/collagen has been broken down and returned into the blood
Osteoblasts Structure- Function- Derivation- shape location
-cuboidal shape on bone surface
-derived from mesenchymal cells in bone marrow-> osteoprogenitor cells-> osteoblasts
can become osteocytes or bone-lining cells
FORM BONE
What are the two fates of osteoblasts
- 2 fates
- become bone lining cells when quiescent (appear flat) or
- become osteocytes (when embedded in ECM)
What are 3 secretions of osteoblasts?
- procollagen for extracellular formation of type 1 collagen
- alkaline phosphatase vesicles promote mineralization
- Ca-binding proteins (OSTEOCALCIN) to bind ECM components together
What are two blood serum markers for bone formation?
Alkaline phosphatase
Osteocalcin
Bone ECM- Structure- function
mineralized/vs non- 2 names
Type 1 Collagen
Non-mineralized bone (Osteoid)
Mineralized bone (hydroxyapatite crystals)
Osteocytes structure. where found? how do they communicate? how do they sense and function?
What cells are the most similar to?
Osteoblasts that become embedded in ECM during bone formation Found in Lacunae & have canaliculi communicate via gap junctions mechanosensitive DIRECTS BONE REMODELING JUST LIKE CHONDROCYTES
What is the Reversal (cement) line?
boundary between pre-existing bone and newly formed bone
How is bone remodeling regulated? 2 ways w examples. Why is bone remodeling important?
regulated by mechanical regulation via osteocytes
and by PTH, CALCITONIN, & ESTROGEN (hormonal).
repairs microfractures, aids in calcium metabolism
Calcitonin - from? (structure) binding site? function- inhibition-
DECREASE BLOOD Ca levels
- secreted by C-cells in thyroid
- bind receptors on osteoclasts
- inhibit osteoclast resorption
PTH- from? binding? secrete? function?
-chief cells of parathyroid
-bind OSTEOBLASTS and secrete RANKL
-RANKL stimulates osteoclasts
INCREASE BLOOD Ca2+ levels
protection mechanism- bind to -blasts to make sure they are around before resorbing bone.
Estrogen- from? bind? secrete? Function?
-secreted by gonads
-bind receptors on osteoblasts & osteoclasts
-osteoblasts secrete OPG (rANKL inhibitor)
BONE MAINTENANCE
OPG
RANKL inhibitor
inhibits osteoclasts
when estrogen levels drop osteoporosis is a concern
Osteopetrosis
Skeletal sclerosis (hardening) caused by osteoclast dysfunction
Osteopenia
Mild form of osteoporosis
Osteomyelitis
inflammation of bone, mostly due to infection
Ricket & osteomalacia
Vit D deficiency, disruption of vit D metabolism
Osteitis deformans (Pagets disease)
Rapid resorption followed by disorganized growth
-caused by slow virus
Osteogenesis imperfecta (brittle bone disease)
Mutation in gene for type I collagen
Where do pelvis, shoulder, limbs, and sternum arise from?
Lateral plate Parietal mesoderm
Where does mandible, and anterior cranium arise from?
Neural crest cells
Where does posterior cranium, vertebrae, and ribs arise from?
Paraxial mesoderm
Calcification vs ossification
Ossification reserved for BONE FORMATION
Calcification can occur in many types of tissues
-ECM calcifies (usually in cartilage)
What affects how mesenchymal cells differentiate?
Two states, what each turns into/forms
Oxygen availability
Hypoxic (like in cartilage); mesenchymal cells-> chondrogenic cells
High oxygen- mesenchymal cells -> osteoprogenitor cells & form ossification centers
What are the two types of ossification?
What is required for each?
- Intramembranous ossification- req vascularized mesenchyme
2. Endochondral ossification- req hyaline cartilage template
3 steps of intramembranous ossification
What 3 types of bone does it form?
-Req-vascular mesenchyme->osteoprogenitor cells (OPC’s) make ossification centers
1. mesenchymal cells differentiate into OPC’s at ossification centers (near bv)
2. OPC’s differentiate into OSTEOBLASTS that form bone trabeculae
3. Trabeculae enlarge and fuse together
Mandible, flat bones of cranium, clavical
Endochondral ossification 5 steps
- mesenchymal cells differentiate into chondrogenic cells (hypoxic environment)
- Chondrogenic cells differentiate into chondrocytes that build Hyaline Cartilage Template
- Blood vessels invade: oxygen rich environment induces chondrocytes to calcify their matrix
- Calcified cartilage starts to be replaced with bone (making ossification centers & growth plates)
- bone Growth ends when plates replaced with bone
What ossification zone supplies/directs proliferation?
- Zone of reserve- Hyaline
What zone for mitosis, ECM secretion?
- Zone of proliferation
What zone for cells enlarge, secrete VEGF for BV growth?
- Zone of hypertrophy
What zone for cartilage ECM calcification and apoptosis?
- Zone of calcification
What zone for calcified cartilage replaced with bone?
- Zone of ossification
What are the 5 zones for endochondral ossification?
- Zone of reserve
- Zone of proliferation
- Zone of hypertrophy
- Zone of calcification
- Zone of ossification
Woven bone- where does it happen- what is it?
Calcified cartilage replaced with bone in zone of ossification :
immature bone that is weaker and more disorganized
1. first type of bone laid down during ossification and also in fracture repair
2. Quickly replaced by lamellar (mature) bone
