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ethan ortho study > Basic Science > Flashcards

Basic Science Flashcards

1
Q

Bone Cells: Osteoblasts

  1. Origin
  2. Structure
  3. Function
  4. Bone non-mineralised matrix consists of: (4)
A
  1. mesenchymal stem cells ->differentiate into osteoprogenitor cells
  2. Contain increased amounts of endoplasmic reticulum, Golgi apparatus, and mitochondria than other cells ◦allows for synthesis and secretion of bone matrix
  3. Form bone by producing non-mineralized matrix and regulate osteoclast function
  4. ◾ALP ◾ Col Type 1 ◾osteonectin ◾osteocalcin ◾stimulated by 1,25 dihydroxyvitamin D
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2
Q

Bone Cells: Osteoblasts
Signaling : osteoblastic differentiation

  1. ___ stimulates mesenchymal cells to become osteoprogenitor cells
  2. . _________ plays a major role in formation of osteoblasts with resulting intramembranous bone formation
  3. GFs ___ and ___ induce osteoblast differentiation
A
  1. BMP
  2. stable beta-catenin
  3. Platelet derived growth factor (PDGF) AND insulin derived growth factor (IDGF) induce osteoblast differentiation

** note: core binding factor alpha-1 (cbf alpha -1: RUNX2) also plays a role in osteoblast differentiation

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3
Q

Bone Cells: Osteoblasts
Signaling : osteoblast bone production

  1. PTH receptor stimulates production of: (2)
  2. 1,25 dihydroxyvitamin D receptor stimulates (3)
A
  1. Stimulates alkaline phosphatase and type I collagen production
  2. Stimulates matrix and alkaline phosphatase synthesis
    and production of bone specific proteins (osteocalcin)
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4
Q

Bone Cells: Osteoblasts
Signaling : osteoblast bone production

  1. Estrogen inhibits ______ and stimulates ________ by inhibiting ________
  2. Glucocorticoids inhibit ______and _____ production
  3. prostaglandins stimulate bone _______ by activating _______
A
  1. (a) bone resorption; (b) bone production; (adenylyl cyclase)
  2. (a) collagen; (b) bone matrix
  3. (a) bone resorption; (b) adenylyl cyclase
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5
Q

Bone Cells: osteoblasts role in–> osteoclast signaling
(note: interconnected signaling allows coupling of bone resorption and formation)

  1. osteoclast activation pathway
  2. osteoclast inhibition pathway
A

◾PTH receptors on osteoblast bind to PTH which when leads to expression of RANKL
◾RANKL binds to RANK receptor on osteoclast and bone resorption

  1. ◾osteoblasts can secrete OPG (osteoprotegrin)
    ◾OPG binds to RANKL on the osteoblast, preventing RANK activation ◾inhibits osteoclast activity
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6
Q

Bone Cells: osteoblasts role in–> regulation of hematopoietic cells and immune response

Occurs through the Jagged1-Notch pathway (explain)

A

◾PTH induces Jagged1 on osteoblasts

◾Jagged1 stimulates Notch receptors on the membrane of hematopoietic stem cells which results in cell proliferation

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7
Q

Bone Cells: osteoblasts

Location

  1. More metabolically active cells at the _________
A
  1. More metabolically active cells at the BONE SURFACE

Note: less active cells in more central bone -> activated by disruption of the more peripheral osteoblasts

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8
Q

Bone Cells: osteoclasts

Function is to reabsorb bone:

  1. regulated by _________
  2. Steps in resorption
A
  1. Osteoblasts regulate osteoclast bone reabsorbtion (see above)
  2. Steps in resorption :
    i) migration to resorption site
    ii) bone attachment
    iii) polarization (formation of membrane domains)
    iv) dissolution of hydroxyapatite
    v) degradation of organic matrix
    vi) removal of degradation products from resorption lacuna
    vii) apoptosis of the osteoclasts or return to the non-resorbing stage.
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9
Q

Bone Cells: osteoclasts

  1. Origin
  2. Cellular anatomy / histology
A
  1. Originate from myeloid hematopoietic cells from monocyte/macrophage cell lineage (Monocyte progenitors fuse together to form mature multinuclear cells)
  2. Multinucleated giant cells
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10
Q

Bone Cells: Osteoclasts
Cellular physiology

  1. Bone reabsorbtion occurs at _______.
  2. What are Howship’s lacunae?
  3. Tartrate resistant acid phosphate:
    a) secreted by ______ ?
    b) Effect on pH ?
    c) Effect on solubility of hydroxyapatite crystals
  4. Proteolytic digestion removes the organic matrix. One of the major proteolytic enzyme that degests organic matrix at ruffled border is _________
  5. Bisphosphonates mechanism? ◾prevents osteoclasts from forming ruffled border and producing acid hydrolases
A
  1. Ruffled border
  2. Site of bone resorption where ruffled border meets bone surface

3a. Secreted by osteoclasts to lower the Ph (utilizing carbonic anhydrase [CA])
3b. increases the solubility of hydroxyapatite crystals (def of CA prevents bone resorption)

  1. Cathepsin K
  2. Prevents osteoclasts from forming ruffled border and producing acid hydrolases
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11
Q

Bone Cells: Osteoclast-osteoblast signaling

Osteoblasts upregulate and downregulate osteoclast activity

Role of:

  1. RANK-L
  2. IL-1
  3. Calcitonin
  4. IL-10
A
  1. Osteoclast activation
    ◾RANKL (NF-kB ligand) ◾expressed by osteoblasts and tumor cells to activate osteoclasts
  2. IL-1 ◾found adjacent to loose total joint implants and known to activate osteoclasts
  3. Osteoclast inhibition
  4. Osteoclast inhibition
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12
Q

Bone Cells: Osteocytes

  1. Origin
  2. Account for _% of cells in mature skeleton
  3. Structure
    a) ____ nucleus to cytoplasm ratio

b) have long cellular processes which communicate with other cells via _______in the bone

A
  1. Former osteoblasts trapped in the matrix they produced
  2. 90%
    3a. High
    3b. Canalculi
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13
Q

Bone Cells: Osteocytes

Function

  1. Maintain ________?
  2. Important in regulation of ____ and ______ concentrations in bone
  3. Do not express __________

Signaling

  1. Stimulated by _______
  2. Inhibited by _____
  3. Communicate with adjacent osteocytes via ___ junctions in _______
A
  1. Maintain bone and cellular matrix
  2. Calcium and phosphorous
  3. Alkaline phosphatase
  4. Calcitonin
  5. PTH
  6. Gap; Canaliculi
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14
Q

Bone Cells: Osteoprogenitor Cells

  1. Origin
  2. Function
    a) become ________ under low strain and high oxygen tension

b) become ________ under intermediate strain and low oxygen tension
c) become _______ tissue under high strain

A
  1. Origin
    ◦originate from MSC’s
    ◦environment will determine their function
  2. Function
    a) Osteoblasts
    b) Cartilage
    c) Fibrous
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15
Q

Bone Matrix

Bone is made up of (2)

A

Bone is made up of

  1. organic component ◾40% of dry weight
  2. inorganic component ◾60% of dry weight
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16
Q

Bone Matrix: Organic component

Components include (4)

A 
1. Collagen
◾90% of organic component
◾primarily type I collagen
◾provides tensile strength
◾it is a triple helix composed of one alpha-2 and two alpha-1 chains
  1. Proteoglycans
    ◾responsible for compressive strength
    ◾inhibit mineralization
    ◾composed of glycosaminoglycan-protein complexes
  2. Matrix proteins
    ◾includes noncollagenous proteins
    ◾function to promote mineralization and bone formation
  3. Cytokines and growth factors
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17
Q

Bone Matrix: matrix proteins

Includes noncollagenous proteins that function to promote mineralization and bone formation

Three main types of proteins involved in bone matrix ?

A
  1. Osteocalcin : most abundant non-collagenous protein in the matrix (10%-20% of total) produced by mature osteoblasts
    ◾promotes mineralization and formation of bone
    ◾directly involved in regulation of bone density
    ◾attracts osteoclasts
    ◾clinical application = marker of bone turnover; can be measured in urine or serum
  2. Osteonectin:
    ◾secreted by platelets and osteoblasts
    ◾function = believed to have a role in regulating calcium or organizing mineral in matrix
  3. Osteopontin ◾function ◾cell-binding protein
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18
Q

Bone Matrix: cytokine and growth factors

  1. Role ?
  2. Include which GF/Cytokine
A
  1. Role of cytokine and growth factors
    ◾small amounts present in matrix
    ◾aid in bone cell differentiation, activation, growth, and turnover
  2. Include
    ◾IL-1, IL-6, IGF, TGF-beta, BMPs
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19
Q

Bone Matrix : Inorganic component

  1. Components (2)
A

Components include

  1. Calcium hydroxyapatite (Ca10(PO4)6(OH)
    ◾provides compressive strength
  2. Osteocalcium phosphate (brushite)
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20
Q

Bone Matrix: Bone Circulation

  1. Bone receives __to__% of cardiac output
  2. Bones with tenuous blood supply (4)
  3. Name the three sources of blood supply to long bones
A
  1. 5-10%
  2. ◦scaphoid ◦talus ◦femoral head ◦odontoid
  3. Blood supply to long bones:
    i) nutrient artery system
    ii) metaphyseal-epiphyseal system
    iii. ) periosteal system
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21
Q

Bone Matrix: Blood Supply

Nutrient Artery System is a high pressure system that branches from major systemic arteries

  1. Enter the cortex through the ______ and enter the _______
  2. Then branch into _____ and ______ branches
  3. Then branch into _______ and supply the inner ___ of mature bone via the haversion system
A
  1. Enter the cortex through the NUTRIENT FORAMEN and enter the MEDULLAR CANAL
  2. Then branch into ASCENDING and DESCENDING branches
  3. Then branch into ARTERIOLES and supply the inner TWO THIRDS (2/3) of mature bone via the haversion system
22
Q

Bone Matrix: Blood Supply

  1. Metaphyseal epiphyseal system ?
  2. Periosteal System
  3. Periosteal System connected by?
  4. Intracortical Vascularization
A
  1. Arteries arise from periarticular vascular plexus ◦e.g. geniculate arteries
  2. Low pressure system that supplies the outer 1/3 of bone
  3. Connected by:
    ◾Volkman’s artery (perpendicular to long axis)
    ◾Haversion system (parallel to long axis)
  4. Intracortical vessels travel within canals ◦Primary Haversian canals
    ◦Secondary Volkmann canals
23
Q

Bone Matrix : blood supply

Direction of Arterial Flow
1. Normal intraosseous blood flow rate is __to__ml/min/100g of bone

  1. Mature bone flow is centrifugal (inside to outside) due to?
  2. Immature bone flow is centripetal (outside to inside) due to:
  3. Factors increasing blood flow (3)
A
  1. 5-20ml/min/100g of bone
  2. Due to high pressure nutrient artery system and low pressure periosteal system
  3. Due to low pressure periosteal system predominates
  4. ◦hypoxia ◦hypercapnia ◦sympathectomy
24
Q

Bone Matrix : blood supply

  1. Direction of Venous Flow in mature bone
  2. Growth Plate:
    ________ artery is the major source of nutrition of the growth plate
A

Flow is centripetal (outside to inside) ◾cortical capillaries drain to venous sinusoids, which drain to the emissary venous system

  1. Growth Plate:
    PERICHONDRAL ARTERY is the major source of nutrition of the growth plate
25
Q

Bone Matrix : Pathoanatomy

Fractures: Patterns of blood flow following fracture

a) immediate phase
◾initial ______in blood flow after fracture
◾flow is ______

b) Hours to days
◾______ in blood flow
◾peaks at ___ weeks and returns to normal in _____ months

A

a) Immediate phase
◾initial DECREASE in blood flow after fracture
◾flow is centripetal (outside to inside)
◦because high pressure nutrient artery system is disrupted ◦ low pressure periosteal system predominates

b) Hours to days
◾INCREASE in blood flow (regional acceleratory phenomenon)
◾peaks at 2 weeks and returns to normal in 3-5 months

26
Q

Bone Matrix : Pathoanatomy
Intramedullary nails

  1. Unreamed intramedullary nails_____ endosteal blood supply
  2. Reaming devascularizes inner __to__% of the cortex and delays revascularization of endosteal blood supply
  3. Loose fitting nails ____ cortical perfusion and allow ________
  4. Tight fitting nails _____ cortical perfusion and ______
A
  1. Preserve endosteal blood supply
  2. 50-80%
  3. Loose fitting nails SPARE cortical perfusion and allow MORE RAPID PERFUSION
  4. Tight fitting nails compromise cortical perfusion and reperfusion is slow
27
Q

Bone Signaling & RANKL
Bone metabolism is a dynamic process that balances bone formation and bone resorption :

  1. bone resorption
    ◾performed by _______
    ◾stimulated by RANKL in _____ process
    ◾stimulated by PTH in _____ process
  2. Bone formation
    ◾performed by inhibiting _____ and stimulating ______
    ◾OPG ______ osteoclasts
A
  1. Bone resorption
    ◾performed by active osteoclast ◾stimulated by RANKL in normal process
    ◾stimulated by PTH in pathologic process (metastatic disease)
  2. Bone formation
    ◾performed by inhibiting osteoCLASTS and stimulating osteoBLASTS
    ◾OPG INHIBITS osteoclasts
28
Q

Bone Signaling & RANKL : Osteoclast Activation

Molecules that stimulate bone resorption (7)

A
  1. RANKL ◾ secreted by osteoblasts; binds to RANK receptor on osteoclast precursor and mature osteoclast cells
  2. PTH (secreted by many cancer cells) ◾activation of its receptor stimulates adenylyl cyclase ◾binds to cell-surface receptors on osteoblasts to stimulate production of RANKL and M-CSF
  3. Interleukin 1 (IL-1) ◾stimulates osteoclast differentiation and thus bone resorption
  4. 1,25 dihydroxy vitamin D ◾stimulates RANKL expression
  5. Prostaglandin E2 ◾activates adenylyl cyclase and stimulates resorption
  6. IL-6 (myeloma)
  7. MIP-1A (myeloma)
29
Q

Bone Signaling & RANKL : Osteoclast Inhibition

Molecules that inhibit bone resorption (5)

A
  1. Osteoprotegerin (OPG) ◾decoy receptor produced by osteoblasts and stromal cells that binds to and sequesters RANKL ◾inhibits osteoclast differentiation, fusion, and activation
  2. Calcitonin ◾interacts directly with the osteoclast via cell-surface receptors
  3. Estrogen (via decrease in RANKL): ◾stimulates bone production (anabolic) and prevents resorption◾inhibits activation of adenylyl cyclase
  4. Transforming growth factor beta (via increase in OPG)
  5. Interleukin 10 (IL-10) ◾suppresses osteoclasts
30
Q

Bone Signaling & RANKL : Clinical Implications

  1. Osteopetrosis
  2. Osteoyltic bone metastasis
A
  1. Osteopetrosis
    ◦condition caused by a genetic defect resulting in absence of osteoclastic bone resorption
    ◦a mouse RANKL knockout model creates a osteopetrosis-like condition
  2. Osteoyltic bone metastasis
    ◦found to be mediated by the RANK and RANKL pathway
    ◦RANKL is produced directly by the cancer cells
    ◦blocking of RANKL by OPG results in decreased skeletal metastasis in animal models
    ◦bisphosphonates decrease skeletal events in cancer metastasis
31
Q

Normal Bone Metabolism

Regulators of bone metabolism:

  1. Hormones (5)
  2. Steroids (2)
A 
1. Hormones  
◾PTH
◾Calcitonin
◾Sex Hormones (eg. estrogen, androgens)
◾Growth Hormone
◾Thyroid Hormones
  1. Steroids
    ◾Vitamin D
    ◾Glucocorticosteroids
32
Q

Normal Bone Metabolism: Properties of bone metabolism

  1. Bone mass: the measure of bone tissue present at the end of skeletal maturity
    ◾peak bone mass occurs between ages __and__ years.
    ◾greater in ____ and _____
  2. Bone loss
    ◾bone mass decreases by __to__% per year after skeletal maturity
    ◾further decreases by __to__% per year for untreated women during the 6th-10th years after menopause
A
  1. Bone mass
    ◾peak bone mass occurs between ages 16 and 25
    ◾greater in men and African Americans
  2. Bone loss
    ◾bone mass decreases by 0.3 to 0.5% per year after skeletal maturity
    ◾further decreases by 2-3% per year for untreated women during the 6th-10th years after menopause

(note: rate of bone loss can be modulated by structural and metabolic factors)

33
Q

Normal Bone Metabolism: Calcium

  1. Location (3)
  2. Function (3)
  3. Forms of calcium in a) bone; b) serum
A
  1. Location: ◦bone (99%); ◦blood and extracellular fluid (0.1%); ◦intracellular (1%)
  2. ◾muscle cell contraction ◾nerve conduction ◾clotting mechanisms
  3. a) majority is hydroxyapatite;
    b) Serum: ◾Ca++ bound to protein (45%) ◾free-ionized Ca++ (45%)◾bound to various anions, eg. citrate, bicarbonate (10%)
34
Q

Normal Bone Metabolism: Phosphate

  1. Location (3)
  2. Function (2)
  3. Forms of phosphate in a) bone; b) serum
  4. Regulation
A
  1. Location: ◦bone (86%); Blood and extracelluar fluid (0.08%); Intracellular (14%)
  2. i) Key component of bone mineral; ii)important in enzyme systems and molecular interactions
  3. a) majority is hydroxyapatite; b) serum ◾mostly inorganic phosphate (H2PO4-)
  4. Regulation
    ◦plasma phosphate is mostly unbound and reabsorbed by the kidney
    ◦may be excreted in urine
    ◦elevated serum phosphate can lead to increased release of PTH and bone resorption
35
Q

Endochondral Bone Formation

Enchondral bone formation occurs in: (3)

A
  1. longitudinal physeal growth
  2. embryonic long bone formation
  3. non-rigid fracture healing (secondary healing)
36
Q

Endochondral Bone Formation : Cell biology

  1. Enchondral bone formation occurs with a cartilage model, steps are:
  2. Type ___ collagen associated with enchondral ossification
A
  1. Cartilage model
    ◾chondrocytes produce cartilage which is absorbed by osteoclasts
    ◾osteoblasts lay down bone on cartilaginous framework (bone replaces cartilage, cartilage is not converted to bone)
    ◾forms primary trabecular bone
    ◾bone deposition occurs on metaphyseal side
  2. Type X
37
Q

Endochondral Bone Formation : Molecular biology

Chondrocytes play a critical role in endochondral bone formation throughout the formation of the cartilage intermediate

Transcription factors involved in regulation of chondrocytes include (2)

A

Transcription factors involved in regulation of chondrocytes include

  1. Sox-9
    ◾considered a major regulator of chondrogenesis, regulates several cartilage-specific genes during endochondral ossification, including collagen types II, IV, and XI and aggrecan
  2. PTHrP
    ◾delays differentiation of chondrocytes in the zone of hypertrophy
38
Q

Endochondral Bone Formation : Biomechanics

  1. Variables that affect growth across the physis ?
  2. Main blood supply to physis ?
A
  1. Hueter-Volkmann Law
    ◾compression across the growth plate slows longitudinal growth
    ◾tension accerelates longitudinal growth
  2. Perichondrial artery
39
Q

Endochondral Bone Formation: Longitudinal Physeal Growth

Zones [from epiphysis to diaphysis]

5.

A
  1. Reserve Zone: Quiescent chondrocytes are found at the epiphyseal end
  2. Proliferative Zone: Chondrocytes undergo rapid mitosis under influence of growth hormone
  3. Hypertrophic Zone: Chondrocytes stop mitosis, and begin to hypertrophy by accumulating glycogen, lipids, and alkaline phosphatase
  4. Primary Spongiosa / Zone of calcification: Chondrocytes undergo apoptosis. Cartilagenous matrix begins to calcify.
  5. Secondary Spongiosa / Zone of ossification : Osteoclasts and osteoblasts from the diaphyseal side break down the calcified cartilage and replace with mineralized bone tissue.
40
Q

Endochondral Bone Formation: Longitudinal Physeal Growth

Physis Periphery

  1. What are the Grooves of Ranvier ?
A
  1. Groove of Ranvier
    - During the first year of life, the zone spreads over the adjacent metaphysis to form a fibrous circumferential ring bridging from the epiphysis to the diaphysis.
    - This ring increases the mechanical strength of the physis and is responsible for appositional bone growths ◦supplies chondrocytes to periphery
41
Q

Endochondral Bone Formation: Longitudinal Physeal Growth

  1. What is the Perichondrial fibrous ring of La Croix?
A

Dense fibrous tissue that is the primary limiting membrane that anchors and supports the physis through peripheral stability

42
Q

Endochondral Bone Formation:
Embryonic Long Bone Formation

Overview: ◦ allows growth in width and length ◦ formed from mesenchymal anlage around 6th week in utero.

Q. Five steps of formation include:

A

◾Step 1: Vascularization
- vascular buds invade the mesenchymal model

◾Step 2: Primary ossification centers form
- (at ~ 8 weeks) osteoprogenitor cells migrate through vascular buds and differentiate into osteoblasts forming the primary ossification centers

◾Step 3: Cartilage model forms
- grows through appositional (width) and interstitial (length) growth

◾Step 4: Marrow forms
- marrow is formed by resorption of central portion of the cartilage anlage by myeloid precursor cells that migrate in through the vascular buds

◾Step 5: Secondary ossification centers form
- develop at bone ends and lead to epiphyseal ossification center (growth plate)

43
Q

Endochondral Bone Formation:
Non-Rigid Fracture Healing

Mechanism of bone formation is similar to physeal enchondral ossification

  1. Cell biology
  2. Examples include (2)
A
  1. Cell biology
    ◦soft callus is the cartilage intermediate
    ◦bone replaces callus via same chondrocyte proliferation, chondrocyte hypertrophy, and finally chondrocyte calcification
  2. Examples include:
    ◦ casting and bracing
    ◦intramedullary nailing
    ◾allows for motion at the fracture site, which promotes bone formation both directly (intramembranous ossification) and through a cartilage intermediate (endochondral ossification)
44
Q

Intramembranous Bone Formation

One of two essential processes during:

  1. ______
  2. ______
  3. Physiology
  4. Examples of intramem ossification (5)
  5. Associated conditions
A
  1. Fetal development bone formation
  2. Fracture healing (also commonly known as contact healing, and Haversian remodelling)
  3. Physiology: occurs without a cartilage model (unlike enchondral ossification)
45
Q

Intramembranous Bone Formation

Examples of intramembranous ossification (5)

A
  1. embryonic flat bone formation (skull, maxilla, mandible, pelvis, clavicle, subperiosteal surface of long bone)
  2. distraction osteogenesis bone formation
  3. blastem bone (occurs in children with amputations)
  4. fracture healing with rigid fixation (compression plate)
  5. one component of healing with intramedullary nailing
46
Q

Intramembranous Bone Formation

Associated conditions

A

Associated conditions = conditions with defects in intramembranous ossification

  1. Cleidocranial dysplasia topic
    ◾caused by defect in intramembranous ossification
    ◾caused by mutation in CBFA1 (also know as Runx2) located on chromosome 6
47
Q

Intramembranous Bone Formation

◾Steps of intramembranous bone formation (3)

◾Regulation and signaling ◦controlled by pathway called canonical Wnt and Hedgehog signaling

A

◾Step 1: aggregation of undifferentiated mesenchymal cells
◾Step 2: osteoblast differentiation
◾Step 3: organic matrix deposition

◾Canonical Wnt and Hedgehog signaling

- beta-catenin enters cells and induces cells to form osteoblasts which then proceed with intramembranous bone formation
- important transcription factors include CBFA1 (also know as Runx2) and osterix (OSX)
- sclerostin, created by the SOST gene, decreases bone mass by inhibiting the Wnt pathway
48
Q

Bone Remodeling

What is Wolff’s Law

A

Wolff’s Law = bone remodels in response to mechanical stress

49
Q

Bone Remodeling

What are Piezoelectic charges

A

Piezoelectic charges
◦bone remodels is response to electric charges
◦compression side is electronegative and stimulates osteoblast formation
◦tension side is electropostive and stimulates osteoclasts

50
Q

Bone Remodeling

What is Hueter-Volkmann Law ?

A

Hueter-Volkmann Law
◦theory that bone remodels in small packets of cells known as Basic Multicellular Units (BMUs)
◦theory suggest that mechanical forces influence longitudinal growth
◦compressive forces inhibit growth
◦may play role in scoliosis

51
Q

Bone Remodeling: Remodeling Mechanism

  1. Cortical bone remodels by osteoclastic tunneling (cutting cone) - explain?
  2. Cortical bone continues to change over time ◾a area decreases with age;
    ◾_b_volume increases as age increases
  3. Cancellous bone remodels by:
    a) _________
    b) _________
A
  1. Cutting cone: ◾osteoclastic resorption > layering of osteoblasts > layering of lamellae > cement line laid down ◾osteoclast make up head of cutting cone, followed by capillaries and then osteoblasts which lay down the osteoid to fill the cutting cone
    ◾sclerostin inhibits osteoblastogenenesis to decrease bone formation
  2. (a) Cortical ; (b) medullary canal
  3. (a) Osteoclastic resorption; (b) osteoblastic deposition of layers of lamellae

ethan ortho study (13 decks)

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