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Histo > Bone Lecture 2 > Flashcards

Bone Lecture 2 Flashcards

1
Q

Intramembranous Ossification is responsible for formation of bone for:

A

Bone healing
Growth of flat bones (i.e. skull, carpals, tarsals)
Thickening of long bones

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2
Q

Intramembranous Ossification

A

Osteoblasts secrete organic matrix (osteoid)

Osteoblasts then directly mineralize the matrix with hydroxyapatite crystals

Once surrounded by calcified matrix, osteoblasts become osteocytes

Osteoblasts are formed by differentiation of cells of the periosteum and endosteum or bone marrow stem cells (mesenchyme)

Osteoblasts secrete an organic bone matrix and then calcify the matrix

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3
Q

Endochondral Ossification

A

Chondrocytes produce cartilage matrix and calcify the matrix

Osteoblasts enter the area and deposit bone matrix (osteoid) over the calcified cartilage matrix

Osteoblasts/osteocytes – remove remnants of cartilage matrix resulting in typical bone matrix

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4
Q

Process of endochondral ossification is responsible for:

A

Growth of long bones (epiphyseal plate)

Bone healing

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5
Q

Epiphyseal Plate: Resting Zone

A

Resting zone

area of normal hyaline cartilage and chondrocytes

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6
Q

Epiphyseal Plate: Proliferative zone

A

Proliferative zone

area of intense mitosis (proliferation) of chondrocytes

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7
Q

Epiphyseal Plate: Hypertrophic zone

A

Hypertrophic zone
area of chondrocyte hypertrophy due to glycogen uptake

Cartilage ECM is partially resorbed

Remnants appear as septa of matrix material between hypertrophic chondrocytes

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8
Q

Epiphyseal Plate: Calcified cartilage zone

A

Calcified cartilage zone
Thin septa of cartilage matrix become calcified
Chondrocytes in this zone die after matrix calcification

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9
Q

Epiphyseal Plate: Ossification zone

A

Osteoprogenitor cells from the bone marrow are delivered to the calcified cartilage
Osteoprogenitor cells differentiate into osteoblasts

Osteoblasts deposit bone matrix over the calcified cartilage matrix = ossification

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10
Q

Endochondral ossification during fetal development is a similar process:

A

Osteoid deposition over cartilage matrix

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11
Q

Basics of Bone remodeling

A

Bone undergoes constant remodeling throughout life

Bone remodeling is dependent on stresses (forces) placed on bones

Bone matrix is deposited and resorbed in accordance with the stresses placed upon it

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12
Q

Wolff’s Law

A

Every change in form and function of bone, or in its function alone, is followed by certain, definite changes in its internal architecture and external form

Bone models and remodels [its internal architecture] in response to the mechanical stresses it experiences, so as to produce a minimal-weight structure that is ‘adapted’ to its applied stresses

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13
Q

Bones response to fx

A

Bone matrix/cells are destroyed

Damaged blood vessels produce a localized clot

Clot material is later removed by macrophages

Periosteum and endosteum respond with intense proliferation of cells

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14
Q

Bone response to fx and repair

A

Periosteal/endosteal fibroblasts differentiate into chondroblasts and form hyaline cartilage model = soft callus

Mesenchyme cells differentiate into osteoblasts and form osteoid

Endochondral and intramembranous ossification occur to form primary (woven) bone = hard callus
Hard callus (woven bone) is replaced by lamellar bone
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15
Q

Healing time table

A

Soft Callus – 2wks
Hard Callus – 4wks
Lamellar Bone – 6wks

Healing bone is influenced by stresses placed upon it during healing

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16
Q

Effects on bone with inactivity

A

Inactivity or decreased loading of bone results in reduced osteoblast activity

Inactivity/decreased loading do not affect osteoclast activity
Osteoclast activity remains at/near normal levels

The overall result of inactivity is increased degradation of bone matrix and increase in serum Ca++ levels
(urine calcium levels increase since calcium is excreted by kidneys)

17
Q

Exercise training: effects on bone

A

Increased loading (mechanical stress) results in improved bone qualities:

Hypertrophy of bone

↑ bone mass/density

↑ load to failure (strength)

17
Q

Exercise training: effects on bone

A

Increased loading (mechanical stress) results in improved bone qualities:

Hypertrophy of bone

↑ bone mass/density

↑ load to failure (strength)

18
Q

Flow for Effects on bone and exercise

A

Mechanical Stress–>Microscopic deformities
–>↑ blood flow & ↑ bioelectric potentials =
(Piezoelectric effect)
—>Increased osteoblast and osteoclast activity

18
Q

Flow for Effects on bone and exercise

A

Mechanical Stress–>Microscopic deformities
–>↑ blood flow & ↑ bioelectric potentials =
(Piezoelectric effect)
—>Increased osteoblast and osteoclast activity

19
Q

Stress Fx

A

Repetitive loading on bone creates microscopic deformities

Deformities are healed and bone repaired with rest

Stress fractures result when loading outpaces bone repair/remodeling

19
Q

Stress Fx

A

Repetitive loading on bone creates microscopic deformities

Deformities are healed and bone repaired with rest

Stress fractures result when loading outpaces bone repair/remodeling

20
Q

Osteopenia

A

reduction in bone mineral density below normal levels, results in decreased bone strength
Osteopenia is often a precursor to the development of osteoporosis

20
Q

Osteopenia

A

reduction in bone mineral density below normal levels, results in decreased bone strength
Osteopenia is often a precursor to the development of osteoporosis

21
Q

Osteopenia occurs as a result of

A

inactivity, aging, low intake of vitamin D and calcium, smoking

21
Q

Osteopenia occurs as a result of

A

inactivity, aging, low intake of vitamin D and calcium, smoking

22
Q

Osteoporosis

A

defined as ↓ bone density and ↓ in overall volume of bone

With osteoporosis, bone resorption > bone formation

Osteoporosis often results in pathologic fractures
Failure of bone in response to normal physiologic stress

23
Q

Bones serves as what reservoir

A

Ca++ reservoir
99% of total body calcium is in the skeleton

Ca++ levels are tightly controlled by the endocrine system

24
Q

Key regulators of calcium metabolism

A 
Parathyroid hormone (parathyroid glands) 
Calcitonin (thyroid gland)
Vitamin D (absorbed thru intestines)
25
Q

Calcium levels in Blood

A

Hypercalcemia (↑ Ca++ level in serum) > 10.5 mg/dL of blood

Typical symptoms = mild to severe proximal weakness of the extremities

Hypocalcemica (↓ Ca++ level in serum ) < 8.5 mg/dL of blood

Typical symptoms = neuromuscular excitability and muscular tetany (especially UE flexion)

26
Q

Parathyroid Hormone (PTH)

A

Secreted from the parathyroid gland in response to low Ca++ levels in the plasma

PTH promotes osteoclast resorption of bone matrix and subsequent liberation of Ca++ into the blood

PTH binds to osteoblasts and stimulates osteoblasts to:
Stop producing bone
Secrete an osteoclast-stimulating factor

PTH also:
Enhances calcium absorption from intestines
Decreases calcium excretion by kidneys

27
Q

Calcitonin

A

Synthesized by the thyroid gland in response to elevated blood (plasma) Ca++ levels

Calcitonin
Inhibits matrix resorption by osteoclasts
Inhibits new osteoclast formation

Calcitonin has no effect on osteoblast activity, thus osteoblasts continue to produce bone matrix (and deposit excess the serum calcium onto new bone)

28
Q

Vitamin D metabolism

A

Vitamin D is necessary for intestinal absorption of Ca++ and PO4- from the small intestine

Vitamin D is necessary for active reabsorption of Ca++ and PO4- from the kidney

Vitamin D formation is stimulated by UV light; initial molecule is inactive

29
Q

VItamin D synthesis

A

Inactive Vit. D is “processed” in the liver and fully activated by the kidneys (hydroxylation)

Activated vitamin D enters the blood stream to assist with calcium absorption from the GI tract

A slight decrease in serum calcium below normal stimulates activation of “inactive” vitamin D

Histo (12 decks)

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