Bone Histology Flashcards
1
Q
Connective tissue characterized by a mineralized extracellular matrix
A
Bone
2
Q
What make up the primary mineralization of bone?
A
Hydroxyapotite crystals
3
Q
What is the primary collagen in bone?
A
Type I collagen fibers
90% of total weight of bone matrix protiens
4
Q
Also contains
Proteoglycan macromolecules, multiadhesive glycoproteins, Vitamin-K dependent proteins, growth factors; make up small compoenent
A
Bone
5
Q
- bone cells, connected via canaliculi.
- Survive 10-20 years.
- Important for maintaining overall structure
- Sense for adaptation
A
Osteocytes
6
Q
1 cause of morbitiy in ppl over 80 occurs after what?
A
bone breakage, seditary
7
Q
Excersise places pressure on bones causing ____ to secrete more hydroxyappotite making bones denser and stronger
A
Osteocytes
8
Q
gives rise to osteoblasts. Respond to markers in ECM, causing htem to differentiaie into osteoblast.
A
Osteoprogenitor cells
9
Q
Differentiated bone-forming cell which secretes bone matrix (osteoid matrix)
A
Osteoblasts
10
Q
Osteoblasts fo to where the Bone matrix is produced and secretes a _____
A
Osteoid matrix
11
Q
Consist of collagen, glycoproteins etc
A
Osteoid matrix secreted by osteoblasts
12
Q
Once osteoid matrix is down, ____ is secreted and traps osteoblast in matrix converting them to ___
A
Hydroxyapotitie, converting to osteocytes
13
Q
- found on bone surface, derived from osteoblasts.
- Provide a foundation of cells that can quicly differentiate into osteoblasts.
- Bones always under stress microfractures, these cell fix these
A
Bone lining Cells
14
Q
- resorb bone they are specialized with enzyme TRAP
A
Osteoclasts
15
Q
What is the physiological marker of osteoclasts?
A
Enzyme TRAP
16
Q
How do osteoclast function?
A
- Seal themselves on bone surface
- Clear zone on edge
- Ruffle zone in center, acid released to break down HA, and TRAP breaks down the rest of the EC components.
17
Q
two types of bone
A
- Compact (dense)
- Spongey (cancellous
18
Q
4 classifications of bone
A
- Long (femur)
- Short (carpals)
- Flat (hip)
- Irregular (vertebrae)
19
Q
Explain three parts of long bone
A
- Diaphysis; main shaft
- Metaphysis on middle end
- Epiphysis; on either end lined with articular cartilage to reduce friction.
20
Q
what part of long bone is cut off with joing replacments?
A
Metaphysis cut off and replaced with prosthetic
21
Q
the outer covering of bones
A
Periosteum
22
Q
articulating surfaces – then covering is ____; reduce fricion
A
cartilage
23
Q
the main component of the periosteum in non-growing bones
A
Fibrous Layer
24
Q
- may become osteoblasts with appropriate stimulus
- Important with repair, major break, disrupt periosteal layer, they can differentiatin into osteoblast. Bone producton
A
Periosteal Cells
25
In long bones, the bone cavites are line with ____ which contains ___ cells
Endosteum, osteoprogenitor cells
26
# What marrow?
**blood producing**
Contains blood cells in different stages of development
red marrow cavity
27
# What marrow?
found in adults, **mostly fat cells**
Can revert to blood producing in cases of extreme blood loss (trauma)
Yellow marrow cavity
28
organized in concentric lamina called ____ (nerve, artery, vein)
osteon
29
* Perpendicular to long axis
* Channal where blood vessle and nerve travel through
* Connect to haversian canal
* Metabolic transfer in/out
* Growth factors in
* Calcium control with blood
Volkmann Canals
30
* parallel with long axis to bone
* Connected to inner and outer surfaces
Haverisian Canal
31
Where do the nutrient **diaphyseal and epiphyseal** arteries arise from?
arise from the periosteal buds
32
Where do the nutrient **metaphyseal** arterry arise from?
From **periosteal vessels** during bone widening
33
Lymphatic drainage only occurs from the ___
Only in the periosteum
| No lymphatic vessels in bone tissues
34
* Not organized – **nonlamellar**
* More cells per unit area than mature
* Random arrangement
* More ground substance
Immature bone
| During development & repair x4
35
?
**Immature bone **
*lack of mineralization
36
?
**Mature bone **
*extensive secondary mineralization, organized
37
**Derived from Mesenchymal stem cells**
Can differentiate into many cell types: fibroblasts, osteoblasts, chondrocytes, muscle cells
Osteprogenitor cells
| Located on **internal and external bone surfaces**
38
Osteoblast are responsible for what?
Calcification of the bone matric
39
How to osteoblast communicate?
Via gap junctions through canaliculi
40
How do osteocytes connect to one another?
Canaliculi
41
Mature bone cell enclosed in bone matrix occupying the lacuna
Osteocytes
42
Osteocytes respond to what?
Mechanical forces via mechanotransduction
43
Mechanotransduction in osteocytes with cause what?
Bone remodeling in response to pressure changes
44
Derived from osteoblast, cover **non-remodeling** bone surfaces
Bone lining cells
45
# what cells?
External bone surfaces
Periosteal cells
46
# What cells?
Internal bone surfaes
Endosteal cells
47
Large multinucleated cellss responsible for bone resorbtion
Osteoclasts
47
what forms as a result of osteoclast activity?
Howship Lacuna
Resorbtion bay
48
What is the purpoe of enzyme **Tartrate-resistant acid phosphatase (TRAP)**
Primary enzyme of bone resorbtion and organic digestion.
| acids digest inorganic element
49
What cells are osteoclast derived from?
Mononuclear hematopoetic progenitor cells
50
What receptor is found in immature inactive osteoclasts?
RANK
51
Explain osteoclast activation
1. RANK receptor on immature oseoclasts
2. RankLigand comes and binds
3. Activates NF-KB
4. Differentiates to mature osteoclasts and commences resorbtion
52
RANK activation can be blocked how?
**Osteoprotegerin** which binds RANK and blocks RL from binding and activating
53
Osteoclast activation depends on amount of what?
Amount of RANKL and Osteoprotegerin
54
Treatment of osteoperosis?
Use OPG to prevent activation of osteoclasrs, less destructuin
55
# Osteoclast bone resorbtion
**increases surface area** and increases efficiency of enzyme release and bone resorption
Ruffle boarder of cell
56
Edge of osteoclast, area of attachment to site being resorbed.
Targeted, controlled digestion
Clear Zone
| sealing zone
57
Inflammation of joints
Arthritis
58
characterized by progressive loss of normal bone density accompanied by the deterioration of its microarchitecture.
Osteoperosis
59
Occurs in post menopausal women, occurs earlier in life so long term effect is more severe.
Type 1 osteoperosis
60
* occurs in the 7th - 8th decade of life
* Leading cause of serious morbidity and functional loss in the elderly
* Due to loss of osteoblastic activity with age.
Type 2 osteoperosis
61
result of drug therapy **(corticosteroids)**or disease process (malnutrition, immobilization, weightlessness, hyperparathyroidism, cancer)
Secondary Osteoperosis
62
What is first line Tx of osteoporosis
* Supplement with VitD & Calcium
* Excersive to increse pressure on bone
63
What is 2nd line Tx for osteoporosis ?
Pharmacologic therapy
64
* For **postmenopausal women** (estrogen and progesterone)
* Increase of risk of CVD, blood clots, breast cancer
HRT tx of osteoporosis
65
** inhibit osteoclastic activity**
* oral vs IV can have increase in **osteonecrosis of the jaw** following tooth extraction
Bisphosphates
66
**neutralizes RANKL;**
* inhibit osteoclastic acivity act like OPG and block!
**Monoclonal antibody therapy** (Denosumab)
67
# Osteoclast Function Regulation
What does parathyroid hormone do?
(PTH)
Indirect effect, **stimulates RankL production** in lymphocytes and osteoblast.
**More osteoclast act**.
* increases blood calcium levels
68
# Osteoclast Function Regulation
What does Calcitonin do?
Reduce osteoclastic activity
* decreases blood calcium levels
69
look
look
70
look
71
**requires Cartilage** model precursor
Endochondral Ossification
72
No cartilage model precursor
Intramembranous ossification
73
Expain intramembranous ossification
1. Increased vascularity
1. **Mesenchymal cell**s condens
2. Differentiation into osteogenic cells and then osteoblasts
3. Osteoblasts deposit osteoid
4. Osteoblasts become surrounded (now osteocytes)
5. Osteoid calcifies into spicules forming trabeculae
6. Salts deposited as HA with cartilage fibers
7. Periostieum & compact bone ofrmed
74
As condensationof bone occurs what penetrates?
Nutrient vessles
75
Explain Endochondra ossification
| within 1 year of birth
1. Start with** hyaline cartilage** model in shape of bone
2. Form **primary ossification center**
3. **Enlargement of chondrocytes** reults in increase length at epiphyseal plate
4. **Secondary oss. centers** establish
76
# Endochondra ossificationn
**Increase in length** is attributed to interstitial growth of ____, forces to either end.
chondorocytes
77
# Endochondra ossificationn
**Increase in width** result of addition of ____ on outside.
cartilage matrix
78
By the late teens to early 20s, all remaining ____ in the epiphyseal plate is generally consumed
**cartilage**
* Gap btwn epihysease and diaphysis closes
* primary & secondary marro cavities unite
* **bone can no longer grow in lenght**
79
Excess of growth hormone **before** closure of epiphyseal plate
Gigantism
80
Once **epiphyseal plate closes**, lots of growth hormone
Acromegaly, bones expand in width.
| Jaws, fingers, larger.
81
what are the 5 zones of epiphyseal cartilage?
1. Reserve Cartilage
2. Proliferation
3. Hypertrophy
4. Calcified cartilage
5. Resorption
82
zone where**# of chondrocyes increases** vastly
Zone of proliferation
83
zone where chrondrocytes **grow in size**
Zone of hypertrophy
84
What two cartilage zones are where **length of bones** originates from?
1. Zone of proliferation
2. Zone of hypertrophy
85
Zone is where **calcification of cartilage occurs**, bone is still weak, 1st step in formation of dense bone
Zone of calcified cartilage
86
Zone where you have turnover, resorb of calcified cartilage by osteoclast that ends depostion of dense bone by osteoblast
Zone of resorbtion
| equals zone of proliferation
87
Zone where you havr restin halyine cartilage
Zone of reserved cartilage
88
89
Responsible for maintaining growth process
Epiphyseal growth plate
| Thickness constant until maturity then it shrinks
90
**Resorbed cartilage** is replaced with ____
spongy bone
91
* Cutting cone (osteoclast)
* Closing cone (osteoblasts)
Bone remodeling unit
92
How is the bone remodeling unit initiatted?
* Microcrack
* Osteocytes signal
* Locak hormones and GF released
93
What are the 3 phases of active bone remodeling unit
1. Cellular actication (recurited at cutting edge)
2. Resorbtion
3. Formation and mineralization
94
# Active Bone-Remodeling Unit
Osteovclasts are active for 12 days and then die, what cleans them?
* death releases IGF, FGF, which recruits what?
PMNL
*recruits osteoblasts*
95
# Active Bone-Remodeling Unit
Osetoid is formed by ____ mineralization begins ____ days later until eroded volume is filled
Formed by osteoblast, mindelization 13 days after, takes uo to 3 months
96
**produced by osteoblasts**
Regulates energy and glucose metabolism through effects on adipocytes and the pancreas
Osteocalcin
97
**bone matrix does not calcify normally**
* Insufficient calcium or Vitamin D
* Results in short stature and skeletal deformities (major is bow legged)
Rickets
98
**insufficient calcium or vitamin D in adults** typically due to improper resorption and malnutrition.
Osteomalacia
99
**Lack of vitamin C** it **reduces calcification** due to collagen synthesis errors catalyzes hydroxylincine
* VitC is not addition of hydroxylicine bad collage synth bad calcification.
Scurvy
100
**suppresses endochondral bone growth**
* Fragility and fractures of long bones
Vitamin A deficiency
101
**fractured bone is surgically stabilized (screws/ rods)**
* Bone undergoes internal remodeling like that of **mature bone**
Direct primary bone healing
102
**responses to signals from the periosteum and surrounding soft tissues**
* Fractures are treated with nonrigid or semirigid bone fixation; bone respond to changes in pressure.
Indirect secondary bone healing
103
Summary of bone healing
| 6-12 week process
1. Disruption of blood supply due to** trauma,** etc
2. **Blood clot** stimulates formation of **soft callus (fibrocartilage scaffold)** (2-3 weeks post fx)
3. **Granulation tissue** form
4. **Inflammatory response**(weak immune system inhibit formation of soft callus) (1 week)
5. **Osteoblast** come in and deposite bone on soft callus to est. spongey bone; **hard callus** (3-4 months)
6. Months later, spongey bone replaced with compact bone, **osteocyte network rest. **
104
What helps expidite bone healing process?
Setting bone!
