MSK L5 Bone and Cartilage Flashcards
Matrix: Made up of
Inorganic/mineral
Organic
Matrix: Inorganic/mineral made up of
Hydroxyapatite
Matrix: Inorganic/mineral Function
Compression strength
→ without = bendy
Matrix:Organic made up of
Collagen and proteoglycans
→ without =brittle bones (osteogenesis impracta
Matrix: Organic part function
Flexible strength
Bones types:
- Cortical or compact – more dense
2. Cancellous (trabecular or spongy) – less dense – bars and plates interconnected
Matrix
Made up of many osteons
Osteon
Concentric layers of lamellae around central blood vessels.
Haversian canal
Contains blood vessels
Interstial lamellae
In between two osteon
Circumferential lamellae
Near matrix at surface
Canaliculi
Radiate from lacunae from mature bones and osteocytes into the haversian canal. Channels provide passageway through compact bone to provide nutrition to the cells.
Volkmann’s canal
Perforating blood vessels – allows them to join in outer membrane
Osteoblast
Forming bone (multinucleated)
Canaliculus
Radiate from lacunar of mature bone cell (osteocyte) into adjacent cavities with blood vessels to obtain nutrients.
2 types of bone development (ossification):
- Intramembranous → ossification of membrane to bone
2. Endochondral ossification→ calcification of cartilage model into bone
Bone Growth:
Apposition growth
Process (width)
Endochonral growth (length) process
Apposition growth
Process (width)
- OB in periosteum secrete matrix and become trapped as osteocytes
- Osteoclasts in crease diameter of medullary cavity
- Increases diameter of bones until skeletal maturity
Endochonral growth (length) process
- Requires interstitial growth from cartilage first
- Occurs at epiphyseal growth plates
- Stops when growth plates ossify
New bone laid down
Woven bone (random collagen)
Remodelled why
More orderly collagen fibres
Remodelling process
Osteoblasts lay down bone Osteoclasts resorbed (remove) bone → Lamellar bone (ordered formed)
Mature bone
Old bone is constantly being replaced by new bone
Bone shape changes in response to changing stresses
Factors influencing bone growth and remodelling:
- Mechanical factors
- Genes
- Hormones
- Aging
- Diseases
Mechanical → influencing bone growth and remodelling:
Wolf’s Law
→ More stress increases osteoblasts activity → more bone
→ Less stress decreases osteoblast activity → less bone
Genes: influencing bone growth and remodelling:
- Determine potential shape and size
- Height and bone mass is multifactorial (many genes involved and other factors)
- Genes influence
a. Growth hormone release
b. Hormone receptor on bone cells
c. Ability to absorb nutrients from the gut - Some genetic disorders influence bone growth e.g. dwarfism (FGFr3 mutation), turners syndrome
Hormones: influencing bone growth and remodelling:
- Growth, sex and thyroid hormones influence cell differentiation and metabolism
- Overactive pituitary gland →excess GH
Ageing: influencing bone growth and remodelling:
- Osteoblast matrix production slows in comparison to osteoclast matrix resorption
- Decreased collagen deposition results in more brittle bone (less flexible strength)
- Bone mass peaks at 25-30 years then falls.
Diseases: influencing bone growth and remodelling:
- Osteoporosis → bone mass is reduced particularly in women after menopause (reduced oestrogen production).
- Other factors affecting oestrogen levels
a. Removal of ovaries
b. Extreme exercise
c. Anorexia nervosa
d. Smoking - Cancellous bone is most affect as it is severly weakened if connections lost.
FGFr3 →
normal proliferation of chondrocytes
Defective = poor proliferation of chondrocytes an abnormal growth of long bones in limb.
Cartilage: types
- Fibrocartilage – strongest and most rigid
a. E.g. minicus - Hyaline cartilage
a. Joint surface
b. Epiphyseal growth plate - Elastic cartilage → balance between structure and flexibility
a. E.g. ear
b. Eustacian tube
Cartilage growth
- Appositional growth
2. Interstial growth
Perichondrium: Outer layer
Dense irregular CT with fibroblasts
Perichondrium: Inner layer
Fewer fibres with chondroblasts
Perichondrium: Appositional growth
Chondroblasts
Perichondrium: Interstial growth
Chondrocytes
Articular Cartilage: Type of
Hyaline cartilage
Articular Cartilage: Found
On articular surfaces of bones
Articular Cartilage:Has no
Perichondrium- as it forms part of the joint.
Articular Cartilage: Growth
Similar to growth plate (but never ossifies)
Columns of cells → calcified cartilage and then form bone
Articular Cartilage: Collagen structure
Arcades – high concentration of collagen on the surface.
Articular Cartilage: Arcades
Type II collagen fibrils anchor proteoglycan matrix to bone
Articular Cartilage: Growth stops
At a similar time to growth plate but never ossifies
Function of Articular cartilage: Smooth
- Reduces friction (heat → protein damage)
2. Low-wear surface
Function of Articular cartilage: Deformable and elastic
Distributes load evenly
• Increased surface area → reduced force (peak contact stress)
• Creep (deformation and load) also increase surface area during sustained loading
Function of Articular cartilage: Visually
- Simple, inert tissue
- Has high stiffness to compression and resilience
- Exceptional ability to distribute load and great durability
Function of Articular cartilage: Adult articular cartilage
Hypocellular
Aneural
Avascular
Cartilage matrix
. Large number of proteoglycans attaching to hyaluronic acid chain → help to maintain the reversible deformity property of cartilage. → Maintains water within the structure 3. Collagen type II (mainly) a. Provide stable structure 4. Collagen (other types)
Matrix Synthesis Promotion
TGF
IGF
Matrix Synthesis Inhibition
IL-1
TNF
Matrix degradation Promotion
IL-1
TNF
Matrix degradation Inhibition
TGF
IGF
Factors influencing cartilage metabolism
- Mechanical factors
- Injury
- Aging
- Diseases
Mechanical → adaptive remodelling
Cartilage is poor at this
➢ High strain = deposition
➢ Low strain = resorption
1. Anabolic and catabolic processes adjusted to adapt matrix to mechanical demands.
2. Low below 1 MPa may be catabolic while load above 1 MPa may be a anabolic stimulus.
Injury and repair:
- Lack capillaries within cartilage.
- Nutrients from diffusion (synovium not bone).
- Chondrocytes do not normally divide in adult but still secrete matrix (repairs normal wear).
- Tears/lesions never fully heal.
Ageing:
- Decreased PG and collagen turnover
a. Collagen disruption
b. PGs lost
c. Water lost on compression
d. Tissue damage - Increase no-enzymatic glycation NEG)
- Impaired joint lubrication
a. Friction/heat
b. Fibrillation
c. Osteoarthritis
Non-enzymatic glycation:
- Cross-linking between collagen and sugars
- Process not controlled by enzymes or cells
- Advanced glycatino end=products (AGEs) make tissue stiffer, more brittle and yellowish (seen with ageing)