Bone Flashcards
What are some important structural features of cortical bone?
Periosteum = membrane of fibrous connective tissue present (except at articulating surfaces)
Haversian canals = run parallel to osteons, contain blood vessels, lymph vessels, and nerves (concentric lamella)
Volkmann’s canals = run perpendicular to osteons, connect Haversian canals with blood vessels, lymph vessels, and nerves (no concentric lamella)
Osteocytes in lamellae of osteons (interstitial and cirumferential lamella)
Immature bone: random arrangement of osteocytes
Mature bone: osteocytes arranged in concentric lamella
What are some of the different components of bone?
Cancellous (spongy) = network of fine bony columns or plates to combine strength with lightness
Cortical (compact) = hard external surfaces of bone (most of skeletal mass)
Bone marrow = haemopoieitc cells & adipose in gaps of cancellous bone
How are the osteocytes connected?
Osteocytes in lacuna.
Extensions of osteocytes connect = canaliculus
Gap junctions pass materials between osteocytes (as there are no blood vessels except in canals)
What are some important structural features of cancellous bone?
No Haversian or Volkmann’s canals (as blood marrow fills the gaps)
Osteocytes lie in irregular lamella
What are trabeculae?
Rods which form with mechanical stress applied on bone.
Osteoblasts are present at trabeculae
What are the different cells in bone? Where do they originate from?
OSTEOCLAST = digest and resorb bone (derived from macrophages)
OSTEOBLAST = secrete bone matrix by depositing osteoid (unmineralised organic portion of bone) (derived from osteoprogenitor cells)
OSTEOCYTE = mature osteoblast surrounded by osteoid
Mesenchymal origin
Outline the process of bone remodelling.
Life-long process where old bone is removed by osteoclasts (resorption) and new bone is deposited by osteoblasts (formation)
Osteoclasts form a cutting cone through the bone by releasing H+ and lysosomal enzymes)
Resting -> Resorption -> Reversal -> Formation -> Mineralisation
How does bone resist fractures?
Lamellae can slip relative to each other, conferring tensile strength, compressive strength, and flexibility
Excessive load causes fractures
Describe the stages of fracture repair.
1) Haematoma formation:
- blood vessels in bone & periosteum break
- bone cells at edge of fracture die due to lack of blood supply
- swelling and inflammation occurs
- phagocytic cells and osteoclasts remove dead/damaged tissue
- macrophages remove blood clot
2) Fibrocartilaginous callus formation:
- new blood vessels infiltrate fracture haematoma
- procallus of granulation tissue rich in capillaries and fibroblasts develops
- fibroblasts produce collagen fibres which span the break, and chondroblasts produce hyaline cartilage to splint the bone
- osteoblasts from periosteum invade fracture site and begin forming cancellous bone
Bony callus formation:
- new bone trabeculae appear in fibrocartilaginous callus
- fibrocartilaginous callus converted to hard callus of cancellous bone
Bone remodelling:
- cancellous bone remodelled to compact bone
- bulging material removed by osteoclasts
- final shape same as original (responds to same mechanical stresses)
What are the two types of ossification? Where do they occur?
ENDOCHONDRAL = replaces hyaline cartilage template with bone (mineralised hyaline cartilage)
Long bones e.g. femur, tibia, humerus, radius, metacarpals, metatarsals, etc.
INTRAMEMBRANOUS = Condensation of mesenchymal tissue (connective tissue converted to bone)
Flat bones e.g. skull bones (parietal, occipital, etc.), pelvis, clavicle
Outline long bone development by endochondral ossification.
Collar of periosteal bone forms by osteoblasts trapped under the perichondrium, which becomes the periosteum
Primary ossification centre forms
Nutrient artery penetrates cartilage and supplies osteogenic cells
Secondary centre of ossification forms
Medulla becomes cancellous bone
Ossification of epiphysis
Growth plates move apart apart, lengthening bone (POSTNATAL)
(Interstitial + appositional growth)
What are the different zone of growth of bone?
RESERVE CARTILAGE: no cellular or matrix proliferation
PROLIFERATION: chondrocytes divide to form columns, cells enlarge and secrete matrix
HYPERTROPHY: cells enlarge, matrix compressed
CALCIFIED CARTILAGE: enlarged cells degenerate and matrix calcifies
RESORPTION: calcified matrix in direct contact with marrow, blood vessels and lymph invade, calcified cartilage forms spicules which lay down bone
Resultant direction of growth ^
What are the features of osteogenesis imperfecta?
Autosomal dominant
Type 1 collagen mutation (affects connective tissue)
Affects skeleton, joints, ears, ligaments, teeth, sclerae, and skin
Can be confused with abuse
How do growth hormone disorders affect bone? What usually causes these disorders?
Growth hormone synthesised and stored in anterior pituitary
Before puberty:
Deficiency = affects epiphyseal cartilage e.g. pituitary dwarfism
Excess = promotion of epiphyseal growth plate activity e.g. gigantism
After puberty:
Excess = promotion of periosteal growth (increased bone width) e.g. acromegaly
Benign tumours of the anterior pituitary
How do sex hormones affect bone growth?
Influences development of ossification centres and stimulates or inhibits osteoclasts and osteoblasts
Increased sex hormones = retardation of bone growth (premature fusion of epiphyses - earlier puberty)
Decreased sex hormones = epiphyseal plates develop longer than normal (prolonged bone growth - later puberty)
Testosterone and oestrogens stimulate osteoblasts (increased bone remodelling)
