Lecture 18 - USE THIS ONE Flashcards
What are the mechanical, synthetic and metabolic functions of bone?
Mechanical = protect important organs, provide overall framework and shape for human body and form basis of levers involved in movement. Synthetic = Haemopoiesis (holds and protects red bone marrow) Metabolic = mineral storage (Ca2+ and PO4), fat storage (yellow bone marrow), acid-base homeostasis (absorbs or releases alkaline salts to help regulate blood pH)
What are the 2 types of ossification and what types of growth do they display?
1) Endochondral ossification: - formation of long bones from a cartilage template, continued lengthening by ossification at epiphyseal growth plates (appositional growth) - growth at edges
2) Intra-membranous ossification: - formation of bone from clusters of mesenchymal stem cells in the centre of bone (interstitial growth) - growth from the middle out
Intramembraneous ossification
- Mesenchymal stem cells (MSCs) form a tight cluster
- The MSCs transform into osteoprogenitor cells and then transform into osteoblasts
- Osteoblasts lay down a osteoid (extracellular matrix containing Type I collagen)
- The osteoid mineralises (crystals of calcium form in and around it) to form rudimentary bone tissue spicules [surrounded by osteoblasts and containing osteocytes]
- The spicules join to form trabeculae, which merge to form woven bone
(6. Trabeculae replaced by the lamellae of mature compact bone)
Cancellous bone conversion to cortical bone
- MSC convert into osteoblast that line recently formed trabeculae
- Lay down osteoid that is mineralised
- Osteoblasts trapped – osteocyte
- Steps 1 to 3 repeat
- Central MSC convert into blood vessels, lymph vessels and nerves
What are the main differences between endochondral and intra-membranous ossification?
Intramembranous takes place within condensation of mesenchymal tissue, endochrondral by replacement of hyaline cartilage template.
Intramembranous ossification forms flat bones, endrochondral ossification forms all other types of bone.
However, intramembranous ossification contributes to bone thickening of long bones, at their periosteal surfaces (appositional growth).
What is the difference between immature and mature bone?
- Immature bone has osteocytes in random arrangements
- Mature bone has osteocytes arranged in lamellae of osteons.
- Resorption canals in mature bone run parallel with osteons’ long axis.
What is the structure of mature compact bone and mature cancellous bone?
Which one of compact or cancellous bone contains Haversian’s and Volkmann’s canals? What do these structures do?
- compact bone HAVE them
- cancellous/spongy bone do NOT HAVE them
- They carry blood vessels, lymph vessels and nerves
Why does bone have great tensile and compressive strength?
Lamallae within cortical bone are able to slip relative to each other to resist fracture
- although excessive load can still cause fractures.
How do osteons remodel themselves: to thicken bones, after a fracture, constant dynamic process
- Bone is dynamic and constantly remodelling itself
- Exercise is a key determinant of bone stranght increased osteon
- Inactivity increases bone resorption (1/3 of mass lost when immobile)
STEPS:
- Osteoclasts make a wide tunnel in the bone (cutting cone), this is because they are resorbing the bone
- Osteoblasts make a smaller tunnel or cortical bone by laying down osteoid, osteoid then mineralises (they are ‘following’ the osteoclasts)
- *Exercise:**
- Osteon will reposit itself along the stress line
- Osteons also get bigger - the bigger concentric circles = the stronger the bone is
- Also lays down a new periosteum on the outside
- Increases the number of trabecula in the middle to try and strength the bone
- *Inactivity:**
- increases resorption
- increased osteoclast activity = bone gets thinner = more bone resorption = loss of bone mass
What are the main factors affecting bone stability?
- Osteoblasts (bone deposition) THICKENING BONES
Stimulated by calcitonin, oestrogen, PTH, thyroid hormones, vitamin A
- Osteoclasts (bone resorption) THINNING BONES
Increased by PTH (think parathyroid learnt in lecture 10 ish), this releases calcium ions into the blood
- A bit - Osteocytes: Can act like osteoblasts and lay down ‘scavenged’ osteoid into their lacunae (increased by oestrogen/thyroid hormone), Can act like osteoclasts and degrade bone (a little) – known as osteocyctic osteolysis (increased by PTH)
- Other important factors include nutrition - Vit D (either absorbed from gut or synthesised in the skin - required for calcium absorption), Vit C (synthesis of collagen)(and Vik K and B12.
Describe the 4 stages of bone repair after a fracture occurs.
1) Blood clot (haematoma) is formed in which granulation tissue arises, eventually removed by macrophage
2) Fibrocartilaginous callus is formed, first a procallus of granulation tissue is replaced by a fibrocalliganous callus in which bony trabeculae are developing.
3) Bonus callus formation - endochondral and intramemranous ossification give rise to a bony callus of spongy/cancellous bone.
4) Cancellous bone replaced by compact cortical bone until remodelling is complete
What is the genetic basis of Osteogenesis imperfecta? What are the clinical features? Who does it mainly affect?
- Mutation in COL1A (collagen type 1) gene, leading to incorrect production of collagen 1 fibres.
- Weak bones, increased risk of fracture, shortened stature, blue sclera
- Neonates + children
What is rickets caused by? What are the clinical symptoms?
- Vit D deficiency, leading to poor Ca2+ mobilisation and ineffective mineralisation
- Leads to soft bones, shortened heigh, bow legs, pain while walking
NB: Rickets is name in children, in adults this is called Osteomalacia.
In picture - can see ineffective mineralisation - osteoid surrounds the trabecula but don’t become mineralised = thin, weak trabecula
What is osteomalacia? Who does it affect?
- ‘Rickets’ in the adult
- Vitamin D deficiency: lower mineralisation, increased osteoid as bones are always remodelling
- increases calcium resorption
Causes of the vitamin D deficiency: - Kidney disease
- Not enough sunlight
- Surgey - Stomach and intestine (may affect absorption of calcium from food)
- Drugs - phenytoin prevents vitamin D absorption
What are the 2 main divisions of osteoporosis? What is each one due to?
1) Primary -
Type 1: occurs in postmenopausal women, due to increased osteoclast number (as there is a loss of oestrogen which keeps osteoclast number under control)
Type 2: occurs in the elderly, due to loss of osteoblast function - also called senile osteoporosis (due to loss of oestrogen/androgen),
2) Secondary - result of drug therapy (corticosteroids), is a major risk factor for bone fracture in elderly, malnutrition, prolonged immobilisation, weightlessness (i.e. with space travel), metabolic diseases like hyperparathyroidism (increased PTH levels, increasing resorption of calcium)
Mechanism of osteporosis
What does the bone look like of someone with osteoporosis?
