Bone Function and Repair Flashcards
What are the functions of bone?
Mechanical such as protection of organs and tissue.
Involved in movement.
Synthesis of cells in haemopoeisis.
Metabolic such as mineral storage of calcium and phosphorus.
Fat storage/energy storage in yellow marrow.
Acid-base homeostasis.
What are the two ossification types?
Endochondral ossification
Intra-membranous ossification
Briefly explain endochondral ossification.
Formation of long bones from cartilage template.
Continued lengthening is by ossification at epiphyseal plates (appositional growth)
Briefly explain intramembranous ossification.
The formation of bone from clusters of mesenchymal stem cells in the centre of the bone. For example how spicules for trabeculae. This is interstitial growth and does not involve cartilage!
What do flat bones develop by?
Intramembranous ossification directly from mesenchymal stem cells.
When can appositional growth occur in intramembranous ossification?
When thickening of long bones occur. This is at the periosteal surfaces.
Are long bones only made from endochondral ossification?
No intramembranous ossification occur as to thicken the long bones. Lengthening however is done by endochondral ossification.
How do blood vessels end up in spongy bone from intramembranous ossification?
As spicules are built and eventually come together they trap blood vessels in between.
Look at page 9.
Yup
What are the stages of intramembranous ossification?
MSCs form a tight cluster.
MSCs become osteoprogenitor cells and then osteoblasts.
Osteoblasts lay down osteoid (ECM containing collagen type 1)
The osteoid mineralises and form bone spicules. Osteocytes are found within the spicules and osteoblasts are found on the outside of the spicules.
The spicules join together to form trabeculae and trap blood vessels.
Trabeculae are then replaced by the lamellae of mature compact bone.
Why are there no Haversian and volksmann canals in cancellous bone?
Because it has red marrow surrounding it.
Why are the lamellae important regarding bone strength?
Because they are thought to be able to slip relative to each other to resists fracture. Works a little bit like a spring then.
What are the factors affecting bone stability/strength?
Activity of osteocytes which can both act as osteoblasts and osteoclasts.
Activity of osteoblasts
Activity of osteoclasts
What are some nutritional factors that affect bone stability?
Vitamin D
Vitamin C (synthesis of collagen, hydroxylation of lysine and proline)
Vitamin K and B12
How does calcitonin work?
Released by thyroid gland to inhibit the action of osteoclasts.
How does PTH work?
Indirectly increases the activity of osteoclasts. (Makes more osteoclasts.)
Mention what steps are involved in fracture repair.
Haematoma formation
Fibrocartilaginous callus formation
Bony callus formation
Bone remodelling
What happens in step 1 of fracture repair?
A haematoma is formed. As the haematoma forms now blood supply reaches the site and tissue dies because of this. Swelling and inflammation occurs as granulocytes enter the site. Phagocytic cells and osteoclasts begin to remove dead and damaged tissue. Macrophages will eventually remove the haematoma.
What happens in step 2 of fracture repair?
A fibrocartilaginous callus is formed. New blood vessels infiltrate the fracture haematoma. The soft callus formed here is rich in capillaries and fibroblasts.
Fibroblasts lay down collagen fibres. Other fibroblasts turn into chondroblasts that will lay down hyaline cartilage.
Osteoblasts near the periosteum and endosteum invade the fracture site and begin bone reconstruction by forming spongy/trabecular bone.
What happens in step 3 of fracture repair?
A bony callus is formed. New bone trabeculae start to appear in the soft callus.
Endochondral ossification replaces cartilage with cancellous bone.
Intramembranous ossification produces new cancellous bone in any gaps.
What happens in step 4 of fracture repair?
Bone remodelling. The cancellous bone is remodelled into compact bone. This is by continuous osteoblastic and osteoclastic activity.
The material bulging from the outside of the bone will eventually be removed by osteoclasts.
What are the two steps of bone remodelling?
Osteoclasts make a wide tunnel in the bone called cutting cone.
Osteoblasts make a smaller tunnel of cortical bone called closing cone.
Look at page 31.
Yup
What are some clinical conditions relating to bone formation?
Osteogenesis imperfecta
Rickets and osteomalacia
Osteoporosis
Achondroplasia
Briefly explain Osteogenesis Imperfecta.
Mutation in COL1A
An incorrect production or close to no production of collagen 1 fibres.
What are symptoms of Osteogenesis Imperfecta?
Weak bones and increased fracture risk Shortened height and stature Blue sclera Poor teeth development Hearing loss
Briefly explain Rickets.
Mainly affects children
Result from a vitamin D deficiency
Poor calcium mobilisation
Ineffective mineralisation
What are symptoms of Rickets?
Weakened bone development
Soft bones
Shortened height and stature
Painful to walk and classic bowed legs.
Briefly explain Osteomalacia.
The same as Rickets but in adults
Vitamin D deficiency
Lower mineralisation
Osteomalacia can be caused by other things than vitamin D deficiency, or indirectly vitamin D deficiency. What?
Increased calcium resorption from:
Kidney disease (Kidneys activate vitamin D)
Protection from sunlight (produces vitamin D)
Surgery (stomach and intestine)
Drugs that prevent vitamin D absorption
What are the main groups of Osteoporosis?
Primary and secondary osteoporosis.
Explain primary osteoporosis type 1.
Occurs mostly in postmenopausal women
This is due to an increase in osteoclast number which means more bones broken down.
The increase in osteoclastic activity is from loss of oestrogen after the menopause.
Explain primary osteoporosis type 2.
Occurs in both older men and women.
This is due to a loss of osteoblast function
This comes from a loss of oestrogen and androgen
What is secondary osteoporosis?
Weak or hollow bone formed ‘external’ factors:
Result of drug therapy
processes after bone remodelling like malnutrition, prolonged immobilisation or weightlessness like space travel.
Metabolic bone diseases like hyperparathyroidism. This causes an increase in PTH which indirectly causes an increase in osteoclast activity.
How can primary osteoporosis be managed?
By increasing the calcium intake of elderly men and women.
How can secondary osteoporosis be treated?
By exercise. Immobilisation leads to weaker bone, then exercise instead.
Explain Achondroplasia.
Inherited mutation in FGF3 receptor gene.
FGF promotes collagen formation from cartilage.
This means that endochondral ossification does not work properly and this results in shorter long bones.
However intramembranous ossification still works properly.
This results in shorted long bones but normally sized short bones, flat bones, irregular bones and sesamoid bones.
