Session 7: Bone marrow, vessels and blood Flashcards
Name the bones of the axial and appendicular skeletons
Axial: Skull, vertebra, thoracic cage(ribcage)
Appendicular: shoulder girdle, pelvic girdle, lower and upper limbs
Explain how a bone is a living tissue
Bones have their own blood vessels, and proteins, minerals which allow them to grow, transform and repair themselves through life
What is the function of bones?
- Protects important and delicate tissues and organs
- Haemopoiesis: holds and protects bone marrow
- Fat storage( yellow BM), acid-base homeostasis absorbs or releases alkaline salts-has Ca, to regulate blood pH)
How are bones formed?
- Endochondral ossification: formation of long bones inside cartiliage. Continued lengthening throughout life by ossification of growth plate- called appositional growth growth at edges)
- Intra-membrous ossification: formation of bones from clusters of mesenchymal(MSC) bone marrow cells from centre of bone. Called intersitial growth- growth begins in middle
How do bones undergo remodelling?
- Bone resorption: osteoclasts digest old bone
- Ossification: bone formed by osteoblasts lay down new bone till resorbed bone is completely replaced
Describe the components of bones( in a fetal skull)
Osteoblasts: bone deposition
Osteocytes: osteoid recycling
Osteoclasts: bone resorption
Periosteum: blood supply for bones( side 1)
Mesenchymal tissue: in bone marrow, make and repair skeletal tissue
Spicule of bone: fragments of bone marrow, connect to form tracbaculae
Osteoid: unmineralised bone tissue
Lacunae: contains osteocyte left behind by osteoblast after remodelling
Canaliculi: links lacunae with one another and with haversian canal. Also found in liver lobule
Lamellae: extracellular matrix around cells that gives compact bones it hardness.
Endosteum: lining membrane of bone marrow cavity, lines haversian canal( side 2)
Trabacular bone: porous bone connected with thin rods and plates
Haversian and Volkmann’s canals: carry blood vessels, lymph vessels and nerves
Describe the structure of cancellous/trabecular/spongy bone and compact/cortical bone which make up every bone in the body
Cancellous: network of fine bony platse called trabeculae to combine strength with lightness. Spaces are filled with bone marrow
Compact: forms externla surfaces of named bones, contains Ca
Explain the importance of Vitamin D in normal bone stability
Vitamin D produces calcitrol which aids in calcium absorption
How does activity of osteocytes affect bone stability?
- Activity of osteocytes( osteoid recycling): can act like osteoblasts and lay down scavenged osteoid into lacunae due to increased oestrogen or thyrois hormones OR can act like osteoclasts and degrade bone, called osteocyctic osteolysis( increased by PTH/parathormone, secreted by parathyroid gland which controls Ca levels in blood)
How does activity of osteoblasts affect bone stability?
Bone deposition is stimulated by oestrogen, testosterone, thyroid hormones, vit A
How does activity of osteoclasts affect bone stability?
Bone resorption is increased by PTH, releases calcium ions into blood. To counteract, calcitonin decreases Ca levels by blocking PTH at PTH receptor.
What biological change generally causes bone disease?
Depletion of bone mass. Loss of mass within trabecular bone is relevant to increased suspectibility to fracture.
Describe the genetic and phenotypical changes in osteogenesis imperfecta
AKA brittle bone disease. Caused due to autosomal dominant mutations in COL1A where produced mutated collagen 1 fibres do not knit together or insufficient collagen is produced. Results in:
weakened bones, short stature, blue sclera, hearing loss, loose joints, flat feet, crowded teeth
Describe the features of bones affected by rickets and phenotypical changes, and compare with osteomalacia
R: mainly in children, due to Vit D deficiency. Leads to poor calcium mobilisation, weak bones, short stature, painful walk, characteristic bowed legs
O: rickets in adults, Vit D def, increased osteoid-unmineralised bone tissue, bones are weak. Leads to increased calcium resorption. Due to lack of sunlight, Ca rich food, esp when preganant. Fetus needs Ca for own tissue development as well.
Describe the radiological and structural changes in primary and secondary osteoporosis
Primary
Type 1: post menopausal women due to increase in osteoclast number, loss of osetrogen in menopause- osteocyte cannot act as osteoblast anymore
Type 2: older people due to loss of osteoblast function AKA senile osteoporosis and loss of oestrogen and androgen. Incomplete filling of osteoclast resorption bay.
Secondary
Due to drugs like corticosteroids( asthma treatment), affects bone remodelling. OR due to malnutrition, space travel, lack of movement OR metabolic bone disease