Bone Remodelling and Osteoporosis Flashcards
What is osteoporosis?
Low bone mass and deterioration of bone tissue, leading to high risk of fracture
When there is not enough type 1 or wrong type 1 collagen, you will have problems
Osteoporosis is due to an imbalance with the cells in the body
Silent disease → if you do not consider the diagnosis when the patient comes in, you will miss the diagnosis!! Esp bc its asymtomatic, blood tests are normal y hay long latent period
Where are the most common sites of osteoporosis fracture?
What are the functions of bone? What are its components?
- Calcium regulation
- Mechanical support and lcocomotion
- Protection of vital organs
Bone is made up of 3 components ⇒ protein matrix, mineral, cells
Expand on the different components of bone, including its constituents and properties
What types of diseases affect the protein matrix, mineral and cell components?
matrix on left, mineral in middle, cells on right
What is the protein matrix?
Protein matrix → osteoid is a matrix material made up of collagen, mycopolysaccharide and organic glue
Soon after the osteoid is laid down, inorganic salts are depositied and allow the formation of mineralised bone, using with Ca, Vitamin D and phosphate → makes bones strong
What are the different bone cell types?
Osteoblasts → synthesise bone
Osteoclasts → resorb bone
Osteocytes → Mechanosensors + paracrine role (RANK-L)
- Mechanosensors will sense exertion in certain places - this causes OCs to produce more bone in the direction that you are exerting on the area
Note → OCs form when OBs become buried in the mineral matrix of bone and develop distinct features
Lining cells → quiescent
Bone marrow cells → in the middle
Compare osteoblasts versus osteoclasts
Osteblasts are derived from mesenchymal stem cells. They synthesise the matrix proteins and form bone mineral
Fate of osteoblasts
- Apoptosis
- Lining of cells - become quiescent
- Osteocytes - go deep into the bone
Osteoclasts are derived from the blood in myeloid lineage - Develop from macrophages
OC produce HCl to resolve bone mineral, then proteolytic enzymes to breakdown the protein matrix, then they digest both matrix and mineral
Labelled this diagram to explain the types of bone
What happens after menopause?
Oestrogen and androgens suppress osteoclastic bone resorption
After menopause, there is no/low oestregen - this means you have excessive resorption of bone due to the osteclasts becoming overactive and bone remodelling is out of sync
Describe the bone remodelling cycle
Which endocrine hormones increase and which hormones decrease bone density?!
GH is usually anabolic anyway
Excess PTH = excess osteclastic bone resorption ⇒ net loss of bone (see the other lecture)
Remember Cushing’s + the glucocorticoids effect
outline the changes in bone mass with age
If you lived in active lifestyle you would have an even higher peak bone mass!!
Bottom line → Lack of mechaniscal stimulation means your bones cannot get stronger
How do we measure bone mass? How do we interpret the results?
DXA scan: Dual Energy Xray Absorptiometry
Measures Bone Mineral Density (BMD)
Bone mass and bone mineral density are synonymous
Measures bone QUANTITY, not bone QUALITY, so DXA not to be used in isolation for diagnosis
What are the limitations of DXA?
Normal T score does not exclude OP
-Artefacts falsely elevate BMD – eg spine OA or fracture
-Bone fragility can be due to poor bone architecture
Low T score is not always due to osteoporosis
-Osteomalacia (undermineralised bone) also causes low BMD
Therefore we now use FRAX first to make an osteoporosis diagnosis.
What are the risk factors for osteoporosis?
Investigations for Osteoporosis?
Describe vertebral fractures
What is the drug treatment for osteoporosis?
Which osteoporosis drugs have a long versus short half life in bone?
When should you also remember to look into calcium and vitamin D?
What are the non-drug treatments for osteoporosis?
How often would you review your osteoporosis patient?
