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75 Cards in this Set

  • Front
  • Back
How many types of bones are there?
-Flat bones(skull,scapula,mandible)
-Long bones(tibia,femur,vertebrae)
Name the 2 distinct mechanisms by which bones are formed.
1.Intramembranous ossification
2.Endochondral ossification
What is important about cortical(compact) bones?
-found on edges
-low surface-to-volume ratio
-80 % bone mass
-rigid and dense
-bone remodelling in cutting cones.
Cancellous bones constitutes
20 % of bone mass.
Rapid response to calcium stress occurs in cancellous bone.
What is the site of most bone remodelling?
Cancellous bone
Is trabecular bone always changing?
Bone remodelling is responsive to what?
-Mechanical stress
-Calcium homeostatic stress
-regulated by hormones/cytokines
Trabecular bone releases Ca2+.
WHat initiates osteoclasts formation?
What happens when bone resorption is > than bone formation?
What happens when bone formation is > than bone resorption?
-Osteopetrosis(little bone resorption)
-Osteosclerosis(excess OB + little marrow space)
Cutting cone implies
turnover in cortical bone.
OC are multinucleate cells that resorb bone.
Cells have a characteristic
Ruffled bone
In OC action, is there a large area for exchange of ions and movement.
WHat is the purpose of H+ secretion by OC ?
Acidify and provide correct pH for lysosomal enz. like cathepsin K + digestion of bone.
What happens to HCO3- during OC action?
Excreted out of cell.
Do you have carbonic anhydrase 2 activity?
OC movement is not essential for bone resorption.
Osteopetrosis leads to
-increased fracture(bone more brittle despite increased density)
-anaemia(little bone marrow)
What could be one cause of osteopetrosis?
c-src deficiency
-carbonic anhydrase 2 deficiency is also another cause
What happens to OC in osteopetrosis?
-OC not motile
-integrin-mediated attachment doesnt release ,OC stay attached to bone surface and resorption doesnt proceed normally.
What happens during rheumatoid arthritis?
Joint destruction due to OC action at inappropriate sites.
Breast cancer metastases to bone cause osteolytic lesions.
OC are overactive in Pagets disease.
What happens to some discrete sites in Pagets disease?
Excess rapid modelling(similar to fracture callus)
In Pagets disease, some areas have too much bone and others have too little.
What does tx. of Pagets involve?
Osteoclast inhibitors-bisphosphonates.
What are OB ?
bone forming/mononuclear cells with high capacity for protein production.
Osteoid matrix is newly formed bone not yet mineralized.
What are osteocytes?
Terminally differentiated OB buried within bone.
Osteocytes constitute
95 % of cells in adult skeleton.
How do osteocytes communicate with each other and with OB?
Via long intercellular processes and gap junctions.
WHat is the role of mechanosensors?
Transduce pressure to activate bone remodelling in response to microfractures.
What are the 2 main extracellular components of bone?
1. Osteoid(organic matrix)-from OB
2. Mineral salts(hydroxyapatite analogue)
Osteoid is made of
85-90 % type 1 collagen.(also binds and orients other proteins)
How much NCPs in osteoid?
10-15 %(albumin,proteoglycans)
Osteoid provides
elasticity and structural organization.
What might NCPs do?
regulate mineral deposition.
What are the mineral salts composed of ?
85 % calcium phosphate
10 % calcium carbonate
1.5 % magnesium phosphate
What is the function of mineral salts?
Confers compressive strength.
Osteoid makes up 30 % of extracellular matrix.
Inorganic matrix(minerals) makes up 65 % of bone.
WHat type of bone is woven bone?
-disorganized collagen arrangement.
-rapidly laid down.
-low Ca2+ content.
Woven bone is replaced by
Lamellar bone.
What is lamellar bone?
-Collagen fibres organized in directions of mechanical strains.
-higher calcium density
-improved mechanical strength.
Collagen fibre content affects
WHat happens in Osteogenesis imperfecta?
Impaired bone formation due to heterogenous collagen 1 mutations----> compromised structural integrity of bone matrix and reduced bone mass.
O. imperfecta leads to
Increased fracture risk and bone deformities.
What are the 2 major processes of bone formation?
1. Secretion of osteoid by OB.
2. Osteoid mineralisation.
What controls rate of osteoid mineralisation?
OB-derived factors
Mineralisation rate =
Osteoid deposition rate
Osteoid matrix accumulates calcium and phosphate.
What are the initial sites of accumulation of mineralites?
Holes between collagen fibres
What happens to the minerals as bone matures?
Crystals grow in the direction and shape dictated by collagen fibres and NCPs.
Mineral content and size of crystals can be altered by diet or therapy.(strontium,fluoride)
What is rickets?
Dysregulated bone formation due to Vit D/Ca/Phosphorus deficiency----> mineralisation rate NOT equal osteoid deposition rate---> increase fracture risk/bone deformities.
While balanced,bone cell activity not always equal througout life.
True(eg. in old age, more resorption than formation)
How do OB know how much bone needs to be formed?
Signals such as IGFs from OC communicate with OB.
Name 2 causes of Osteoporosis in women.
Age and hormones.
Name some anti-resorptive therapies to Osteoporosis.
Calcitonin,Bisphosphonates,Src inhibitors,Androgens----> can prevent further bone loss but not increase BMD.
PTH treatment increases OB activity in osteoporotic patients.
Bone remodelling is
process of bone renewal.
Bone modelling is
Growth and reshaping of bones.
What are the 2 methods of osteogenesis involving replacement of pre-existing CT with bone?
1. Endochondral ossification-formation of bone within a cartilage model
2. Intramembranous- formation of bone directly on or within fibrous CT membranes.
What happens during intramembranous ossif. and where does it occur?
Growth in width in long bones.
-flat bones of skull
-facial bones
In endochondral ossification,primary ossification centre is in the diaphysis and secondary centre is found in the epiphysis.
From what does trabecular bone arises from?
From growth plate
NAme the diff. parts of the growth plate.
-Resting zone
-Proliferative zone
-Hypertrophic zone
-Zone of calcification
What determines bone length?
Chondrocytes proliferation
What is Laron syndrome?
Growth hormone receptor mutation.(GH deficiency)----> premature slowing of chondrocyte proliferation(early growth plate closure)
What are the 3 main stages of fracture repair?
1. Inflam.-recruitment of mesenchymal cells.
2. Reparation-mesenchyme becomes cartilage & endochon. ossif. begins
3.Bone remodelling with bony callus refined to appropriate shape in response to mechanical forces.
What does rigid fixation do?
Eliminates the cartilage phase(more rapid healing by intramembranous ossif.)
Bone formation requires balanced osteoid formation and matrix calcification.