Bone 4 Flashcards
1st step in bone repair
1) Blood vessels at the fracture site will break
Hematoma (mass of clotted blood) forms @ grace and tissue swells, inflammation, bone cells are dying
2nd step in bone repair
Hematoma is removed by macrophages. Replaced by soft callus. Periosteum re-grows if necessary.
Fibroblasts and osteoblasts migrate in through growing capillaries
-Soft callus, rich in collagen and fibroblasts. Made of both hyaline cartilage and fibrocartilage. Amount of type I collagen increases over time
-Hyaline cartilage and fibrocartilage will link the broken ends of the bone
3rd step in bone repair
Soft callus is invaded by blood vessels and osteoblasts. Soft tissue is replaced by spongy bone, forming a hard callus
- First bone to be formed is woven bone (spongy). Irregular trabecular unite the broken ends of bone
- Endochondral ossification (at location of callus) and intramembranous ossification (at the periphery)
Soft callus=?
Hard callus =?
soft- cartilage
hard- bone
4th step in bone repair
Bone of hard callus is remodeled
- Compact or spongy bone as appropriate
- Full vasculature is re-established
- excess material is removed
Decreased mineralization
- Calcium or vitamin D deficiency (rickets, osteomalacia)
- Bone resorption exceeds bone formation due to increased osteoclast activity or decreased osteoblast activity (osteoporosis)
Increased mineralization
Bone formation exceed bone resorption; decreased osteoclast activity or increased osteoblast activity (osteopetrosis)
Problems with organic matrix
impaired collagen formation (scary, osteogenesis imperfecta)
Rickets
Softening and weakening of bones in children usually due to vitamin D difficiency (absorption of calcium)
- Calcium or phosphate or both is sufficient in concentration of properly mineralized bone
- Vitamin D deficiency -> intestinal mucosa can’t absorb calcium
- Poorly calcified bone matrix, distortion at epiphyseal plates
- Bones can become deformed because they can’t bear body weight
Osteomalacia
Similar to rickets but in adults
Lack of available calcium or phosphorous (or both) for mineralization of newly formed osteoid
-Decrease in the amount of calcium per unit of bone matrix
Scurvy
vitamin D deficiency which is needed for proper type 1 collagen matrix
- Prevents hydroxylation of proline and lysin -> collagen contains only non-hydroxylated proline and lysine –> collagen fibrils lack hydrogen bonding and lose mechanical stability
- Leads to failure of collagen synthesis and osteoid formation
Osteoporosis
Uncoupling of resorption and deposition
Bone is histologically normal but there is too little of it
Most common metabolic bone disorder, especially common in post menopausal women
Estrogen prolongs osteoblast lifespain and suppresses M-CSF and RANKL (also inhibits osteoclast activity)
-Diminished estrogen -» osteoclast activity greater than osteoblast activity –> decreased bone density
Osteogenesis imperfects
aka brittle bone disease
Genetic disorder
Usually autosomal dominant
caused by mutations in the genes that code for type I procollagen
Osteopetrosis
aka marble bone disease
Genetic disorder; several forms
Mutation in genes that regulate osteoclast function
results: increased bone density and thickening
- Bone may be brittle and fracture easily
Paget’s disease (osteitis deformans)
Increase in osteoclastic activity followed by a compulsory increase in osteoblastic activity.
Increased bone density in some locations, decreased bone density in others
