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23 Cards in this Set

  • Front
  • Back
what is the structure of type I collagen?
- triple-helical supercoil made up of 2 α1 chains and 1 α2 chain
- gly-pro-hypro
what is released when type I collagen is degraded
- hydroxyproline
- indicator of bone resporption
what links collagen in bone and cartilage?
- intramolecular and intermolecular (most critical) cross-links
- hydroxylysine w/ cartilage
- lysine and hydroxylysine w/ bone
what do serum derived proteins do?
- they are part of non-collagenous proteins of the bone
- acidic and bind to the mineral of bone
- this can provide local []'s of serum-derived GF's like PDGF and IGF-1
what are the 3 groups of non-collagenous proteins that are NOT serum derived, and where do they come from?
- cell attachment and Ca binding proteins (Gla proteins)
- growth and diff proteins (TGF-B like BMPs, IGF-1)
- AP, which initiated mineralization
- they are secreted by blasts
what are the proteoglycans of bone?
- both are GAGs
- chondratin sulfate - does early bone formation w/ blast pericellular environment
- heparin sulfate - helps blast interactions
lipids in bone
- TGs, FFAs, CHL, PL's
- may be involved in ossificication
- b/c they can ind Ca
where does Ca from bone come from?
- less than 1% from bone is available
- from lining of H canals and resorption cavities
- vitamin C deficiency
- prevents normal OH of proline and lysine, so decreased quantity and quality of collagen
- New bone formation is prevented and older bone becomes brittle
- Skin collagen affected too
what is the mineralization lag time
5-10 days after osteoid is laid down
Ehlers-Danlos syndrome
- inherited collagen disorder, seven different types
- hyperextensible joints, hyperelastic skin
- poor wound healing and easy bruising
- due to delicate collagen fibers in multiple locations
what is nuclation in bone?
- when the seed of hydroyapitate is deposited
- initiated by blast-derived matrix vessels from the
whats the deal w/ osteocytes?
- they can make collagen, control mineralization, and respob bone
- they do too much resprotion in many diseases like hyperPT, pagets, or disuse osteoporosis
- they are the 1o site for Ca exchange
- matrix metalloproteinases
- secreted by clast in resorption
- dissolve the various parts of bone (substrate specific)
all about a BMU
- takes 4 months
- the unit that forms in bone remodeling
what controls clast stem cells
- from hematopoetic cells of BM (CFU-GM)
- IL-1 and 6
- TGF a and b
what controls blast stem cells
from local CT mesenchyme or BM
used to monitor bone resorption
- osteocalin
- hydroxyproline (urine)
- pyridinoline (urine) - more specific
- deoxypyridinolin (urine) - most specific
what amount of Ca is transferred per day?
- in most places, 200-500 mg
- BUT from serum to bone, 6g
parathyroid hormone
- released when Ca is low
- for fine tuning
- causes release of Ca from bone
- for long term control
- stimulated intestinal Ca absorption
- buffering system for Ca
- can act act to lower Ca, but not when is superhigh
- controls for postprandial high Ca to keep PTH secreting
order of Ca removal from body
- leaky dike
- then bone surfaces in contact w/ bone fluid
- then, when PTH really high, activation of clasts that just take it randomly