alveolar bone and cementum Flashcards

1
Q

what is intra-membranous ossification?

A

E.g. body of mandible & maxilla

Main mechanism of bone formation here

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2
Q

what occurs during intra-membranous ossification?

A

Bone formation directly within the mesenchyme

  • Mesenchymal stem cells differentiation into osteoblasts.
  • ECM synthesis / secretion (osteoid).
    • From osteoblasts
  • Matrix-mediated mineralisation.
    • Remodelling
  • Remodelling / turnover
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3
Q

what is endochondral ossification?

A

E.g. mandibular condyle & symphysis, long bone

Alternative mechanism

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4
Q

how is hyaline cartilage formed?

A

Chondrocytes undergo proliferation & hypertrophy.

& Enlarge

Cartilage ECM forms trabeculae & mineralises.

Chondrocytes die.

Bone marrow cells & blood vessels enter tissue

Lining osteoblasts form lamellae & ECM = bone.

Which become mineralised to form bone

Mineralised cartilage degraded.

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5
Q

Which types of bone are lamellar bone?

where are these bones found?

A
  • found in post-natal tissues
  • cortical / compact bone
  • trabecular / cancellous / spongey bone
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6
Q

properties of cortical / compact bone

A
  • Strongest in alveolar process
    • Protection from external environment and trauma
  • High density / low porosity (5-30%).
  • High mineral content
  • Osteons!
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7
Q

what are osteons?

A

Haversian canal system with concentric lamellae.

  • Rings of type 1 collagen
  • Blood & nerve supply to the bone

Cylindrical structures, consisting of concentric layers (lamellae), surrounding central Haversian canal.

  • Osteons connected to each other & the periosteum by Volkmann’s canals.
  • Some osteoblasts develop into osteocytes embedded in spaces (lacunae).
    • Osteocytes make contact with the cytoplasmic processes of their counterparts, via network of small canals (canaliculi).
    • Mature osteoblasts embedded
    • Exchange nutrients / metabolic waste in different regions of bones
    • Bone formation, Ca2+ homeostasis.
  • Between adjoining osteons occupied by interstitial lamellae.
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8
Q

properties of cancellous bone?

other names for this bone?

A

tracbeular / cancellous / spongey bone

  • Forms majority of the alveolar process
    • Flexibility
  • Low density / high porosity (30-90%).
    • Vast bone marrow space
  • Softer, weaker, more flexible.
    • Reduced mineral content
    • Flexible - allows withstand mechanical forces put on the teeth
  • Trabeculae surrounded by bone marrow spaces.
  • Blood & nerve supply.
  • Collagen fibres run in parallel to bone marrow spaces .
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9
Q

properties of woven bone

A
  • Not present in alveolar process
    • Formed during bone development
    • Only found in post-natal tissues during fracture repair
  • Immature bone.
    • Not well mineralised
    • No mechanical strength
  • Fewer collagen fibres, arranged in haphazard manner.
  • Low density / mechanical strength.
  • Produced when osteoblasts produce osteoid rapidly.
    • e.g. foetal bone, adult bone fractures.
  • Evident as fibrous matrix.
  • Later replaced by lamellar (cortical or cancellous) bone in foetal tissues.
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10
Q

which types of bone make up alveolar bone

A
  • cortical bone (lamellar)
  • cancellous bone (lamellar)
  • bundle bone (lamina dura)
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11
Q

properties of bundle bone

A
  • Lining the tooth socket
  • Immature bone (similar to woven bone).
  • Inner alveolar plate / lamina dura.
  • Rapid deposition with random collagen fibre orientation.
  • Apparent at Sharpey’s fibres from the PDL, through the alveolar bone proper.
  • High remodelling capacity.
  • Formed the quickest
    • Least mineralised - not well organised collagen fibres
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12
Q

how are osteoblasts formed

A
  • Migration / proliferation of bone marrow-derived, MSCs (Osteoinduction)
    • Migration to target - then proliferate
    • Enhanced by TGF-bs, BMPs, PDGF, VEGF.
  • MSC differentiation into mature osteoblasts (Osteoconduction).
    • Induced by BMPs, TGF-b, VEGF.
    • Inhibited by PDGF & bFGF.
  • Osteoblast is formed
    • Not until osteo progenitor cells express transcription factor called RUNX2
    • (RUNX2 is required for osteoblast to be fully formed)
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13
Q

how is mineral deposited in alveolar bone

A
  • framework of type I collagen
  • mineral crystal initiation within the gap zone between collagen fibrils
  • Collagen sulphate substitute decorin
    • involved in formation of collagen fibres
    • As core protein interacts with the collagen fibres
      • Regulates the process
  • GAG chains - chondroityn sulphate chains
    • Extrude out and help attract calcium and phosphate to the regions for mineralisation to occur
    • Get incorporated into hydroxyapatite crystals
  • Bone glycoproteins - roles in mineralisation
    • Regulate hydroxyapatite crystal growth
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14
Q

what are the properties of bone glycoproteins

how do they contribute to mineralisation?

A

Glycoproteins of mineralised tissues often very acidic in nature.

  • High negative charge - allows them to bind to hydroxyapatite
  • High acidic amino acid content - aspartate, glutamate, γ-carboxyglutamate.

Some glycoproteins carry sulphate groups.

Some glycoproteins are phosphorylated.

Correct arrangement of ionised groups in glycoproteins act as nucleators for HAP crystal growth

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15
Q

what is mineralised bone composed of?

A

Mineral content = 70%.

Hydroxyapatite - Ca10(PO4)6OH2.

Impurities = Mg2+, F-, CO32-.

Collagen = 90% of organic matrix.

  • Mainly type I collagen,
  • Also type III collagen.

Non-collagenous matrix = 30%.

Chondroitin sulphate-substituted, decorin & biglycan.

Bone sialoprotein, osteonectin, osteopontin, osteocalcin.

Mineral deposition, crystal size & morphology.

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16
Q

how do osteoblasts regulate the formation of osteoclasts?

A
  • Osteoblasts express surface Receptor Activator of NF-kB Ligand (RANKL)
  • RANKL binds to RANK receptor on osteoclast precursor surfaces
    • = osteoclast differentiation and bone resorption
  • osteoblasts produce OPG - osteoprotergerin
    • prevents RANKL-RANK interaction by binding to RANK
    • = reduced osteoclast numbers and reduced bone resorption
    • therefore more net bone formation
17
Q

how do osteoclasts cause resorption?

A
  • Migration to resorption site & attachment to underlying bone.
  • Formation of sealing zone & ruffled border.
    • Seal off surrounding environment
    • Ruffled border - where resorption takes place
  • Hydroxyapatite dissolution.
    • HCL release through pumps in cell membrane
      • Low pH 4
    • HCL accumulated in the osteoclasts
      • Cells accumulate high levels of chloride ions within the cell
      • Enzyme -carbonic anhydrase 2- catalyses reaction - formation of carbonic acid
      • Dissociation into H+ & HCO3-
      • H+ & Cl- released and form HCl to dissolve mineral within the resorption pits
  • ECM degradation by cysteine proteinases and MMPs & removal from resorption pit.
  • Apoptosis or return to non-resorbing state.
18
Q

composition of mineralised cementum in comparison to alevolar bone

A
  • Mineral content = 50%.
    • Less than bone
  • Hydroxyapatite - Ca10(PO4)6OH2.
    • Impurities = Mg2+, F-, CO32-.
  • Collagen = 90% of organic matrix.
    • Same as bone
    • Type I collagen, type III collagen = Sharpey’s fibres.
    • No collagen in acellular, afibrillar cementum near dentino-enamel junction.
  • Non-collagenous matrix = 30%.
    • Same as bone
  • Chondroitin sulphate-substituted, decorin & biglycan.
    • Bone sialoprotein, osteonectin, osteopontin, osteocalcin, tenascin, fibronectin.
      • Bone has similar matrix components
19
Q

cementum matrix compared to bone

A

Different fibre formation within cellular / acellular intrinsic / extrinsic fibre cementum.

Lower mineral content.

Slower deposition rate.

Resistance to resorption.

Lacks vascularity.

Lacks innervation.