Tissue Reactions to Orthodontics Flashcards
Tooth movement
osteoblast is pivotal cell
excessive ortho forces can cause inefficient tooth movement and adverse tissue reactions
Bioelectric Theory
tooth movement changes in bone metabolism controlled by electrical signals that are produced when the alveolar bone and collagen flex and bend
stress-generated electric signals do not fully explain tooth movement, electric and electromagnetic influences can modify the bone remodelling on which tooth movement depends
Piezoelectric potentials
phenomenon observed in many crystal structures in which the deformation of the crystal structure (due to applied force) produces a flow of electric current, as electrons are displaced from one part of the crystal to another
Bioelectric potentials
observed in bone that is not being stressed
metabolically active bone or connective tissue cells in areas of active growth or remodelling produce electronegative charges that are generally proportional to how active they are.
Pressure-Tension theory
Tooth movement to changes in bone metabolism controlled by chemical rather than electric signals:
- Alteration in blood flow associated with pressure within the PDL
- Formation and/or release of chemical messengers
- Activation of cells
Impact of blood compression
alteration in blood flow quickly create changes in the chemical environment. These chemical changes, acting either directly or by stimulating the release of other biologically active agents, then stimulate cellular differentiation and activity.
Changes in the PDL following orthodontic loading?
Compression side
- compression of bv
- attraction of osteoclasts
- resorption of bone (Howship’s lacunae)
- production of fibrous tissue in Howship’s lacunae
Tension side
- stretching of PDL fibres
- stimulation of osteoblasts
- deposition of bone
Osteoblasts
derived from mesenchymal/stromal cells (CT cells found in bone marrow)
- construct ECM of bone
- demonstrate inc levels of intracellular messenger Camp when stimulated
- control osteoclast function
Osteoclasts
large multinucleated cells, of the monocyte-macrophage lineage
- adhere to the bone surface and secrete acid/hydrolytic enzymes into it
- found in well-defined pits known as ‘howship’s lacunae’
What is bone remodelling controlled by?
Systemic hormones - parathyroid
local factors - prostaglandins
How do osteoblasts control osteoclasts?
RANK Ligand and OPG
Factors (e.g., PTH) induce the expression of RANK ligand on osteoblasts
RANK ligand in combination with other factors (M-CSF and VEGF) induce the differentiation of osteoclasts from their precursors
Osteoblasts secrete OPG which opposes the effects of RANK ligand
RANK ligand is a member of the TNF superfamily and is expressed on the cell surface of osteoblasts. It binds to a receptor (RANK) on the osteoclast.
Opposing its actions is OPG, a soluble member of the TNF superfamily that is secreted by osteoblasts.
Osteoclastogenic molecules stimulate expression of RANK ligand and blunt production of OPG.