2, biology of ortho movement Flashcards
what are the injuries of tissues and their subsequent remodeling and repair?
- resorption/apposition of bone
- resorption of root surfaces
- hyalinization of the PDL
under heavy forces what occurs in and around the tooth?
- PDL compression on the pressure side with bone bending and transduction of a signal to cells: 1-2 seconds
- the fluid is expressed from the PDL space and the tooth moves within the PDL
- the blood vessels are occluded: 3-5 seconds
- blood flow is cut off: minutes
- cell death-hyalinization: hours
- cell differentiation from bone marrow spaces: 3-5 days
- undermining resorption and tooth movement: 7-14 days
how does the tooth move during the initial and secondary periods?
initially, the tooth will move a little bit, but then not really for a week or two. Then in the secondary period, there is pretty steady movement
lag phase
2-10 week, undermining resorption
progressive tooth movement
after lag phase, frontal resorption
Light forces
- blood vessels partially compressed and PDL fibers are distorted: 3-5 s
- blood flow is altered, oxygen tension is changing and release of PROSTAGLANDINS AND CYTOKINES: minutes
- metabolic changes: chemical messenger to alter cell activity, enzyme levels change: hours
- Increased cAMP levels, cellular differentiation starts: 4 h
- tooth movement occurs with osteoblasts/clasts coupling: 2 days
- frontal resorption
- NO SIGNIFICANT hyalinization zone observable
what is the hyalinized zone?
- it is a zone of “cellular necrosis” in the PDL that looses all organization or structure and looks like cartilage
- under a light microscope, the hyalinizaed zone looks like ground glass
- no tooth movement occurs until this zone has been remodeled
- hyalinization is also observed during physiologic tooth migration
which cells are the first ones to invade the hyalinized PDL?
“pioneer cellls”
- mononuclear cells with numerous processes and small inclusions
- blood vessels are commonly the primary invading structures
- the tissue that was away from the advancing edge of the hyalinization was typically invaded by larger mononuclear cells
- CONCLUSION: hyalinized tissue is replaced by cellular and vascular invasion from surrounding undamaged PDL
what are the vascular changes on the pressure side?
- at the ultrastructural level, 3 phases are seen (per rygh, 1972):
1. intact blood vessels walls are filled with erythrocytes (30 minutes)
2. Partial disintegradation of the blood vessels, degradation of the erythrocytes and formation of cryst-like structures (2h-48h)
3. complete disintegration of blood vessels, amorphous necrotic cell remnants and degradation of crytal-like structures (1-7 days)
what hormones play a role?
the first messanger
PTH and calcitonin may play a role: both hormones are mediated by cyclic nucleotides and calcium
-prostaglandins(?), VIP, CGRP
what does physical distortion of the cellular membrane do?
-alters its polarity and increases permeability and activates membrane bound enzymes?
The second messanger
cAMP
- Davidovitch and shanfel have reported that an increase in levels of cAMP is associated to tooth movement
- increased levels of cGMP have also been reported
- Somjen (1980) reported that the increase in cAMP coincides with the stretching of cells and is prostaglandin dependent
what i messanger is associated with cell stretching?
prostaglandins
-PGE2 levels increase on both tension and compression sides
what would injections of PGE2 do to the tooth/bone?
yamasaki showed that local injections of PGE2 may increase the rate of bone resorption (?) PGE2 may influence bone growth
which cytokines increase bone resporption?
iL 1 alpha and 1 beta
what does TNF alpha do?
induces increased IL production by monocytes, enhances PGE and collagenase production
how many compartments does the PDL have during tooth movement?
4, from bone to cementum
-there is a net migration of cells from zone III to I (osteoblasts are observed at 21 h and bone formation starts as early as 42 h)
what does bone bending do to deposition?
bone bending creates negative fields in the concave aspect of the bone surface and this leads to bone deposition
what is the mechanism of action for bisphosphonates and its derivatives?
ex: fosamax (alendronate)
- inhibition of bone resorption via actions on osteoclasts and osteoclast precursor cells
- this decreases the rate of bone resorption
in postmenopausla women, what considerations for ortho?
- slower rate of tooth mevement bc bone is not as effectively resorbed and remodeled
- perio concern?
- retention phase is enhance bc of limited bone resorption
what type of bisphosphonates are the most likely to accumulate in the alveolar bone?
nitrogen-containing bisphosphonates (alendronate)
after third molars, which teeth are the most impacted?
maxillary canines
% of maxillary canines impacted and where
85% of max impactacted canines are palatal and 15% are labial(crowding)
-85% of palatally displaced canines have adequate space to erupt, etiology related to size of max lateral incisors
how can impacted canines be made to erupt spontaneously?
surgically uncover them
what are different biological and etiological factors for root resorption?
- individual susceptibility
- genetics
- chronological age
- gender
- systemic factors
- bone density
what are some of the systemic factors for root resorption?
- hypothyroidism, hypopituitarism, hyperpituitarism
- hyperparathyroidism, hypopara.. and pagets disease(?)
mechanical factors for root resorption
- appliances
- types of tooth movement
- orthodontic force
- treatment duration
which roots have a higher incidence of resorption?
single-rooted teeth
how does age affect root resorption?
-it doesn’t
what direction of forces will increase the occurrence of root resorption?
intrustion, A_P
Retention:
- “secondary tooth movement”
- PDL fibers will remodel for 15-232 days
- the upper third of the PDL will remodel for a longer period of time (up to 232)
- the apical third is more stable faster
- free gingival and marginal fibers as well as transseptal fibers are very critical during retention
