Drugs And Tooth Movement

Prepared by
Dr. Sajid Al-badri
M.Sc.(Ortho.); Certified Trainer (MOH).
Lecture Outlines:
• Pressure - Tension Theory.
• Physiological Response To Sustained Pressure
Against A Tooth.
• Approaches Of Tooth Movement Acceleration.
• Promoter Drugs.
• Suppressor Drugs.
Tooth Anatomy
Pressure – Tension Theory
Classic theory of tooth movement depends upon chemical rather than electrical signals as stimulus for cell
differentiation and tooth movement.
In essence, there are three stages in tooth movement:
• Alterations in blood flow associated with pressure in the PDL.
• Formation and release of chemical messengers.
• Activation of cells.
Pressure Side

vessel
s

Bone
Tension Side
Pressure
Tension
Theory
 Physiological Response To Sustained Pressure Against A Tooth
Light force
 Less than 1 sec.: PDL incompressible, alveolar bone bends, piezoelectric signals generated.
 1-2 sec.: PDL fluid (clavicular fluid) expressed, tooth will move within PDL space.
 3-5 sec.: blood vessels within PDL partially compressed on pressure side and dilated on tension side; PDL
fibers and cells mechanically distorted.
 Minutes: blood flow and O2 ↓↓↓ in pressure side and ↑↑↑ in tension side while CO2 vice versa; and chemical
messengers ( prostaglandins and cytokines) released.
 Hours: chemical messengers will stimulate the activity of osteoblasts on tension side and osteoclasts on
pressure side and enzyme levels change.
 Within 4 hours: cyclic adenosine monophosphates (cAMP) levels ↑↑↑ leading to ↑↑ cells function and
differentiation.
 Within 2 days: tooth movement will begin as osteoblasts and osteoclasts remodel bony socket.
 Heavy Force

• 3-5sec.: blood vessels within PDL occluded on pressure side.

• Minutes: blood flow cut off to compressed PDL area.
• Hours: cells death in compressed area.
• 3-5 days: cell differentiation in compressed side;
undermining resorption begins.
• 7-14 days: undermining resorption remove lamina dura
adjacent to compressed PDL, tooth movement occurs.
 Force

Blood flow alteration + cell distortion

Phospholipids mobilization in cell

membrane

Formation of arachidonic acid

Prostaglandin E And Other Chemical Inflammatory

Mediators Formation

Stimulation Of Osteoblasts And Osteoclasts

Bone Remodeling
Tooth movement
Approaches of Tooth
Movement Acceleration
Micro-Perforation of Cortical Bone
Distraction Osteogenesis
Cortictomy
Low Intensity Laser
Hyperbaric Oxygen
Therapeutic Ultrasonic Device
Vibration Device
Phototherapy Device/ A Prototype Biolux Device

Intraoral
Extraoral
Nicot
Psychological Stress Reduction
Menstrual Cycle
Static Magnetic Fields
Note
Drugs that promote or suppress tooth movement are unlikely to
be encountered, although efforts to produce them continue.
Major problem is how to applied them to local area to stop or
facilitate tooth movement, because administration of them
systemically associated with many side effects in vivo.
 Promoter Drugs
 Prostaglandin: if injected locally to PDL will be very painful as bee sting.
 Vitamin D: regulate both bone formation and resorption.
 Leukotrienes: also comes from arachidonic acid conversion, but this mediator associated
with contraction bronchi increase it secretion leads to Asthma ( singular anti-
leukotriene drug).
 Local administration of vascular endothelial growth factor (A,B,C,D,F) if give locally in
rats increase osteoclasts activity .
 Osteocalcin: non- collagen protein facilitate tooth movement by acting as molecule
induces chemo- attraction to recruit osteoclasts at sites of greater pressure and act
as a key factor helping bio-mineralization locations at tension side.
 Oral administration of evening primrose oil: increase number of osteoclasts in rats.
Suppressor Drugs
NSAIDS: inhibit conversion of arachidonic acids to prostaglandin so regarded as prostaglandin inhibitors.
e.g. Indomethacin used in treatment of arthritis, Acetaminophen( paracetol) members of NASIDS family.
Alternatives: aspirin, ibuprofen just in case.

Corticosteroids: inhibit formation of arachidonic acid.

e.g. hydrocortisone, predinsolone, cortisone.

Bisphosphonates: used in treatment of osteoporosis by preventing bone loss by stopping action of

osteoclasts.
e.g. alendronate (Fosamax), risedronate (Actonel).
Alternative: Evista prevent bone loss, but has little effect on tooth movement.
Tricyclic anti- depressants: doxaepin, amitriptyline, imipramine.
Anti-arrhythemic agents: procaine.
Anti- malarial drugs: quinine, quinidine, chloroquine and methylxanthine.
Anti- convulsant drug: phenytoin.
Doxycycline: doxydar.

 Thyroid hormones: given in hypothyroidism which impaired bone formation decrease osteoclast activity.
 Relaxin: pregnancy hormone facilitate delivery, reduce collagen synthesis so effect on PDL health
casing teeth mobility.
 Sex hormones: estrogens increase osteoblasts activity in female while testosterone in male.
 Parathyroid hormones: increase osteoblasts activity and decrease osteoclasts activity
 Morphine.
 Immune suppressant drugs (cyclosporine A): as in renal failure and kidney transplantation.
 Systemic fluoride administration.
 Strontium: substitute the calcium in bone
 Anti-cancer drugs: chemotherapeutic drugs damage precursors cells involved in bone remodeling.