This tells us about pain pathway and it's management.

1. Pain In Orthodontics
Guided By – Dr Priyanka Niranjane Presented By – Dr. Nikita Soni

2. Learning Objectives
• In the end of today’s seminar the learner should be able to –
Describe the causes of orthodontic pain.
Describe the mechanism of orthodontic pain.
To manage the orthodontic pain.

3. Contents
• Introduction
• Types of pain
• Characteristics of orthodontic pain
• Causes of orthodontic pain
• Mechanisms of orthodontic pain
Vascular Events
Cellular Events
Chemical Events
• Management of orthodontic pain
• Conclusion
• References

4. Introduction
• Pain is defined as –
“An unpleasant emotional experience usually stimulates by noxious stimuli and
transmitted over a specialized neural network to CNS where it is interpreted as
such”.
- Monheim.
• With no exception, orthodontic pain is perceived as discomfort, dull pain and
hypersensitivity in affected teeth.

5. • Pain includes sensations evoked by noxious stimuli due to inflammatory
responses.
• On the contrary it is also an essential stimulus to prevent the further damage of
the tissues in play.

6. Types of Pain
• It is classified depending upon the duration of action into two –
• Fast Pain – Felt within about 0.1 second. Which occurs due to Aδ fibers with the
speed of 6 – 30 m/sec.
• Slow Pain – It Begins after 1 second or more and is transmitted by type C fibers
with the speed of 0.5 - 2 m/sec.

8. Pathway of
Pain:

9. Mechanism of Pain:
Transduction
Noxious stimuli lead to electrical activity in the sensory nerve endings.
Transmission
Neural events that carry the nociceptive input into the CNS for proper
processing.
Modulation
Ability of the CNS to control the pain transmitting neurons.
Perception
Nociceptive input reaches the cortex, perception occurs, which immediately
initiates a complex interaction of neurons between the higher centers of the brain.

11. Orthodontic Pain transmission Pathways
• Orthodontic force once applied, received by
periodontal sensory endings as nociceptive
stimuli.
• These nociceptive stimuli transmitted ultimately
to somatosensory cortex via three-order
neurons.

12. • The first order neurons are trigeminal
neurons that are located at trigeminal
ganglia with having two processes – central
and peripheral.
• Peripheral processes run peripherally to
facial skin, periodontal tissue and oral
mucosa and forms sensory endings to receive
nociceptive, mechanical and thermal
sensations.

13. • Central process of trigeminal neuron projects to synapse
with second-order neurons, the trigeminal nucleus
caudalis located in medulla oblongata.
• The trigeminal nucleus caudalis send fibers to form
trigeminothalamic tract and ascends to make synapse
with postero-ventricular nucleus of the thalamus.
• Thalamus in turn sends fibres to various areas of brain
including hippocampus and somatosensory cortex.

14. Characteristics of Orthodontic Pain
• Orthodontic pain with a prevalence of 72% - 100% is
perceived as soreness, pressure and tension in the
affected teeth.
• Orthodontic force activated the sensory receptors in
the periodontal tissues and results in a cascade of
nociceptive pain processing and transduction.

15. The perception of orthodontic pain is due to
changes in blood flow caused by the
appliances
Force application causes compression of
periodontal ligament, ischemia, inflammation
and edema.

16. Upon vascular compression and local ischaemia
which leads to hypoxia(diminished oxygen
tension). .
Periodontal cells, mainly fibroblasts, undergo
anaerobic respiration and cause local acidosis.
Secrete local biologic mediators including,
Substance P, IL1B, TNFa, PGE2, Histamine,
Enkephalin, Dopamine, Serotonin, Glycine,
cytokines etc.
The proton ion (H+) binds to ASIC3 receptors on
sensory endings to generate pain.

17. Causes of Orthodontic Pain
• Causes for orthodontic pain are –
Arch-wire placement and activations
Separator placement
Debonding procedures
Application of orthopaedic forces, etc.
• It is also clear that fixed appliances produce more pain than removable or
functional appliances. Stewart et al. (1997)

18. • Orthodontic separation and pain – Results in painful
experience for almost all patients.
• The discomfort associated with separator placement usually
starts within 4 hours of insertion.
• Increases over the next 24 hours which peaks at day 2 and
• Decreases to pre-placement level within 7 days.

19. • Arch-wire placement and activation – Jones (1984)
reported that pain is experienced by majority of patients is at 4
hours after arch-wire placement, will peaks 24 hours and then
gradually declines from 5th – 6th day.

20. • Debonding – Williams and Bishara (1992) found
intrusive forces to produce less pain during debonding in
comparison with forces applied in a mesial, distal, facial,
lingual or extrusive direction.
• They also suggested applying finger pressure or asking
patient to bite on a piece of cotton roll to minimize pain
while debonding.
• Use of an occlusal rim wax for pain-free debonding.

21. • Orthopaedic forces and sutural strain – Patients
often experience discomfort after 24 hours of headgear
with sharp decline in pain after 3 days.

22. Mechanisms of Orthodontic Pain
• A cascade of self-limiting inflammatory reaction which includes - cellular,
vascular, neural and immunological events, acts in a way to cause pain.
• The products of local inflammation like, prostaglandin and bradykinin act on
sensory nerve endings to incite painful sensations.
• Orthodontic forces leads to periodontal inflammatory response.

23. • This periodontal inflammatory response includes three
components: Vascular, Cellular and Chemical events -
• Vascular Events – Optimal orthodontic force that is 20-25 g/cm2
when applied leads to change in tissue pressure that is
approximated with capillary blood pressure.

25. • Cellular Events – after local inflammation,
increased vascular permeability leads to
recruitment of neutrophils, mast cells,
macrophages, T-cells and monocytes.
• Periodontal mast cells and macrophages
releases mediators like histamine and tumor
necrosis factor-alpha (TNF-α) which facilities
leucocyte adhesion and transmigration.

26. • Chemical Events – Inflammatory cells release abundant inflammatory
mediators, chemokines and cytokines within periodontal tissues.
• It includes – IL-1, IL-6, prostaglandin, TNF-α, interferon-gamma, macrophage-
colony-stimulating-factor (M-CSF) and VEGF.
• These mediators act in concert to incite and amplify local inflammation.

27. • M-CSF stimulates the conversion of monocytes to macrophages and also the
recruitment and differentiation of osteoclasts.
• This enhances local inflammation and pain sensations.

28. Management of Orthodontic Pain
• Prostaglandin is a pro-inflammatory
mediator that causes painful
sensations by binding with sensory
endings and promote tooth
movement by stimulating bone
remodeling.
MOA Of
NSAIDS
MOA Of
Steroids

29. • Pharmacological approach – by the means of NSAIDS, which blocks the
prostaglandin synthesis by inhibiting the activity of cyclooxygenase enzyme.So
the pain is relieved.
• On the other hand, it also reduces local inflammation and inhibits osteoclasts,
reducing tooth movement.
• NSAIDS also impede tooth movement by interfering with collagenase activity and
procollagen synthesis, which results in impeded periodontal remodeling.

32. • Simmons and Brandt (1992) were the first to
recommend use of “acetaminophen” for
managing orthodontic pain.
• Another drug which is selective COX-2 inhibitor
and has no effect on PGE1 levels is “rofecoxib”.
Can be used safely for pain control during
orthodontic mechanotherapy.

33. • Mechanical approach – it has been proposed to relieve orthodontic pain.
• It activate mechanoreceptors that transmit tactile signals while suppressing the
transmission of painful signals.
• As orthodontic forces squeeze periodontal vascular vessels and cause local
ischemia, vibrations restore the normal circulation and thus reduces pain.
• Chewing gum during 1st few hours of appliance activation in order to reduce pain
has been suggested. (Proffit, 2000)

34. • Roth and Trash (1986) evaluated the effect of TENS
(Transcutaneous electrical nerve stimulation) in
reducing periodontal pain after separator placement
within 6 seconds of electrode placement.
• Low-level laser therapy – by applying laser
irradiation to the whole dental arch.
• It acts by increasing the blood flow which flushes
noxious stimuli by heat generation at tissue level.

35. • Behavioral approach – to relieve orthodontic
pain include Cognitive Behavioral Therapy, physical
activity and music therapy.
• It reduces pain by reducing anxiety and by
production of endogenous opioids.

36. Difference between Orthodontic pain and Other pain
Orthodontic Pain Other Pain
Type Pain which happens due to
sterile inflammation.
Pain that elicits due to
inflammation caused by
bacterial invasion.
Duration Acute in nature, then
gradually subsides within 4-5
days.
Mostly chronic in nature
Patient Perception Pain which builds anxiety.
Pressure and tension type.
Dull excruciating type of pain
or gnawing type.
Management Can be managed by
prescribing acetaminophen,
or selective COX-2 inhibitors.
Can be managed by
prescribing antibiotics with
NSAIDS (COX-1 or COX-2).

37. Conclusion -
• Orthodontic pain, an inflammatory pain, shares many similar features with
common inflammation, but it has specific hallmarks.
• This inflammation is perceived as pain by the patient. Both the
phenomenon are interrelated to each other and nether can be eliminated.
• The changes in the mechano-therapy and drug therapy along with newer
advancements, the perception of pain by the patient is reduced and along
with effective orthodontic treatment, the results can be obtained.
• Hence, the painful experience is converted to pleasure.

38. References:
1. Al-Ani, Reem & Saleem, Alan & Faleh, Alaa & Nahidh, Mohammed.
(2020). Orthodontic Pain (Causes and Current Management) A
Review Article. International Medical Journal (1994). 25. 1071-1080.
2. Guyton and Hall textbook of Medical Physiology- 12th edition.
3. Wall P. Melzach r. Textbook of pain. Third edition. 1984

39. Thank You