PAIN PATHWAYS

INTRODUCTION

 

Orofacial pain is the presenting symptom of a broad spectrum of diseases. As a symptom. It may be

due to diseases of orofacial structures, generalized musculoskeletal or rheumatic disease, psychological

abnormality or pain may be referred from other sources. OFP may also occur in the absence of detectable physical, imaging or laboratory abnormalities. The

possible causes of orofacial pain are considerable and cross the boundaries of many medical and dental disciplined. An inter-disciplinary approach is often

required to establish a diagnosis and for treatment

DEFINITIONDEFINITION

The most recent definition of pain, produced by task force on Toxonomy of the international association for the study of pain (IASP) is

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in term of such damage.

Incidence of PainIncidence of Pain :- :-

According to Cohen – it was found that 21.8% of adult in the United States experience orofacial pain symptoms within 6 months of study. The most common pain was toothache, which was estimated to have occurred in 12.3% of the population

Factors influencing behavior responses elicited by the painful

stimuli are:

Physical

Psychological

Social factors.

PAIN PATHWAYSPAIN PATHWAYS

Detection of Pain Pain sensation from the intraoral and extraoral structure of head and face is carried to CNS by primary afferent neurons through trigeminal ganglion to synapse with second order neuron, in the trigeminal brain stem complex. This complex also receive afferent axons from the facial (VII), glossopharyngeal (IX), vagus (X) and upper cervical (C2, C 3) nerve (this connection between the upper cervical nerves and trigeminal spinal tract nucleus may be a mechanism involved in facial pain and headaches).

Pain ReceptorsPain Receptors :- :-

Bare nerve ending serve as pain receptors whereas other

cutaneous receptors when stimulated excessively may

cause pain. From tooth, pain sensation is carried by A delta

fibres and C fibres.

A-Delta FibresA-Delta Fibres :- :-

These are myelinated, relatively large fibres, with fast conduction velocities. They

enter the root canal and divide into smaller branches, coursing coronally through the pulp. Once beneath the

odontoblastic layer, the A- delta fibers loose their myelin sheath and anastomose in to a network of nerves referred as the

plexus of Raschkow

This circumpulpal layer of nerves sends free nerve endings on to and through the

odontoblastic cell layers, extending up to 200um into the dentinal tubules, while also conducting the odontoblastic cell process.

Disturbances of pulp dentinal complex in a vital tooth initially affect the low thresholds A-

Delta fibers.

Nociceptive signals, transmitted through fast conducting fibers are perceived as a

quick, sharp, momentary pain.

The clinical symptoms of A delta fiber pain signify that the pulp dentinal complex is intact and

capable of responding to an external disturbance

A-Beta Nerve FiberA-Beta Nerve Fiber :- :-

They are among the fastest conducting fibers. They may function as

mechanoreceptors that trigger withdrawal reflexes so that potential damaging forces

may be avoided, but the role of A beta fiber is not clearly understood

C-Nerve FibersC-Nerve Fibers: -: -

Small, unmyelinated nerves that innervate the pulp. They are high threshold fibers, course

centrally in the pulp stroma. The pain associated with C-fiber is dull and poorly localized. C fiber have a high threshold and can be activated by

intense heating or cooling of the tooth crown or mechanical stimulation of the pulp. Once

activated, the pain initiated by C fibers can radiate to anywhere in the ipsilateral face and

jaw.

ProcessingProcessing :- :- Pain is perceived and recognized in the cortex, because of incoming nociceptive

input. The primary afferents neurons enters the brainstem at the level of the pons. The

cell bodies of the trigeminal nerve are located in the gasserian ganglion. Trigeminal brain stem sensory nuclear complex can be

separated in to trigeminal main sensory nucleus and trigeminal spinal tract nucleus, also Known. as nucleus of desending tract

The spinal tract nucleus is composed of three separate nuclei processing

from rostral to caudal direction, subnucleus oralis, interpolaris and caudalis. Caudalis is located in the medulla, at times extending to the level of C2 or C3 and is the principal brain recognizing site of nociceptive

information arising from the orofacial region.

Both incoming nociceptive signals to subnucleus caudalis and projecting signals on their way to thalamus can

be modified by descending nerve fibers from higher levels of CNS or by drugs.

Convergence of Neurons within Convergence of Neurons within Trigeminal Spinal TractTrigeminal Spinal Tract

Nerve fibers from different areas in the mouth may all synapse on

another neurons in the spinal cord, thus sending a signal to the brain.

Due to convergence factors, the brain may experience more difficulty in

localizing the pain.

Trigeminal Second Order NeuronsTrigeminal Second Order Neurons :-

These second order nociceptive neurons in Nucleus caudalis can be classified in to two main categories:

Nociceptive specific (NS) neurons

Wide dynamic range (WDR) neurons

NS neurons respond exclusively to noxious stimuli i.e heat and pinch. Their receptive fields are small and

may include skin and muscle.

WDR neurons are excited by both noxious stimuli and non-noxious

tactile stimuli over a wide range of intensities. Their field are large.

In addition nucleus caudalis also contain low threshold

mechanoreceptors (LTM) which are activated by light tactile stimuli. Axon from the spinal nucleus cross to the opposite side and ascend to nuclei of

thalamus

A delta fibers from pulp synapse in the lamina-I area of SC and C fiber

synapse in the lamina II and III areas. A-delta fiber pass to the thalamus directly, by way of the

neospinothalamic tract and is said to carry fast pain.

The 2nd order C-fiber neuron carries impulse by paleospinothalamic tract. This passes through the reticular formation,

where the impulse are influenced by many modulator interneurons before they reach

the thalamus, this type of pain is called slow pain

Third Order NeuronsThird Order Neurons :- :-

The next major synaptic connection in pain transmission is in the thalamus, where axon traveling in the trigeminothalamic tract synapse with third order neurons.

Thalamus act as primary relay station between the brainstem and different

parts of somatosensory cerebral cortex.

For all nerve pathway from thalamus to cerebral cortex, there are reciprocal connections from the cortex to the thalamus. In the thalamus, action

potential will be subjected to extensive processing through interactions among its

various nuclei and by inter connections with the limbic, hypothalamic and cortical

regions of the brain.

Pain ModulationPain Modulation :- :-

Definition

Human nervous system has an inherent ability to alter the intensity of

nociceptive signals and reduce the pain experience.

The key pathway start in the pre-aqueductal gray region in the mid brain.

Signals from this area of the brain descend to the spinal cord dorsal horn where further neuron inter connection serve to reduce the transmission of the

primary pain signal.

This modulation also takes place within the spinal trigeminal nucleus.

Pain PerceptionPain Perception :- :-

The final process of perception of pain take place in the

posterior parietal cortex of the brain.

.

Cranial and cervical nerves that Cranial and cervical nerves that provide somatic and visceral sensation provide somatic and visceral sensation

to the orofacial areato the orofacial area.

1.Trigeminal Nerve 2. Facial Nerve 3. Gloss pharyngeal Nerve2. Vagus Nerve3. Cervical Nerve-24. Cervical Nerve-3.  

MEASURMENT OF PAIN AND MEASURMENT OF PAIN AND

DISABILITY:-DISABILITY:-

There is no simple method of measuring pain. In assessing OFP patients, pain

intensity, emotional distress, and associated disability are important and cannot be captured with one scale or questionnaire. Pain intensity can be measured by using rating such as a

visual analog scale (VAS).

A VAS consist of a 10cm line on which 0cm is “no pain” and 10cm is pain as bad as it could be”. The patient marks

the point along the line that best represents his or her pain and score is measured from the no pain end of the scale. Visual analog scale are sensitive

to treatment effects, can be incorporated into pain diaries and can

be used with children.

MC Gill Pain Questionnaire (MPQ)MC Gill Pain Questionnaire (MPQ)

It is used to measure the motivational, affective and the cognitive evaluative qualities of pain, in addition to the sensory experience. It provides quantitative measures of clinical pain

that can be treated statistically.

The questionnaire enables patients to choose from 78 adjectives that describe pain, the form is designed to assess the sensory (Group-10), affective (Gp-11-15)

and evaluative (Gp 16) dimensions of pain and to produce a pain rating index. VAS and numeric scales require no specific forms and are easily administered. The MPQ is available from the (IASP) and is

used in pain clinics and by clinicians focusing on pain management.

The scales and rating provide help in diagnosis, treatment planning,

treatment program and out come assessment. It also give the patient a method for keeping a pain diary to

provide insight in to what activities and events make pain better or worse.

PAIN MEDIATORS PAIN MEDIATORS

Nociceptors can be activated by intense thermal and mechanical stimuli,

noxious cold and noxious chemicals. They are also activated by stimulation

from endogenous algesic chemical substances (Inflammatory mediators) produced by the body in response to

tissue injury.

Pain mediators includePain mediators include:

bradykinin (BK) potassium (K+) histamineserotonin arachidonic acid and others

BradykininBradykinin :- :- develops asdevelops as :-

Factor XII Factor XII a act on– prekallikrein kallikrein-HMW Kininogen - Bradykinin

Bradykinin strongly stimulate nerve ending that transmit pains and produce a burning

sensation when they injected intraperitoneally, brachial artery produce

intense transient pain and has been used in analgesics testing. It also act as potent

vasodilator. It act synergistically with other chemical mediators to increase plasma

extravasations and produce edema. This replenishes the supply of inflammatory

mediators so BK act directly and indirectly by increasing PG production

HistamineHistamine :- :-

It is an amine derivative from histidine. It is synthesize locally and store in mast cell.. It cause increase permeability of capillaries which lead to exudation and release of inflammatory mediators.. It act on sensory nerve ending cause pains, act as

pain transmitter. Non mast cell histamine has been implicated, sp in hypothalamus and midbrain and appear to act as transmitter regulating body

temperature, cardiovascular function and hormonal function. It is also implicated in certain vascular headache. Its release in stimulated by

tissue damage, antigen-antibody reaction, polymer like dextran, some drugs i.e. morphine, atropine,

polymyxin B etc.

Arachidonic Acid Metabolites (AAM)Arachidonic Acid Metabolites (AAM)

AA is processed by two different enzyme systems to produce prostaglandins and leukotrienes. PGS, TXs and LTs are all derive from eicosanoids. They lead to vasodilatation, contraction of visceral

smooth muscle, acid secretion, and have diuretic effect.

PGs sensitize afferent nerve ending to pain inducing chemical and mechanical stimuli.

They irritate mucous membrane and produce long lasting dull pain on intradermal injection. They cause

tenderness and amplify the action of other algesic. In the brain PGs may function as neuromodulators by regulating neuronal excitability. Sympathetic nerve terminals

will release PGs in response to own neurotransmitters nor epinephrine.

LeukotrienesLeukotrienes :- :-

In addition to direct stimulation of afferent carrying pain sensation also

act indirectly by causing PMNs leucocytes to release other chemicals

which in turn stimulates the nociceptor.

Platelet Activating Factors :-

Produced at the site of inflammation. PAF appears to cause

vasodilatation, exudation, cellular infiltration and hyperalgesia.

Substance P and Cacitonin gene Substance P and Cacitonin gene Related Peptide (CGRP)Related Peptide (CGRP) :- :-

Activation of C fibers cause their cell bodies to synthesize the

neuropeptides, substance P and calcitonin gene-related peptide

(CGRP).

neuropeptides are then antidromically transported along the axon branches to

the periphery by an axon transport system, where they induce further plasma extravasations and increase inflammation. The release of these algogenic substances

at the peripheral axon injury site produces the flare commonly seen around

an injury site and is referred to as neurogenic inflammation or the axon

reflex

SerotoninSerotonin

Derive from amino acid tryptophan. When it act on 5HT3 receptor, it produce

pain and itching and mediate indirect and reflex effects of 5HT. 5HT is said to initiate the vasoconstrictive phase of

migraine and to participate in the neurogenic inflammation of the affected

blood vessels.

VARIOUS THEORIES DESCRIBING VARIOUS THEORIES DESCRIBING PAINPAIN

Specificity Theory In the late 19th century Vonfrey develop the concept of specific cutaneous receptors for the mediator of touch, pain, cold and heat.

According to this theory pain is a specific sensation, such as vision and

touch with its own substrate of anatomically distinct receptors, primary

afferent nerve fibers nerve tracts and relay and receptors present in the brain.

Present day proponents of this theory have had to discard the anatomic aspect of specificity because receptor structure

specific for pain can not be found. Nevertheless, there is also recent

evidence that suggests that some central neurons and primary afferent fibers which respond to non-noxious stimuli, may also

play a role in pain, other inadequacies are its inability to explain some characteristics of clinical pains, i.e. trigeminal neuralgia,

which can be elicited not by noxious stimuli but by tactile stimulus.

Other mediators include lysosomal components which

include neurotrophils granules, granules of monocytes and tissue

macrophage which on release elaborate a variety of mediators

of inflammation.

INTENSIVE OR SUMMATION THEORYINTENSIVE OR SUMMATION THEORY

Develop by Goldscheilder in 1894. According to this theory pain depends

not on specific pathways but on excessive stimulation involving all types of receptors, with resultant

central convergence and summation of activity. Pain results when total output of the cells exceeds a critical level e.g.

touch plus heat plus pressure might add up in such a manner that pain was

the modality experienced

GATE CONTROL THEORY

It is proposed by Melzach and wall in 1965 and recently

reevaluated Gate control theory postulates

following:-

Information about the presence of injury is transmitted to the CNS

by small peripheral nerves.

Cells in the spinal cord or nucleus of Vth cranial nerve, which are excited by these

injury signals are also facilitated or inhabited by other large peripheral

nerves that also carry information about innocuous events (e.g. temperature or

pressure).

Descending control systems originating in the brain modulate the excitability of

cells that transmit information about the injury.

Therefore brain receives message about injury by way of the gate control

system, which is influence

(1) injury signals

(2) afferent impulses

(3) desending control.

The gate control theory was postulated primarily in terms of spinal cord

mechanisms of pain but it can also be viewed within the frame work of the

trigeminal system

CHARACTERISTICS OF PAINCHARACTERISTICS OF PAIN

Threshold and Intensity :-

If the intensity of the stimulus is below the threshold, pain is not felt. As the

intensity increases more and more, pain is felt ,pain sensation begin to spread

i.e. it begin to be felt in the neighbouring region.

Distraction of mind, excitement and net emotion can alter the threshold value of

pain

Adaptation Pain receptors show no adaptation and so the pain continue as long as

the receptors continue to be stimulated.

Localization of Pain Pain sensation is somewhat poorly

localized. However, superficial pain is comparatively better localized than deep pain. Visceral pain is usually

referred

Emotional Accompaniment

Pain sensation is usually accompanied by emotional component which as a rule are

unpleasant.

Influence of rate of damage on the Intensity

if the rate of tissue injury is high, intensity of pain is also high and vice-versa.

Therefore, a very slowly growing tissue damaging agent may not produce any pain

at all.

First (Fast) and Second (Slow pain)First (Fast) and Second (Slow pain) :- :-

The pain sensation transmitted by A delta fibers are felt earlier whereas that

due to C fibers are felt after a longer interval. They are called fast ,first pain due to A delta fibers and slow or second

pain due to C fiber. Usually the pain due to C-fibers stimulation, is

particularly unpleasant and out last the period of stimulation second pain is also spoken of as pathological pain.

Besides, the fast pain is better localized while slow pain is not.

REFERRED PAINREFERRED PAIN

Pain occurring in a visceral structure is usually not felt in the viscus itself but

on the surface of the body or in some other somatic structure that may be

located quite some distance away. Such type of pain is said to be referred pain. It is commonly observed in all type of deep pain both visceral and somatic

pain e.g. the pain of angina pectoris is often felt in the left arm or the jaw and diaphragmatic pain is often felt in the

shoulder or neck.

The two most popular theories explaining mechanism of referred pain

are

Convergence-Projection Theory

Convergence Facilitation Theory

Convergence-Projection Theory Convergence-Projection Theory

The sympathetic afferent fibers carrying the pain sensation emerges from the viscus and via dorsal root ganglion ends in the posterior horn

of the spinal cord. Afferent somatic nerve, emerging from the pain receptor, of the

corresponding dermatome of the viscus, enters the same segment and terminates on the very

same cell where sympathetic nerve is terminating i.e. these two different neurons converge on the same next order neuron. Therefore when the next order neuron is

stimulated – the impulse reaches the brain and person feel pain, but he feels as if the pain is

coming from the dermatome.

Convergence Facilitation TheoryConvergence Facilitation Theory

According to this theory, nociceptive input from the deeper structure causes the resting activity of the second order

neurons pain transmission in the spinal cores to increase or be facilitated. The resting activity is normally created by

impulses from the cutaneous afferents, facilitation from deeper nociceptors

causes the pain to perceived in the area that creates the normal, resting

background activity.

The theory tries to incorporate the clinical observation that blocking sensory input from the reference area with either L.A. or cold, can

sometimes reduce the perceived pain e.g. in myofacial pain, application of

a vapocoolant spray is actually a popular and effective modality used

for pain control.

Subliminal Fringe EffectSubliminal Fringe Effect

The afferent sympathetic nerve bringing pain sensation from the viscus

terminate on the second order neuron, but at the same time it also via

collateral, stimulate another second order neuron. This second order neuron is synapse with somatic neuron of the corresponding dermatome. Therefore, when the pain is felt by the patient, he feel as if the pain is coming from the

corresponding dermatome.

Dermatome Rule Dermatome Rule When pain is referred, it is usually to a structure that developed from the same

embryonic segment or dermatome as the structure in which the pain originate. This is called dermatome rule e.g. during embryonic

development the diaphram migrates from neck region to the adult location between the chest and abdomen and take its nerve supply, the

phrenic nerve with it. One third of the fibers in the phrenic nerve are afferent and they enter the spinal cord at the level of IInd to IV the

cervical segments, the same location at which afferents from the tip of the shoulder enter.

Pain Inhibiting Pain Inhibiting MechanismMechanism

It can be--Endogenous Exogenous

Endogenous pain inhabiting mechanismEndogenous pain inhabiting mechanism Activation of Enkephalinergic neurons (EN) and

serotonergic neurons (5NS). ENS arise from periaqueductalgray matter in the

midbrain (PAG). The SNs arise from Magnus raphae nucleus of the medulla. Magnus raphae nucleus act as

intermediate relay station from Pag to substantia gelatinosa (SGR), both types of fibers terminate on

the SGR. Also fibers carrying pain from periphery (A delta and C) terminate at SGR and the spinothalmic

tract which carries pain to the thalamus. Stimulation of these descending fiber can cause synaptic inhibition

as a result of which STT is no more stimulated

The stimulation of these descending fibers are The stimulation of these descending fibers are caused bycaused by

(1)Local application of encephalin and

endorphin.

2) Exogenous opioid (morphine when applied locally at these site do the same).

3) Electrical stimulation of these fiber (TES)

4)Collateral from STT with raphae nucleus can stimulates descending pathway.

5)Stimulation of the limbic systemic occur during (rage, panic etc) can stimulate these fibers. This factor explains why a soldier who sustains a serious injury in the battle field may not feel the pain at all during the heat of the battle

6)Acupuncture Method – these fibers can be stimulated

Second mechanism can be explained by gate control theory of pain. The

principle is that signals passing from primary afferent neurons to second

order cells have to pass through a gate which may be wide open (in which case

resulting pain may be severe), closed (in which case no pain is felt), or more

commonly partly open.

Gate consist of several interneurons which can inhibit activity beyond

the first synapse either by decreasing release of the excitatory

transmitters or by inhibiting the 2nd order cells. There inhibitory

activity is mediated by GABA, substance P, enkephalin, endorphin

etc

Also activity of AB afferent fibers from same neural segment can inhabit

activity in second order nociceptive neurons. These neuron can be activated

by rubbing close to an injury. These receptors are very sensitive to physical stimuli. Any damage to these receptors

can open the gate. This may explain whey reestablishment normal mobility may contribute to successful treatment

of some chronic pain.

The activity of these fibers give rise to principle of transcutaneous electric nerve stimulation (TENS) whereby

selective activation of AB nerves with electric stimulation has been used to relieve pain. When TENS is used at

relatively high intensities, it may exert its effects via descending pathways.

Endogenous Method of Controlling Endogenous Method of Controlling Pain Includes - Pain Includes -

(1) Removing the cause :- It is a desirable methods. It is imperative that

any removal leave no permanent environmental changes in tissue, since

this condition would then be able to create the impulse, even though the original causative factor had been

eliminated

Blocking the pathways of painful Blocking the pathways of painful ImpulsesImpulses

This can be done by injecting drug

possessing local analgesic property in proximity to the nerve involved.

Thus preventing those particulars fibers from conducting any impulses

centrally beyond that point. These two method act by altering pain perception.

Raising the pain threshold :- Raising the pain threshold :- Raising pain threshold depends on the pharmacological activity of drugs

possessing analgesic properties. These drugs raise pain threshold and therefore alter pain reaction,

conceptually there are two components of pain (a) Nociceptive (b) affective component. The path of nociceptive component is spinothalmic tract

Thalamus – past central groups. This component is purely physical

component of pain.

Affective ComponentAffective Component is the psychological component associated

with pain. The path is that some fibers from STT to thalamus terminate in some

intermediate stations in the reticular formation of brain stem and are called spinoreticular thalamic system. Non-

narcotic analgesic like aspirin can inhibit the nociceptive but not the affective component of pain whereas opioid

(Morphine) inhibit affective as well as nociceptive components of the pain. They act centrally at cortical and sub cortical centers, to change patient mind and his

reaction towards pain

Preventing pain reaction by cortical depression –

eliminating pain by cortical depression is by the use of general anesthesia.

Using Psychosomatic Method This method affects both pain perception and pain reaction. It

include audio analgesia

TRIGEMINAL NERVETRIGEMINAL NERVE

The largest cranial nerve contains both sensory and motor fibers. It contains both

general somatic afferent fibers convey both exteroceptive and propioceptive impulses and special visceral efferent

fibers supply motor innervations. It has two roots, motor and sensory. The two

roots enter the middle cranial fossa and attach to the lateral part of the pons.

SENSORY ROOT OF TRIGEMINAL NERVESENSORY ROOT OF TRIGEMINAL NERVE The fibers of sensory root arises from the semilunar ganglion (gasserian). Develop from neural crest cells. It contain unipolar neurons with central and peripheral processes. Peripheral branches form – ophthalmic, maxillary and mandibular division of the nerve. Central fibers form sensory roots, they enter the pons where they form ascending and descending fibers. Ascending fiber terminate in the upper sensory nuclei. These fiber carries light touch, tactile discrimination, sense of position and passive movement. The spinal nucleus extends caudally from the main sensory nucleus to the second cervical segment. They give rise to fibers of ventral trigerminothalamic tract which cross toward opposite side and go to cortex and conveys sensation of pain temperature

Motor RootMotor Root :- :- Its fibers derive from motor nucleus and it

passes through foramen ovale through which it passes to join the mandibular

division. The nerve is chiefly motor and its fibers supply the muscle of mastication. It

is often called the masticator nerve.Mesencephalie Root of the trigeminal Mesencephalie Root of the trigeminal

nervenerve :- :- It contain afferent fibers accompanying

motor root. Afferent fibers convey propicoceptive impulses from the TMJ,

PDL, maxillary and mandibular teeth and hard palate, muscles of mastication.

DIVISIONS OF THE TRIGEMINAL NERVE DIVISIONS OF THE TRIGEMINAL NERVE

Ophthalmic Nerve :- Ist division, sensory nerve. It is smallest of the three division and enter the orbit

through superior orbital fissure. Its fibers are sensory or afferents from the scalp,

the skin of the forehead, the upper eyelid lining of the frontal sinus, the conjunctiva of the eyeball, the lacrimal gland and the skin of the lateral angle of the eye , lining

of the ethamoidal cells and also durameter.

Maxillary DivisionMaxillary Division :- :-

It is entirely sensory in function. It enter in the pterygopalatine fossa through foramen

rotundum. It enter in to orbit through inferior orbital fissure and then emerges on the anterior surface of the maxilla through the infraorbital foramen where it divide.

Branches and areas supply by them :-

1. Middle Cranial Fossa Middle meningeal nerve supply dura with

sensory fibers.

2. Pterygopalatine fossa Zygomatic nerve Zygomaticofacial &

zygomaticotemporal nerve supply prominence of the zygomatic bone and

anterior temporal fossa region

B. Pterygopalative Nerves and orbital branches supply periosteum of orbit,

ethamoidal cells and sphenoid sinus. Nasal branches supply mucous

membrane of the nasal septum and posterior ethamoidal cells.

C.C. Palatine BranchesPalatine Branches

greater or anterior palatine nerve supply major part of hard palate and

palatal gingiva and extends as far forward as the premaxillary palatine

mucosa. Middle Palatine Nerve mucous

membrane of soft palatePosterior palatine nerve mucous

membrane of the tonsillar area.

3. Posterior Superior Alveolar nerve :- Gingival Branches supply buccal

gingiva of the upper molar and mucous membrane part of the cheek.

Alveolar Branches :- Supply maxillary molar except the MB root of the upper first molar and their gingiva, mucous

membrane of maxillary sinus. Middle Superior Alveolar Nerve :- Maxillary

bicuspids and the MB root of the first molar, lining of the maxillary sinus

Anterior superior alveolar nerve:-supply incisors and cuspid and maxillary sinus.

Terminal branches:-supply skin of the lower eye lid side of the nose and upper lip.

MANDIBULAR NERVEMANDIBULAR NERVE

Larges of the 3 division contains both sensory bundle of fibers and a small motor

bundle of fibers.

Benches from Undivided nerve :- Nerve spinosus supply the dura and mastoid

cells. Nerve to internal pterygoid muscle –

a branch of motor root.

Anterior DivisionAnterior Division : :

have both sensory and motor fibers – it supply motor fiber to - External pterygoid

muscle, massater muscle, temporalis muscle and supply sensory buccal nerve (long buccal) – it is sensory from the mucous

membrane and the skin of the cheek membrane and gingiva of the mandibular

molar region.

Posterior DivisionPosterior Division :- :- It is mainly sensory but also carries some

motor components. It give rise to :- Auriculo temporal nerve :- It provide

sensory supply from the skin over the areas supplied by facial nerve (VII) that is

zygomatic, buccal and mandibular area.Sensory from the parotid gland

Skin lining the external auditory meatus and from the lateral surface of the

tympanic membrane. From the skin and scalp over the upper part of the external ear and side of the head up

to the vertex of the skull.

Lingual NerveLingual Nerve :- :- Sensory from the anterior two third of the tongue, mucous membrane of the floor of

the mouth and lingual side of the mandibular gingival, sensory from

submandibular and sublingual gland and their duct.

Inferior Alveolar nerveInferior Alveolar nerve :- :- Dental branches – sensory from all the

lower molar and bicuspid teeth and their PDL.

Mental Branch – from the skin of the lower lip and chin regions and mucous membrane

lining the lower lip region.Incisive Nerve :- Sensory from Incisors,

cuspid teeth and their periodontal membranes.

CLASSIFICATION OF PAINCLASSIFICATION OF PAINPAIN PAIN

Somatic (Samasthetic) Visceral (from viscera)

e.g. angina pectoris

peptic ulcer

Intestinal colic

Renal colic etc.

Superficial Deep (from skin & subcutaneous (from muscle/ bonetissue) e.g. superficial joint/fascia periosteum)cuts/burns etc e.g. fracture/arthritis/ fibrositis/disdislocation etc.

PRACTICAL CLINICAL CLASSIFICATION OF PRACTICAL CLINICAL CLASSIFICATION OF CARNIO FACIAL PAINCARNIO FACIAL PAIN

General Classification

Origin of Pain Quality of Pain

Extra cranial Structure

Craniofacial region Varies

Referred pain from remote pathologic sites

Distant organs and structures

Aching and pressing

Intracranial pathosis

Brain and related structures

Varies

Neurovascular Blood Vessels Throbbing, pulsing or pounding

Neuropathic Sensory nervous system

Shooting, sharp, burning pain

Causalgic Sympathetic nervous system

Burning

Muscular Muscles Deep aching, tight

Unclassifiable Etiology unknown Any

It can be also classified as:- It can be also classified as:-

Typical Pain Disorders Atypical Pain Disorders

Periodontalgia

Neuralgic (trigeminal neuralgia)

Vascular (migraine, cluster headache)

Otic (Otitis media)

Sinus (Sinusitis)

Heart (cariogenic jaw pain)

Salivary gland Disorder

Musculo skeletal disorder

Causalgia

Reflex sympathetic dystrophy

Atypical facial pain

Phantom tooth pain

Neuralgia including cavitational osteonecrosis

Diagnosis based on specific questions Diagnosis based on specific questions and testsand tests

questions asked-two type

General questions

Specific questions

Some general questionsSome general questions are- are-

What can I do for you? Pt give response in three ways- historical, Diagnostic, &factual

What sort of pain are you having ?Varied response effected by

physical, psychological , social factors

Do you have any reaction to hot Do you have any reaction to hot cold and sweetness-?cold and sweetness-?

this questions differentiate between dental pain or pain due to

non dental causes & we have to analyze the responses and have to get an impression of the severity

of the response

Pain to sweetness

Pain to cold

pain on application of cold but relieved by hot

Delayed response to heat

Unexplained sensitivity to cold in posterior teeth

Root filled teeth sensitive to cold

pain on biting-vital posterior teeth pain on biting-vital anterior teeth

Pain on eating

pain relieved by placing hand on the side of the face

Pain on ascent or descent

Pain ass. with exertion or after exertion

Pain on swallowing Bilateral pain

Pain on waking in the morning

Pin in the afternoon or evening

Pain at a particular time each day pain when the Pt goes out in the cold

SITE OF PAINSITE OF PAIN Observation of the manner in which the Pt

uses there hands And fingers while describing the pain provide information

About the origin of pain

Placing a fingernail between the tooth

Moving a fingernail on the tooth

Holding one tooth

Placing a finger over the apex of the tooth

Pressing over the gingival margin

Holding or moving several teeth

Pressing over the zygoma

Pressing under the maxilla

Pressing on side of maxilla with rotary movement or pressing on the body of mandible with finger in motion

Using more than one finger for describing the pain

bilateral pain

Pain on percussion of more than one tooth

Holding a hand on side of face

Moving finger in line under the mandible

pointing to an area but reluctant to touch

Complaining of altered sensation

When Pt describe his pain by two hand

Pain in and around the eyes

Pain in between the eyes

OTHER QUESTIONS AREOTHER QUESTIONS ARE

When did the pain start ?

where did the pain start ?

Does any thing relieve the pain?

Have you been able to sleep?

Pulpal PainPulpal Pain :- :- It is the most commonly experienced

pain in and near the oral cavity. Pulpal pain can be diagnose by based

on clinical signs and symptoms histological finding.

Clinically pulp is referred as healthy, reversible pulpitis, irreversible pulpitis

histological as acute, chronic&hyperplastic.

HyperemiaHyperemia

The increased pressure against the sensory nerve endings in the pulp might well produced the sensation of pain. Application of cold produce a sharp hypersensitive response and heat produce true transient hyperemia and a dull pain

An assessment of pain intensity at the time of stimulation, dental history& a through dental examination allow the clinician to

differentiate among the normal pulp, dentin hypersensitivity, and the reversible inflamed

pulp

Hyperactive pulpalgia :- It is characterized by a short, sharp,

shock ,pain is feel as a sensation of sudden shock. It is never spontaneous. It

includes :-

Dentin Hypersensitivity :- Pain arise in response to thermal, chemical, tactile or osmotic stimuli and is not caused by any

other dental defect or pathology. This pain is explained by, hydrodynamic theory

postulated by Brannstrom.

Characteristic features of irreversible Characteristic features of irreversible pulp condition are :pulp condition are :

Hyperalgesia in the initial stage

Dull throbbing ache in the later stage

Lingering pain on application of stimuli

Pain is spontaneous

Cause referred pain in other areas

Relief is provided by cold

Acute Pulpagia :- Pain is nagging or boring pain which may at first be localized but finally becomes diffuse or referred to another area in mild pulpalgia but in advanced lesion, pain is excruciating and relived by cold.

Chronic Pulpagia :- Mild pain that is quite diffuse and is difficult to locate source of pain. It is likely to cause referred pain ;which is also mild.Hyper active pulpitis :- Pain or slight discomfort from food coming against the tooth or on taking extreme of hot & cold

Internal resorption :- Pain is mild and at tolerable level and closely resemble chronic pulpalgia.

Incomplete fracture or split tooth :Pain range from those of constant unexplained hyper sensitive pulp to constant unexplained toothache. The most frequent complaint is that of a tooth painful to bite on, with occasional mild ache.

In general periodontal pain areIn general periodontal pain are

-localized, deep throbbing painInvolving inflammation of PDL around one or more teethMobilityLocalized bleeding Presence of pocketIn radiograph loss of bone is therePain last for hour or dayInvolve tooth is tender on percussion

If pain involve multiple teeth including opposing teeth then occlusal trauma

should considered

Periradicular painPeriradicular pain :- :-

Acute apical periodontitis. The pain has been described as constant, gnawing, throbbing and pounding. Tooth is tender and slightly elevated in its socket. The pain is most persistent, lasting 24 hours a day.

Acute apical abcess :- Pain is similar to AAP but somewhat lower in intensity. Involved tooth is painful to movement or mastication

Chronic apical periodontitis Chronic apical periodontitis :- :- It is seldom painful.Chronic apical abcess/suppurative apical Chronic apical abcess/suppurative apical periodontitisperiodontitis :- :- it is generally symptoms free. When draining fistula close, dis comfort ensue.

Periodontal lesion painPeriodontal lesion pain :- :- Acute gingival or periodontal abscess. Tooth is painful to bite on and is not so deep seated or throbbing as that of apical abscess. Pain is spontaneousAssociated localized swelling is there Presence of deep PDL pocket is there.

PericoronitisPericoronitis :- :-

Severe radiating pain in posterior mouth region and inability to

comfortably close or open mandible. Tissue distal to

erupting molar is most painful to touch.

Salivary gland disordersSalivary gland disorders :- :-

Siolithiasis pain ass. With sub mandibular gland is more prone to mimic endodontic pain in posterior aspect of mandible

The occluded duct often lead to swelling of sub mandibular area hence it may mimic lymphadenitis ass. with an endodontic infection of a posterior mandibular tooth

Characteristic feature of pain:Characteristic feature of pain:

Location of pain

Pain exacerbated by salivation

Palpation of duct yield no saliva

Pt feel stringent drawing in the area

Panoramic radiograph reveal radio opacity

Ear pain :-Ear pain :-

Odontogenic infection of posterior teeth may refer pain to the ear/TMJ area.

Similarly middle ear infection/otitis media/mastoiditis may be confused with odontogenic pain. In otitis media pain is acute, sever, throbbing and exacerbate on lowering the head. Pain may be referred to tooth, TMJ, tonsils, tongue, throat, trachea and thyroid.

It is unlikely for the middle ear infection/otitis media/mastoiditis pain to be exclusively

expressed as jaw pain

Sinus and Para nasal painSinus and Para nasal pain :- :-

In acute maxillary sinusitis pain may be stabbing, with severe aching pressure. Pain is frequently referred upward under the orbit and downward over the maxillary posterior teeth. Pain is referred in all the teeth in the quadrant and exacerbated when head is placed below the knee

In chronic sinusitis there is dull constant pain. The location of these symptoms may vary from the maxilla and maxillary teeth in maxillary sinusitis, to the upper orbit and frontal process in frontal sinusitis and at the junction of the hard and soft palate, occipital and mastoid process in sphenoid sinusitis.

Temporo mandibular joint articular Temporo mandibular joint articular disordersdisorders :- :-

Capsulitis and synovitis

chief complaint is continuous pain over the joint aggravated by function. Swelling may be evident and patient

may complaint of acute malocclusion, restricted mouth opening and teeth

pain.

Internal DerangementInternal Derangement :- :-

It includes meniscus displacement, formation of intra articular adhesion and various forms of

arthritis.

There occur limited jaw opening, deviation on opening, joint clicking, crepitus and pain

directly localized to the joint area in front of the tragus of the ear. The pain is dull, boring ache but may be more acute when exacerbated by wide mouth opening. The symptoms become

progressively worse and the degree of pain increase. TMJ pain is often referred into

temple, cheek and posterior dental area of the maxilla and mandible

NEUROPATHIC PAINNEUROPATHIC PAIN It results from an abnormality in one or more components of the nervous system i.e. peripheral, central or autonomous. They are characterized as :- - Do not required presence of noxious stimuli in contrast to somatic pain which does .- Pain manifestation are usually maintained by neuroplasticity that is change in nervous pathway carrying pain. When neuroplasticity is prolonged the result in a state of chronic or path physiologic pain. - Hyper excitability of IInd order neuron i.e. central sensitization - Allodynia- Hyperalgesia- Pain is bright, stimulating and burning - Pain that is relatively unresponsive to low doses of narcotic analgesic

Neuropathic painNeuropathic pain :- :-Neuralgias Neuralgias :-:-

Trigeminal Neuralgia Etiology:

Precise cause is unknown. Evidence indicates it may be due to vascular compression of gasserian

ganglion, viral infection of neuron or nerve sheath may be there.

Neuropathic painNeuropathic pain :- :-Neuralgias Neuralgias :-:-

Trigeminal Neuralgia It primarily involves either maxillary or the mandibular division but sometime it may involve ophthalmic division. Pain is severe and lancinating, shooting into the bone and teeth. Electric like quality of pain is unique and is rarely encountered in odontogenic infections. The pain episode last only second at a time. Although paroxysms may occur in rapid succession. A trigger zone exists somewhere on the facial skin or occasionally in the oral cavity.

Treatment:Treatment:It is essential to establish diagnosis and avoid

any invasive procedure.Carbamazipine (Tegretol) Peripheral neurectomy Rhizotomyalcohol injectionCryotherapyRadiofrequency lesioningLaser therapySurgical decompressionTrans cutaneous ganglionic neurolysisDental extractions and endodontics is contra

indicated

Post herpetic NeuralgiaPost herpetic Neuralgia This disease represent a recrudescence of a

latent virus located in sensory ganglion. The painful lesions of shingles cause a deep, boring ache involving not only the superficial mucosal and cutaneus tissues but also the maxillary and

mandibular bones. Occurrence of prodromal pain obscure the diagnosis. Prodromal pain is acute and electric like and the pain associated

with vesicular eruption is deep and boring. Once the vesicles clear, the residual pain is of

burning quality and chronic. The quality of pain may be confused with odontogenic pain but the

history of vesicular eruption is sufficient to make a diagnosis

Treatment of post herpetic Treatment of post herpetic neuralgia:neuralgia:

TENS Anti seizure drugs Analgesics Topical preparation Refer to neurologist

Glosso Pharyngeal NeuralgiaGlosso Pharyngeal Neuralgia : :-

It include unilateral rarely bilateral stabbing pain in the lateral posterior

pharyngeal and tonsilar area , the base of the tongue, down in to the throat, the

Eustachian tube or ear and down the neck. Sometime pain radiate into vagus

region and may be associated with salivation, flushing, sweating, tinnitus,

cardiac arrhythmias, hypertension, vertigo or syncope.

Eagle’s SyndromeEagle’s Syndrome : : It is similar to those of gloss pharyngeal neuralgia but involve compression of the

area of Ixth nerve by a calcified elongation of stylohyoid process of the temporal bone. Precipitating factors

include fast rotation of head, swallowing, pharyngeal motion from talking and

chewing.

Vasogenic craniofacial painVasogenic craniofacial pain

In general pain is deep, throbbing, pulsing or pounding quality, occasionally sharp and with an aching and

burning background.

Migraine

Classic migraine headache begin as ache but usually develops in to pain of a throbbing, pulsating or bating

nature. One episode can last for several hrs today. Somatosensory areas are most common field and consist of dysesthesias that start in one hand and

spread up to involve the ipsilateral side of the face, nose and mouth. The headache itself is predominantly

unilateral in the frontal, temporal, or retro bulbar areas, although it may occurs in the face or in a single

tooth.

Cluster headache (Spheno palatine neuralgia)

It can be classified as: CLASSIC and CHRONIC TYPE

CLASSIC type affect patient mostly in spring season

.CHRONIC type occurs through out the year.

It is often mistaken for acute pulpits of maxillary posterior teeth.

Cluster headacheCluster headache :- :- It have temporal pattern. They tend to occur in “Clusters” a series of one to eight 20-180 minute attack/day lasting for several week

or months.

The pain is a severe, unilateral, continuous intense ache or burning that often occur at

night.

The most common sites are either around and behind the eye radiating to the forehead and temple, infraorbitatly in to maxilla and occasionally into the teeth and rarely to the

lower jaw and neck.

TreatmentTreatment

Use of oxygen at the time of attack relieves pain and used for diagnosis of pain. Ergotamine tartarate may cause vaso constriction and contra indicated in hypertensive patient. CCBs like Nifedipine prevents pain paroxysms. Corticosteroids alleviating pain and preventing pain occurrence. Dry Sumatriptin succinate

Myofacial PainMyofacial Pain The most common form of musculoskeletal pain affecting the head, neck and face. The main characteristic features is ->

Myofacial trigger point

Muscle affected have a reduced active range of movement

Referred pain in reproducible patterns remote from the site of the rigger point.

A jump sing and verbal response or reflex reaction occur on palpation of the trigger point

Pain is deep, dull, aching and provocable.

ATYPICAL ODONTALGIA ATYPICAL ODONTALGIA

The most likely mechanism involved in atypical odontalgia (AO) is related to deafferentation

following injury to a nerve. Deafferentation refer to the partial or total loss of an afferent nerve

supply from a particular area, following trauma during dental procedure. Nerve damage in

reversible in most patient but in some patient (3%). It is permanent. Pain may not appears for week, month or even a year after the procedure. It has been hypothesized that there is genetic predisposition towards pain in these patients.

Involvement of sympathetic nervous system (SMP) in AO has been suggested.

Characteristic of pain in atypical Characteristic of pain in atypical odontalgia are:odontalgia are:

Chronic aching pain

Pt feel it is deep with in the bone & it is hard to localized it.

In many Pt symptoms appears to wonder from site to site

Intensity of pain also varies