describes briefly about conditions causing oro facial pain other than neuralgias

1. ORO-FACIAL PAIN
(OTHER THAN NEURALGIAS)

2. CONTENTS
• Introduction
• Definition
• Terminologies
• Neural pathways
• Classification
• Evaluation of Orofacial pain patient
• General Treatment principles
• Common facial pain disorders(other than neuralgia)
• References

3. INTRODUCTION
• OFP – presenting symptom of a broad spectrum of diseases
• As a symptom may be due to:
– Diseases of the oro-facial structures
– Generalised musculoskeletal disease
– Psychological abnormalities
– may be referred from other sources
– May also occur in the absence of detectable physical, imaging or
laboratory abnormalities.
• An interdisciplinary approach is required to establish
diagnosis and for treatment.

4. WHAT IS PAIN ?
 Task force on Taxonomy of IASP
 “Pain is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage or described
in terms of such damage”
 Traditional Approach (Bio medical Model)
 embraced a dualistic viewpoint that conceptualized the
mind and body as functioning separately and
independently.
 Biopsychosocial model

5. TERMINOLOGIES
 Nociceptors: Receptors that are sensitive to painful stimulus and are
responsible for initiating the generation of pain
 Nociception: Mechanism that provides for the conversion of noxious or
potentially noxious stimuli into neural impulses
 Allodynia: Pain that is produced by a stimulus that is not normally painful
 Pain threshold: the minimum intensity of a stimulus that is perceived as
painful.
 Pain tolerance is the maximum level of pain that a person is able to tolerate

6. TERMINOLOGIES
 Hyperesthesia: is an increased sensitivity to stimuli and does not imply a
painful sensation but rather an augmented response to specific sensory
mode
 Hyperalgesia: Increased sensitivity to painful stimulus. It is a special case of
hyperesthesia
 Hypoesthesia: Reduced sensation in response to stimulus
 Causalgia: burning pain often associated with trophic skin changes in the h
and or foot, caused by peripheral nerve injury. may be exagerated by
slightest stimuli or it may be intensified by the emotions.

7.  Neuralgia: intense burning or stabbing pain caused by irritation of /
or damage to a nerve. The painis usually brief but maybe sever. Pain is
usually felt along the area of distribution.
 Neuropathy:
Anyof numerous functional disturbances and pathologic changes in th
e peripheral nervous system
 Referred pain: heterotopic pain that is felt in an area that is
innervated by a nerve different from the one that mediates the primary
pain.

8. NEURAL PATHWAY OF PAIN
 Fields has noted that the subjective
experience of pain arises by 4 distinct
process:
 Transduction
 Transmission
 Modulation
 Perception

9.  Transduction:
 process – noxious stimuli lead to electrical
activity in the appropriate sensory nerve endings.
 Several type of sensory receptors:
1. Merkels corpuscles- tactile receptors –submucosa
of tongue and oral mucosa
2. Meissners corpuscles:tactile recptors in skin
3. Ruffnis corpuscles: pressure and warmth receptors
4. Krausse’s corpuscles or end-bulbs: cold receptors

10. 5. Nociceptors or free nerve endings:
- found in almost all tissues
- identifies tissue injury
- may respond to multiple stimulus- polymodal
All sensory receptors are attached to afferent neuron(first-order
neurons)which vary in their Dm and conduction velocity:
 Type A fibers
 Alpha
 Beta
 Gamma
 Delta
 Type C fibers
Carry tactile and proprioceptive
impulse not pain
Carries pain sensation.Pricking pain is
mediated A-delta and dull aching burning is
mediated by Type C fibers

11.  Transmission:
 Neural events that carry nociceptive inputs to CNS for
processing.
 3 basic components:
 First order neurons:-
 Carries nociceptive from the sensory receptor to the spinal cord
 Second order neuron
 Carries the input to higher centres
 Involves a no. of neurons that send the input upto thalamus
 Interactions between thalamus , cortex and limbic system

12.  Modulation:
 Refers to ability of CNS to control the pain-transmitting neurons.
 Several areas of cortex and brainstem have been identified –can
either enhance or reduce nociceptive input arriving by way of the
transmitting neurons
 Perception:
 When the nociceptive input reaches the cortex perception occurs
 Immediately initiates a complex interaction of neurons between
the higher centres
 Suffering and pain behaviour begin

13. SOMATIC PAIN PATHWAY
 Information from the tissue outside the
CNS needs to be transferred into the CNS-
on to the higher centers-once evaluated-
sends down impulses down the spinal cord
–to efferent organ.
 Primary afferent neurons (1st order
neuron)recieves impulses form the sensory
receptor-pain mediated by a-delta and C-
fibers.
 Primary neuron synanpses at dorsal
horn(substantia gelatinosa) of the spinal
cord with a second order neuron

14.  Most of second order crosses the midline to enter
the antero-lateral spinothalamic tract (carries
broder spectrum –pain warmth cold crude
tactile)which ascends to the higher centers
 Some remain on the same side of dorsal column
and ascend by way of lemniscal system(touch
pressure vibration and proprioception)

15. The trigeminal Pathway
 Sensory input from face and oral structures is carried by Vth cranial
nerve.
 Cell bodies of the afferent neurons are located in the large gasserian
ganglion.
 Impulses carried by TN enter directly into the brain stem – pons –to
synapse with Trigeminal spinal tract nucleus
 Trigeminal brainstem nucleus complex consists of
 Main sensory nucleus located rostrally
 Spinal tract nucleus located caudally
 Subnucleus oralis
 Subnucleas interpolaris
 Subnucleus caudalis
 Motor nucleus

16. OKESONS CLASSIFICATION
 Axis I(physical conditions)
1. Somatic pain
 Superficial
 Cutaneous
 Mucoginigival
 Deep somatic pain
 Muculo skekelatal pain
 Muscle pain
 Protective contraction
 Local mucle soreness
 Myofascial pain
 Myospasm
 Centrally mediated myalgia
 TMJ pain
 Ligamentous
 Retrodiscal
 Capsular
 Arthritic
 Osseous and periosteal pain
 Soft connective tissue pain
 Periodontal dental pain

17.  Visceral pain
 Pulkpal dental pain
 Vascular pain
 Arteritis
 Carotidynia
 Neurovascular pain
 Visceral mucosal pain
 Glandular , ocular and auricular pain
 Neuropathic Pain
 Episodic
 Paroxysmal neuralgia opain
 Trigeminal neuralgia
 Glossopharyngeal neuralgia
 Geniculate neuralgia
 Superior laryngeal neuralgia
 Nervus intermedius
 Occipital neuralgia
 Continous
 Peripherally mediated(entrapment neuropathy, deafferentation, peripheral neuritis)
 Centrally mediated ( BMS,atypical odontakgia,PHN,CRPS, sympathetically maintained pain)
 Metabolically mediated(Diabetic ,hypothyroid,alcoholic,nutritional )

18.  Axis II(psychological condition)
 Mood disorder
 Depression
 Bipolar disorder
 Mood disorder resulting from medical condition
 Anxiaety disorder
 Generalised anxiaety disorder
 Post traumatic stress disorder
 Anxiety arising from a medical condition
 Somatoform disorder
 Undifferentiated somatoform disorder
 Conversion disorder
 Pain disorder
 Hypochondriasis
 Other conditions
 Malingering
 Psychological affecting a medical condition
 Personality traits or coping style
 Maladaptive health behaviour
 Stresss-related physiological response
 Any other mental disorders not mentioned in this classification

19. Part One: Primary headache
1. Migraine
2. Tension-type head ache
3. Cluster head ache and other trigeminal autonomic cephalgias
4. Other primary Headaches
Part Two: secondary headache
5. Attributed to head/neck trauma
6. Attributed to cranial or cervical vascular disorder
7. Attributed non-vascular intra-cranial disorder
8. Attributed to substances or their with drawal
9. Attributed to infection
10. Attributed to disorder of homeostasis
11. Attributed to disorder of cranium, neck , eyes,ears, nose,sinuses,teeth , mouth or other facial or
cranial strutures
12. Attributed to psychiatric disorder
Part Three: cranial neuralgias,central and primary facial pain, and other head aches
13 cranial neuralgias and central causes of facial pain
14 Other headache, cranial neuralgia cantral or primary facial pain.
CLASSIFICATION OF HEAD ACHE(IASP)

20.  History
 Clinical examination
History
 Chief complaint
 History of present illness
1. Chronology of onset
2. Location of symptoms as pointed by the patient
3. Quality of the symptoms:-
• Aching/ Dull/pressure pain- represents musculoskeletal
category
• Throbbing /stabbing/pounding-neurovascular
• Itching/burning/electric shock like pain-neuropathic pain
Evaluation of Orofacial pain patient

21. 4. Behaviour of pain:
 Temporal behaviour- frequency and periods between episodes
 Intermittent
 continous
 Duration
 Momentary
 Long-lasting
 Protracted
 Localization behaviour
5. modifying factors
 effect of functional activities
 Effect of physical modalities
 Effect of medication
 Effect of emotional stress
6. Associated symptoms(tearing,nasal congestion,
nausea,vomitting,sensitivity to light,parasthesia,otalgia,headache)

22. 7. medical history:
 Comorbid systemic diseases
 History of trauma to head and neck
 History of previous treatments and outcomes
8. psychological and social history:
 Routine psychologic evaluation-may not be necessary for acute pain- but
essential chronic pain
 Evaluated and managed by a multidisciplinary approach
 Variety of measuring tools that can be used to assess psychologic status-
 Multidimensional pain inventory(MPI)
 Evaluate three pain profiles:
 Adaptive coping
 Interpersonal distress
 Dysfunctional chronic pain
 Synptom Check List(SCL-90)
 Provides two scales
 a depression scale
 Scale measuring the severity non specific physical
symptoms(somatization scale)

23.  Psychological conditions that can contribute to 0r
actually be responsible for pain disorders:
 Somatoform disorders :
 Characterised by complaints of physical symptoms like pain-no
demonstratable organic findings
 Conversion disorder:
 Alteration or loss of physical functioning-suggests a physical
disorder-but actually apparent expression of psychological
conflict or need
 Hypochondriasis:
 preoocupation with fear or belief of having a serious disease.

24. General examination
1. Vital signs - BP, pulse rate
respiratory rate , temperature
2. Cranial nerve evaluation

25. 3. Eye evaluation:
4. Ear evaluation:
Muscle evaluation:
Masster muscle
palpation
Temporalis muscle
SCM

26. Masticatory evaluation:
Deviation Deflection
Comfortable
mouth
opening
Maximum mouth
opening
Normal range of mouth opening(inter-
incisally)-53-58mm
Restricted mouth opening -<40mm

27. PAIN ASSESSMENT METHODS
 Assist in the process of D/d and evaluation of treatment
effectiveness
 Pain experience- subjective-cannot be objectively measured by a
single test
 Most rely on pts ability to express the experience of pain ,
questionaire , diary or interview
Pain intensity measurement methods:
 Visual analog scale(VAS)
 Numerical Rating Scale(NRS)
 Verbal Rating Scale(VRS)

28.  Visual Analog scale
 Linear scale on which patients specify their level of
pain by indicating the position along a continous
10cm line b/w 2 end points
 Distance from the low end of VAS to the patients mark
is mearured- numerical index of pain severity.
 Disadvantages: requirement to have a minimal motor
skill and visual and cognitive ability
 Failure of VAS is related to educational level ,
cognitive impairment and motor disability and not age
per se

29.  Numerical Rating Scale:
 Involves asking the patient to rate the pain 0 to
10 or 0 to 100 -0 represents no pain and 10 or
100 represents pain as bad as it could be.
 Advt: good sensitivity
 Easy to administer
 Generates data that can be statistically analysed
 Useful geriartic patients and those with impaired motor
skill

30.  Verbal Rating scale
 Consist of a series of verbal pain description from least to most intense
 Many different VRS lists have been created with adjectives –gradual
change in pain intensity
 For eg: 4- point scale by Seymore
 Score 0 – No pain
 Score 1 – mild pain
 Score 2 – moderate
 Score 3 – severe pain
 Advt- simple to understand
 Preferred for older adults –requires to interpret and express their
pain verbally
 Disadvt: time consuming – if the list is too long to
review
less reliable among illitrates

31.  Mcgill pain Questionairre
 Widely used self-rating instrument for measurement of pain in
clinical and research settings
 Takes into account motivational-affective-cognittive
psychological aspects- sensory physiological aspects
 Enables the pt to choose from 78 adjectives –arranged in 20
groups:
 Group 1 to 10- assess the ssensory dimensions
 Group 11 to 15-assess the affective dimensions
 Group 16-assess the evaluative dimensions
 Group 17 to 20- describes miscellaneous dimensions
 Rank value for each descriptor is based on its position –sum
total of which gives pain rating index(PRI)
 Additionally there is rating scale for Present Pain Intensity

32.  Diagnostic imaging:
 Use of a specific diagnostic imaging depends on DD
after history and examination have been completed
and evaluated
 Needs to consider the cost, potential benefits,
radiation dose and availability of various imaging
techniques
 Plain films , panoramic radiographs, conventional and
computed tomography- osseous morphology and
disorders of the joint
 MRI is most specific and sensitive for interpretation of
soft tissue and inflammatory condition in the joint
 Because 10% of patients with symptoms of TN have
underlying CNS disorder- MRI of brain with thin
sections through the brain is indicated.

33.  Diagnostic Nerve Block
 Helpful in establishing a diagnosis-when used to distinguish
peripheral disease from more centrally acting neuropathic pain.
 If pain does not resolve- neuropathic changes are likely to be
central in origin
 Information gathered from diagnostic nerve block can be
ambigous :
 LA may induce systemic effects
 Proximity of other neural structures to the nerve , ganglion or plexus
being blocked
 Placebo effects
 Technical limitattions- accurate diagnostic nerve block
 Anatomic variations
 Pts may premedicate themselves before the diagnostic nerve blocks

34. GENERAL PRINCIPLES OF TREATMENT
 Pain management (also called pain medicine or algiatry)- branch of
medicine employing an interdisciplinary approach for easing the suffering
and improve the quality of life of those living with pain.
 Interdisciplinary therapies include:
 Education and counselling
 Pharmacological measures
 Pain management techniques such as:
 Electric nerve stimulation techniques
 Nerve – blocking procedures
 Acupuncture
 Psychological therapy: cognitive , behavioural
 Relaxation training via biofeedback, mental imagery, yoga and meditation
 Hypnotherapy
 Occupational therapy
 Physical therapy modlaities
 Stretching strengthening and conditioning programs

35.  Treatment goals usually focus on:
 Managing medication misuse or abuse
 Increasing function
 Reducing the use of medical resources
 Decreasing pain intensity
 Managing associated depression and anxiety

36.  COGNITIVE THERAPY:
 Individuals affect and behaviour are largely determined by the manner
in which he/she structures the world
 In chronic OFP,not unusual encounter patients – express ideas that are
based on false assumptions.
 Maladaptive thoughts lead to behaviour that contribute to the disease
 Cognitive- behavioural model suggests that pts develop negative and
distorted convictions regarding functional capactiy ,diagnosis ,
prognosis and future- affect behaviour and reinforced when activity or
recondtioning proves to be painful;
 Four basic components:
 Education
 Skill acquisition
 Cognitive and behavioural rehearsal
 Generalization and maintenance

37.  Relaxation therapy:
 Relaxation techniques are used for non-directed
calming rather than achieving a specific therapeutic
goal
 Do not always reduce pain intensity and are
recommended as an adjunctive traetment
 GUIDED IMAGERY: (involves recall of a pleasant or
peaceful experience) and YOGA are examples:
 Relaxation techniques share 2 basic components:
 Repetitive focus on a word sound, prayer, phrase, body
sensation or muscle activity
 Adoption of a passive attitude toward intruding thoughts and a

38.  Drug therapy:
 Significant part of OFP management
 Analgesics are generally divided into 3 groups:
 Non-opiods(acetaminophens &NSAIDs)
 Opiods
 Adjuvants
 Often involves simultaneous use of more than one drug
 Takes advantage of different mechanisms of action of different
drugs
 Also allow the use of smaller dose –
 May reduce adverse effects or risks
 Oral route of administration is preferred for compliance
and convenience
 Drug dose titration is required to establish proper

39.  Acetaminophen
 Nacetyl-p-amino phenol- OTC analgesic and anti-pyretic
drug
 Also available in controlled formulations in combination with
codeine and other opiods
 Fewer side effects compared to otherNSAIDs
 Mechanism of action;
 The main mechanism proposed is the inhibition of
cyclooxygenase (COX), and recent findings suggest that it is highly
selective for COX-2.
 In 2011, Anderson et al, metabolites of paracetamol e.g. NAPQI, act
on TRPA1-receptors in the spinal cord to suppress the signal
transduction from the superficial layers of the dorsal horn, to alleviate
pain.

40.  NSAIDs
 class of drugs that provides analgesics antipyretic effects, and, in
higher doses, anti-inflammatory actions
 Most NSAIDs inhibit the activity of (COX-1) and (COX-2), and
thereby, the synthesis of PGs and thromboxanes- inhibiting COX-
2 leads to the anti-inflammatory, analgesic and antipyretic effects-
inhibiting COX-1 may cause gastrointestinal bleeding and ulcers.
 selective COX-2(celecoxib and rofecoxib) inhibitors pose less
risk of GI bleeding and do not inhibit platelet aggregation.
 Combination of NSAIDs increse the risk of side effects
 Treatment with cox-2 inhibitors-pose increased risk for
cardiovascular problems

41.  Opiods
 Largest group of opioids that used for analgesia consists of morphine-
like agonists
 Their most important effects are on the CNS and GI system
 Mechanism of action:
 Bind to m-opiod receptors –actions that lead to analgesic effect
 At membrane level- opening of K+ channels and inhibiting voltage gated Ca2++
channels-decresae in neuronal excitability.
 At spinal level: inhibits transmission of nociceptive impulses through the dorsal
horn
 Use of opiod therapy in moderate to severe acute pain and cancer pain
is well established
 Concern regarding administering for non-malignant pain relates to risk of
additional disability and anti-social behaviour with long term opiod use
 Agonist-antagonist drugs(pentazocine,buprenorphine,butorphanol)-
moderate to severe acute pain-may cause withdrawal symptoms in pts
taking mu agonists-psychomimetic effects-agitation dyphoria and
confusion

42.  Adjuvant drugs:
 TCAs(Tri Cyclic Antidepressant) like amytriptyline-most frequently
studied in clinical trials in chronic OFP treatment-
 Better off than 74% of chronic OFP pts receiving a placebo
 Mechanism of Action:
 Seratonin and Norepinephrine –play role in desecending inhibitory
transmissions from brain to the dorsal horns-modulating nociceptive impulses
 TCAs block the reuptake of seratonin and NE-enhance central inhibitory
system in pain processing-at doses less than those required anti-dpressive action
 Usually introduced at lower dose-gradually increased to reduce adverse
effects
 SEs: dry mouth, increased apetite and weight gain , cardiac effects
sedation and dysphoria

43.  Anticonvulsant drugs
 Effective in the treatment of TN, , diabetic neuropathy and
for migraine prophylaxis
 Mechanism of Action:
 Carbamazepine(tergetrol) stabilizes the inactivated state of voltage-
gated sodium channels- leaves the affected cells less excitable until
the drug dissociates
 also GABA receptor agonist- potentiate GABA receptors- may
contribute to its efficacy in neuropathic pain and manic-depressive
illness.
 Frequent side effects: sedation, dizziness, ataxia
 The starting dose to treat TN is 100 mg twice daily.control of pain is
maintained in most patients with a dosage of 400to 800 mg daily
 Newer drugs like felbamate, lamotrigine produce fewer SEs

44.  Gabapentin:
 Become commonly used in pain management partly
because of its relatively few side effects
 Mechanism of action:
 Binding to cal cium channels and modulating calcium influx as well as
influencing GABAnergic neurotransmission
 A new newer drug similar to Gabapentin konown to have
fewer side effects is pregablin.
 A variety of other adjuvant drugs are used in pain
mangement such as mexiletine, clonidine,
clonazepam and alprazolam- though there is only
limited clinical trials conducted regarding its role chronic
OFP management.

45.  Topical medications:
 Has the advantage of reduced systemic absorption and thereby
reducing the SEs
 Capsaicin:
 Used a topical cream-effective for the management of Post- herpetic
neuralgia(PHN)
 Natural product extracted from pungent red chilli pepper.
 Single application- causes burning sensation- resolves after repeated
application
 Mechanism of action:
 Blocks C-fiber conduction-inactivates release of neuropeptides from peripheral
nerve endings-depletes stores of substance P from sensory neurons-decresing
the inputs to the CNS neurons
 Doxipine clonidine , ketamine, cyclobenzaprine and
carbamazepine- used topically for chronic OFP-not subjected to
clinical trials so far
 Topical NSAIDs like diclofenac effective for musculoskletal pain

46. COMMON FACIAL PAIN DISORDERS
(OTHER THAN NEURALGIAS)

47. CUTANEOUS AND MUCOGINGIVAL PAINS OF
THE MOUTH
 Categorised under superficial somatic pain:
 Bright , stimulating quality
 Excellent subjective localization and anatomically
accurate.
 Site identifies –correct location of its source
 Topical application of LA-temporarily arrests the pain

48. CUTANEOUS PAIN OF THE FACE:
 Usually described as itching, pricking, stinging, burning.
 Initially felt as fast, sharp, pricking pain-mediated by A-delta
 Later slightly delayed, less sharp, burning, less precisely located-
C-fibers
 Diagnosis is easy-precisely felt at the site of cause
 If not immediately evident- might be a heterotopic-topical
application of LA at the site of pain helps in such cases.

49. MUCOGINVIAL PAINS OF THE MOUTH:
 Features of superficial somatic pain
 Usually described as stinging, burning sensation.
 Pain from lining tissue precisely located.
 Is an expression of primary hyperalgesia of tissues that are hurt.
 Pain due to – trauma, allergic responses, local infections, systemic
conditions, burning mouth syndrome.
 Allergic responses – stomatitis venenata, Stomatitis medicamentosa
 Systemic conditions – nutritional deficiencies, anaemia, blood
dyscrasias, intoxification, infections, diabetes

50. BURNING MOUTH SYNDROME:
 Reserved for describing oral burning that has no detectable cause.
 Do not follow anatomic pathway-no mucosal lesions or known neurologic or systemic
disorders-no characteristic laboratory findings
Etiology :
 Cause remains unknown
 Can be a symptom of local factors or systemic deseases including hormonal and allergic
disorders,salivary gland hypofunction,chronic low-grade trauma and psychiatric
abnormalities.
 May also be a complication of drug therapy with ACE inhibitors.
 Depression is frequently asso with psychological disorders in many studies.-not sure wether
its is the cause or effect or BMS

51.  Features:
 Women affected 7 times more frquently than men
 10 to 15 % of postmenopausal women are found to have ahistory of BMS –
most prevalent 3 to 12 years after menopause.
 Tongue is the most common site of involvement.
 Can be intermittent or contimous.
 Drinking or placing candy or chewing gum characteristically relieves the
symptoms
 Generally anxious and high-strung-less appetite- insomnia
 Other causes of burning symptoms of oral mucosa must be eliminated.
 Combination of xerostomia with BMS must be evaluated for salivary gland
disorder.
 Lab tests –detect undiagnose Diabetic neuropathy, anemia or Fe –
deficiency, folate or vitamin B12

52.  Management:
 Once diagnosed, pt should be reassured of the benign
nature of the condition.
 Pts with more severe symptoms may require drug therapy
that includes:
 Low dose of TCAs or clonazepam (clinician prescribing these
should familiarize with SEs)
 A 2-month course of 600mg daily of alpha-lipoic acid –shown
to reduce BMS pain
 Systemic capsaicin(0.25% capsule 3/d for 30 days)

53. DENTAL PAIN
 Types:
 Odontogenic tooth
ache
 Pulpal origin:
 Acute pulpal pain
 Chronic pulpal pain
 Recurrent pulpal pain
 Periodontal origin
 Non odontogenic tooth
ache:
 Sinus/nasal mucosal
origin
 Neurovascular origin
 Neruropathic origin
 Cardiac origin
 Psychogenic origin

54. TOOTH ACHE:
 Odontogenic tooth ache:
 Pulpal origin
 Pain is of visceral character –threshold type-as opposed to graduated response compared
to musculoskeletal pain
 Respond to impact, shock, thermal & chemical irritants, direct exploration.
 Non localizable.
 Classified : acute , chronic, recurrent, mixed .
 Do not remain the same
 Acute pulpal pain
 Non localizable.
 Cause –responds to injury-inflammatory changes-may be reversible unless congestion
occurs-pulpal necrosis-threshold is decreased
 Response
 Pain – hypersensitivity, throbbing. Aggravating factors. Progress

55.  Chronic pulpal pain
 Injured pulal tissue may progress from an acute to
chronic inflammatory phase –neithr resolution – nor
necrosis.
 Pain is milder . Symptomless
 Recurrent pulpal pain
 Sensed as Recurrent hypersensitivity
 Asso with changes in vascular pressure or fluid balance
 So- called high-altitude tooth ache fall into this category.

56.  Periodontal origin:
 Deep somatic pain of the musculoskeletal type.
 More localised-related to biomechanical function.
 Arise due to local cause like trauma, occclusal overloading, or may result from
spreading inflammatory reaction through apical canal / lateral root
canal(causing peripaical/periodontal abscess)
 quality is dull aching and occasionally throbbing
 Indentifiable periodontal condition.
 Pain proportional to provocation of the tooth
 Pain is reduced or eliminated by a local anesthetic injection of the tooth region

57.  Tooth ache of non odntogenic origin:
 Features:
 Failure of local provocation of site of pain
 Failure of local anesthetic agent to reduce the pain
 They include:
 Muscular toothache
 Neurovascular toothache
 Cardiac toothache
 Neuropathic toothache
 Sinus toothache
 Psychogenic toothache

58. TOOTH ACHE OF MYOFASCIAL RORIGIN:
 Myofascial pain –regional myogeneous pain characterised by local areas of firm
, hypersensitive bands of muscle tissue –trigger points.
 Etiology – complex-simons et al described certain local and systemic factors –
trauma , hypovitaminosis,poor physical conditioning, fatigue and viral infections-
also emotional stress
 Recent studies-pointed toward genetic polymorphism of gene coding for
catechol-o-methyltransferase –involved in catecholamine metabolism.

59.  Features :
 Pain is relatievely constant, dull, aching, non –pulsatile
 Pain is not altered by local stimulation of the tooth
 Examination reveals the presence of localised
firm,hypersensitive bands within the muscle tissue
 Increased with funstion of invovlved muscle
 Palpation and stimulation of the trigger points increase the
tooth ache
 Confirmed anesthesia of tooth doesnot relieve the tooth
ache
 LA inj of involved muscle (trigger points) reduces the tooth
ache

60.  Management of myofascial pain:
 Eliminate any source of ongoing deep pain input
 Reduce the local and systemic factors
 If sleep disorder is suspected,proper evaluation and referrel
should be made
 Treatment and elimination of the trigger points.following
techniques can be used to achieve this:
 Spray and stretch –vapocoolant spray(ethyl chloride) –actively
stretching
 Pressure and massage
 Ultrasound and electrogalvanic stimulation
 Pharmocological therapy-using muscle relaxant

61. NON-ODONTOGENIC TOOTHACHE OF
SINUS/NASAL MUCOSAL ORIGIN
 Pain arising from the nasal mucosa –resullt of viral, bacterial or
allergic rhinitis-expressed as referred pain throughout the maxilla
and maxillary teeth .
 Inflammation of the ostium-compresses nociceptors –refers pain to
maxillary teeth

62.  Features:
 Reports pressure felt below the eyes
 Incresed by applying pressure over the involved sinus
 Tooth is sensitive to percussion
 Increased by lowering the head
 In creased by stepping hard on to the heel of the foot
 LA of tooth-partially reduce the pain or it may fail to reduce any pain
 Diagnosis confirmed by CT scan or Waters view
 Management considerations:
 Bacterial sinusitis is often treated with β-lactamase-resistant antibiotics such as
amoxicillin with clavulinic acid-Allergic rhinitis –antihistamines or
decongestnatss

63. TOOTH ACHE OF CARDIAC ORIGIN
 Cardiac ischemia can refer pain- arm,neck,face and even teeth.
 Likely related to convergence of nociceptive input originating
from myocardial ischeamia carried by vagus and thoracic nerves
as they enter the CNS and ascend to the cortex.
 Important to appreciate this pattern of pain referral-immediate
diagnosis and referral to appropriate HCP is critical

64.  Features:
 Deep,diffuse toothache that may sometimes pulsate
 Has a pressure burning quality
 Has a temporal behaviour-increases with physical exertion or exercise
 May/may not be asso with chest pain, anterior neck pain, throat pain,
and/or shoulder pain.
 History of CVS disease
 Decreased with nitorglycerine tablets
 Management considerations:
 Complete health history is essential
 When cardiac origin is suspected-referral to proper medical personnel is
mandatory

65. TOOTH ACHE OF PSYCHOGENIC
ORIGIN(SOMATOFORM TOOTH ACHE)
 Term somatoform pain disorder is used to describe a cognitive perception of
pain –no demonstrable physical basis.
 Pose a significant diagnostic problem
 Not associated with any obvious source of local somatic tissue changes

66.  Features:
 Pain is reported in many teeth and/otr other sites
 Pain jumps from tooth to tooth or to other locations
 General departure from normal or physiological patterns of pain
 Lack of response to reasonable dental treatment
 Unusual and unexpected response to treatment
 Chronic and often unchanging
 Presents with chronic pain behaviour
 Frequent use of health care systems
 Unusual dependence on others
 Reclusive non-functional lifestyle
 Significant use of medications
 Management considerations:
 Somatoform disorders are mental disorder –best treated by psychologists or
psychiatrist
 Any irreversible dental procedures should be avoided

67. VASCULAR PAIN:
 Pain originating from vascular structures may
cause facial pain that can be mis diagnosed and
mistaken for other oral disorders.
 They include:
 Cranial arteritis
 Cluster head ache
 Migraine
 Chronic paroxysmal hemicrania

68. CRANIAL ARTERITIS
 Also called temporal arteritis
 Inflammatory disorder involving medium-sized branches of carotid arteries-
temporal artey most involved-localised to head and face
 Etiology:
 Immune disoders that affect cytokines and T-lymphocytes –inflammatory
infiltrate in the walls of the arteries-characterised by multinucleated giant cell
formation-underlying trigger is unknown

69.  Features:
 Affects adults above the age of 50 years
 Throbbing headache-accompanied by generalized symptoms, including
fever, malaise , loss of appetite.
 Examination of temporal artery-thickened pulsating vessel
 Since mandibular and lingual arteries may be involved –throbbing pain
in jaw or tongue-early sign
 Serious complication-lead to progressive loss of vision or sudden
blindness
 Lab diagnosis:
 Elevated ESR and anemia
 Abnormal C-reactive protein
 Definitive diagnosis-biopsy-characteristic infiltrate and multinucleated
giant cell

70.  Treatment:
 Systemic corticosteroids-prednisone(40-60mg / day)
 Tapered once the signs are controlled
 ESR-helps in monitoring the disease status
 Maintainance of systemic steroids for 1 to 2 years after
symptoms resolve.
 Supplemented by adjuvant therapy with
immunosuppressive drugs –cyclophosphamide-

71. CLUSTER HEAD ACHE
 Distinct pain syndrome –episodes of severe unilateral head pain –
occuring aroun the eye –accompanied by number of autonomic signs.
 “Cluster”-indivual experience multiple head aches per day for 4 to 6
weeks and then may be without pain for months
 May originate in the hypothalamus and vascular systems in the braon –
or in the cavernous sinus.

72.  Features:
 80 % of pts are men.
 Attacks-sudden,unilateral and stabbing-causing pts to pace,cry out, or
even strike objects
 Most commonly affect the area supplied by first division of TN-2 nd
division may also occur-dental consultation
 Begins with aura –become excritiating within a few minutes
 Each attack- lasts for 15 min to 2 hrs several times daily-majority at night.
 Asso with autonomic symptoms-nasal congestion and tearing-sweating
of face,ptosis,hypersalivation,edema of eye-lid are also common signs

73.  Treatment:
 Acute attack aborted by breathing 100% o2
 Inj sumatriptan or inhaled ergotamine may also be effective
 Lithium is effective –long-tem use can cause renal toxicity
 Other drugs include-prophylactic predisone, calcium channel blockers
 Chronic paroxysmal hemicrania
 Form of CH-occurs predominantly in women-30 to 40
yrs of age
 Episodes tend to be shorter-5 to 20 minutes-upto 30
times daily
 CPH tend to be become chronic overtime
 Responds dramatically with indomethacin

74. MIGRAINE
 Migraine is the most common of the vascular headaches-may
also cause pain of the face and the jaws.
 My triggered by foods,stress,sleep deprivation,or hunger.
 More common in women
 Etiopathogenesis:
 Classic theory : migraine is caused by vasoconstriction of
intracranial vessels(neurologic symptoms) followed by
vasodialation(pounding headache)
 Triggering of neurons in the midbrain –activation of trigeminal
system –release of neuropeptides like substance p-acts on
receptors of cerebral vessels- vasodialation and vasoconstriction

75.  Types:
 Classic:
 Starts with a prodromal aura-usually visual-includes flashing lights or
scotoma.photophobia, hemianesthesia , aphasia can be part of aura.
 Aura is followed by increasingly severe head ache –unilateral throbbing asso with nausea
and vomitting.-lasts for hours to 2 or 3 days
 Common:
 Not preceded by aura
 Pain resembles classic migraine
 Basillar
 Most common in young women
 Neurologic symptoms aphasia taxia blindness vertigo confusion-accompanied by occipital
head ache
 Facial(carotidynia)
 Throbbing pain face, jaw ,neck
 Involvement of caotid artery branches
 Usually begins in individual of 30 to 50 years
 Pts often seek dental consultation-but is not continous –lasts minutes to hours
 Examination of neck reveals tenderness of caroitid artery

76.  Treatment:
 Should be carefully assessed to determine common food trigers
 Attempts to minimize reaction to stress –relaxation techniques
 Drug therapy:
 May be used either prophylactically or acutely at the first sign
of attack
 For abortive therapy:ergotamine, sumatriptan(5HT agonists)
 For preventive therapy: propranolol, verapimil, and TCAs.

77. COMPLEX REGIONAL PAIN SYNDROME(CRPS)
 Chronic systemic disease – severe pain, swelling, and changes in the skin.
 often worsens over time- initially affect an arm or leg and spread throughout the
body
 Types:
 Type I, formerly known as reflex sympathetic dystrophy (RSD)
 does not exhibit demonstrable nerve lesion
 Type II, formerly known as causalgia, has evidence of obvious nerve damage.
 feature the more painful and difficult-to-control symptomes of CRPS

78.  Etiology:
 Result from changes after trauma –that causes coupling of sensory nerve fibres
with sympathetic stimuli.
 Evidence for this includes the studies that shows that surgical or drug-induced
blockades of sympathetic nervous system relieve the symptoms.
 Features:
 Spontaneous chronic burning pain and tenderness, accompanied by motor
dysfuncstion, sweating and cutaneous atrophy
 Involved skin-edematous and erythematous-changes in blood flow-underlying
bone is demineralised.
 Allodynia and hyperesthesia are common

79.  Treatment:
 Multidisciplinary approach includes physical therapy,
nerve blocks and drug therapy
 Blockades of regional sympathetic ganglion or regional
IV blockade with guanethidine, reserpine,or
phenoxybenzamine combined with LA,successfully
employed
 Bisphosphonates given IV –decreased pain in some pts

80. ATYPICAL FACIAL PAIN (ATYPICAL ODONTALGIA)
 Type of chronic facial pain which does not fulfill any other diagnosis
 No objective signs, negative results with all investigations/ tests, no obvious
explanation for the cause of the pain, and a poor response to attempted treatments
 the term AO may be used where the pain is confined to the teeth or gums, and AFP
when the pain involves other parts of the face.
 are umbrella terms for a heterogenous group of misdiagnosed or not yet fully
understood conditions- unlikely to each represent a single, discrete condition.

81.  Causes:
 One theory considers AFP and AO to be a form of deafferentation or phantom tooth pain
 Also theorised that –form of vascular neuropathic or sympathetically maintained pain.
 Others have proposed a strong psychogenic component –depressive, somatization and
conversion disorders have been described as major factors
 Features:
 Constant aching pain without apparent cause that can detected
 Most frequent among women -4th and 5th decades of life
 No trigger zones-some report pain coincided with dental procedure-oral surgry/endontic
 May can be unilateral or bilateral
 A thorough history and examination –evaluation of cranial nerves ,muscles of
mastication, oropharynx and teeth must be done rule out a definite cause-
 Pateints with AO and AFP –normal radiographic and clinical lab findings

82.  Management:
 Should be counseled regarding the nature of AO and reassured that
they do not have any undetectable life-threatening disease and can
be helped without invasive procedures
 TCAs such as amitryptyline,desipramine and doxepin – low to
moderate dose-effective reducing the pain
 Some clinicians report benefit from topical densensitization with
capsaicin, topical anesthetics or topical doxepin

83. CONCLUSION

84. References
• Bell’s Orofacial pains 5th, 6th edn – Jeffrey P.Okeson
• Oral Medicine – Diagnosis and Treatment 11th edn – Burket’s
• Orofacial pain- a primerDent cln N Amr. 2013;57: 383-392
• Andersson DA, Gentry C, Alenmyr L, Killander D, Lewis SE, Andersson A,
Bucher B, Galzi J-L, Sterner O, Bevan S, Högestätt ED, Zygmunt PM
(2011). "TRPA1 mediates spinal antinociception induced by acetaminophen
and the cannabinoid Δ(9)-tetrahydrocannabiorcol". Nat Commun 2:
551. doi:10.1038/ncomms1559
• Claesson, A. "On the mechanism of paracetamol's analgesic activity and a
note on related NSAID pharmacology“
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