1.1 Introduction

Pain in the head, neck and mouth region is a common affliction, affecting up to 26% of the population (MacFarlane et al 2002). Acute pain is a protective reflex in health and stops us damaging ourselves. In addition once injured the increased sensitivity from the swelling (inflammation) caused by the region helps to remind us to protect the region from unnecessary movement and further trauma thereby helping maximise healing capacity. If the pain persists beyond the healing phase it is known as “chronic” pain. If chronic pain develops it is thought that a large proportion of this type of pain is due to subtle changes in the peripheral and central nervous system that mean the pain sensing nerves (nociceptors) process normal and painful information differently. A good explanation of how pain can become chronic can be found on this link or this video:


We are therefore evolutionarily programmed to interpret pain as a warning sign of tissue being damaged and often protective reflexes will ensue. The fact is that we now understand it is possible to have pain without visible damage or pathology and science is beginning to unpick the nerve-based mechanisms behind this.

The facial region contains structures vital for living: eyes for sight, mouth for breathing, communicating and eating, and ears for hearing. In addition the essential organ, the brain, is also obviously in close proximity. It should be of no surprise, therefore, that any threat of damage to this region is likely to initiate primitive survival instincts and this may amplify the psychological and physiological consequences of pain in this region. This coupled to the level of sensory supply to the face probably helps explain the highly distressing nature of pain in this region. Please see this link.

This partly explains as to why pain in the orofacial region causes such fear and emotion in patients. The face and head include many structures (ears, joints, eyes, sinuses, teeth to name a few) so it’s often very complicated getting the diagnosis right. It takes time and patience, a multidisciplinary team and plenty of support.

1.2 What is pain? 

So what is pain?  It is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”.  This is an over- simplification of the complex, entirely subjective, sensation with physical and psychological effects. The pain mechanism involves nociception (the transmission of the painful stimulus to the sensory cortex), sensation (arrival of the stimulus at the sensory cortex and recognition of pain), pain behaviour and suffering (the results of engagement of the affective and Limbic systems). Pain is formed of 4 key stages;

  • Nociception – the basic neuro protection mechanism
  • Sensation- conscious recognition of pain
  • Behaviour- resultant behavior caused by acute and ongoing pain
  • Suffering- resultant suffering

The initial sensation (nociception resulting in the sensation of pain) is simultaneous to the emotional reaction to pain (anxiety, stress, fear) and they cannot be separated from each other. This then leads to the resultant behavior and suffering as a result of the pain ‘experience’.  Pain experience is dependent upon age, gender, ethnicity, culture, pain experience, personality, stress, depression and anxiety.

Figure 1.1 The Biopsychosocial model of pain influencing factors

Figure 1.1 The Biopsychosocial model of pain influencing factors

The biopsychosocial model applies to pain management (Fig 1.1) and various settings can affect your pain levels including whether you are stressed, anxious and or tired, whether you trust in your clinician.  It is known that soldiers in military zones have higher pain thresholds in combat than off duty; and rugby players continue to score tries even having just sustained a fracture during a tackle.

Downward modulation of pain is key and the ultimate example of complete control of pain modulation (both behavior and suffering), with a full onslaught of nociceptive input, is the self-emolliating Tibetan monk. Whether due to hypnotism, meditation or acupuncture, blocking of the limbic reaction to the overwhelming sensory input is a skill, which happens in all of us during sleep. If only we could harness the elements of the sleep downward modulation blocking pain signals, we would win the battle against pain!

Pain can be caused by organic and psychological causes.  Herta Flor’s pain psychology group in Mannheim have eloquently shown with MRI studies in man that a significant vascular activity in reaction to pain is initiated due to the affective components of pain rather than the physical nociceptive process.

Measuring pain is near impossible.  Pain experience is an entirely individual response.  No other person can derive your own experience of pain because you alone experience it; and due to its complexity, conveying your total pain experience to others is impossible.  Unless your clinician is equipped with Dr Spock’s (from Starship Enterprise not paediatrics) ability to key into your experience using bi-temporal palpation, sharing your pain experience will depend upon your clinician’s talent for listening and empathising that may, in part, allow him/her to begin to understand your pain.  We attempt to gain an idea of the affective component of your pain experience using questionnaires for psychometrics and we use questionnaires to assess your functionality, disability and behaviour.  Scoring pain using a Lickhert scale is standard but it massively over simplifies the complex pain experience.The patient may be fit and well or have significant co-morbidity including medical history complexities or have difficulty managing their anxiety and fear during the procedure. Fear and anxiety may require adjunctive therapy including behavioural and medical techniques .

Consulting a patient in pain requires specific skills and excellent communication. The patients are often anxious visiting the dentist without pain. Whilst in pain their anxiety levels are increased potentially related imminent treatment necessary to treat the cause of their pain. Communication is key to eliciting an appropriate history from your patient and the clinician must be a good listener. The patient must also be able to communicate clearly and this is often not the case (children, Intellectual disability in general population 2.5%, Cerebral palsy, Dementia in  8% of people over 65 years, Brain damage:  5 - 1.9 million head injuries per year with 10% of these being serious). These people are all vulnerable to pain even more so because of their inability to communicate it.

1.3 Mechanism of pain

We now understand that specific and general receptors and transmitters at the primary, secondary and tertiary sensory neuron interface play a role in regulating pain.  We understand that the key primary sensory nerves transmitting painful stimuli are A Delta (cold and pain) and C fibres (warm and pain).   They synapse with the secondary order sensory neurons a specific region of the spinal cord (Lamina I of the Distal Root Ganglion).  These secondary order neurons convey pain to the contra-lateral tertiary sensory neurons in the sensory cortex.  Other specific areas of the brain play a role in pain although their roles are not yet fully understood (thalamus, anterior cingulate cortex, insula and brainstem) (Figure 1.2).

fig1.2

Figure 1.2 Pain Pathways

1.4 Nociception

The first stage of nociceptive pain is the initiation of an action potential in one of the pain specific fibres caused by local mediators in traumatized tissue.  Inflammatory ‘soup’ resulting from tissue damage causing elicitation of action potential in local nociceptor neurons. Pain mediators such as bradykinin, cytokines and serotonin (5-hydroxytryptamine, 5-HT) are specific chemicals that stimulate nociceptors, and are released at the site of tissue damage. These nerve endings are further sensitized by prostaglandins, which can contribute to the pain experience considerably. The combination of mediators and prostaglandins at the site of tissue trauma is sometimes referred to as "inflammatory soup". These chemical mediators are an extremely important component of the pain experience, as they constitute the initiation of the pain cascade. LOCAL anaesthetics work at this level preventing response to the Inflammatory ‘soup’ preventing elicitation of action potential in local nociceptor neurons.

Pain mediators such as bradykinin, cytokines and serotonin (5-hydroxytryptamine, 5-HT) are specific chemicals that stimulate nociceptors, and are released at the site of tissue damage. These nerve endings are further sensitized by prostaglandins, which can contribute to the pain experience considerably. The combination of mediators and prostaglandins at the site of tissue trauma is sometimes referred to as "inflammatory soup". These chemical mediators are an extremely important component of the pain experience, as they constitute the initiation of the pain cascade.

Many factors are involved in tissue healing after injury and many have an algesic effect resulting the classic signs of inflammation (Tubor -RED, Dolor- PAIN, Calor-HEAT and Tumor-SWELLING).

The specific peripheral tissues involved in pain include tissue injury, ischemia, or cellular stress generates an array of pro-algesic and pro-inflammatory agents, collectively referred to as the “inflammatory soup.” This includes extracellular protons (H+), bradykinin (BK), and nerve growth factor (NGF), as well as reactive oxygen species (ROS) that convert polyunsaturated fatty acids into reactive carbonyl species, such as 4-hydroxy-trans-2-nonenal (HNE). Some factors, such as HNE and protons, activate PAIN RECEPTORS including sodium channels (NaV1.3, 1.4, 1.7 and 1.8), Vanilloid recepors (TRPA1 or TRPV1) directly, while others, such as Bradykinina (BK) and Nerve Growth Factor (NGF), modulate channel gating indirectly by binding to cognate receptors (Bradykinin Receptors  and  tropomyosin-receptor-kinase TRKA, respectively) to activate cellular signaling cascades, most notably those downstream of phospholipase C (PLC). Some receptors, TRPA1 and TRPV1 function as polymodal signal integrators capable of detecting chemically diverse products of cell and tissue injury. In doing so, these channels promote pain hypersensitivity by depolarizing the primary afferent nerve fiber and/or lowering thermal or mechanical activation threshold. In addition sodium channel receptors are activated by similar pathways.

injury

Figure 1.3 Activation of Pain Receptors

Figure 1.3 Activation of pain receptors on nociceptive fibres (c and A Delta neurons) and resultant intracellular calcium changes and resultant membrane depolarisation

1.5 Neural response to insult (Nociception)

The function of a nerve is to carry messages from one part of the body to another. These messages, in the form of electrical action potentials, are called impulses. Action potentials are transient depolarisation of the membrane that result from a brief increase in the permeability of the membrane to sodium and usually also from a delayed increase in the permeability to potassium.

Impulses are initiated by chemical, thermal, mechanical or electrical stimuli. Once an impulse is initiated by a stimulus in any particular nerve fiber, the amplitude and shape of that impulse remain constant. Regardless of changes in the quality of stimulus or its strength, the impulse remains constant without losing strength as it passes along the nerve because the energy used for its propagation is derived from the energy that is released by the nerve fiber along its length and not solely from the initial stimulus.

1.6 Pain Afferents

Pain afferents can be myelinated or unmyelinated.

  • The unmyelinated pain fibers belong to the class of afferent fibers called the C fibers and conduct from about 0.5 to 2.0 meters/second.
  • The myelinated pain afferents belong to the class of afferent axons termed the A-delta fibers and conduct action potentials between about 5 to 30 meters/sec. These are the smallest and slowest of the myelinated axons. (By contrast, myelinated axons for fine touch and proprioception conduct between 35 to 120 meters/sec.)

A C fiber can respond to a broad range of painful stimuli, including mechanical, thermal or metabolic factors. The pain produced is slow, burning, and long lasting. The neurotranmitter in the dorsal horn is glutamate along with certain peptides such as substance P. The receptors for glutamate are not only fast, five subunit ligand gated ion channels, but also NMDA receptors. The latter do not open immediately, but only following prolonged depolarization. Thus, continual stimulation of C fibers eventually causes greater excitation in the postsynaptic neurons in the dorsal horn as the NMDA receptors start adding to the response.

An A-delta fiber responds to either mechanical stimuli or temperature stimuli in the painful realm and produces the acute sensation of sharp, bright pain. Their neurotransmitter in the dorsal horn is glutamate acting on fast, five subunit ligand gated ion channnels.

The receptor for capsaicin, which is found in hot peppers, is located in the C fibers. This ion channel normally is opened by hot stimuli.

nerves

Figure 1.4 Nerve Fibres, their structure and upward connections

C fibres transmit heat and pain
Aδ fibres transmitting pain and cold
Any larger myelinated fibres (A beta) for proprioception and mechanosensory function may play a role in pain.

On the basis of their diameter, nerve fibers are categorized into 3 types. Type A fibers are the largest and are responsible for conducting pressure and motor sensations. Type B fibers are myelinated and moderate in size. Type C fibers, which transmit pain and temperature sensations, are small and unmyelinated. As a result, anaesthetics block type C fibers more easily than they do type A fibers. As nocioceptive fibres tend to be small and highly active (especially when you are drilling a hole in a tooth) LAs will tend to act on these rather than large, less active motor fibres. Therefore, patients who have blocked pain sensation still feel pressure and have mobility because of the unblocked type A fibers.

membrane

Figure 1.5 Membrane Stabilization

Nerves transmit sensation as a result of the propagation of electrical impulses; this propagation is accomplished by alternating the ion gradient across the nerve cell wall, or axolemma.

In the normal resting state, the nerve has a negative membrane potential of -70 mV. This resting potential is determined by the concentration gradients of 2 major ions, Na+ and K+, and the relative membrane permeability to these ions (also known as leak currents). The concentration gradients are maintained by the sodium/potassium ATP pump (in an energy-dependent process) that transports sodium ions out of the cell and potassium ions into the cell. This active transport creates a concentration gradient that favors the extracellular diffusion of potassium ions. In addition, because the nerve membrane is permeable to potassium ions and impermeable to sodium ions, 95% of the ionic leak in excitable cells is caused by K+ ions in the form of an outward flux, accounting for the negative resting potential. The recently identified 2-pore domain potassium (K2P) channels are believed to be responsible for leak K+ currents.

The Na channel has two gates: an activation ("voltage sensor") or "m-gate" and an inactivation or "h-gate". The voltage-dependend activation leads to closing of the inactivation-gate ("h-gate") within 1-2 milliseconds. Repolarization leads to conformation changes (= closing) of the "m-gate" (now, both gates are closed), which forces the "h-gate" to re-open within 2-5 ms (= refractory period). When a nerve is stimulated, depolarization of the nerve occurs, and impulse propagation progresses. Initially, sodium ions gradually enter the cell through the nerve cell membrane. The entry of sodium ions causes the transmembrane electric potential to increase from the resting potential. Once the potential reaches a threshold level of approximately -55 mV, a rapid influx of sodium ions ensues. Sodium channels in the membrane become activated, and sodium ion permeability increases; the nerve membrane is depolarized to a level of +35 mV or more.

impulse

Figure 1.6 Impulse activation and action potential

Once membrane depolarization is complete, the membrane becomes impermeable to sodium ions again, and the conductance of potassium ions into the cell increases. The process restores the excess of intracellular potassium and extracellular sodium and reinstates the negative resting membrane potential. Alterations in the nerve cell membrane potential are termed the action potential. Leak currents are present through all the phases of the action potential, including setting of the resting membrane potential and repolarization. Local anaesthetics act by preventing action potential development in all nerves both motor and sensory.

salatatory

Figure 1.7 Transmission ‘saltatory’ conduction / Modulation of the impulse

Saltatory (latin Saltare to jump)  is the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials. The uninsulated nodes of Ranvier are the only places along the axon where ions are exchanged across the axon membrane, regenerating the action potential between regions of the axon that are insulated by myelin, unlike electrical conduction in a simple circuit. This form of neural transmission is very energy efficient and fast.

1.7 Sensation

When the action potential reaches the third order neuron at the sensory cortex, then pain is recognized consciously. The sensory cortex activation occurs simultaneously to activation of the limbic and affective components of the brain resulting in behavioural and suffering dependent upon the many biopsychosocial, phenotypic and genotypic factors.

1.8 Behavioural and suffering due to pain

As explained the pain response is predominantly emotional and not due to the ‘nociceptive’ sensory neurological process. Thus management of both acute and chronic pain conditions involves a holistic approach often using good patient management skills, patient education, psychological and medical (sedation) methods.  Acute nociceptive pain is managed holistically understanding that reduced stress and anxiety maximises the pain relief for the patient with the added benefit of LA techniques providing excellent nociceptive pain management. Chronic pain management require different skills with more emphasis on psychological and medical management of the patient’s behavioural and suffering caused by their pain experience.

However our comprehension of the mechanisms behind the complex peripheral and central nervous system interaction has only just begun.  Translational research methods including functional MRI, biomolecular and genetic assays are rapidly improving our ability to research these mechanisms in man.  Psychometric studies (social, illness behaviour, psychological distress, beliefs and attitudes, personality traits, drug abuse) will enhance our understanding of the affective components of pain.

1.9 Types of pain

A recent article highlighted that there 4 types of pain (Figure 1.8). Two ‘healthy’ protective types of acute pain (Nociceptive and inflammatory please see link) and 2 types of chronic pain whereby the pain is symptomatic of a diseased neuromatrix and persist long after the protective pain mechanisms have subsided. Woolf et al (2010 Figure 3) described nociceptive pain by which tissue damage is registered centrally and reflexes result in order to protect your body from threat. The inflammatory pain that results after tissue damage has occurred and results mainly from local nerve instigating neurogenic inflammation and drawing healing mechanisms to the damaged site to expediate and facilitate tissue healing (increased vascularity, nerve growth, tissue repair by phagocytes and collagenesis and wound healing). These are both protective neural mechanisms at the frontline of  defence and immunological responses.

dentine

Figure 1.8 Types of pain and related dental conditions

The chronic pain states include neuropathic pain when there is a lesion of the sensory system (in PNS and or CNS) resulting in chronic pain resulting from a tissue insult. Many causes including; viral infections (Post herpetic neuralgia), surgery (post traumatic neuropathy), Diabetes (metabolic insufficiency of nerves), chemotherapy, tissue damage due to (chemical, thermal and radiation damage), vitamin deficiencies (Vit B complex and E) and demyelination (due to malignancy, motor neurone disease, multiple sclerosis). All these mechanisms can cause neural lesions leading to persistent neuropathic pain in some patients. If your patient is a migraineur, has existing neuropathic or dysfunctional pain conditions (Back pain, Irritable bowel for example) is over 50 then the risk is increased.

The second type of chronic pain is idiopathic or dysfunctional pain. This typically presents as long term chronic pain unresponsive to all known drugs and remedies. The various tyes of pain with their trigeminal correlates are shown in Figure 3.When pain affects the trigeminal system the patients life is miserable as the trigeminal nerve is the largest sensory nerve in the body represeneted on over 50% of the sensory cortex. In addition the trigeminal nerve is the main primordial sensory nerve of the cranial nerve system. It is protective of the vital organs that underpin our existence (brain, airway, sight, smell, gustatory). Thus chronic pain in the trigeminal system can affect the patients identify and perception of self.

The issues specific to trigeminal pain include the problematic impact on daily function.  By nature of the geography of the pain (affecting the face, eyes, scalp, nose, mouth) interference with just about every social function we take for granted is significant.  It is no wonder that pain within the trigeminal system in the face is often inescapable.

It is often forgotten that there are several types of dental pain. Because inflammatory pain is by far the most common send in the dental clinic, dentists are occasionally ‘fooled’ into treating non inflammatory or neuropathic dental pain by surgery, which will be ineffective and cause unnecessary harm to the patient.

dentalpain

Figure 1.9 Types of Dental Pain

Management of dental pain includes management of 4 aspects:

  • Prevention of dentine sensitivity
  • Intraoperative- managing patients undergoing surgical procedures of the face, jaws and mouth requiring anaesthesia (general or local) will require intra-operative pain management
  • Post-surgical pain management.
  • Patient presenting with pain (usually caused by acute infection) as a symptom. The pain may be chronic (lasting over 3 months) or acute (lasting under 3 months) usually a symptom of ongoing pathology.

Management of intraoperative pain –Must be holistic and involves many skills and may include; preoperative analgesia, Local anaesthesia with or without adjunctive sedation (for anxiolysis) and general anaesthesia for prolonged or extensive surgical procedures.

This guide does not attempt to cover:

  • Management of anxiolysis, non-medical (behavioural) and medical (sedation) Management of acute post-surgical pain
  • Management of acute orofacial pain-patient presenting with dental pain as  a symptom
  • Management of chronic trigeminal pain conditions

1.10 Treatment planning

In order to provide each patient with the most suitable treatment plan to address individual needs it is essential to discover as much information as possible about each patient’s experience, expectations, health and quality of existing dentures.

The cornerstones of treatment planning in Dentistry are:

  • Thorough history ( Social, dental and medical)
  • Careful examination
  • Appropriate special tests ( Radiographic, MRI, Blood, Histological, Psychometrics etc)
  • Correct Diagnosis or occasionally a list of likely differentials

In order to ensure that your diagnosis is correct you must ensure that you have the correct diagnosis. A detailed pain history will often confirm diagnostic features (Table 1.1). Often within the trigeminal system diagnosis can be challenging and a differential diagnosis list must be made. Investigations (Table 1.2) will enhance deriving the diagnosis. Remember, understanding your neurology and neural supply is fundamental to identifying the correct diagnosis (Section 2). Don’t forget using diagnostic LA block when appropriate can also facilitate diagnosis in complex cases.

Please see more information on Pain Assesssment.

It is imperative that the clinician establishes the correct diagnosis based on the history, investigations and examination of the patient in order to provide the appropriate and optimal treatment.

Table 1.1 Pain History

Character
Severity
Site, radiation
Duration, periodicity
Provoking factors Importantly for dental pulpal pain and periapical periodontitis
Relieving factors
Associated factors (functionality, disability, psychological effects)

Table 1.2 Examination with reference to pain and Special tests required for pain patients

Diagnostic requirements:
Identify signs of; Inflammation Redness swelling heat pain (tenderness)Response to anti inflammatoriesResponse to antibiotics if initiated by infectionTenderness to percussion of a tooth-indication of periapical periodontitis
Loss of function Trismus, inability to bite on tooth, difficulty swallowing
Pulpal testing (ethyl chloride) non response does not signify pulpal necrosis, positive response may be complicated in multi rooted teeth with varying rates of pulpal death in different canalsHyper- responsiveness to cold may indicate that the pulp is inflamed reversibly and hyperaemicHyperresponisveness to heat may indicate irreversible pulpitisPain with sweetness may indicate leakage into the pulpal cavity via caries or fractured breached crownIntermittent hypersensitivity on biting may indicate ‘cracked tooth syndrome’ using a ‘tooth sleuth’ or simply a mirror handle between the tooth cusps..pain will often be elicited on biting down on the instrument
Neuropathic signs Mechanical allodynia (pain to touch)Hyperalgesia ( increased pain to painful or noxious stimulus)
Radiographs Long Cone periapical for individual to 3 teeth in single quadrantIf multiple quadrants or impacted teeth use DPTRarely additional radiographs are required (spreading infection covered in Oral Surgery Section)
Differential diagnosis with Trigeminal neuralgia mimicking toothache
Haematological investigations required for patients with chronic pain ESR CRP levels in acute spreading infections (see Oral Surgery section)For Chronic pain pains with pain of unknown causeFBC with Haematinics (Fe, B12, Folate)Zinc (required for Fe absorption)CRP levelThyroid function testsHBA1c (exclude Diabetes)Autoantibody screen (ENAs and ANAs)
Signs sinister disease Over 50yrsSudden recent onset and intensePainless trismus, Worsening trismus despite therapyNeuropathyAsymmetry

2.1 Types of Orofacial pain

Pain diagnosis is complex. See the separate sections on Pain Diagnosis and Dental Pain.

Orofacial pain is pain within the trigeminal system. The trigeminal nerve supplies general sensory supply to face, scalp, and mouth. A vast proportion of the sensory cortex represents the trigeminal input (over 40%).

somato

Figure 2.1

The trigeminal sensory region is very complex, incorporating the cranium, ears, eyes, sinuses, nose, pharynx, infratemporal fossa, jaw joint, teeth, jaws, salivary glands, oral mucosa, and skin. As many medical students are rarely exposed to ear, nose, and throat (ENT), otolaryngology, and dentistry, this region remains an enigma to most, with their singular experience of trigeminal pain being based on trigeminal neuralgia in relation to neurosurgical procedures.

2.2 Aetiology of acute orofacial pain

See more on acute orofacial pain.

Orofacial pain can be associated with pathological conditions or disorders related to somatic and neurological structures. There are a wide range of causes of acute orofacial pain conditions, the most common being dental pain (toothache) due to dental caries (tooth decay) the most common human infective disease worldwide. Interestingly periodontal disease (gum disease) the second most common infection is painless similar to other chronic macrobacteria infections for example Leprosy.

2.3 Prevalence

The prevalence of dental pain and its characteristics were recorded using standard measures of pain. Dental caries, dental trauma and dental plaque were assessed using WHO criteria. Multiple logistic and ordinal polytomous regression were used to assess which factors were associated with the dental pain outcomes. Results: 1,052 individuals participated in the study. The prevalence of reported toothache in schoolchildren in the last six months was 33.6% (31.1-36.8, 95% CI). The fully adjusted regression models showed a significant relationship between lower social class, later birth order, failure at school and attendance at the dentist only when in trouble with both the prevalence and severity of dental pain. The major predictor of the prevalence and severity of pain was pattern of dental attendance (p<0.001).

Goes, P.S.A. and Watt, R.G. and Hardy, R. and Sheiham, A. (2007) The prevalence and severity of dental pain in 14-15 year old Brazilian schoolchildren. Community Dental Health, 24 . pp. 217-224.

2.4 Odontogenic pain

Odontogenic pain refers to pain initiating from the teeth or their supporting structures, the mucosa, gingivae, maxilla, mandible or periodontal membrane.

insult

Figure 2.2 The stages and characteristics of dental pulpal pain.

2.5 Dental pulpitis (‘toothache’)

In health teeth are only perceive pain often due to dentine sensitivity on cold, sweet or physical stimulus. Dental pulpitis may be due to infection from dental caries close to the pulp, inflammation caused by chemical or thermal insult subsequent to dental treatment, and may be reversible or non-reversible. Intermittent sharp, shooting pains are also symptomatic of trigeminal neuralgia, so care must be taken not to mistakenly label toothache as neuralgia.

mouth

Figure 2.3

Initially the tooth after insult due to caries (causing bacterial products infiltrating the pulp via the dentine tubules) or iatrogenic insult (dental restoration close to the dental pulp or trauma) will cause pulpal inflammation and results in extreme sensitivity to cold and sweet flavours with short sharp ‘neuralgic’ pain. Protection of teh pulp to bacterial infection and chemical irritation by dietary and salivary content must be undertaken promptly to minimise persistence of acute pulpitis thus evolving into chronic irreversible pulpitis

Fractured tooth If the crown of a tooth is fractured by trauma and the broken fragment is available, it should be stored in a physiological medium until a dentist can assess the patient. Coverage of exposed dentine on the fractured crown with a temporary restoration is desirable to protect the underlying pulp tissue.

Placement of temporary restorations Although it is unlikely that many general medical practitioners will have temporary filling materials available in their surgeries, dentine that has been exposed by caries, a lost filling or tooth fracture can be covered relatively easily with glass ionomer cement (GIC) or zinc oxide eugenol (ZOE) materials. Most GIC materials are dispensed in capsules but a hand-mixed material is available, consisting of a powder, liquid and conditioner. The surface of the cavity is painted with the conditioner, then rinsed and dried, before placement of the filling. Zinc oxide eugenol materials consist of a powder and liquid (oil of cloves) that are mixed to a putty-like consistency before placement in the tooth.

If the insult persists the pulpitis will become irreversible with increased pulpal vascularity and resultant pressure, inducing ischaemia causing sensitivity to heat with prolonged pain. Once necrosis of the dental pulp has occurred, the infection spreads through the apex of the tooth into the surrounding bone and periodontal membrane, initiating periodontal inflammation and eventually a dental abscess causing spontaneous long lasting pain on biting on the tooth. Typically the pain associated with an abscess is described as spontaneous aching or throbbing and if associated with swelling in the jaw, trismus or lymphadenopathy it may be indicative of an acute spreading infection. Thus different stages of infection have different clinical presentations (Figure 2.3).

Management for dental pulpitis is excavation of the tooth decay with restoration (filling)  If the puplitis becomes irreversible then pupectomy (pulp removal) and root canal treatment will be required.

2.6 Which tests can assist in diagnosis?

There are several simple tests that may assist in diagnosis of dental pain.

Pulp sensitivity test Dry ice, or an ordinary ice stick (made in a plastic or glass tube), is placed on the cervical third (neck region) of the tooth crown. A response to the stimulus indicates that the pulpal tissue is capable of transmitting nerve impulses. No response may indicate pulp necrosis.

lower-molar

Figure 2.4

Percussion test Using an instrument handle, the tooth is tapped in the longitudinal axis. A painful response suggests possible periapical inflammation.

Probing Placing a fine, blunt probe gently into the gingival sulcus surrounding the tooth enables the health of the gingival tissues to be assessed. Bleeding and/or sulcus depths greater than 3-4 mm indicate gum disease.

Mobility test Holding a tooth firmly on the buccal (cheek) and lingual sides between the fingers enables mobility to be assessed. All teeth have a small amount of mobility (<0.5 mm), but visible movement suggests loss of bone support around the root of the tooth.

Palpation Careful palpation around the area of concern may reveal tenderness and the type and extent of swelling.

Radiographic examination If it is possible to obtain a screening radiograph, such as an orthopantomograph (OPG), this may assist in the diagnosis and localisation of the cause of the pain. The radiograph should show clearly the apical and periapical structures of teeth and associated tissues. The relationship of the maxillary molars and premolars to the floor of the maxillary sinus can be examined, and radiographs may reveal recurrent caries or periapical radiolucencies associated with an established infection.

2.7 Exposed cementum or dentine

There is tooth sensitivity from cold fluids and/or air, a reflection of a healthy pulp. With gingival recession, recent scaling, or tooth wear due to a high acid diet or gastric reflux, there may be generalised dentine sensitivity. However, with caries, fractured fillings and cracked cusps, the pain tends to be localised to the affected tooth. The tooth root surface comprises of a thin layer of cementum overlaying dentine, is exposed from excessive and/or incorrect tooth brushing. Dentine underlying the enamel crown is constituted of tiny tubules which are fluid filled and connect directly to the nerve ending in the dental pulp. The current hypotheses for dental pain include the osmolality theory whereby the dentine fluids elicit an action potential within the A delta and C fibres in the pulp caused by mechanical stimulation.

Management  For root sensitivity the use of a desensitising toothpaste and a reduction in acid in the diet will help resolve the symptoms. The use of a fluoride mouth-rinse may also help. In the case of caries, a lost filling or fractured tooth, coverage of the exposed dentine with a temporary restoration will usually relieve the symptoms. Pericoronitis Pain commonly arises from the supporting gingivae and mucosa when infection arises from an erupting tooth (teething or pericoronitis). This is the most common cause for the removal of third molar teeth (wisdom teeth). The pain may be constant or intermittent, but is often evoked when biting down with opposing maxillary teeth. This elicits pain in the inflamed mucosa and gingivae surrounding the partially erupted tooth. If recurrent, then pericoronitis is the main NICE indication for removal of wisdom teeth, however if the infection is acute and spreading then antibiotics must be prescribed. Chronic periodontitis with gradual bone loss, rarely causes pain and patients may be unaware of the disorder until tooth mobility is evident. There is quite often bleeding from the gums and sometimes an unpleasant taste. This is usually a generalised condition, however, deep pocketing with extreme bone loss can occur around isolated teeth. Food impaction in these areas can cause localised gingival pain. Poor contact between adjacent teeth and the presence of an occluding cusp forcing food into this gap can also cause a build-up of food debris and result in gingival inflammation.

Acute pericoronitis involves bacterial infection around an unerupted or partially erupted tooth and usually affects the lower third molar (wisdom tooth). The condition is often aggravated by the upper molar impacting on the swollen flap of soft tissue covering the unerupted tooth. There may be trismus.

2.8 Apical pain

Apical pain can be caused by infection spreading through the apical foramen of the tooth into the apical periodontal region causing inflammation (apical periodontitis) and ultimately a dental abscess if left untreated. Iatrogenic apical pain may result after dental treatment including premature contact if a restoration is left high in occlusion. This is characterized by an initial sharp pain which becomes duller after a period. The pain is due to a recent tooth restoration that is ‘high’ compared with the normal occlusion when biting together and Postendodontic surgery pain This is severe aching pain following endodontic treatment such as root canal therapy or apicectomy. While the majority of patients improve over time (weeks), a few will develop a chronic neuropathic pain state (see section on persistent post surgical trigeminal pain). There is considerable variation in the pain reported by patients, but it commonly starts as a sharp stabbing pain that becomes progressively dull and throbbing. At first the pain may be caused by a stimulus, but it then becomes spontaneous and remains for a considerable time after removal of the stimulus. The pain may radiate and be referred to other areas of the mouth. This type of pain tends to cause the patient to have difficulty sleeping and may be exacerbated by lying down. Heat may make the pain worse whereas cold may alleviate it. The pain may be intermittent with no regular pattern and may have occurred over months or years. If there is periapical infection present, patients may no longer complain of pain in response to a thermal stimulus, but rather of sensitivity on biting.

Management. Advise the use of an analgesic to relieve symptoms (Ibuprofen, or paracetamol if ibuprofen is contraindicated or unsuitable, is recommended first-line and Paracetamol and ibuprofen can be taken together if pain relief with either alone is insufficient. For adults, if taking paracetamol and ibuprofen together does not provide enough pain relief, consider adding codeine phosphate or switching to an alternative nonsteroidal anti-inflammatory drug (NSAID). For women who are pregnant or breastfeeding, paracetamol is preferred. A short course of codeine may be added if paracetamol alone is insufficient. Antibiotics are generally not indicated for otherwise healthy individuals when there no signs of spreading infection. Only prescribe an antibiotic: For people who are systemically unwell or if there are signs of severe infection (e.g. fever, lymphadenopathy, cellulitis, diffuse swelling).

Dental management for dental abscess is either root canal with removal of the necrotic pulp or tooth extraction, Periapical inflammation can lead to a cellulitis of the face characterised by a rapid spread of bacteria and their breakdown products into the surrounding tissues causing extensive oedema and pain. If systemic signs of infection are present, for example, fever and malaise, as well as swelling and possibly trismus (limitation of mouth opening), this is a surgical emergency. Antibiotic treatment alone is not suitable or recommended. If pus is present, it needs to be drained, the cause eliminated, and host defences augmented with antibiotics. The microbial spectrum is mainly gram positive including anaerobes. Appropriate antibiotics would include a penicillin or a ‘first generation' cephalosporin, combined with metronidazole in more severe cases.

2.9 Alveolar osteitis

After extraction, the most common complication is a ‘dry socket’ which is a condition whereby the clot formation within the socket fails at 3–5 days; healing fails, resulting in an empty socket which traps food and debris. The resultant pain is caused by necrotic foodstuff aggravating bony nerve endings, causing intense pain following extractions. Interestingly this condition is devoid of the usual acute inflamammtory markers (absence of lymphadenopathy, local inflammation and swelling). dull throbbing pain develops two to four days after a mandibular tooth extraction. It rarely occurs in the maxilla. Smoking is a major predisposing factor as it reduces the blood supply. The tissue around the socket is very tender and white necrotic bone is exposed in the socket. Halitosis is very common. The incidence of this condition is between 1-9% associated with patientsundergoing mandibular surgical tooth removal. Patients should be routinely warned of a possible incidence of 5%.

Management Irrigation of the socket using saline or chlorhexidine and then an obtundant dressing usually soaked in bacteriorstatic solution (alvogyl paste, BIPP paste, cotton wool or gausze soaked in iodofrom). Immediate pain relief is usually attained and rarely patient re present for additional treatment. Patients should be shown how to irrigate the area and told to do this regularly. Analgesics are indicated, but pain may persist for several days. Although opinion is divided as to whether or not dry socket is an infective condition, we do not recommend the use of antibiotics in its management If the patient returns recurrently with ongoing pain then osteomyelitis should be excluded and localised bony sequestrate should be excluded.

2.10 Maxillary sinusitis

Recurrent maxillary sinusitis may cause widespread pain in the maxillary teeth. The pain tends to be increased on lying down or bending over. There is often a feeling of `fullness' on the affected side. The pain is usually unilateral, dull, throbbing and continuous. Quite often the patient feels unwell generally and feverish. It can mimic the maxillary sinusitis-like symptoms in temporomandibular disease (TMD) (see below) or neuropathic pain. These dental conditions rarely present as chronic pain unless misdiagnosed. Inflammation of the maxillary sinuses is best treated using local and systemic decongestants and if persistent then antibiotics may be prescribed. Pain originating from the sinus arises mainly from pressure. Decongestants can help sinus drainage. Antibiotics probably have only a minor role in mild cases. Referral to an otorhinolaryngologist for endoscopic sinus surgery may be indicated in chronic cases.

2.11 Non-odontogenic facial pain

Non-odontogenic facial pain can be caused by inflammation due to tumour, infection, or trauma. Topographical classification is often applied to this complex region. Regions often presenting as orofacial pain complaints include the sinuses, salivary gland, ears, eyes, throat, mandibular, and maxillary bone pathology.

2.12 Acute necrotising ulcerative gingivitis

Acute necrotising ulcerative gingivitis is a rapidly progressive infection of the gingival tissues that causes ulceration of the interdental gingival papillae. It can lead to extensive destruction. Usually young to middle-aged people with reduced resistance to infection are affected (diabetes, HIV infection, chemotherapy). Males are more likely to be affected than females, with stress, smoking and poor oral hygiene being predisposing factors. Halitosis, spontaneous gingival bleeding, and a `punched-out' appearance of the interdental papillae are all important signs. The patients quite often complain of severe gingival tenderness with pain on eating and tooth brushing. The pain is dull, deep-seated and constant. The gums can bleed spontaneously and there is also an unpleasant taste in the mouth and obvious halitosis.

Management As there is an acute infection with mainly anaerobic bacteria, treatment follows surgical principles and includes superficial debridement, use of chlorhexidine mouthwashes and a course of metronidazole tablets. Treating the contributing factors should prevent a recurrence.

References

  1. Hapak L, Gordon A, Locker D, Shandling M, Mock D, Tenenbaum HC. (1994) Differentiation between musculoligamentous, dentoalveolar, and neurologically based craniofacial pain with a diagnostic questionnaire. J Orofac Pain, 8(4), 357–68. OROFACIAL PAIN 295
  2. Abbott PV. Selective and intelligent use of antibiotics in endodontics. Aust End J 2000;26:30-9.
  3. Okeson JP. Management of temporomandibular disorders and occlusion. 4th ed. St. Louis: Mosby; 1998.
  4.  Wormald PJ. Treating acute sinusitis. Aust Prescr 2000;23:39-42.

 

3.1 Persistent pain after dental surgery

See more information on Neuropathic Pain  

Chronic orofacial pain syndromes represent a diagnostic challenge for any practitioner. Patients are frequently misdiagnosed or attribute their pain to a prior event such as a dental procedure, ENT problem or facial trauma. Psychiatric symptoms of depression and anxiety are prevalent in this population and compound the diagnostic conundrum. Treatment is less effective than in other pain syndromes, thus often requires a multidisciplinary approach to address the many facets of this pain syndrome1.

3.2 Aetiology of orofacial pain

Facial pain can be associated with pathological conditions or disorders related to somatic and neurological structures2. There are a wide range of causes of chronic orofacial pain and these have been divided into three broad categories by Hapak et al.3—musculoligamentous, dentoalveolar, and neurological and vascular. The commonest cause of  chronic orofacial pain is temporomandibular disorders, principally myofascial in nature4.

As mechanisms underlying these pains begin to be identified, more accurate classifications which are mechanism-based may come to be used. A major change in mechanism has been that burning mouth syndrome probably has a neuropathic cause using the newly defined definitions rather than being a pain owing to psychological causes.

3.3 Incidence

Chronic orofacial pain is comparable with other pain conditions in the body, and accounts for between 20 and 25% of chronic pain conditions.

A 6-month prevalence of facial pain has been reported by between 1% and 3% of the population. In the study by Locker and Grushka6, some pain or discomfort in the jaws, oral mucosa, or face had been experienced by less than 10% in the past 4 weeks.

In 1987, Bonica estimated that 5–7 million Americans suffer from chronic pain in the face and mouth, and between 25 and 45% are affected at some time of life.

Most population-based studies have shown that women report more facial pain than men, with rates approximately twice as high among women compared to men10. In clinic populations the rates for women are even higher1. On the other hand, other studies have found no sex difference in the prevalences of orofacial pain. Several studies have also shown variability in the prevalence across age groups. The age distribution of the facial pain population differs from that of the most usual pain conditions.

In contrast to chest and back pain, for example, facial pain has been suggested to be less prevalent among older persons than younger ones. Conversely, in 1993 Lipton et al. found the prevalence of facial pain to remain relatively constant across the age groups, while in a study in 2001 by Riley and Gilbert, no difference in prevalence was observed between the age groups of 45–64 years and older.

3.4 Diagnosis

The International Headache Society (IHS) has published diagnostic criteria for primary and secondary headaches as well as facial pain. Criteria have also been published by the International Association for the Study of Pain (IASP) and by the American Academy of Orofacial Pain (AAOP), and the Research Diagnostic Criteria for Temporomandibular Disorders (RDCTMD). The impact of trigeminal pain must not be underestimated. Consequences include interruption with daily social function such as eating, drinking, speaking, kissing, applying makeup, shaving, and sleeping. Burning mouth syndrome has been reported to cause significant psychological impact in 70% of patients. In temporomandibular joint (TMJ) pain, 29% patients report high disability resulting in unemployment18,19. A recent validated tool has been developed for the assessment of disability related to oral function (Oral Health Impact [OHIP 14]).

3.5 Classification of orofacial pain  

See more information on Classification of Pain

The aim of this chapter is to address the causes of chronic orofacial pain (lasting >3 months). However, the most common causes of acute dental pain are due to trauma or infection of the dental pulp which contains the nerves and vessels supplying the tooth. Dental disease of the hard tissues (caries of enamel, dentine, and cementum), and soft tissues and supporting bone (gingivitis/periodontitis) are recognized as the most common diseases to afflict the general population. These conditions are largely diagnosed and treated by dental practitioners by history, dental clinical examination, and radiographs. By far the most common forms of oral pain are them acute form of pain that tend to last for short periods of time. These include toothache (dental pulpitis), gum pain (pericoronitis in 80% of the population), periapical periodontitis (owing to apical infection or postendodontic therapy of high occlusal contact). Dentine sensitivity affects 40% of the adult population; dry socket is postsurgical intense pain that affects 10% of patients after extraction of their teeth. Other orofacial acute pain conditions include trauma or infection of the orofacial tissues22.

Chart illustrating a suggested classification for chronic orofacial pain (from Woda et al. 2005 23)

classification

Figure 3.1 - Classification of chronic orofacial pain

3.6 Chronic orofacial pain

The various suggested classifications of chronic orofacial pain do conflict with each other. Several classifications of chronic orofacial pain have been presented and the authors will use the fourth classification for this chapter as it presents a pragmatic and clinically useful alternative.

Group 1: neurovascular (predominantly VI pain)

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Short-lasting unilateral neuralgiaform conjunctival irritation and tearing (SUNCT) This is possibly a variation of the cluster tic syndrome. It is characterized by brief (15–120 seconds) bursts of pain in the eyes, temple, or face. The pain is usually unilateral and is described as burning, stabbing, or electric. It occurs frequently in a 24-hour period (>100 episodes). Neck movements can trigger the pain. SUNCT syndrome is refractory to medical therapy but there is increasing evidence for treatment with lamotrigine.

Temporal arteritis Temporal arteritis is characterized by daily headaches of moderate to severe intensity, scalp sensitivity, fatigue, and various non-specific complaints with a general sense of illness. Ninety-five per cent of patients are over 60 years old. The pain is usually unilateral, although some cases of bilateral or occipital pain do occur. Pain may also be felt in the tongue and is a continuous ache with superimposed sharp, shooting head pains. The pain is similar to and may be confused with that of CH, but CH tends to occur in younger patients. The two may also be distinguished on physical exam, when dilated and tortuous scalp arteries are noted. The erythrocyte sedimentation rate (ESR) is markedly elevated in temporal arteritis. Definitive diagnosis is made by artery biopsy from the region of the pain, although negative biopsy may be caused by the spotty nature of the disease and does rule out the diagnosis. High dose steroid therapy usually precipitates a dramatic decrease in head pain. Failure to respond to steroid therapy with a negative biopsy should call the diagnosis into question. If the diagnosis seems likely based on history and physical examination, steroids should be started immediately to avoid vision loss, the most common complication of the disorder, occurring in 30% of untreated cases. The biopsy remains positive for 7–10 days from starting steroid therapy. Steroids may be tapered to an every other day maintenance schedule when the pain resolves and ESR normalizes. The disease is usually active for 1–2 years, during which time steroids should be continued to prevent vision loss.

Group 2: Neuralgia   

See more information on Trigeminal Neuralgia and Neuropathic Pain

This group includes primary neuropathies -trigeminal neuralgia (typical or atypical), glossopharyngeal neuralgia, and secondary neuropathies including postherpetic neuralgia and post-traumatic V neuralgia, and other peripheral neuropathies affecting the trigeminal system (nutritional neuropathy, diabetes mellitus, human immunodeficiency virus (HIV), chemotherapy, and multiple sclerosis (MS) are not covered in this review but can present as orofacial pain.

Primary neuropathies

Glossopharyngeal neuralgia Glossopharyngeal neuralgia is characterized by pain attacks similar to those in trigeminal neuralgia, but is located unilaterally in the distribution of the glossopharyngeal nerve. Pain is most common in the posterior pharynx, soft palate, base of tongue, ear, mastoid or side of the head. Swallowing, yawning, coughing or phonation may trigger the pain. Management is similar to that for trigeminal neuralgia.

Secondary neuropathies

Many conditions can cause peripheral sensory neuropathies that may present with pain, these include;

  • Diabetes
  • Post herpetic neuralgia
  • Human Immunodeficiency Virus
  • Chemotherapy
  • Muliple Sclerosis
  • Post surgical traumatic neuropathy
  • Parkinson’s
  • Malignancy
  • Drugs - Growth hormone injections
  • Nutritional neuropathy

The most common causes of trigeminal neuropathy would include post traumatic neuropathy, PHN and idiopathic persistent post surgical pain.

Postherpetic neuralgia In patients over 50 years of age there is a 60% incidence of developing postherpetic pain42. Herpetic skin eruption is caused by the reactivation of latent varicella zoster virus from the sensory nerve ganglia. The reactivated virus is carried via the axons distally to the skin where it produces a painful rash with crusting vesicles in a dermatomal distribution. The trigeminal nerve is the second most commonly affected after nerves in the thoracic region. Ramsay Hunt syndrome occurs when herpes zoster infection of the geniculate ganglion causes earache and facial palsy. Pain that persists 2 or more months after the acute eruption is known as postherpetic neuralgia. The pain is neuropathic in nature, severe, and it is associated with allodynia and hyperalgesia, most commonly affecting the VI distribution of the trigeminal nerve. High doses of antivirals, steroids, and amitriptyline are often used for the acute eruption in otherwise healthy individuals. Antivirals, NSAIDs, and opiates are often used in immunocompromised patients. More recently, there is evidence that topical 5% lignocaine patches (Versatis) worn alternatively every 12 hours are very effective.

Post-traumatic trigeminal neuropathy The most problematic outcome of dental surgical procedures with major medico-legal implications is injury to the trigeminal nerve (Caissie, 2005). The prevalence of temporarily impaired lingual and inferior alveolar nerve function is thought to range between 0.15–0.54% whereas permanent injury caused by injection of local analgesics is much less frequent at 0.0001–0.01% (Hillerup, 2007). Traumatic injuries to the lingual and inferior alveolar nerves may induce a pain syndrome owing to the development of a neuroma. The most commonly injured trigeminal nerve branches, the inferior alveolar and lingual nerves are different entities, whereby the lingual nerve sits loosely in soft tissue compared with the IAN that resides in a bony canal. Injury to the third division of the trigeminal may occur due to a variety of different treatment modalities, such as major maxillofacial and minor oral surgery (Blackburn, 1990; Kraut & Chahal, 2002; Wismeijer et al., 1997; Hillerup and Jensen, 2006; Grotz et al., 1998). Peripheral sensory nerve injuries are more likely to be persistent when the injury is severe, if the patient is older, if the time elapsed between the cause of the injury and the review of the patient is of longer duration, and when the injury is more proximal to the cell body.

Subsequent to iatrogenic trigeminal nerve injury, the patient often complains about a reduced quality of life, psychological discomfort, social disabilities and handicap (Lam et al. 2003). Patients often find it hard to cope with such negative outcomes of dental surgery since the patient usually expects significant improvements not only regarding jaw function, but also in relation to dental, facial, and even overall body image after oral rehabilitation (Kiyak et al, 1990). Altered sensation and pain in the orofacial region may interfere with speaking, eating, kissing, shaving, applying make up, tooth brushing and drinking; in fact just about every social interaction we take for granted (Ziccardi and Zuniga, 2007).

In a recent prospective assessment of 252 patients with iatrogenic trigeminal nerve injuries (Renton & Yilmaz 2010 in press) most were caused by third molar surgery but implants and local anaesthesia were significant contributors - see figure 3.2 below:

graph

Figure 3.2

The diagnosis of posttraumatic neuralgia/ neuropathy is based upon a history of surgery or trauma temporally correlated with the development of the characteristic neuropathica pain. Age, poor wound closure, infections, foreign material in the wound, haematoma, skull fracture, diabetes mellitus or peripheral neuropathy elsewhere in the body predispose to neuroma development. The pains commonly persist 2– months after the injury and can be permanent. Medical therapy is similar to that used in neuropathic pain conditions depending on the patients’ symptoms. In a recent survey of 252 iatrogenic trigeminal nerve injuries related to dental treatment, 70% of patients presented with pain (Figure 3.3). This highlights the problems related to postsurgical neuropathy aggravated by the fact that many patients may not have been warned at all about nerve injury or told that they would risk numbness.

pain

Figure 3.3

Any patients experienced significant daily disability predominantly caused by elicited mechanical or cold allodynia resulting in pain on eating, drinking, kissing sleeping and other essential functions (figure 3.4).

graph2

Figure 3.4

Current management of these nerve injuries is inadequate. The focus remains on surgical correction or laser therapy with little or no attention to medical or counselling intervention and the patients’ psychological, functional or pain related complaints. The fault partly rests with how we assess these patients. Assessment tends to show little regard for the functional or pain evaluation with the main focus on basic mechanosensory evaluation, which is not necessarily reflective of the patients’ difficulties. Oral Surgery specialists assessing these injuries should therefore follow guidelines from the World Health Organisation, which suggest that nerve injury outcomes should be assessed in terms of impairment, activity limitations, and participation restrictions (MacDermid, 2005). Guidelines set out by the International Association for the Study of Pain and European Federation of Neurological Societies should also be followed (Cruccu et al., 2004). Without exception these recommendations are holistic when compared with reports evaluating the management of trigeminal nerve injuries.

Traumatic injuries to peripheral nerves pose complex challenges and treatment of nerve injuries must consider all aspects of the inherent disability. Pain control is of paramount importance and rehabilitation needs to be instituted as first-line treatment. Early intervention is important for optimal physiologic and functional recovery (Robinson & Shannon, 2002). Reparative surgery may be indicated when the patient complains of persistent problems related to the nerve injury, however there remains a significant deficiency in evidence base to support this practice. The patients presenting complaints may include functional problems due to the reduced sensation, intolerable changed sensation or pain the latter being predominantly intransigent to surgery (Rutner et al., 2005; Hillerup and Stoltze, 2007; Robinson et al., 2000) and less often expressed psychological problems relating the iatrogenesis of the injury and chronic pain. Generally for lesions of the peripheral sensory nerves in man, the gold standard is to repair the nerve as soon as possible after injury (Birch et al., 1991). However, the relatively few series of trigeminal nerve repair on human subjects relate mainly to repairs undertaken at more than 6 months after injury.

It is evident from the literature review that there needs to be a cultural change in the choice of intervention, timing and outcome criteria that should be evaluated for interventions for trigeminal nerve injuries. To date, there have been a very limited number of prospective randomised studies to evaluate the effect of treatment delay, the surgical, medical or counselling outcomes for trigeminal nerve injuries in humans.

Persistent post surgical pain without demonstrable neuropathy

See more information on persistent idiopathic pain

This is defined as present at 1 year post-op or longer, unexplained by local factors and best described as neuropathic in nature

Nonodontogenic dentolalveolar pain is often difficult to diagnose because it is poorly understood. Even defining and categorizing such persistent pain is challenging. Nonodontogenic pain is not an uncommon outcome after root canal therapy and may represent half of all cases of persistent tooth pain. A recent systematic review of prospective studies that reported the frequency of nonodontogenic pain in patients who had undergone endodontic procedures. Nonodontogenic pain was defined as dentoalveolar pain present for 6 months or more after endodontic treatment without evidence of dental pathology. Endodontic procedures reviewed were nonsurgical root canal treatment, retreatment, and surgical root canal treatment. 770 articles retrieved and reviewed, 10 met inclusion criteria with a total of 3,343 teeth were enrolled within the included studies and 1,125 had follow-up information regarding pain status. We identified nonodontogenic pain in 3.4% (95% confidence interval, 1.4%-5.5%) frequency of occurrence.

(Nixdorf N et al Frequency of Nonodontogenic Pain after Endodontic Therapy: A Systematic Review and Meta-AnalysisJ Endod 2010;36:1494–1498)

The prevalence of persistent pain post surgically in the trigeminal system may be low compared with other surgical sites (Kehlet et al, 2006 Lancet)

amputation

Figure 3.5

However when one considers the significant frequency of dental surgical procedure undertaken (Figure 3.5) then significant numbers of individuals may be affected by both post traumatic neuropathy and persistent post surgical pain.

Risk factors for developing persistent post surgical pain include; Genetics (catecholamine-O-methyltransferase), preceding pain (intensity and chronicity), psychosocial factors (i.e. fear, memories, work, SES, physical levels of activity, somtatization), Age (older = ­ risk), Gender (female = ­ risk) and the surgical procedure and technique (tension due to retraction).

All these persistent post surgical pain conditions may be attributable to post traumatic neuropathy but it is difficult to be conclusive without a demonstrable neuropathic area in relation to the previous surgery. The significant decreased ncidence in this condtion in the trigeminal region may reflect the lack of central sensitization due to most procedures being undertaken under local anaesthetic (Woolf et al 2010).

Group 3: Idiopathic chronic orofacial pain 

This group includes preauricular pain related to the TMJ , burning mouth syndrome (BMS), and persistent idiopathic facial pain.

Persistent idiopathic facial pain The term atypical facial pain was first introduced by Frazier and Russell in 1924. It has since been renamed persistent idiopathic facial pain (PIFP). PIFP refers to pain along the territory of the trigeminal nerve that does not fit the classic presentation of other cranial neuralgias12. The duration of pain is usually long, lasting most of the day (if not continuous). Pain is unilateral and without autonomic signs or symptoms. It is described as a severe ache, crushing or burning sensation. Upon examination and workup no abnormality is noted.

Definition According to the International Association for the Study of Pain (IASP), chronic facial pain refers to symptoms which have been present for at least 6 months. ‘Atypical’ pain is a diagnosis of exclusion after other conditions have been considered and eliminated (i.e. it is idiopathic), and is characterized by chronic, constant pain in the absence of any apparent cause in the face or brain. Many information sources suggest that all ‘unexplained’ facial pains are termed atypical facial pain but this is not the case. Categories of idiopathic facial pain conditions include neuropathic pain due to sensory nerve damage, chronic regional pain syndrome (CRPS) from sympathetic nerve damage and atypical facial pain. Atypical odontalgia, or phantom tooth pain, is a variation of atypical facial pain where intense discomfort is centred around a tooth or group of teeth with no obvious dental or oral disease.

Epidemiology Atypical facial pain is more common in women than in men; most patients attending a facial pain clinic are women aged between 30 and 50 years. Although any area of the face can be involved, the most commonly affected area is the maxillary region. In the majority of patients there is no disease or other cause found. In a few patients the symptoms represent serious disease. In a small number of patients the pain may be one consequence of significant psychological or psychiatric disease.

Clinical presentation Atypical facial pain has a very variable presentation. Often it is characterized by continuous, daily pain of variable intensity. Typically, the pain is deep and poorly localized, is described as dull and aching, and does not waken the patient from sleep. At onset the pain may be confined to a limited area on one side of the face, while later it may spread to involve a larger area. Atypical facial pain is a diagnosis of exclusion for pain not meeting the diagnostic criteria of other facial pain syndromes. Mongini et al refers to the term atypical facial pain as outdated and includes its description in psychogenic facial pain. Indeed, the description of the pain may be inconsistent with bilateral pain that often changes locations over weeks to months. The pain is not triggered and is not electrical in quality. Intensity fluctuates but the patient is rarely pain-free. Pain is typically located in the face and seldom spreads to the cranium in contradistinction to tension headache. It is more common in women aged 30–50 years old. Between 60 and 70% of these patients have significant psychiatric findings, usually depression, somatization or adjustment disorders, therefore psychiatric evaluation is indicated. Treatment is with antidepressants, beginning with low dose amitriptyline at bedtime and increasing the dose until pain and sleep are improved. Accurate figures are difficult to obtain because of the lack of agreement on classification criteria. Estimated incidence is 1 case per 100 000 population, although this number may be underestimated. PIFP affects both sexes approximately equally, but more women than men seek medical care. The disorder mainly affects adults and is rare in children. PIFP is essentially a diagnosis of exclusion. Daily or near-daily headaches are a widespread problem in clinical practice. According to population-based data from the United States, Europe, and Asia, chronic daily headache affects a large number (approximately 4–5% of the population) of patients. Importantly, PIFP must be distinguished from various other chronic daily headache syndromes, including hemicrania continua, TMJ syndrome, sidelocked migraine, chronic cluster headache, SUNCT, TN, and many others. A careful history and physical examination, including a dental consultation, laboratory studies, and imaging studies, may be necessary to rule out occult pathology. Underlying pathology such as malignancy, vasculitis, infection, and central or peripheral demyelination may manifest early as neuralgia, and, not until focal neurological deficits, imaging abnormalities, or laboratory abnormalities are discovered, does the diagnosis become evident. Rare cases of referred pain must also be considered. Atypical odontalgia (AO) is characterized by continuous, dull, aching, or burning pain of moderate intensity in apparently normal teeth or endodontically treated teeth and occasionally in extraction sites. AO is not usually affected by testing the tooth and surrounding tissues with cold, heat or electrical stimuli. The pain remains constant despite repeated dental treatment, even extractions in the region, often rendering patients with persistent pain but whole quadrants stripped of dentition. Moreover, the toothache characteristics frequently remain unchanged for months or years, contributing to the differentiation of AO from pulpal dental pain. Occasionally, the pain may spread to adjacent teeth, especially after extraction of the painful tooth. These patients are defined as having pain in a tooth or tooth region in which no clinical or radiological findings can be detected. Several studies have been conducted to define this group more clearly. AO patients have more comorbid pain conditions, higher scores for depression and somatization, significant limitation in jaw function, and lower scores on quality of life measures when compared with controls. When compared to patients with TMD, AO patients were more likely to describe their pain as aching, find rest relieving but cold and heat aggravating. Over 80% relate the onset of their pain to dental treatment. Both groups show worsening of symptoms on chewing, but more patients with TMD have other chronic pain. These patients have somatosensory abnormalities, suggesting that generalized sensitization of the nociceptive mechanism may be occurring. The relationship with previous surgical intervention infers that this condition may, in some cases, be partial postsurgical neuropathy of the superior alveolar nerves.

The lack of RCTs makes evidenced-based care in AO difficult. One of the major problems with this condition is convincing the patient, and informing their dentist, that there are no dental causes for their pain, so avoiding unnecessary irreversible invasive dental treatment. AO patients are often diagnosed late and therefore need a multidisciplinary approach. In her recent review, Baad-Hansen presents a sensible progressive approach to managing AO, beginning with topical lignocaine or capscasian, then TCAs. Ulltimately, the drugs used in neuropathic pain are often gabapaentin and pregablin, and finally tramadol or oxycodone.

Medical care Medical treatment of PIFP is usually less satisfactory than medical treatment for other facial pain syndromes. Medications used to treat PIFP include antidepressants, anticonvulsants, substance P depletion agents, topical anaesthetics, N-methyl-D-aspartate (NMDA) antagonists, and opiate medications. Of these classes of medications, anticonvulsants and antidepressants appear to be the most effective. The neuropathic component of pain responds well to anticonvulsants and antidepressants. Pharmacotherapeutic knowledge is paramount in the treatment of this refractory pain syndrome. A multimechanistic approach, using modulation of both ascending and descending pain pathways, is frequently necessary. The goal of therapy is to manage the pain effectively with the fewest adverse medication effects. Anticonvulsants and antidepressants are the mainstays of medication treatment. Alternative therapies such as acupuncture and neuromuscular re-education have been tried and should be considered as part of a comprehensive treatment plan. Psychiatric treatment is important in the overall management of a patient with chronic pain. Holistic approach as many has other chronic pain. Available data on alternative treatments are limited.

Surgical care Details of neurosurgical interventions are beyond the scope of this review. Analgesic surgery should be considered at a centre well versed in these procedures.

Consultations Psychometric testing may be of benefit in the evaluation and treatment of patients with headache and facial pain. Many tests have been applied, but probably the most widely used is the Minnesota multiple personality inventory (MMPI). While especially useful in the evaluation of chronic headache and facial pain patients, a thorough discussion of psychometric testing is beyond the scope of this discussion and is mentioned here only for completeness. Consultation with a dentist may be of benefit. All treatments should be provided in cooperation with the patient’s primary care physician.

Future novel treatments in development include several phase three trials assessing specific pain receptor and channel blocking agents for neuropathic pain. Several studies have reported upregulation of peripheral TRPV receptor and sodium channel receptor expression in the human trigeminal system. Recent recognition of genetic factors contributing to nociception, pain behaviour, and suffering may also lay the foundations for future strategies for improved treatment of patients with chronic pain. Of the 3.16 billion base pairs comprising the 23 pairs of chromosomes, the Human Genome Project has sequenced about 2.8 billion base pairs to date. Only 3% of the human genome actually codes for proteins, and about 15% of the non-coding DNA in humans is conserved (has functional importance). It is estimated that there are approximately 25 000 genes in the human genome and it is as yet unknown how many genes are involved in pain mediation, perception, and behavioural response. To date, gene coding for TRPV1 channel is associated with altered pain responses, and sodium ion channels coded by an SCN9A mutation was found in a Pakistani family with an inability to experience pain. Catechol-O-methyltransferase and the cytochrome P450 variant allele CYP3A5 have been linked with pain behaviour attributed to dopamine metabolism which defined how patients coped with their pain experience. The ability to evaluate the phenotype and genotype of the patient with pain may enable to clinician to provide specific and tailor-made treatment in the future.

Conclusion Chronic orofacial pain continues to present a diagnostic challenge for many practitioners. Patients are frequently misdiagnosed and they suffer from psychiatric symptoms of depression and anxiety. Treatment is less effective than in other pain syndromes and a multidisciplinary approach treatment is desirable.

A condition that does not cluster due to the fact that it includes many conditions is Temporomandibular joint pain  - see the link for more information.

3.7 Pain Management

Pain management is summarised after each section.

Additional useful information is supplied here

3.8 Pain Curriculae and Strategy

Pain Curriculae differ depending upon training needs and national pain strategy.

3.9 Pain Guidelines

Guidelines for OFP

  1. TMD  (RCS and BDA)
  2. PTN trigeminal: NICE neuropathic pain guidelines 
  3. BMS diagnosis & management
  4. Headache NICE
  5. TN NICE

Description:

Persistent facial pain that does not have the characteristics of the cranial neuralgias described above and is not attributed to another disorder.

Diagnostic criteria:

  1. Pain in the face, present daily and persisting for all or most of the day, fulfilling criteria B and C
  2. Pain is confined at onset to a limited area on one side of the face1, and is deep and poorly localised
  3. Pain is not associated with sensory loss or other physical signs
  4. Investigations including x-ray of face and jaws do not demonstrate any relevant abnormality

Note:

  1. Pain at onset is commonly in the nasolabial fold or side of the chin, and may spread to the upper or lower jaw or a wider area of the face and neck.

Comments:

Pain may be initiated by surgery or injury to the face, teeth or gums but persists without any demonstrable local cause.

Facial pain around the ear or temple may precede the detection of an ipsilateral lung carcinoma causing referred pain by invasion of the vagus nerve.

The term atypical odontalgia has been applied to a continuous pain in the teeth or in a tooth socket after extraction in the absence of any identifiable dental cause.

Management  Gary Klasser, DMD, Cert Orofacial Pain : J Can Dent Assoc 2013;79:d71