Received Date : 10-Jul-2016

Accepted Date : 11-Jul-2016

Accepted Article
Article type : Invited Concise Review

Chronic Orofacial pain

Tara Renton Professor Oral Surgery Kings College London

Email Tara.renton@kcl.ac.uk

The issues specific to trigeminal pain include the complexity of the region, the problematic
impact on daily function and significant psychological impact (Shueb SS et al., 2015). By
nature of the geography of the pain (affecting the face, eyes, scalp, nose, mouth) it may
interfere with just about every social function we take for granted and enjoy (Renton and
Yilmaz, 2011). The trigeminal nerve is the largest sensory nerve in the body, protecting the
essential organs that underpin our very existence (brain, eyes, nose, mouth). It is no wonder
that pain within the trigeminal system in the face is often overwhelming and inescapable for
the affected individual.

Pain is “An unpleasant sensory and emotional experience associated with actual or
potential tissue damage, or described in terms of such damage” (IASP, 1994) reinforcing
that pain often occurs without actual physical harm, with overlay of the brain pain on the
affected limb or tooth. Perpetuation of this phenomenon when the tissue damage is healed
and the painful stimulus is removed, is symptomatic of a ‘disconnect’ with the brain
continuing to overlay the pain leading to chronicity. Woolf (2010) classifies pain into 2
groups: Healthy acute adaptive and protective pain including nociceptive (detects noxious
stimuli) and inflammatory pain. The second group, both evidence of a diseased neuro matrix
or maladaptive, pathological pain including neuropathic (with a lesion or disease present)
and dysfunctional or centralised pain (with no identifiable cause) (Flor et al., 2005). Table 1
is an attempt at listing various conditions that can present as persistent pain in the orofacial
region attributed to the various types of pain.

This article has been accepted for publication and undergone full peer review but has not
been through the copyediting, typesetting, pagination and proofreading process, which may
lead to differences between this version and the Version of Record. Please cite this article as
doi: 10.1111/odi.12540
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 The most common chronic orofacial pain conditions are related to poorly-managed acute
recurrent dental pain or temporomandibular disorders. Recurrent or persistent dental
nociceptive or inflammatory pain must be excluded primarily and this requires a dental
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practitioner. The challenge of an ageing increasingly dentate population, often with multiple
complex restorations, is likely to increase the number of patients presenting with difficult to
diagnose ‘cracked cusp syndrome’ or low level irreversible pulpitis, both easily resolved with
simple dental restorative intervention.

Temporomandibular (TMJ) disorders comprise of three main groups. Of these myofascial or

arthromyalgic pain and dysfunctional joint pain (clicks, crepitus and or locking) are the most
common followed rarely by arthritides. These conditions are predominantly nociceptive and
inflammatory in nature with some patients displaying some elements of centralised pain in
phenotypic predisposed patients (Schiffman and Ohrbach 2016).

Another group of OFP conditions present with an autonomic component likely driven by
interaction with cervical nerves whose close relationship with the Vth and related cranial
nerves may explain the associated symptoms (Bartsch and Goadsby, 2003). It has been
postulated that the autonomic symptoms as part of the trigemino-autonomic reflex are
perhaps more likely in first-division more specific for trigeminal autonomic cephalalgias
(TACs) compared to Trigeminal Neuralgia however, it is likely that there is spectrum
between these conditions (May and Goadsby,1999). These ‘neurovascular pain conditions’
include headaches, giant cell arteritis and TACs. Headaches affect many individuals and
those regularly assessing patients with chronic orofacial pain should be familiar with
headache diagnosis. Tension, Medication over use and Migraine headaches formulate the
most common conditions and due to the meninges, being partly innovated by the second
and third divisions of the Vth cranial nerve, mimicking of toothache or misdiagnosed
idiopathic facial pain is possible (Alonso and Nixdorf, 2006). TACs include Cluster
headache, SUNCT, Hemicranial continua and Paroxysmal hemicranias, again conditions
that frequently mimic toothache, trigeminal neuralgia and other conditions that dentists are
less familiar with. A high percentage of patients presenting at a multidisciplinary orofacial
pain clinics will be diagnosed with TACs rather than Trigeminal Neuralgia (TN) or
persistent idiopathic facial pain (PIFP) (VanderPluym and Richer, 2015).

Neuropathic pain is defined as “pain caused by a lesion or disease of the somatosensory

nervous system” (Treede et al.,2008), is the first of the chronic pains as described by
Woolf.4 Neuropathic pain is characterised by altered sensation within a specific
dermatome(s), constant or intermittent (elicited) pain which may be spontaneous or evoked.

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 Mechanical and thermal (particularly cold) allodynia are common features and descriptors
include; sharp, shooting, stabbing, burning, tingling or pins and needles. The diagnosis and
assessment of neuropathic pain still require a consensus however, a specialist subgroup of
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the International Association for the Study of Pain (IASP) have published guidance
(Haanpää et al., 2011). The same group have also made recommendations with regard
phenotyping patients with neuropathic pain (van Hecke et al., 2015). The prevalence of
neuropathic pain in the population is unknown but increasingly recognised as one of the
most common causes for chronic pain in the orofacial region (Renton and Yilmaz, 2011,
Klasser and Gremillion, 2012).

Neuropathy (dysfunction of the nerve) may present with or without neuropathic pain and
onset may be spontaneous or subsequent to various types of lesions or trauma. In the
orofacial region neuropathic pain unrelated to a disease or traumatic event may be
diagnosed as primary trigeminal painful neuropathy, non-odontogenic pain, phantom tooth
pain, atypical odontalgia or persistent dentoalveolar pain type I (PDAPI), and is often difficult
to diagnose because it is poorly understood (Nixdorf and Moana-Filho, 2011). Exclusion of a
condition termed ‘pretrigeminal neuralgia’ is required as there is increasing recognition that
neuropathic toothache may precede the onset of TN (Wright and Evans, 2014). Burning
mouth syndrome, not attributable to a known cause (Symptomatic burning mouth), is now
recognised as a neuropathic pain condition presenting with three group that are either
peripherally driven, mixed or centrally driven (Jääskeläinen, 2011).

Trigeminal neuropathic conditions that present as a result of a disease or lesional

interferences in neural function include; classical trigeminal neuralgia with evidence of
vascular compromise, non-classical symptomatic Trigeminal neuralgia [TN], post herpetic
neuralgia [PHN], symptomatic burning mouth syndrome [BMS} and post traumatic
neuropathies with pain [PPTTN] (Table 1). A more appropriate name for this group may be
secondary neuropathic pain in the trigeminal system. There are many systemic causes for
peripheral neuropathy that may be associated with neuropathic pain in the trigeminal
system. Nerve lesions causing neuropathic pain can be caused by many conditions
including;
 Compression by a space occupying lesion centrally or peripherally
o Neoplasia (any case of spontaneous sensory or motor neuropathy must be
suspicious of neoplasia)
o Bone compression due to Acromegaly
o Other benign lesions (e.g. dentigerous cysts, cemento osseous dysplasia)

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  Nutritional deficiencies (Fe, B12, Ferritin, Zinc, Vit D, Vit E)
 Hormonal neuropathy (Hypothyroidism, Diabetes),
 Infarction (stroke, sickle cell hypoxic neural damage, giant cell arteritis)
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 Demyelination (Multiple sclerosis)
 Post viral neuropathy (Post herpetic neuropathy)
 Local bacterial infections (medical related osteonecrosis, periapical lesions close to
the inferior dental canal)
 Auto immune disease: Lupus, Rheumatoid disease
 Sarcoidosis and Amyloidosis
 Parkinsons disease
 Leprosy

Painful neuropathy occurring after insult, or post traumatic neuropathy and can be caused by
surgical or physical trauma, chemical, irradiation and thermal insults. Persistent pain after
endodontic therapy (PDAPII) is more commonly reported, as it is estimated 3-4% of patients
may experience persistent pain after root canal therapy (Nixdorf et al., 2012). The IHS (III)
term this painful posttraumatic trigeminal neuropathy (PPTTN) (Benoliel et al., 2012) is better
known in the medical literature as Chronic post-surgical neuropathic pain (CPSP) (Macrae,
2008). Recently it has become evident that significant numbers of patients suffer from
chronic pain as a result of routine surgery with over 20-40% of patients presenting in chronic
pain clinics being diagnosed with CPSP.20 CPSP is known to be caused by a number of
common surgical procedures for example; thoracotomy, breast surgery, limb amputation and
herniorraphy (Macrae, 2008). Within the trigeminal system, CPSP has been reported
following local anaesthetic administration, dental extractions, endodontic procedures, dental
implant placement and seemingly benign facial cosmetic procedures (Renton and Yilmaz,
2011; Benoliel et al., 2012; Gay-Escoda et al., 2015). Neuropathic area may not be present
and is not included in the diagnostic criteria (Renton and Yilmaz, 2011; Haanpää et al.,
2011; van Hecke et al., 2015).

Possible mechanisms for developing chronic pain (Woolf, 2010; Ossipov et al., 2014)
Neuropathic and dysfunctional chronic pains may be attributable to various peripheral and
central mechanisms;

• Sensitization of peripheral nociceptors

• Central sensitization
• Altered bulbospinal modulation or diffuse noxious inhibitory control (DNIC) system

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 – Both descending facilitatory and inhibitory influences run from brainstem to
spinal cord. In chronic pain, levels of descending inhibition can be reduced
while facilitation is enhanced. There are established techniques for evaluating
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the degree of descending pain modulation in operation in volunteers or
patients.
• Altered cortical circuitry and connectivity (Plasticity)

Recent studies have demonstrated that reduced pain modulation is demonstrable in patients
with PPTTN (Nasri-Heir et al., 2015). The low incidence of CPSP in the trigeminal region
may reflect the lack of central sensitization due to most procedures being undertaken under
local anesthetic thus preventing central sensitization (Woolf, 2010; Ossipov et al., 2014). It
is also recognized that post traumatic neuropathy is more resistant to medical management
compared to other chronic pain conditions (Nasri-Heir et al., 2015).

Risk Factors for developing chronic pain after routine surgical intervention
Prevention of CPSP with or without neuropathy may be possible and risk factors are
becoming evident including;
 preoperative screening for neuropathic is recommended, to prevent inappropriate
surgery and possible escalation of pain. Many validated diagnostic screening tools
are available including; the Leeds Assessment of Neuropathic Symptoms and Signs
(LANSS), the Self-reported LANSS (S-LANSS), the Neuropathic Pain Questionnaire
(NPQ), the Douleur Neuropathique en 4 (DN 4) questions, pain DETECT and ID-
Pain. A recent review reported that he DN4 and Neuropathic Pain Questionnaire
were most suitable for clinical use (Mathiesonet al., 2015). However their sensitivity
and specificity for chronic pain in the trigeminal system is poor (Elias et al., 2014).
 preoperative medical screening for existing conditions including (Katz and Seltzer,
2009; Kehlet et al., 2006);
o Raynaud’s disease
o Erythromelalgia
o Irritable bowel syndrome
o Migrainous headaches
o Fibromyalgia
 preoperative screening for specific patient factors including (Macrae, 2008);
o Age (Younger = risk breast surgery and herniorrhaphy / older =  risk other
surgery), Gender (female =  risk)
o Genetics (catecholamine-O-methyltransferase),
o preceding pain (intensity and chronicity),

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 o Sleep disorders also interfere with the DNIC system, and management of
sleep disorders has been shown to improve chronic pain syndromes
o Excessive nociceptive stimulation during early childhood impairs development
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of the DNIC system. At adolescence, children born prematurely present twice
as many trigger points compared to children born at term
o Psychosocial factors are recognised increasingly as the most important risk
factor for developing chronic pain with or without surgery. Previous
psychological stressors in childhood and personality or anxiety disorders
appear to reduce the capacity of the pain modulation system (Kehlet et al.,
2006; Macrae, 2008; Schreiber et al., 2014).
 Cognitive -Fear of surgery and anxiety and fear of pain (Kehlet et al.,
2006; Macrae, 2008; Schreiber et al., 2014).
 Personality disorders (increased preoperative anxiety, Introverted
personality, Catastrophizing, Poor coping skills, Hypervigilance states)
(Kehlet et al., 2006; Macrae, 2008; Schreiber et al., 2014).
 Psychological vulnerability – pain related fear (Kehlet et al., 2006;
Schreiber et al., 2014).
 Social support (Kehlet et al., 2006).
 Solicitous responding -Empathetic spouse encouraging negative
behaviour and Munchausen (Schreiber et al., 2014).
 Post-Traumatic Stress disorder (PTSD) is reported in post-traumatic
neuropathy with pain in the trigeminal system (Elias et al., 2014), and is
also reported with chronic pelvic pain syndromes, particularly if iatrogenic.
Post-traumatic stress disorder (PTSD) is a major anxiety disorder initiated
by exposure to a traumatic event.
o Family history of anxiety and or depression, a personal or family history of
depression is found in 66% of cases of fibromyalgia and it may decrease
the patient’s capacity to inhibit pain. Patients with higher psychological
distress and perception of unhappy childhood are more likely to report
orofacial pain. The presence of documented depression, with decreased
involvement in activities, chronic fatigue, and sleep disorders exacerbates
and perpetuates both PTSD and the clinical features of chronic pain.
o A strong relationship between a history of sexual abuse (generally within
the family, by the father or spouse with physical or psychological trauma)
and chronic pelvic pain has been reported in relation to developing
chronic pelvic pain and IBS. Symptoms are maintained by anxiety and

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 pain, which increase vulnerability and traumatic re-experiencing (PTSD)
(Schreiber et al., 2014).
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Assessment Holistic assessment of the patient is required including likely cause, duration,
pain, psychological and functional or social impact (Axes I-III) (Haanpää et al., 2011; van
Hecke et al., 2015). Sensory examination confirming a neuropathic area, may include
mechano-sensory tests (response to light touch, temperature, painful, moving and vibratory
stimuli), reflex assessment and quantitative neuroosensory techniques (QST). Associated
signs including autonomic changes in colour, temperature, sweating and swelling must be
assessed. Investigations including; Haematology to exclude systemic causes of neuropathy
including; full blood count (FBC), erythrocyte sedimentation rate (ESR), glucose, creatinine,
alanine transaminase (ALT), vitamin B12, serum protein immunoelectrophoresis and thyroid
function. Assessing glycaemic control with an HbA1c is useful in patients who are diabetic. A
glucose tolerance test may be helpful if diabetic status is not known. Imaging techniques
may be required to exclude local causes of nerve damage usually with plane films and
CBCT or magnetic resonance imaging (MRI) if a central lesion is suspected.

The second type of maladaptive pain alluded to by Woolf (2010) termed dysfunctional or
centralised pain is likely characterized by failure of the diffuse noxious inhibitory control
(DNIC) system (Kehlet et al., 2006; Schreiber et al., 2014). DNIC dysfunction is not a
characteristic of all chronic pain syndromes, but includes tension headache, irritable bowel
syndrome, restless legs syndrome, TMD arthromyalgia and persistent idiopathic facial pain
(Woolf, 2010).

Management of chronic trigeminal pain

The pain and cause (first axis) that the patient is experiencing must be assessed on the
functional (second axis) and psychological impact (third axis) basis. These important
features must be managed alongside the pain where possible with physical and
psychological interventions where appropriate. The painful element or neuropathic pain due
to neuropathy is sometimes considered to be of two types – neuralgic (sharp, stabbing pains
as in TN) or neuropathic (altered sensations such as burning, tingling, ‘pins and needles’)
and so sometimes different treatments are given according to which type of pain is felt most
often. Medical management of neuropathic pain (NICE 2014), may include tricyclic
antidepressants, gabapentin and or pregabalin, topical drugs applied to the skin (local
anaesthetic or capsaicin) or Botoxin injections where applicable. Surgery is indicated
URGENTLY for post traumatic neuropathy related to wisdom teeth, implant or root canal

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 surgery within 30 hours and rarely up to 3 months but not later to maximise resolution of
traumatic nerve injuries (Renton and Yilmaz 2011).
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The second axis consists of psychological therapy with the use of cognitive behavioral
therapy (CBT), acceptance commitment therapy (ACT), hypnosis, relaxation, or even EMDR
(Eye Movement Desensitization and Reprocessing) (in patients with a documented history of
trauma), or family therapy when the family repercussions are predominant. However, the
evidence for these various treatments remains scant.

Finally, the socio-occupational approach, in collaboration with the occupational health

physician, is designed to promote return to work for patients on sick leave, and especially
maintenance at work, if necessary by quantitative (part-time), or qualitative (adapted seat,
adapted working schedules, etc.) adjustment of the patient’s job.

In conclusion chronic pain within the trigeminal system is complex to diagnose, assess and
manage. Importantly, pain caused by surgery, a well-recognised phenomenon in the medical
setting, but remains mainly unrecognised and poorly diagnosed in dentistry. Fortunately, it is
very rare in the trigeminal system, likely due to the regular use of local anaesthetic
injections. However, in order for our specialty to reliably develop evidence based
management of these conditions alignment and rationalisation of the current nomenclature
must be undertaken. A refreshing approach to apply the Research diagnostic criteria used
for TMD will be applied to other chronic orofacial pain conditions, allowing clarification of
diagnostic terminology promoting improved consensus in assessment and management
(Durham et al., 2015; Ceusters et al., 2015).
Chronic pain may be preventable, improving the awareness of healthcare personnel
concerning the importance of doing no harm by procedures which can be considered by the
patient to constitute a new form of abuse or aggression is essential.

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ccepted Articl
Acute
Table 1 Conditions presenting as chronic pain in the orofacial region

Acute inflammatory Neurovascular Neuropathic Neuropathic Dysfunctional Referred

nociceptive Intermittent or unknown identifiable
Intermittent persistent cause cause
Dentine Dental Primary Headaches Persistent Peripheral Association Cardiac
sensitivity  Reversible  Migraine dentoalveolar neuropathy with Multiple
Cracked pulpitis  Tension pain type 1 with identified pain
tooth  Irreversible  Chronic daily (PDAPI) or peripheral or conditions
syndrome pulpitis  Medication neuropathic central
 Periapical overuse dental pain disease: for Fibromyalgia
periodontitis Or Pre TN example PHN Pelvic pain
Or Irritable
Post traumatic bowel
neuropathy syndrome
with pain Tension
(PPTTN or PTN) Headaches
OR
Persistent
dentoalveolar
pain type 2
(PDAPII)
Post endo
persistent pain
TMJ Disc Temporomandibular Trigeminal autonomic Classic TN with Classic TN with TMD Cervical
entrapment joint (TMJ) disorders cephalalgias no vascular vascular arthromyalgi
associated  Arthromyalgi  Cluster compromise compromise a
with a/ headache Or
Dysfunction myofascial  SUNCT Symptomatic
group TMDs  Dysfunction  Paroxysmal TN
clicks hemicranias
crepitus  Hemicrania
 Arthritides continua

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ccepted Articl
Recurrent
traumatic
Mucosal
Recurrent traumatic
Giant Cell arteritis Burning
Mouth
Symptomatic
Burning mouth
Centrally
Driven BMS
geal
Oesopha

ulcer ulcer Syndrome

Aphthous Aphthous ulceration (BMS)
ulceration Lichen planus
Geographic tongue

Salivary Salivary gland Other cranial Persistent Tonsillar

gland disease neuralgias idiopathic
obstructive Obstructive Glossopharyng facial pain
disease Inflammatory eal
‘Meal time Nervous
syndrome’ intermedius
Dermatological CPSP Lung
infections
Lymph node
inflammation
Chronic Sinusitis

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