Australian Dental Journal 2009; 54: 84–93

REVIEW
doi: 10.1111/j.1834-7819.2009.01099.x

Burning mouth syndrome and psychological disorders

LM Abetz,* NW Savage*
*Oral Medicine and Oral Pathology, School of Dentistry, The University of Queensland.

ABSTRACT
Burning mouth syndrome (BMS) is an oral dysaesthesia that causes chronic orofacial pain in the absence of a detectable
organic cause. The aetiology of BMS is complex and multifactorial, and has been associated in the literature with
menopause, trigger events and even genetic polymorphisms. Other studies have found evidence for mechanisms such as
central and peripheral nervous system changes, with clinical and laboratory investigations supporting a neuropathologic
cause. These physiological explanations notwithstanding, there is still much evidence that BMS aetiology has at least some
psychological elements. Somatoform pain disorder has been suggested as a mechanism and factors such as personality,
stress, anxiety, depression and other psychological, psychosocial and even psychiatric disorders play a demonstrable role in
BMS aetiology and symptomatology. In order to treat BMS patients, both physiological and psychological factors must be
managed, but patient acceptance of possible components of psychological disease basis is a major hurdle. Clinical signs of
patient stress, anxiety or depression are a useful reinforcement of clinical discussions. The current paper proposes a number
of clinical signs that may be useful for both clinical assessment and subsequent patient discussions by providing visible
supportive evidence of the diagnosis.
Key words: Aetiology, burning mouth syndrome, clinical signs, oral dysaesthesia, psychological disorders.
Abbreviations and acronyms: BMS = burning mouth syndrome; HRT = hormone replacement therapy; OSC = oral sensorial complaints.
(Accepted for publication 20 August 2008.)

INTRODUCTION the continuation of the condition. A number of muco-

sal alterations will also be discussed, together with
Oral dysaesthesias or abnormal sensations such as their possible use in clinical evaluation and patient
burning mouth syndrome (BMS) present a difficult discussions.
diagnosis for many clinicians. Diagnostic criteria are
not consistent and the aetiology of BMS is multifacto-
Burning mouth syndrome
rial and poorly understood. It seems likely that both
physiological and psychological factors play a role in There are a number of oral symptom complexes and
causing, perpetuating and ⁄ or exacerbating BMS, but presentations for which there is no readily detectable or
the interaction between these and the relative signifi- clinically visible organic cause. This group of conditions
cance of each remains largely speculative. Clinical is clustered under the general heading of idiopathic oral
management is correspondingly complex and there is dysaesthesias and cause chronic orofacial pain in the
no uniform treatment protocol, but in each case, both form of disturbance in oral sensation. A common
the physiological and psychological components of the example is BMS. This condition presents a useful model
patient’s symptoms must be addressed. The acceptance for discussion of the dysaesthesias as it is increasingly
of psychological factors by the patient is often an recognized due to informational articles and a devel-
important element of BMS management, but this in oping body of research.
itself can present a clinically challenging situation. BMS is a chronic oral dysaesthesia characterized by
If there were oral signs or symptoms indicative or a burning sensation of the oral cavity with clinically
predictive of psychological disturbance, both the normal mucosa and in the absence of any detect-
patient and clinician would be aided in terms of able organic cause.1–3 It has variously been called
diagnosis and management of oral dysaesthesias such glossodynia, glossopyrosis, stomatodynia, stomato-
as BMS. The objective of this paper is to review the pyrosis, sore tongue, or burning tongue4 although
clinical presentation of BMS and to focus on fac- these are not helpful diagnostic terms, describing
tors contributing to both the initial presentation and symptoms rather than the disease. BMS has been
84 ª 2009 Australian Dental Association
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Burning mouth syndrome and psychological disorders

described by patients as a burning, tingling, or numb Aetiology of burning mouth syndrome

feeling in the oral cavity. A burning sensation may
also occur at other sites, e.g., the anogenital or vulval Physiological factors
region2,5 (one of the reasons for the designation
‘‘syndrome’’). Intra-oral burning can occur at any site BMS mainly affects post-menopausal women and,
and it is common for it to occur at more than one because of this, it has been postulated that menopause,
site. The tongue is most commonly affected, princi- the cessation of menopause, or hormonal disruption is a
pally the anterior two-thirds and tip on the dorsum precipitating factor. Around 20 per cent of oophorec-
and at the anterolateral margins.2 The anterior hard tomized and menopausal women experience BMS-like
palate, mucosal aspect of the lip,2 and mandibular oral symptoms,5,7 but it is difficult to draw meaningful
alveolar regions can also be affected, while sites such conclusions about BMS incidence in these groups as
as the buccal mucosa and floor of the mouth are none were examined clinically for detectable pathology.
rarely involved. BMS burning is almost always However, women with BMS do not have more
bilateral and symmetrical and does not follow the hormonal abnormalities than those without, and hor-
anatomical distribution of a peripheral sensory nerve.1 mone replacement therapy (HRT) used to treat BMS
This is an important part of the clinical examination has not been effective, though this may be related to the
in order to exclude any anatomical distribution to the variable presence of oestrogen receptors in the oral
dysaesthesia, which may indicate a neurogenic pain. mucosa. The designation of the typical BMS patient as
Symptoms such as itching, drawing and crawling a post-menopausal female has, in the authors’ opinion,
sensations of the mucosa and teeth have also been unfairly categorized patients with this syndrome. It is
described.2 BMS patients will also often report common for patients to be described as neurotic, and
subjective conditions such as xerostomia and dysgeu- the condition as existing only in their mind. This is
sia, as well as sialorrhoea, globus hystericus, halitosis neither a realistic or professional stance, and the reader
or dysphagia.2 In fact, the frequent concomitant or should not suppose that there is any such simplistic
overlapping presentation of burning mouth, dysgeusia approach in the discussion of psychogenic factors in
and xerostomia has led some researchers to group this paper.
these symptom complexes together as one entity under A recent study has suggested that genetic polymor-
the name oral sensorial complaints (OSC).6 phisms associated with increased production of inter-
BMS can be classified as mild, moderate or severe leukin-1b, a pro-inflammatory cytokine that plays a
depending on the intensity of pain symptoms, but most role in several chronic diseases and has been implicated
patients experience burning sensations of moderate to in the modulation of pain sensitivity, are also impli-
severe intensity with mean severity of about 5–8 cm on cated in BMS patients.8 The success of topical clonaze-
a 0–10 cm visual analogue scale1 or of similar intensity pam in reducing BMS symptoms may indicate that
to toothache pain. An important clinical parameter in alteration in the density of GABAa receptors in
this context is the reported impact the pain is having peripheral tissues due to hormonal, age and stress-
on a patient’s ability to cope and perform their nor- related changes may be an aetiological factor in the
mal daily routine and the variation in pain percep- disease.1 However, the success of alpha lipoic acid
tion during periods of mental preoccupation with therapy supports the view that BMS may be a
other tasks. BMS has also been divided into three neuropathy, and suggests this may be related to free
distinct categories based upon the occurrence of oral dis- radical production and low levels of intracellular
comfort and pattern of symptom presentation and glutathione.3 BMS has also been successfully treated
progression.1,5 with olanzapine, which exerts its effects through
Type 1 BMS is characterized as a burning sensation antagonism at serotonin and dopamine receptors.9
that is not present upon waking, but which develops in Neurological changes seen in BMS patients include
the late morning and progresses during the waking change in the eye-blink reflex which appears to be
hours, with the greatest intensity of discomfort in the related to longer disease duration.10 Additionally,
evening. This sensation is present every day. positron emission tomography seems to indicate
Type 2 patients awake with a burning sensation that decreased dopaminergic inhibition in BMS patients.11
is constant throughout the day, which often prevents One study compared superficial biopsies of the lateral
patients from falling asleep. This discomfort is present aspect of the anterior two-thirds of the tongue between
all day, every day. BMS patients and healthy controls and found a
Type 3 patients report intermittent symptoms and significantly lower density of epithelial nerve fibres
symptom-free periods, with variable presence between and axonal degeneration in the BMS patients.12 This
days and may experience the symptoms at unusual suggests that the aetiology of BMS may have a
oral sites such as the floor of the mouth and buccal component of trigeminal small-fibre sensory neuro-
mucosa.5 pathy.
ª 2009 Australian Dental Association 85
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LM Abetz and NW Savage

One hypothesis proposes a comprehensive mecha- Psychological factors

nism for BMS, taste disturbances and ⁄ or xerostomia
based on a regional neuropathy.6 The mechanism Psychological abnormalities are associated with BMS in
suggested is via either a regional small-fibre idiopathic numerous studies,3,15,16 but the precise relationship
neuropathy affecting salivary secretion and oral sen- between these factors and any predisposition to BMS
sation, or a primary idiopathic neuropathy causing remains unclear. Assuming this relationship, the initial
sensory neural dysfunction at the receptor level by prescription of a low dose anxiolytic will usually
changing the oral cavity environment.6 Sensory provide some level of dampening of symptom intensity
changes in the tongue6 and changed salivary compo- and so confirm the diagnosis, as well as strengthen the
sition with normal salivary flow rates have been basis of clinical discussion and decisions concerning
demonstrated in patients with BMS, xerostomia and ongoing management.
dysgeusia.6,13 Differences in salivary composition are Several studies suggest the important role of psycho-
also found between these groups.6,13 Higher concen- logical factors such as anxiety and depressive disorders
trations of salivary K and amylase were associated in unexplained somatic symptoms and the prevalence of
with increased warm thresholds, providing a link non-specific somatoform symptoms is higher in psycho-
between neuropathy and saliva.6 In BMS, dysgeusia logically disturbed patients than in the general popula-
and xerostomia, there may be a common taste tion.17 BMS patients have poorer self-reported overall
perception profile that differs significantly from con- health and complain of more illnesses,18,19 gastrointes-
trols, again pointing to a neurological dysfunction tinal problems, chronic fatigue, disturbed sleep pat-
mechanism for these complaints.13 terns,18 headaches and pain in other locations19 and are
Patients will very often associate the onset of burning more likely to display a cancer phobia.2,5,18 An inter-
symptoms with a particular life event ranging from a esting proposed link is that cancerophobia, chronic
temporal association with dental procedures, illness, fatigue and disturbed sleep can be thought of as
a course of medication, or stressful events.1 It is emotional concomitants of anxiety, while gastrointesti-
suggested that certain dental treatments may cause nal disorders could be a physical concomitant of
injury to orofacial tissues and nerves, leading to anxiety.18 The implication is that BMS may be indica-
undesirable neuroplastic changes, which lead in turn tive of distress that causes vulnerable individuals to
to BMS symptoms. Central sensitization producing experience emotional distress as pain. Studies suggest
long-lasting neuroplastic changes in central nociceptive SSRIs and amisulpride may be effective in reducing BMS
neurons, including increased excitability and occasional symptoms,20 supporting the somatoform pain disorder
spontaneous tonic activity, has also been suggested as a model for BMS. However, to regard BMS as merely a
mechanism, as has damage to the taste system, causing somatic symptom of an underlying psychiatric disorder
oral phantom pain.1 is inappropriate.
This raises further considerations concerning the Chronic stress, post-traumatic stress, depression and
origin of pain in BMS and probable variance between chronic anxiety have been prevalent states in ‘‘func-
the initiating and perpetuating factors in this pain tional pain disorders’’ which are a group of conditions
syndrome. By definition, BMS presents as a spontane- such as BMS, irritable bowel syndrome, fibromyalgia
ous dysaesthesia with no detectable organic cause. and chronic fatigue syndrome. A hypothesis linking
Many patients, however, report a range of exacerbating psychological and somatic aspects of so-called func-
factors including dietary items, particularly hot drinks ⁄ tional pain conditions (such as BMS) has been proposed
foods, direct touch to the dorsum and lateral margins of based on aspects of the physiology and neurochemistry
the tongue and, to a lesser extent, other site involve- of anxiety and response to stress.18 Chronic stress,
ment. There is some clinical evidence to suggest this is a anxiety and depression can cause changes in the control
secondary cause of pain following habitual trauma to of cortisol secretion. Permanent changes in the hypo-
the site. For example, in many BMS patients as well as thalamic-pituitary-adrenal axis, resulting in changes to
some asymptomatic patients, the lateral tongue margins the level of glucocorticoid already produced, along with
are scalloped and the anterior dorsum and tip of the constant modifications in the level of gonadal steroid,
tongue show a traumatic abrasion of the filiform could help to trigger the pain. The primary trigger may
papillae against the coincident palate and dentition, be damage to neural cells caused by abnormal cortisol
and resultant prominence of the usually bland fungi- levels. It has also been shown that maternal distress can
form papillae. sensitize children to react with increased circulating
One case control study found no significant differ- cortisol in response to stressful events in later life.18
ence between BMS patients and controls with respect to Psychological factors could help explain BMS in at
various physiological factors; the only significant dif- least 50 per cent of patients.21 Results of studies into
ferences found were with respect to self-reported treatment of BMS by cognitive behavioural therapy
depression and anxiety.14 indicate that, in some cases at least, BMS does have
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Burning mouth syndrome and psychological disorders

components of psychological origin.22 A Cochrane vulnerability.26 The severity of burning symptoms

review of interventions for BMS found that cognitive correlates with neuroticism as well as extroversion,
behavioural therapy was one of only three interventions openness and conscientiousness.26 All facets of neuro-
resulting in the reduction of BMS symptoms.23 Cogni- ticism that are significant in BMS are significantly
tive behavioural therapy is currently used to treat a related to the negative affect and lower life satisfaction
variety of mental disorders including depression, anx- and complaints of pervasive psychological distress.26
iety, phobias and pain complexes. A cognitive therapist There also seems to be a direct relationship between a
identifies, reality-tests and corrects dysfunctional beliefs worsening of physical symptoms, increased functional
underlying the patient’s suffering in order to replace impairments and a lowering of the quality of life with
these dysfunctional cognitive structures (attitudes or progression to depression and anxiety in a cause and
assumptions about the world) with more realistic and effect relationship.18 This is supported by a study on
functional ones.22 More evidence for components oral health-related quality of life in oral medicine
of psychological origin in BMS is provided by the outpatients which found that the greatest impairment
observation that reassurance alone can be an effective to quality of life was registered on the physical pain
treatment, resulting in a reduction of symptoms in 24 subscale.15
per cent of patients, and that improvement of psycho- As with all chronic pain sufferers, it is challenging to
logical status often relates directly to a reduction in distinguish whether depression and anxiety are causes
symptoms.16 One study found that the onset of BMS or effects of the symptoms of oral dysaesthesias such as
was preceded by acutely stressful events superimposed BMS.1 Depression and psychological disturbance are
on pre-existing psychological factors.24 common in chronic pain populations and may be
There is an accumulating body of evidence that BMS secondary to chronic pain rather than the cause of
patients differ from the general population in their BMS. Mood and sleep disturbances and a decreased
psychopathologic profile.25 Psychological disorders desire to socialize may also be secondary, but nonethe-
possessed by BMS patients include personality dis- less contributing factors, rather than the primary
orders, uncommon depression, emotional instability,5 precipitating factors of BMS. The results of the
and chronic anxiety.5,16 BMS patients may have Multiphasic Personality Inventory observed for BMS
significantly higher experiences of adverse early life subjects in one study was typical of chronic pain
experiences compared to controls.18 A high percentage patients suffering from ‘‘reactive depression’’ caused by
of BMS patients have been hospitalized for psychiatric their chronic pain.27 In addition, symptoms of dyspho-
illness in the past, and show greater tendency to be ria and anxiety may develop after the onset of BMS
under current psychological treatment, often initiated symptoms and remit fully upon pain relief. It has also
prior to the appearance of BMS symptoms.24 A high been proposed that because studies usually involve
proportion of BMS patients have an associated psychi- samples of care-seeking patients, higher rates of psy-
atric disorder, usually in the form of mixed anxiety and chological symptoms are found in samples of BMS
depressive symptoms forming part of a complex picture patients than would be found in BMS sufferers within
of social as well as psychological problems.21 Patients the general population as psychologically distressed and
with BMS have significantly higher incidence of anxiety depressed individuals are more likely to seek care.28
and depression compared to both the general popula- The presence of both physical and psychological
tion18,21 and to patients suffering chronic organic symptoms points to a psychogenic-physical aetiological
orofacial pain.7,15 continuum.18 It is therefore likely that there are both
Psychiatric assessment has identified abnormal per- ‘‘affective and cognitive dimensions of chronic pain’’
sonality profiles in 40 to 50 per cent of patients with and to treat chronic pain such as BMS, a clinician must
BMS while personality trait assessment has indicated take into account both axes. Management and out-
that BMS patients tend to be anxious, introverted and comes depend at least equally upon addressing psycho-
self-reliant, have low self-esteem, are fearful, prone to logical factors as well as addressing the disease entity.
worry, nervous and tense.26 They are more concerned
with bodily function, depressed, emotionally repres-
Patient acceptance of psychological aetiological
sed, angry, distrustful, anxious, socially isolated,27 and
factors
have a tendency to experience anger and related states
such as frustration and bitterness.26 They also score A primary clinical goal in the treatment and manage-
significantly higher on the scales of somatization, ment of any patient complaint is the development of a
obsession-compulsion, personal sensitivity, depression, common level of understanding between clinician and
anxiety, hostility, phobic anxiety, and psychoticism.25 patient. This is relatively easily accomplished when the
Patients with BMS have significantly higher levels major complaint is a well-defined entity, e.g., toothache,
of neuroticism in all its facets: anxiety, anger, hos- a visible lesion, or a lip lump. Patient expectation of an
tility, depression, self-consciousness, impulsiveness and anticipated and readily understood diagnosis such as
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LM Abetz and NW Savage

dental caries or a mucocele is realized and the treatment reliability. A Japanese study examined this issue using
proceeds along a route readily accepted by the patient: a multiple logistic regression models and found that age
dental restoration or removal of the lump. However, (over 30 years), personality traits (neuroticism and
the aetiology, diagnosis and treatment of dysaesthesias extroversion) and choice of certain pain expression
are significantly more abstruse, and patients often seem terms (‘‘sickening’’) could help to predict anxiety
expectant of a ‘‘real’’ diagnosis rather than being or depression in patients.29 However, these are not
receptive to the suggestion that the condition may have symptoms that necessarily have significance to the
components of a psychological aetiology,4 which must patient, and cannot be used by the patient for the same
be addressed as part of successful treatment. There may purpose as the oral signs listed previously. The lack of
also be concern on the part of the clinician that the clinical indicators of a specific psychological profile is
diagnosis of an oral dysaesthesia may not be correct, a significant gap in current knowledge, as the man-
and there is a real need to provide additional indicators agement of oral dysaesthesias frequently involves the
that a clinician can use in these situations. Acceptance of use of a range of potent psychoactive medications
the role of psychological factors in the development and including tricyclic anti-depressant and anti-convulsant
progression of a dysaesthesia is an important element in medications.2,4
patient understanding. Any clinical signs that patients
can confirm for themselves in the privacy of their own
The oral cavity and psychological profile
homes are a useful reinforcement of clinical discussions.
Such signs might include: (1) frothy saliva indicating a The inherited psychological characteristics and current
parotid hypofunction and dominance of mucoid sub- psychological profile of a patient influence their body in
mandibular saliva over the serous parotid saliva (anx- many ways. For example, the response to stressors
iety is the most common cause of both acute and chronic modifies numerous physiological responses such as
xerostomia); (2) dryness of the inner aspect of the lower pulse rate, skin resistance, blood pressure and blood
lip from minor labial gland hypofunction; (3) scalloping distribution. The oral cavity is also affected. For
of the lateral lingual margins secondary to habitual example, a study of university students found that
pressure against the adjacent teeth; (4) buccal mucosal during stressful periods (examinations) a small, stan-
irregularity often with leukoedema, translucent kerato- dardized wound of the oral mucosa took 40 per cent
sis and linea alba, also due to pressure against the longer to heal than during vacation periods, and this
adjacent teeth; (5) low grade erythema of the anterior coincided with a 68 per cent decline in IL-1b mRNA in
dorsum of the tongue as a result of traumatic abrasion of peripheral blood mononuclear cells.30 An example of
the filiform papillae against the adjacent teeth and an orofacial manifestation of stress modified immune
palate and exposure of the sensitive fungiform papillae; dysfunction is the observation that oral lichen planus is
(6) low grade erythema and often slight sensitivity of the exacerbated by stress. Subjective complaints regarding
coincident anterior hard palate; and (7) low grade linear migratory glossitis are also often associated with stress.
erythema of the inner aspect of the lip coincident with
the edges of the incisor teeth, mainly on the lower lip.
Xerostomia and sialorrhoea
This listing, used clinically by the authors, has proved
extremely useful both at initial consultation in the The relationship between stress and salivary flow has
assessment of dysaesthesic conditions with presenting been known for some time. Investigations of the stress
symptoms and sequence consistent with BMS, and response associated with particular situations including
subsequently at review. The authors have found that examinations and fear of pain show reduced flow rates,
patients are highly likely to accept that anxiety or an decreased pH values, and increased protein and amy-
associated condition is related to their dysaesthesia if lase concentrations.31 Psychological and physiological
they can agree that the visible presentation of clusters stress exacerbated by examinations or menstruation
taken from this list have no real cause other than can also cause an increase in oral volatile sulphur-
anxiety or other psychological ⁄ psychiatric bases. How- containing compounds31 and variation in total ion
ever, the basis for this list is merely clinical observa- concentration. Numerous studies have confirmed the
tion and experience. There is little in current or past relationship between anxiety, stress and particularly
literature to support the use of these or other oral depression with a lowering of unstimulated salivary
observations as clinical indicators of particular psycho- flow rates,32 and most readers will relate to both acute
logical profiles and there is a need to objectively assess onset oral dryness in situations such as unexpected
whether the presence of these signs is actually associ- public exposure or to slower onset in situations such as
ated with psychological disturbance in the general the lead-up to a planned public exposure, e.g., giving a
population. speech.
Other predictors of anxiety or depression in orofacial Patients with symptoms allegedly caused by abnor-
outpatients have proven more difficult to use with mal sensitivity to dental fillings and ⁄ or to electro-
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Burning mouth syndrome and psychological disorders

magnetic fields and other environmental factors thickness and length of each secondary protrusion of the
frequently report a range of oral complaints and connective tissue core of the filiform papilla decreases
dysaesthesias including burning mouth, taste aberra- roughly proportionally with age34 and specific condi-
tions and subjective oral dryness. Many medications tions may further contribute to this. These include
can alter salivary flow by both sympathomimetic and Sjogren’s syndrome, which dermoscopically demon-
parasympathomimetic actions or by acting directly on strates flattened filiform papillae,35 anaemia, vitamin
salivary cellular processes, so it is often challenging to or iron deficiency, chemotherapy, radiotherapy, or
distinguish between physiological and psychological because of infection such as candidosis. Immune-based
causative factors associated with hyposalivation and atrophy of the filiform papillae is also common in
subjective oral dryness. A reduced salivary flow rate defined mucocutaneous diseases including lichen planus
is difficult to diagnose as it varies widely between and pemphigoid as well as in less well-defined condi-
patients. Increased age and medications, e.g., psycho- tions including erythema migrans and the inappropriate
tropics, anti-asthmatics and diuretics, seem to be more use of potent corticosteroids to treat these conditions.
important in objective hyposalivation, while gender and The clinical picture is often complicated by the presence
psychological factors feature more in subjective oral of tongue fissuring and clefting, with the former
dryness.31 Low unstimulated salivary flow, coupled presenting with smooth surfaced filiform papillae and
with subjective oral dryness, is associated with age, very atrophic and often sensitive mucosa lining these
female gender and medication.32 Low unstimulated clefts and fissures. The depapillation has varying
salivary flow without subjective dryness is associated patterns, but in many cases there is some specificity in
with age and medication (anti-hypertensives and anal- relation to cause. For example, mucosal disease-related
gesics), while purely subjective oral dryness is associ- atrophy is defined by the extent of disease and may
ated with depression, perceived stress, state and trait range from the entire dorsum to focal but usually
anxiety, female gender and anti-hypertensives.32 Med- bilateral sites. Trauma or lichenoid stomatitis is focal
ications and psychological factors may have a recipro- and specific to the causative area such as a prominent
cal effect in reduction of salivary flow and causation of tooth cusp or an amalgam restoration. In areas sub-
subjective oral dryness.32 Late life depression is asso- jected to habitual and repetitive trauma by rubbing
ciated with, among other conditions, diminished sali- against adjacent tissues, usually the palate or anterior
vary flow and oral dysaesthesias particularly chronic mandibular teeth, the atrophy is bilateral and restricted
facial pain or a burning sensation of the oral mucosa to the anterior dorsum or the lateral and anterolateral
and tongue.33 The summation of this information is margins of the tongue. Examples of this pattern of
that xerostomia is almost never the result of a single filiform papillae abrasion are shown in Figs 1–3.
causative factor. Great caution is required to not only Hyperplasia and hyperkeratosis of the filiform papil-
confirm a subjective xerostomia, but also to ensure lae also occurs in response to a number of causes. A
patient understanding of the multifactorial nature of common but frequently unrecognized cause is simply a
this symptom, and to establish expectations regarding reactive hyperplasia in response to habitual irritation of
any treatment. Cure, at least in the short term, is
unrealistic in many patients, but any level of improve-
ment can be used as a positive indicator of overall
progress in management of conditions such as BMS.
Sialorrhoea or excessive saliva is a rare complaint
and may be a misinterpretation of xerostomia.2
Depressed parotid flow and resultant pooling of viscous
submandibular saliva alters normal oral clearance
patterns and some patients will interpret this as
excessive saliva. Drooling can also occur in patients
with reduced vertical dimension, as overclosure can
cause commissural contours ideal for the escape of
saliva.2 Again, this is a likely multifactorial scenario
with obvious areas to be addressed, but also more
subtle contributors to be reviewed.

Tongue morphology and taste

Fig 1. Clinical photo showing elongation of filiform papillae in a
The dorsum of the tongue changes with age in bilateral linear pattern on the dorsum of the tongue commonly
referred to as black hairy tongue. The anterolateral margins show a
many patients, with a loss of density and shortening modest degree of filiform papillae atrophy with prominence of the
and flattening of the filiform papillae. The number, fungiform papillae.
ª 2009 Australian Dental Association 89
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LM Abetz and NW Savage

anatomical form changes. There is also some evidence

for a relationship between increased inflammation
and erythema of the fungiform papillae and atopy.37
However, in the context of the current discussion,
the prominence of fungiform papillae restricted to the
anterior dorsum of the tongue with an essentially
normal distribution elsewhere seems related to repeti-
tive habitual abrasion of the normal tongue surface
against the adjacent tissues and exposure of underlying
fungiform papillae. Figures 1–3 provide examples of
this.
Tongue scalloping (multiple lateral glossal indenta-
tions resulting from molar compression) is usually
ascribed to tongue-sucking habits, macroglossia, or
excessive lingual inclination of the teeth. It can also be
Fig 2. Clinical photo of tongue showing scalloping of lateral lingual observed after placement of complete dentures with a
margins and traumatic abrasion and atrophy of filiform papillae on resultant combination of altered volume available to
anterior dorsum and anterolateral margins with prominence of
fungiform papillae. The mid dorsum shows low-grade hyperkeratosis accommodate the tongue and persistent pressure on the
of filiform papillae. lower prosthesis to aid stability and retention. One
study found it predictive of sleep pathology in high-risk
patients.38 The proposed link is that tongue scalloping
is caused by either glossopalatal disproportion alone
or in combination with macroglossia.37 The current
authors’ position supports a revision of this listing,
with an upgrading of the importance of tongue
scalloping in patients with oral dysaesthesias. In many
patients there is a gradual progression from a low-grade
leukoedema on the posterolateral and lateral margins of
the tongue to a prominent scalloping on the antero-
lateral and anterior margins. As an example, scalloping
is common in highly stressed groups such as university
students at examination times with some level of
resolution following this period (Fig 3). Although not
the usual sequence, if persistent in the medium to longer
term, in a small percentage of cases this may progress to
the level of a reactive hyperplasia and hyperkeratosis
Fig 3. Clinical photo of tongue in a young patient during school with a fine linear tissue fold or hyperkeratotic band
examinations showing marked scalloping of the lateral lingual obvious clinically and overlying the lingual aspects of
margins and prominence of the fungiform papillae. The anterior
dorsum is sensitive due to habitual irritation.
the adjacent teeth. In combination with other indicators
of increased personal stressors, it seems unlikely that
these clinical signs are not a direct result of habitual
the tongue, usually against the anterior and mid hard pressing of the tongue against the adjacent teeth in a
palate. The surface appears dry and rough and is direct cause-and-effect relationship with stress.
reported subjectively as such by the patient. This There may also be an association between depres-
change is similar in cause but different in execution to sion, anxiety and somatoform symptoms and number
the traumatic abrasion of the filiform papillae previ- and type of traumatic life experiences. In particular,
ously discussed. Black hairy tongue presents due to experience of sexual abuse leads to significantly more
accumulation and staining of surface keratin. This somatoform symptoms, and these include bad taste in
condition is distinct from the roughness and hyper- the mouth and an excessively coated tongue.17 In rats,
keratosis just discussed and a range of possible causes stress alters taste, and individual differences in taste are
have been identified. Fungiform papillae density can be related to measures of emotion.39 It has been demon-
an indicator of taste function, and a loss of taste acuity strated that after exposure to a mild stressor, col-
following medications or neural damage can correlate lege students’ sensitivity to saccharin’s bitterness is
with a decrease in the number of papillae.36 Like increased.39 Incidentally, in highly arousable individ-
filiform papillae, the connective tissue cores of fungi- uals, the increase was higher and, relative to high-
form papillae become thin with age34 and their pleasure individuals, low-pleasure students gave higher
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Burning mouth syndrome and psychological disorders

Table 1. Examples of causes of dysgeusia

Physiological Infections Acute necrotizing
gingivitis

Candidosis
Neuropathology Chorda tympani
injury
CNS lesions
Oral diseases
Medications
Systemic diseases Endocrine
Neurologic
Gastrointestinal
Cardiovascular ⁄
hypertension
Heavy metal
intoxication
Zinc deficiencies
Idiopathy
Fig 4. Clinical photo of lower lip showing multiple linear
Non-physiological Psychological fibro-epithelial hyperplasias, representing a reactive tissue process to
disorders habitual sucking and trauma against adjacent dentition. These
correspond precisely to the inter-incisal line.

bitterness ratings and lower sweetness ratings after

stress.39 Dysgeusia, or altered taste, can be caused by Table 2. Factors associated with cheek biting
organic conditions ⁄ factors as well as psychological Physiological Reduced buccal overbite (prosthetic or
disorders, and these are outlined in Table 1. natural teeth)
Reactive hyperplasias
Mucosal oedema ⁄ disease
Buccal and labial mucosa
Non-physiological Psychological Stress
A range of mucosal changes can occur from habitual Anxiety
Conditions associated Autism
cheek, lip and tongue abrasion and repetitive dental with self-injurious
trauma. Buccal mucosal linea alba is a common form of behaviour
so-called frictional or traumatic keratosis resulting from Mental disability
syndromes
this and according to one study, present in 13 per cent of (e.g. Tourettes,
the population.40 It is typically bilateral and scalloped, Lesch-Nyhan)
and is most likely associated with pressure, frictional Psychiatric disorders
irritation, or sucking trauma from the facial surfaces of
teeth. This, along with an increased prominence in
Other sensory complaints
bruxism or clenching, and an association with tongue
scalloping, could point to a possible psychological Globus sensation (aphonia, the sensation of a lump in
contribution. These changes are reactive and range the throat, difficulty swallowing, a sensation of chok-
from leukoedema with faint translucent keratosis, ing, dyspnoea, or suffocation) may be an oral and
through translucent surface hyperkeratosis, to those oropharyngeal manifestation of a psychological dis-
presenting as opaque but homogeneous keratotic order and is then termed globus hystericus.42 It has
plaques. Figure 4 shows a patient whose lower lip been explained variously as a conversion disorder,
demonstrates multiple linear fibro-epithelial hyperpla- which is a type of somatoform disorder with symptoms
sias due to habitual sucking and trauma against adjacent derived from psychological conflict that unconsciously
dentition. Leukoedema is regarded as a variation of presents as neurological symptoms, a depressive disor-
normal and is identifiable in the majority of individuals. der, a somatoform disorder, and a personality disorder.42
Chronic lip and cheek biting (morsicatio buccarum) Studies of cases of globus sensation find elevated levels
is a habitual form of self-injurious behaviour. Cheek of psychological distress, including anxiety, low mood
chewing is most commonly seen in people who are and somatic concern.43 However, globus sensation is
under stress or in psychological situations in which the not necessarily indicative of psychological disease. A
condition becomes habitual with many patients being psychological cause cannot be ascribed until all organic
unaware of the habit. It has been described as a com- causes, of which there are many, are excluded.42 One
pulsive neurosis, and is reported in 0.12 to 10 per cent study has even shown physiological changes in globus
of the general population41 as a result of stress or hystericus cases, showing an association with laryngeal
anxiety. Table 2 outlines some factors associated with penetration (entrance of material into the top of the
cheek biting. airway that is subsequently ‘‘stripped out’’ during the
ª 2009 Australian Dental Association 91
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LM Abetz and NW Savage

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200 Turbot Street
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2:96–102. Email: [email protected]

ª 2009 Australian Dental Association 93