Burning Mouth Syndrome
Oral Pathology

Author: Alberto Iuso
Date: 28/05/2007


Burning mouth syndrome or stomatopirosys has been defined as burning pain in the tongue or oral mucous membranes, usually without accompanying clinical and laboratory findings or mucosal lesions. If pain is located on the tongue it is called glossopyrosis.

Based on the makeup of most studies published to date, oral burning appears to be most prevalent in postmenopausal women. It has been reported in 10 to 40 percent of women presenting for treatment of menopausal symptoms. Major incidence in patients over 50 with a ratio around 1 to seven and average age of 62 yo (Lamey PJ 1996). 3.7% of the whole population. Never seen among children.


In more than one half of patients with burning mouth syndrome, the onset of pain is spontaneous, with no identifiable precipitating factor. Approximately one third of patients relate time of onset to a dental procedure, recent illness or medication course (including antibiotic therapy). Regardless of the nature of pain onset, once the oral burning starts, it often persists for many years.
In many patients with the syndrome, pain is absent during the night but occurs at a mild to moderate level by middle to late morning. The burning may progressively increase throughout the day, reaching its greatest intensity by late afternoon and into early evening. Patients often report that the pain interferes with their ability to fall asleep. Perhaps because of sleep disturbances, constant pain, or both, patients with oral burning pain often have mood changes, including irritability, anxiety and depression. If pain is present from early in the morning the prognosis is worst. Earlier studies frequently minimized the pain of burning mouth syndrome, but more recent studies have reported that the pain ranges from moderate to severe and is similar in intensity to toothache pain. Can lead to geographic tongue.


ConditionCharacteristic pattern
Mucosal disease (e.g., lichen planus)Variable pattern
_Sensitivity with eating
Menopause (26% of women Van der Waal I 1996)Onset associated with climacteric symptoms
Nutritional deficiencyMore than one oral site (e.g., vitamins B1, B2, B6, B12 also called cobalamin, folic acid and niacin
Possibly, mucosal changesDry mouth Xerostomia (e.g., in Sjögren's syndrome or subsequent Alteration of taste to chemotherapy
or radiation therapy);
altered salivary content Sensitivity with eating
Cranial nerve injuryVariable pattern
Usually bilateralDecreased discomfort with eating
Medication effectOnset related to time of prescription

• Case reports have linked burning mouth symptoms to the use of angiotensin-converting enzyme (ACE) inhibitors used to deal with high pressure, antihistamine and antidepressant drugs or beta-blockers. Once these medications were reduced or discontinued, oral burning was found to remit within several weeks. Interestingly, loss of taste sensation has also been reported with the use of ACE inhibitors.
• Candidal infections are also purported to cause burning in patients with dental prothesis.
• Stomatitis caused by acrylic components of mobile ptrotesis
Parafunctional habits (bruxism, high tongue mobility) due to low calcium levels
• Esophageal reflux
• Disgeusia
Depression and emotive disorders
• Cancerophobia
Sideropenic anemia
• Diabetes
• Aids

Open Questions

* hypothyroidism

* hyperparathyroidism

* bisphosphonates

* association with hearing loss

Nicotine acid ester and sorbic acid
Role of various cytokines has been implicated in the development of BMS. The aim of this study was to evaluate levels of salivary IL-2 and IL-6 in patients with BMS, compared with age-matched healthy volunteers (control group). Saliva IL-2 concentrations in BMS IS significantly increased in patients compared to healthy subjects: mean 34.1 +/- 9.7 versus 7.3 +/- 3.0 pg/mL. Patients with BMS had significantly higher concentrations of IL-6 compared to control: mean 30.8 +/- 5.6 versus 5.2 +/- 2.8 pg/mL. In patients with BMS, IL-2 and IL-6 levels in saliva are elevated, correlating with the severity of illness.
The loss of iron has been related to the rise of stomatopyrosis but this situation is rare. Diabetes through a pathogenic mechanism in relationship with neuropathy and microangiopathy could be responsible of burning.
A theory to know how pain rises could be considering Magnesium levels. In fact low levels of this element can lead to hypocalcemia which can cause muscle contraction and parafunctional habits of lower jaw muscles.
Magnesium is an important factor also in the conduction of nervous signals. Its deficiency can cause disorders mostly in the trigeminal nerve and give origin to a huge pain into the mouth like BMS' pain.

The role of taste in burning mouth syndrome is not straightforward, although recent studies by one set of investigators19 demonstrated a possible relationship between taste activity and the disorder. There is an increased prevalence of so-called "supertasters" (persons with enhanced abilities to detect taste) among patients with burning mouth syndrome.
In addition to alteration of taste functions there cuold be an interesting theoty which detect the possible origin of pain in the glossopharyngeal neuralgia. In fact, the pain in glossopharyngeal neuralgia has been described as sharp, shooting and stabbing or “ like a needle” and commonly lasts from a few seconds to a minute. However, Dandy (1936) noted that pain in glossopharyngeal neuralgia can be more constant and a substantial number of patients will experience a dull aching or burning sesation or even a painful feeling of pressure that persists for several minutes or even several hours rather than tipical tic-like pain. Is the burning pain, indeed, that makes us to think that an alteration of the conduction of the electric signal in the putative verves can lead to the pain tipical of BMS.
On the other hand, instead, glossopharyngeal neuralgia is not just a painful condition. At times, it may be life-threatening as a result of associated cardiovascular consequences. Even in the absence of life-threatening consequences, it can be a severe debilitating disease with depression, suicidal tendencies, fear of swallowing, loss of weight and under-nutrition.

Other investigations have found that the ability to detect bitter taste decreases at the time of menopause. This reduction in bitter taste at the chorda tympani branch of the facial nerve (cranial nerve VII) results in intensification of taste sensations from the area innervated by the glossopharyngeal nerve (cranial nerve IX) and the production of taste phantoms. It has been suggested that damage to taste might also be associated with loss of central inhibition of trigeminal-nerve afferent pain fibers, which can lead to oral burning symptoms.
Possible effect also on chorda timpani


Difenidramine syrup1 spoon, rinse for 2-3 min, than swallow (before meals)
Xylocaineviscous solution topic application for 2-3 times/die
NistatineRinse for 4-5 times/die
Ketoconazol2 tablet 1 cpr/die for 7 days
Clordiazepossidtablet 5-10 mq os 3 times/die
Diazepamtablet 6-15 mg/die os
Amitriptilinetablet 25-75 mg /die per os
Levosulpiridesystemic (Levopraid®, gtt/cpr)
Hypericum perforatum(RCT)

ALA: alpha-lipoic acid
Gabapentin but with a low effect

The treatment of burning mouth syndrome is usually directed at its symptoms and is the same as the medical management of other neuropathic pain conditions. Studies generally support the use of low dosages of clonazepam (Klonopin), chlordiazepoxide (Librium) and tricyclic antidepressants (e.g., amitriptyline [Elavil]). Evidence also supports the utility of a low dosage of gabapentin (Neurontin). Studies have not shown any benefit from treatment with selective serotonin reuptake inhibitors or other serotoninergic antidepressants (e.g. trazodone [Desyrel].

Topical clonazepamlocale (Rivotril®, cpr 2mg) and cognitive therapy have been proven efficacious in some patients. Emerging evidence supports the effectiveness of the antioxidant, alpha lipoic acid, with further studies of this agent being warranted. Additional research into mechanisms, diagnostic criteria, and randomized controlled interventional studies are needed.

Differential Diagnosis

Oral Herpes


Pemphigus and Staphylococcus toxins

Squamous cell carcinoma

Oral Candidiasis

2007-06-29T10:40:27 - Alberto Iuso


Dopaminergic pain is involved in central pain modulation. Atypical facial pain is a chronic pain condition of the face. Symptoms do not follow peripheral nerve distribution although pain is often initially localized to one division of the trigeminal nerve.
Animal studies suggest that striatal, limbic and cortical dopaminergic system partecipate in pain transmission or modulation. Presynaptic dysfunction of the nigrostriatal dopaminergic pathway can be responsable of the burning mouth pain. The inhibitory role of dopamine in pain modulation is mediated by dopamine D2 receptors but D1 are not involved.
So, diminished levels of dopamine metabolites are tought to be found in the cerebrospinal fluid of the trigeminal cistern in patients with facial pain.
The less presence of dopamine in the putamen is reflected by the increased D2 receptor binding.
The D1/D2 ratio in patiens with burning mouth is strongly lower in the right and a bit less lower in the left putamen if compared with healthy people due to the increased uptake in those patients of the C-raclopride, a dopamine D2 receptor antagonist which binds to striatal D2 recetors.
Another possible explanation of the lower level of this ratio might be an imbalance between D1 and D2 receptor mediated pathways, maybe due to the early disruption of the interaction of D1 and D2 receptors in patological conditions involving the basal ganglia area.
Increased C-raclopride uptake and subsequent decrease in the D1/D2 ratio, may indicate a decline in endogenous dopamine levels in the putamen in BMS patients which suggest the less effect of striatal dopamine in central pain modulation.
C-raclopride increased uptake in the medial thalamus, suggest that alterations in the nigrostriatal dopaminergic system may be involved in atypical facial pain.
The medial pain pathway, including the medial nuclei of thalamus, is involved in the affective component of pain, which could be an important feature in atypical facial pain.
The dopaminergic neurons of the nigrostriatal pathway originate from the substantia nigra and project to medium spiny neurons in the striatum.
Postsynaptic striatal D1 and D2 receptors mainly reside on different output neurons, and neurons projecting to internal globus pallidus express D2 receptors.
Dopamine D2 receptor binding has been shown to decline with age.
However, the impact of aging on D1/D2 is unclear, so that at the moment there’s no association between striatal D1/D2 ratio and age either in burning mouth syndrome patients nor in hot ill people.
Increased striatal activity during pain can be attributed to the inhibition or preparation of motor activity; however, altered striatal uptake of dopamine receptor ligands may reflect plastic changes in striatal neurons in chronic pain.
Plastic changes in synaptic neurotransmission in the brain are tought to play an important role in chronic pain.
High D2 receptor availability in the putamen is associated with low cold pain threshold and high pain modulation capacity induced by conditioning stimulation. High D2 receptor availability ca be demonstrated in the putamen in a chronic orofacial pain state, such as, for example, the burning mouth syndrome. Depression and mild sensory disturbances frequently accompany pain. Patients with this kind of pain exhibit abnormalities in brainstem reflexes such as increased threshold of the R1 component and deficient habituation of the R2 of the blink reflex suggesting diminshed dopaminergic inhibition. The habituation of the R2 componet of the blink reflex is under inhibitory dopaminergic control and similar deficient habituation has been demonstrated in dopaminergic hypofunction.
Other causes of this alteration are still to know, also if viruses or other enviromental factors can be involved. At the moment dopamin is very important in the ethiology of the Parkinson's disease.

2007-06-01T13:50:21 - Alberto Iuso

Parafunctional habits

A broad consensus does exist among main authors on the importance of parafunctional habits in the etiopathogenesis of temporomandibular disorders (TMD). Mechanisms through which an intense parafunctional activity determined a pathological effect on the temporomandibular joints (TMJs) and their related structures have still not been definitively clarified; nevertheless, before investigating those mechanisms, it's useful to study predisposing, triggering and/or worsening factors of parafunctions themselves. At present the theory, once widely accepted, according to which occlusal interferences can trigger a muscular hyperactivity through the activation of periodontal receptors, has lost a lot of credit. Recently, the hypothesis that bruxism and other parafunctions have a central etiology has become more and more accepted. In such a context, the role of the psychic component assumes a strong relevance, particularly for its relation with the limbic system, which is the part of the central nervous system (CNS) that regulates emotions. Such a hypothesis is confirmed by clinical practice, but it doesn't explain why some patients have reported a worsening of parafunctional activities after occlusal adjustment. The aim of this study is to investigate this issue through a critical review of the literature, indicating how the 2 theories might be complementary for the development and worsening of a parafunctional habit. From this review, despite the number of clinical opinions, there emerges a lack of methodologically appropriate associative works and controlled clinical trials which consent to clarify the effective importance of psychic and/or occlusal factors in the etiopathogenesis of parafunctional habits.

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