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.
EPIDEMIOLOGY
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.
PREVALENCE
PAIN CHARACTERISTICS
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.
POSSIBLE CAUSES:
| Condition | Characteristic 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 deficiency | More than one oral site (e.g., vitamins B1, B2, B6, B12 also called cobalamin, folic acid and niacin |
| Possibly, mucosal changes | Dry 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 injury | Variable pattern |
| Usually bilateral | Decreased discomfort with eating |
| Medication effect | Onset related to time of prescription |
OTHER POSSIBLE CAUSES:
• 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
• Alexithymia
• 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.
TASTE FUNCTIONS
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
MEDICAL MANAGEMENT
| Difenidramine syrup | 1 spoon, rinse for 2-3 min, than swallow (before meals) |
| Xylocaine | viscous solution topic application for 2-3 times/die |
| Nistatine | Rinse for 4-5 times/die |
| Ketoconazol | 2 tablet 1 cpr/die for 7 days |
| Clordiazepossid | tablet 5-10 mq os 3 times/die |
| Diazepam | tablet 6-15 mg/die os |
| Amitriptiline | tablet 25-75 mg /die per os |
| Levosulpiride | systemic (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
Phemphigus
Pemphigus and Staphylococcus toxins
Squamous cell carcinoma
Oral Candidiasis
