Where does the tongue begin?

When the tongue catches fire

Burning tongue describes complex symptoms that have different names in the literature, such as: B. "Burning tongue", "Glossodynia", or "Stomatopyrosis". In the course of time, the term Burning Mouth Syndrome (BMS) became established.

The International Headache Society [1] defines BMS as an intraoral burning sensation or sensory disorder (dysesthesia) that occurs daily for more than two hours for three months without any clinically detectable causal changes. This type of definition is reminiscent of the definitions of irritable bowel syndrome (IBS) [2]. Here, too, there are defined complaints for which no tangible causes can be found. In IBS it has now been proven that there are organic causes and that there are numerous subgroups with different pathophysiologies [3, 4, 5]. A similar constellation can be assumed for the BMS. Typical symptoms are the sensation of burning, stinging or itching, which is mainly localized in the area of ​​the tongue and lips and less in the area of ​​the cheek mucosa [6]. Associated complaints such as a bitter or metallic taste (60%), taste disturbances (35%) or a feeling of dry mouth (xerostomia, 63%) are often found. The onset is spontaneous with no apparent triggering cause. BMS occurs more frequently, depending on the specialist discipline and the patient collective examined, although the prevalence data are given in the literature with a large variation of 0.7–15% due to the likely very heterogeneous patient collective [7]. The mean age is 27-87 years, with peri- and postmenopausal women in particular being predisposed. There is a high level of suffering, also because the patients are often not taken seriously and this results in high indirect and direct costs in the health system.

Oral cavity anatomy

The epithelium of the oral cavity consists of non-keratinizing squamous epithelium, which is moistened by the secretion of the salivary glands. The somatosensory innervation of the oral mucosa is provided by the trigeminal nerve (V) and the glossopharyngeal nerve (IX). The anterior two-thirds of the tongue are supplied by the mandibular nerve of the trigeminal nerve, and the posterior third by the glossopharyngeal nerve (IX). In this way, the mechanical, thermal or tactile stimuli received via the papillae of the tongue are passed on. The taste receptors of the front two thirds of the tongue are transmitted via the notchorda tympani of the facial nerve (VII), those of the posterior third of the tongue via the glossopharyngeal nerve (IX). Taste receptors are also found on the soft palate and in the larynx (N. laryngeus des N. vagus) [6].


Classifications of diseases whose causes are still unclear or which consist of several subgroups are of course artificial. There are also attempts to classify the BMS. These include, on the one hand, the pragmatic differentiation between primarily without a recognizable cause and secondarily with triggering causes or a classification based on the symptoms.

A secondary BMS can include be associated with thyroid diseases (hypofunction), diabetes mellitus, gastrointestinal or urogenital diseases, psychiatric diseases (including depression, anxiety, hypochondria), personality changes (cluster A disorders), Parkinson's disease, mouth infections (Candida species, coliform Enterobacter, Klebsiella), medication (ACE inhibitors, angiotensin receptor inhibitors, nevirapine, efavirenz, levodopa, topiramate), dental treatments, vitamin deficiency (B1, B2, B6, B12, folic acid), mineral deficiency (zinc) or nicotine. An attempt to classify on the basis of symptoms suggests different pathophysiologies, for which, however, no valid data are available (Table 1).

Etiology and pathogenesis

The pathophysiology of BMS is still unclear. Neuropathy is preferred today, although it is discussed whether a peripheral or central manifestation is present (Table 2). Depending on the patient collective, there are probably both forms, possibly also a combination. A peripheral sensory neuropathy / axonopathy of the small sensory nerve fibers in the mouth (50-60%) or the trigeminal nerve (20-25%) is indicated by lower thresholds for temperature-pain stimuli, a decreased density of epithelial or subpapillary nerves, an axonal Degeneration, increased levels of nerve growth factor (NGF), an increased density of TRPV1 ion channels and P2X3 receptors on nerve fibers, dysfunction of the notochord tympani branches of the facial nerve, changes in the blink reflex, a positive influence through stimulation of the taste system and a drop in neuroprotective gonadal and adrenal steroids during menopause. Central neuropathy (20-30%) is indicated by a change in the central processing of stimuli (pain, temperature) in the thalamus (fMRI), dysregulation of the nigrostriatal dopaminergic system (Parkinson's disease) or increased scores for anxiety and depression (50%) of patients) [6, 8, 9].

Clinical diagnostics

Clinical diagnosis is still a challenge, as there are no generally accepted criteria, the clinical symptoms can be variable and the patient population is heterogeneous [10]. A BMS can be suspected if there is bilateral burning sensation of the oral mucosa that occurs daily, of continuous or increasing intensity for at least four to six months, which is not made worse by food or fluid intake, but rather improved and is independent of sleep [11]. Additional criteria are changes in smell and / or xerostomia, alterations in sensory or chemosensory perception or psychopathological abnormalities [12].

Since the primary BMS is a diagnosis of exclusion, all secondary causes must be clarified in each individual case (Table 2). These include a detailed inspection of the nasopharynx, the dental status, a nutritional history or a medical history. The laboratory tests should be able to reveal a deficiency in iron, trace elements, vitamins B1, B12, diabetes mellitus or autoimmune diseases. Measuring the flow of saliva can also be helpful. If necessary, a swab of the oral mucosa can provide information on bacteria or fungi.


Therapy for BMS is difficult and individual [13]. The primary goal is to differentiate between primary and secondary forms (Table 2). In individual cases, this means that the potential secondary factors must be worked through and treated using a checklist in the hope of a causal therapy option [14, 15]. As with functional bowel diseases, this is naturally time-consuming and costly. The drug therapy strategies are numerous and are determined by the heterogeneous patient population (Table 3). After excluding the secondary forms with appropriate specific therapy, under the V. a. a primary BMS different therapy concepts can be tried. There is currently no biomarker that favors a therapy concept in advance. A practicable therapy strategy was proposed by Kääskeläinen et al. [10] proposed (figure). When making therapy decisions, unnecessary action should be avoided. Studies show that the course without therapy over 18 months shows a spontaneous remission in 10% and a moderate improvement in 26%. 37% of the patients show no change, 26% a worsening of their symptoms. These results are formally no worse than the course with therapy over 18 months: 29% improvement, 56% no change, 15% deterioration [16].


Although there are only a few follow-up studies, it can be assumed that a "rule of three" applies. This means that approx. 30% of the patients will show a spontaneous remission or an improvement in their symptoms, another third will show no change and another third will show their symptoms worsening.

What is the gastroenterologist interested in?

Patients with BMS are often referred to gastroenterologists under the V. a. presented gastroesophageal reflux disease. However, this is unlikely in the absence of typical reflux symptoms (heartburn, acid regurgitation), so that in general no further reflux diagnostics have to be carried out. If there are clinical signs of reflux disease, especially volume reflux or high reflux, esophagogastroscopy can be performed to detect reflux esophagitis or esophageal function diagnostics using a combined 24-hour pH-metric impedance measurement. The significance of the oropharyngeal acid measurement with the Restech® probe is currently unclear [17, 18]. Experience with the functional examination of globus feeling or sore throat suggest, however, that this specialized functional diagnosis is of no clinical relevance. Corresponding scientifically validated data are currently not available. Studies on the relevance of gastric mucosal heterotopias in the proximal esophagus or the significance of eosinophilic esophagitis are also lacking. However, these factors should be excluded in individual cases.

Burning tongue describes a complex symptom that is referred to in the literature under the term Burning Mouth Syndrome (BMS). The heterogeneous patient collective shows a high level of suffering, also because the patients are often not taken seriously. This creates high indirect and direct costs in the health system. In the primary form, a peripheral or central neuropathy is favored today. A secondary BMS can be associated with various endocrinological, gastrointestinal, urogenital, neurological, psychiatric diseases, oral infections, dental treatments, medication, vitamin or trace element deficiencies or nicotine abuse. Therapy for BMS is difficult and individual. After excluding the secondary forms with appropriate specific therapy, under the V. a. a primary BMS different therapy concepts with local therapy of clonazepam or capsaicin or systemically with clonazepam or gabapentin can be tried. There is currently no biomarker that favors a therapy concept in advance.

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General internal medicine with gastroenterology, hepatology, neurogastroenterology, infectiology, hematology, oncology and palliative medicine

Conflicts of Interest: The author has not declared any

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