Primary burning mouth syndrome (BMS) is severe, disabling and chronic intraoral 
pain condition for which no local or systemic cause can be found and clinical 
examination is normal. It mostly affects elderly citizens, especially 
postmenopausal women with prevalence up to 12-18%. In addition to spontaneous 
burning pain, patients may complain of taste alterations. Recent 
neurophysiologic, psychophysical, neuropathological, and functional imaging 
studies have elucidated that several neuropathic mechanisms, mostly subclinical, 
act at different levels of the neuraxis and contribute to the pathophysiology of 
primary BMS. Demonstration of loss of small diameter nerve fibres in the tongue 
epithelium explains thermal hypoesthesia and increase in taste detection 
thresholds found in quantitative sensory testing. As in neuropathic pain, 
decreased brain activation to heat stimuli has been demonstrated with fMRI in 
BMS patients. However, it seems that the clinical diagnosis of primary BMS 
encompasses at least three distinct, subclinical neuropathic pain states that 
may overlap in individual patients. The first subgroup (50-65%) is characterized 
by peripheral small diameter fibre neuropathy of intraoral mucosa. The second 
subgroup (20-25%) consists of patients with subclinical lingual, mandibular, or 
trigeminal system pathology that can be dissected with careful neurophysiologic 
examination but is clinically indistinguishable from the other two subgroups. 
The third subgroup (20-40%) fits the concept of central pain that may be related 
to hypofunction of dopaminergic neurons in the basal ganglia. The neurogenic 
factors acting in these subgroups differ, and will require different treatment 
strategies. In the future, with proper use of diagnostic tests, BMS patients may 
benefit from interventions specifically targeted at the underlying 
pathophysiological mechanisms.