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  • Title: Pathophysiology of primary burning mouth syndrome.
    Author: Jääskeläinen SK.
    Journal: Clin Neurophysiol; 2012 Jan; 123(1):71-7. PubMed ID: 22030140.
    Abstract:
    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.
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