Aims. Burning pain is considered characteristic of chronic neuropathic pain condition in general, and so me recent data seem to suggest peripheral or central nervous system involvement as possible underlying factor in BM3. This study was designed to determinate if burning mouth symptoms could be originated from a peripheal neuropathy of small diameter nerve fibres. Material and methods. The material of the study consisted of 25 patients (18 female, 7 male, 30-75 years; means 54 years). In all patients there were not: oral muco membranes lesions, oral muco membranes diseases, oral correlated diseases, oral dysfunctions, dental and periodontal diseases. Besides there were: no evidence of central nervous system pathology, no evidence of peripheral nervous system pathology, no presence of organic body disfunctions. AIIpatients didn't show significant alterations of blood investigations. AIIpatients were undermitted to our protocol including: oral and facial c1inicalexaminations, neurological exam, blood investigations, Mc Gill Pain Questionnaire, VAS(visual analogical scale), biopsy of tongue mucosa with hystological and immunofluorescence exams, quantitative somatosensory thermotest and teletermography examination of tongue mucosa. ResuIts. These examinations have showed subclinical polineurophaty in 50% of patients. In particular were observed a loss of function in small diameter nervous fibres in about 50% of patients. Hystological exam of mucosal tongue revealed a moderate atrophy and alterations of structures. Conclusion. Etiology, pathogenetic processes, c1inicaland diagnostic approaches, therapeutical resolutions and researches of burning mouth syndrome are not c1ear yet. The local alterations of small diameter sensitive nerve fibres could cause an increase of oral burning, without muco membranes pathologies. These locallesions could justify the bms c1inicalsymptomatology. The hystological alteration of small diameter sensitive nerve fibres could involve meaningful alterations of thermal reactivity of oral and body surfaces. These c1inicalreactivities are evident in chronic peripheal neuropathy (diabetes). These conclusions and our study results are still provisory. It will be necessary to estend and to increase our results, comparing our research with other bms etio-pathogenetic hypotesis.
Calzavara, D., Lauritano, D., Papagna, R., Baldoni, M., Bascones, A. (2003). Evidencia del sindrome neuropático en un estudio neurofisiológico e inmunohistoquímico de las fibras nerviosas en pacientes con síndrome de boca ardiente. In VII Congreso Nacional de SEMO (Sociedad Espanola de Medicina Oral). Evidencia del sindrome neuropático en un estudio neurofisiológico e inmunohistoquímico de las fibras nerviosas en pacientes con síndrome de boca ardiente.
Evidencia del sindrome neuropático en un estudio neurofisiológico e inmunohistoquímico de las fibras nerviosas en pacientes con síndrome de boca ardiente
LAURITANO, DORINA;Baldoni, M;
2003
Abstract
Aims. Burning pain is considered characteristic of chronic neuropathic pain condition in general, and so me recent data seem to suggest peripheral or central nervous system involvement as possible underlying factor in BM3. This study was designed to determinate if burning mouth symptoms could be originated from a peripheal neuropathy of small diameter nerve fibres. Material and methods. The material of the study consisted of 25 patients (18 female, 7 male, 30-75 years; means 54 years). In all patients there were not: oral muco membranes lesions, oral muco membranes diseases, oral correlated diseases, oral dysfunctions, dental and periodontal diseases. Besides there were: no evidence of central nervous system pathology, no evidence of peripheral nervous system pathology, no presence of organic body disfunctions. AIIpatients didn't show significant alterations of blood investigations. AIIpatients were undermitted to our protocol including: oral and facial c1inicalexaminations, neurological exam, blood investigations, Mc Gill Pain Questionnaire, VAS(visual analogical scale), biopsy of tongue mucosa with hystological and immunofluorescence exams, quantitative somatosensory thermotest and teletermography examination of tongue mucosa. ResuIts. These examinations have showed subclinical polineurophaty in 50% of patients. In particular were observed a loss of function in small diameter nervous fibres in about 50% of patients. Hystological exam of mucosal tongue revealed a moderate atrophy and alterations of structures. Conclusion. Etiology, pathogenetic processes, c1inicaland diagnostic approaches, therapeutical resolutions and researches of burning mouth syndrome are not c1ear yet. The local alterations of small diameter sensitive nerve fibres could cause an increase of oral burning, without muco membranes pathologies. These locallesions could justify the bms c1inicalsymptomatology. The hystological alteration of small diameter sensitive nerve fibres could involve meaningful alterations of thermal reactivity of oral and body surfaces. These c1inicalreactivities are evident in chronic peripheal neuropathy (diabetes). These conclusions and our study results are still provisory. It will be necessary to estend and to increase our results, comparing our research with other bms etio-pathogenetic hypotesis.
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