ETIOPATHOGENESIS OF BURNING MOUTH SYNDROME

In clinical practice, a dentist is faced with a paradoxical situation: the patient complains of burning and pain in the oral cavity, which significantly reduce the quality of life, while an objective examination does not reveal any pathologies on the mucous membrane. Burning mouth syndrome remains (BMS) an exceptional diagnosis requiring a long-term differential diagnostic search. Subject. This study examines the complexity of managing patients with BMS, which is compounded by the multifactorial nature of the disease. The pathogenesis involves mechanisms of peripheral small fiber denervation, overexpression of nociceptors, hormonal imbalance, and microbiome disturbances. To develop patient management algorithms and select pathogenetically based therapy, it is necessary to systematize information on the etiopathogenesis of BMS, which determines the relevance of this review. Aim. The objective of this study was to conduct an analytical review of the literature on the multifactorial mechanisms underlying the development of BMS to identify the most significant etiopathogenetic factors and support personalized approaches to patient care. Methodology. A systematic literature search was conducted, including studies dated from 1992 to 2025. The search was conducted in the electronic databases PubMed, eLibrary, and CyberLeninka. Search results were integrated using EndNoteWeb bibliographic referencing software to remove duplicate articles. The following search terms were used: "burning mouth syndrome," "oral dysesthesia," "neuropathic pain," and "microbiome." Articles were excluded for the following reasons: titles and abstracts irrelevant to the topic of the study; and full texts did not match potentially relevant articles. Results. It has been established that the leading mechanism in the pathogenesis of BMS is neuropathic dysfunction, including peripheral denervation of small fibers and central sensitization due to overexpression of nociceptors. The course of the syndrome is modulated by estrogen deficiency, oral dysbiosis, and depressive disorders, which lower the pain threshold.