# Photobiomodulation as a Therapeutic Strategy in Burning Mouth Syndrome: A Scoping Review  
[PERSON]  
1 Department of Biomedical Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; [EMAIL_ADDRESS] (F.S. ); [EMAIL_ADDRESS] (M.P. ); [EMAIL_ADDRESS] (M.B.) [PERSON]  
1 Department of Biomedical Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; [EMAIL_ADDRESS] (F.S. ); [EMAIL_ADDRESS] (M.P. ); [EMAIL_ADDRESS] (M.B.) [PERSON]  
3 Section of Dentistry, Department of Clinical, Surgical, Diagnostic and Pediatric Sciences, University of Pavia, 27100 Pavia, Italy; [EMAIL_ADDRESS]  
[PERSON]  
1 Department of Biomedical Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; [EMAIL_ADDRESS] (F.S. ); [EMAIL_ADDRESS] (M.P. ); [EMAIL_ADDRESS] (M.B.) [PERSON]  
1 Department of Biomedical Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy; [EMAIL_ADDRESS] (F.S. ); [EMAIL_ADDRESS] (M.P.) and ulcerative lesions of the mucosa, oral infections, inappropriate prostheses, and para-functional habits [5; 6]. When we have an oral burning pain condition, without clinical signs and with an unknown origin, we will speak instead of primary BMS or idiopathic BMS [6; 7; 8]. The various etiological and pathophysiological aspects would lead to considering primary BMS as a complex multifactorial clinical condition, although it has also been associated with psychological and endocrinological disorders [9; 10; 11; 12]. In the late 1980s, neurophysiological, neuropathological, and imaging studies led to the hypothesis that BMS could be a neuropathic pain condition [13; 14; 15; 16]. Therefore, we can consider at least three lines of research that have characterized the studies on the etiology and pathogenesis of idiopathic BMS: a peripheral and central neurological basis, and an endocrinological and psychological matrix [8]. The pathophysiology of BMS is still unknown [8]. Three distinct subclasses of primary burning mouth syndrome (BMS) can be identified. The first subgroup (50-65%) is characterized by peripheral neuropathy affecting the small diameter fibers of the intra-oral mucosa. The second subgroup (20-25%) comprises patients with subclinical trigeminal lingual nerve system pathology, which clinically resembles the other two subgroups. The third subgroup (20-40%) aligns with the concept of central pain, potentially linked to the reduced function of dopaminergic neurons in the basal ganglia [8]. The development of neuropathic pain in primary BMS is thought to be closely related to small fiber damage. Recent studies in primary BMS have emphasized the role of small myelinated A8 fibers and unmyelinated C fibers [15; 17; 18]. Additionally, approximately 50% of patients with primary BMS experience significant pain relief after lidocaine anesthesia of the lingual nerve, suggesting a peripheral origin of the pain [18]. The taste and pain neurological circuits appear to be intricately interconnected. Damage to the chorda typnari results in the inhibition of its function, leading to reduced control over the activity of other nerves. Consequently, deafferentation of the A8 gustatory fibers of the chorda typnari nerve may result in lingual burning pain symptoms [19; 20]. Alternatively, the diminished signaling of A8 channels with preserved C-fiber function could also contribute to the burning pain experienced in primary BMS [8; 21]. Patients with BMS often report dysgeusia or phantom taste sensations. [8; 22; 23; 24; 25]. In the pathogenesis of primary BMS, the possible involvements of the central nervous system related to the sensorium of the mouth and face regions have been considered [26; 27]. Alterations in the basal ganglia would cause signs of dopaminergic system dysfunction, like [PERSON]'s disease, and bilateral oral pain distribution. The dopaminergic system has a pain-inhibitory role [25; 26; 27; 28; 29; 30].