## 3 Discussion  
The presence of white lesions of the oral mucosa is a relatively frequent occurrence in clinical practice; in fact, many oral diseases appear in the oral cavity as \"white patches\". This is a diagnostic and therapeutic challenge for clinicians because the same clinical appearance can be shared among different lesions with different aetiopathogenetic and prognostic significance. Oral lichen planus, OLLs, proliferative verrucous leukoplakia, homogeneous leukoplakia, frictional keratosis, benign alveolar ridge keratosis, white sponge naevus, candidiasis, and leukoedema may be clinically confounded with each other, and only an accurate and careful examination allows for the correct diagnosis [10]. This case report highlights how completely different nosological entities affecting the margins of the tongue, such as OLLs, OHL or frictional keratosis, can appear the same to clinicians. Clinical investigation, even before histopathological sampling, could lead to a  
Figure 3: Left border of the tongue two weeks after the amalgam removal. Mucosal signs were strongly improved. The patient reported no symptoms. Figure 2: Composite resin restorations on 3.6 and 3.7 teeth after the removal of the amalgams. diagnosis and resolution of the lesions with a less invasive and uncomfortable approach for patients. OLLs, described for the first time 40 years ago by [PERSON] et al., have a low prevalence and have been diagnosed in about 0.15% of patients with at least an amalgam filling [11; 12]. OLLs induced by amalgam restorations can appear as white patches, atrophic erosive areas, or with mixed aspects. Different localisations of OLLs were described by [PERSON] et al. [13], who reported on 467 patients with amalgam-triggered OLLs. Three different types of oral lesions were described: (a) oral lesions topographically in contact with the amalgam; (b) oral lesions extending beyond the contact zone between the oral mucosa and the amalgam; and (c) oral lesions without any contact with the amalgam filling. The different clinical responses of the oral mucosa can be explained by the different pathogenetic mechanisms through which amalgam fillings cause damage. The mechanisms by which amalgam fillings can determine the onset of OLLs remain debated, and several hypotheses have been postulated. The first hypothesis considers OLLs as a delayed type IV, cell-mediated immune response to mercury, copper, tin, zinc, or one of the other constituents of a dental amalgam [14]. Skin patch testing is a valuable tool to confirm clinically suspected oral lichenoid reactions, although other authors do not consider patch tests reliable in diagnosing OLLs [15; 16]. A second pathogenetic hypothesis concerns the presence of non-specific toxic reactions to amalgam components (especially those with a high zinc content) developed over the years. These reactions could also explain why OLLs are very often seen in correspondence with old fillings [17]. A third hypothesis concerns the presence of electrogalvanic phenomena that could arise between the metal components present in a filling and salivary ions, with saliva as the conducting medium [18]. In the present case, the presence of an OLL mimicking OHL led us to suppose that the patient was immunosuppressed. OHL is an oral mucosal disease associated with Epstein-Barr virus infection, which predominantly occurs in immunocompromised patients (e.g., from untreated HIV, haematological malignancy, and organ and bone marrow transplantation) [19; 20]. However, OHL lesions have also been sporadically described in healthy subjects [21] and are quite common, unlike OHL. Frictional keratosis must also be considered as it can affect the margins of the tongue. The careful evaluation of sharp dental margins or cuspid fractures and incongruuous fillings can cause hyperkeratatio traumatic reactions at the site where they persist [22].