## 4 Discussion  
Numerous studies have tried to find a possible association between microbiome and autoimmune diseases, like primary Sjogren's syndrome [68; 69], systemic lupus erythematosus [70], rheumatoid arthritis [71], and brain autoimmunity [72], trying to understand if a specific bacterial infection may play a role in the aetiopathogenesis of the disease [73]. Mucous membranous pemphigoid and pemphigus vulgaris are multifactorial genetic disorders. Genetic predisposition is necessary for developing these diseases, but it is not the only cause. Finding a possible association between these diseases and different bacteria, as well as identifying the actual prevalence of bacterial infection and whether a specific bacterial infection may play a role in the aetiopathogenesis of the disease, is a current and very intriguing topic. Not long ago, thanks to next generation sequencing, scientists began to study microbial communities and sequence them faster, making them more accessible and more searchable, and coming to define the contours of the microbiome's contribution to health and disease. Any dearth of variety can lead to dysbiosis, a critical disproportion between commensal and pathogenic bacteria. These commensals supply an essential niche by regulating the immune response and supporting a homeostatic environment. The bacteria that make up the oral microbiota come into contact with the oral mucosal immune system with numerous consequences. The mechanisms by which the microbiome can potentially influence the host's immune system include molecular mimicry, epitope spreading, and constitutive stimulation of Toll-like receptors [74; 75]. Microbes can also cause epigenetic changes, including post-translational modification of histones, micro-RNA alteration without changes in DNA sequence, and changes in gene function through DNA methylation [76]. In the present review, we identify very few scientific studies that evaluated the oral microbiome in patients with pemphigus vulgaris and mucous membranous pemphigoid. The three studies that analyzed samples from the oral cavity of patients with PV reported the presence of _P. intermedia_, _T. denticola_, _T. forysythemensis_, _P. gingivalis_, _Fusobacterium nucleatum_, _Capnocytophaga leadbetteri_ and _Parumomas micra_. At the phyla level, [PERSON] et al., record a prevalence of Firmicutes and Fusobacteria. These data agree with those presented in a recent paper by [PERSON] et al. [66]. The authors searched for peptides common to a set of eight periodontaltopathogenic bacteria (_Aggregatibacter actinomycetemcomitans_; _Campylobacter rectus_; _Eikenella corrodens_; _Fusobacterium nucleatum_; _Parumomas micra_; _Porhyromonas gingivalis_; _Prerotella intermedia_; _Tannerella forysthia_)and DSG3. The PV autoanti and the eight bacterial proteomes share 23 heptapeeptides; the bacterial proteomes most involved in sharing are _E. corrodens_, _F. nucleatum_ and _T. forysthia_. Similarly to PV, a very small number of studies have been identified for mucus membranous pemphbigoid, in this case only one [62]: that of [PERSON] et al., The authors reported a subgingival colonization of _F. nucleatum_, _E. corrodens_, _Capnocytophaga_ spp. in the 14 patients analyzed with MMP. Again, these experimental data are in agreement with a recent research paper [68]. In this study, the authors investigated a possible relationship between the immune response directed against pathogenic bacteria colonizing the oral cavity and the aetiopathogenesis of MMP. They hypothesized that immune responses against these pathogens may cross-react with MMP's autoantigens. Based on the study by [PERSON] et al. [68], they searched for peptides common to a set of eight oral bacteria representing periodonopathogenic bacterial species, and BP180 and BP230. Subsequently, they searched for potentially immuno-crosslinked shared sequences. The authors reported 12 peptides shared between BP180 and the bacterial proteome of _Tannerella forysthia_ and _Eikenella corrodens_[67].