## 5 Conclusions  
Recent literature has established the role of dysbiosis in several diseases, like type 1 diabetes [86], rheumatoid arthritis [80], psoriatic arthritis, ankylosing spondyloarthritis [87], systemic lupus erythematosusous [88], multiple sclerosis, osteoporosis [34; 89], Crohn's disease (CD) and may even contribute to the late onset of schizophrenia [90]. Several mechanisms have been proposed to explain how microbiota contribute to the development of autoimmune diseases. As previously mentioned, the oral microbiota is physiologically in a state of equilibrium to maintain the state of health of the host. Without perturbations within this balance, colonization by several microorganisms cannot occur. _C. albicans_, for example, is not a passive player. Indeed, in a predisposing immunological condition, it promotes a subversion of the oral microbiota, increasing the prevalence of some bacterial species to the detriment of others. For example, with the increase in the number of enterococci, there is a negative impact on tissue barriers, thus facilitating their colonization [91]. Significant variations exist between the composition of the \"healthy\" microbiota and the one of a subject suffering from candidiasis. Colonization by _C. albicans_ is therefore combatted by a number of factors that act synergistically. A note should be made about the microorganisms that produce short-chain saturated fatty acids (SCFA), which have a profound impact on the formation of the biofilm by _C. albicans_ and, therefore, on its passage from yeast to hypha, both by inhibiting the metabolic activity of the fungus and by reducing the environmental pH [92]. The same goes for lactobacilli, which through the production of certain acids and inducing the production of IL-22 by the host, hinder colonization by _C. albicans_[93]. That said, it is therefore easy to deduce that this infection is associated with the loss of mucosal bacterial diversity [91]. It is, therefore, clear that the interactions between _C. albicans_, host, and microbiota have an important impact on both the development and spread of infection and its severity. Being aware of all these interactions gives us the opportunity to reflect on the appropriate use of certain drugs, such as antibiotics, antifungals, and probiotics. Hence, dysbiosis should not be viewed only as a biomarker of inflammatory diseases but even as a promoter of inflammatory diseases and autoimmune responses [94; 95]. It is unclear whether it could trigger a cascade in the autoimmune response that leads to the onset of the disease. Still, some bacterial species' predominance seems protective against pathology manifestation [96; 97]. Research data are insufficient to determine whether dysbiosis of the oral cavity is the consequence or the cause of autoimmune bullous diseases. However, the role of commensal bacteria in modulating the immune system is evident, which could lead to autoimmune inflammation. This fascinating topic acquires increasing relevance and consequently encourages further analysis of the correlation between the microbiome and autoimmunity, also intending to provide additional scientific support for antibiotic therapy in treating diseases with oral involvement, such as MMP [98; 99]. Additional studies are required to investigate the possible role of antibiotics as adjuvant therapy for oral autoimmune diseases and their possible clinical role. The ultimate goal is always to enhance the quantity and quality of the data to boost the translation of research into clinical practice.  
Conceptualization, R.S. and F.D.S.; methodology, R.S.; validation, M.C.M.; formal analysis, F.F.; investigation, A.R.; writing--original draft preparation, R.S.; writing--review and editing, F.D.S.; supervision, F.F. All authors have read and agreed to the published version of the manuscript.  
This research received no external funding.  
Not applicable.  
Data Availability Statement: Data is contained within the article.  
The authors declare no conflict of interest.