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Down syndrome (DS) is a genetic disorder associated with early-onset periodontitis and other periodontal diseases (PDs). The present work aimed to systematically review the scientific literature reporting studies in vivo on oral microbiota features in subjects with DS and related periodontal health and to highlight any correlation and difference with subjects not affected by DS, with and without PDs. PubMed, Web of Science, Scopus and Cochrane were searched for relevant studies in May 2021. The participants were subjects affected by Down syndrome (DS) with and without periodontal diseases; the study compared subjects with periodontal diseases but not affected by DS, and DS without periodontal diseases; the outcomes were the differences in oral microbiota/periodontopathogen bacterial composition among subjects considered; the study design was a systematic review. Study quality was assessed with risk of bias in non-randomized studies of interventions (ROBINS-I). Of the 954 references retrieved, 26 studies were considered. The conclusions from the qualitative assessment of the papers revealed an increasing knowledge over the last years of the microbiota associated with DS and their periodontal diseases, in comparison with healthy subjects and subjects with other kinds of mental disabilities. Few data have emerged on the mycobiome and virobiome of DS, hence, further investigations are still necessary.

Background: Gingival hyperplasia could occur after the administration of cyclosporine A. Up to 90% of the patients submitted to immunosuppressant drugs have been reported to suffer from this side effect. The role of fibroblasts in gingival hyperplasia has been widely discussed by literature, showing contrasting results. In order to demonstrate the effect of cyclosporine A on the extracellular matrix component of fibroblasts, we investigated the gene expression profile of human fibroblasts after cyclosporine A administration., Materials and Methods: Primary gingival fibroblasts were stimulated with 1000 ng/mL cyclosporine A solution for 16 h. Gene expression levels of 57 genes belonging to the "Extracellular Matrix and Adhesion Molecules" pathway were analyzed using real-time PCR in treated cells, compared to untreated cells used as control., Results: Expression levels of different genes were significantly de-regulated. The gene CDH1 , which codes for the cell adhesion protein E-cadherin, showed up-regulation. Almost all the extracellular matrix metalloproteases showed down-regulation ( MMP8 , MMP11 , MMP15 , MMP16 , MMP24 , MMP26 ). The administration of cyclosporine A was followed by down-regulation of other genes: COL7A1 , the transmembrane receptors ITGB2 and ITGB4 , and the basement membrane constituents LAMA2 and LAMB1 ., Conclusion: Data collected demonstrate that cyclosporine inhibits the secretion of matrix proteases, contributing to the accumulation of extracellular matrix components in the gingival connective tissue, causing gingival overgrowth. Patients affected by gingival overgrowth caused by cyclosporine A need to be further investigated in order to determine the role of this drug on fibroblasts.

Gingival overgrowth is a serious side effect that accompanies the use of amlodipine. Several conflicting theories have been proposed to explain the fibroblast's function in gingival overgrowth. To determine whether amlodipine alters the fibrotic response, we investigated its effects on treated gingival fibroblast gene expression as compared with untreated cells., Materials and Methods: Fibroblasts from ATCC ® Cell Lines were incubated with amlodipine. The gene expression levels of 12 genes belonging to the "Extracellular Matrix and Adhesion Molecules" pathway was investigated in treated fibroblasts cell culture, as compared with untreated cells, by real time PCR., Results: Most of the significant genes were up-regulated. ( CTNND2 , COL4A1 , ITGA2 , ITGA7 , MMP10 , MMP11 , MMP12 , MMP26 ) except for COL7A1 , LAMB1 , MMP8 , and MMP16 , which were down-regulated., Conclusion: These results seem to demonstrate that amlodipine has an effect on the extracellular matrix of gingival fibroblast. In the future, it would be interesting to understand the possible effect of the drug on fibroblasts of patients with amlodipine-induced gingival hyperplasia.