RESUMO
Keratinized mucosa in oral cavity plays an important role in periodontal health. The defect of keratinized mucosa may increase the risks of complication of oral implant surgery and restoration. Graft of keratinized tissue and connective tissue are still the gold standard for treating keratinized mucosa defect now. The current research focus on how to modulate non-keratinized mucosa to highly-efficient and minimally-invasive keratinized mucosa. Keratinocytes are critical components of oral mucosa and its final differentiation into keratinized mucosa is controlled by the connective tissue microenvironment involving a variety of molecules and ions. To fully understand keratinized differentiation of keratinocyte, this review focuses on its influence factors and possible mechanisms under the differentiation.
RESUMO
FimA has been characterized as an important virulence factor for Porphyromonas gingivalis (Pg). These structures play a major role in the mechanisms of adhesion and invasion of Pg to host cells, and can induce cellular activation and cytokines release. FimA can also promote biofilm formation and induce immuno-inflammatory response of host cells. Many studies have characterized FimA to be associated with periodontitis and cardiovascular disease. Pg strains are classified into six types based on divergent nucleotide sequences of the fimA gene (types Ⅰ、Ⅰb、Ⅱ、Ⅲ、Ⅳ andⅤ). The expression of fimbriae is regulated by the fimA gene, which may be the key factor that leads to virulence diversities of Pg, At present, the research on the pathogenesis of FimA mainly focuses on periodontitis and atherosclerosis, which is of great significance for the prevention and treatment of diseases. This paper reviewed the pathogenic effect of FimA in the development of above mentioned two diseases and its application in the prevention.