Research continues in this field, though there is also no biochemical diagnostic test clinically available to detect the progression of gingivitis or periodontitis as of yet. Prevention and Maintenance
The best management of peri-implant mucositis is preventing it from occurring through maintenance of the implants. This involves regular cleaning from both the patient and a dental professional and antibacterial mouthwashes may help reduce plaque and bleeding around dental implants. Self-care
Various mechanical ways of removing bacteria from around implants are available to be used by patients in their own homes, including but not limited to nylon-coated interdental brushes, soft-bristled toothbrushes and hard plastic cleaning instruments. These are all designed to prevent damage of the implant abutment, which would roughen the surface and lead to the accumulation of more bacteria on the surface which would contribute to the formation of more biofilms in the area. However, it was found that there were no statistically significant differences between some types of self administered antimicrobials, as they were all equally successful at maintaining the health of the soft tissues. One study was done comparing hyaluronic acid gel and chlorhexidine gel and another compared amine fluoride/stannous fluoride mouthwash to chlorhexidine mouthwash, but neither study showed either antimicrobial to be more effective at preventing peri-implant mucositis.It was found that there was no statistically significant difference between the effectiveness of using a powered/sonic toothbrush and using a manual toothbrush, although participants reported that they preferred the sonic toothbrush as they felt that it was better at keeping the areas around the implants clean.
Factor VIII (FVIII) is an essential blood-clotting protein, also known as anti-hemophilic factor (AHF). In humans, factor VIII is encoded by the F8 gene. Defects in this gene result in hemophilia A, a recessive X-linked coagulation disorder. Factor VIII is produced in liver sinusoidal cells and endothelial cells outside the liver throughout the body. This protein circulates in the bloodstream in an inactive form, bound to another molecule called von Willebrand factor, until an injury that damages blood vessels occurs. In response to injury, coagulation factor VIII is activated and separates from von Willebrand factor. The active protein (sometimes written as coagulation factor VIIIa) interacts with another coagulation factor called factor IX. This interaction sets off a chain of additional chemical reactions that form a blood clot.Factor VIII participates in blood coagulation; it is a cofactor for factor IXa, which, in the presence of Ca2+ and phospholipids, forms a complex that converts factor X to the activated form Xa. The factor VIII gene produces two alternatively spliced transcripts. Transcript variant 1 encodes a large glycoprotein, isoform a, which circulates in plasma and associates with von Willebrand factor in a noncovalent complex. This protein undergoes multiple cleavage events. Transcript variant 2 encodes a putative small protein, isoform b, which consists primarily of the phospholipid binding domain of factor VIIIc. This binding domain is essential for coagulant activity.People with high levels of factor VIII are at increased risk for deep vein thrombosis and pulmonary embolism.