Average 29.1 bleeding events per year are serious enough to require factor replacement in F VIII-deficient patients which 9% involved oral structures.

[11] In 1990, George Brownlee and Merlin Crossley showed that two sets of genetic mutations were preventing two key proteins from attaching to the DNA of people with a rare and unusual form of haemophilia B – haemophilia B Leyden – where patients experience episodes of excessive bleeding in childhood but have few bleeding problems after puberty.

[10] This lack of protein attachment to the DNA was thereby turning off the gene that produces clotting factor IX, which prevents excessive bleeding.

[11] Factor IX deficiency leads to an increased propensity for haemorrhage, which can be either spontaneously or in response to mild trauma.

[6] Surgical treatment, including a simple dental extraction, must be planned to minimize the risk of bleeding, excessive bruising, or haematoma formation.

Soft vacuum-formed splints can be used to provide local protection following a dental extraction or prolonged post-extraction bleed.

[14] In July 2022 results of a gene therapy candidate for haemophilia B called FLT180 were announced, it works using an adeno-associated virus (AAV) to restore the clotting factor IX (FIX) protein, normal levels of the protein were observed with low doses of the therapy but immunosuppression was necessitated to decrease the risk of vector-related immune responses.

[20] He emigrated to Toronto, Ontario, Canada, with his family, and was there at the age of two years that hemophilia was diagnosed at the Hospital for Sick Children.

He became an active worker for the Canadian Hemophilia Society and campaigned for transfusion safety ever since getting infected, but developed AIDS and died from it in 1993.

[20] In the 1950s and 1960s, with newfound technology and gradual advances in medicine, pharmaceutical scientists found a way to take the factor IX from fresh frozen plasma (FFP) and give it to those with haemophilia B.

Though they found a way to treat the disease, the FFP contained only a small amount of factor IX, requiring large amounts of FFP to treat an actual bleeding episode, which resulted in the person requiring hospitalization.

With the rise of these deadly viruses, scientists had to find improved methods for screening the blood products they received from donors.

Queen Victoria was a carrier of haemophilia B who later passed these onto other ruling families from Russia, Spain and Germany.