These indicate that the vital inflamed pulp is not capable of healing and it is often indicated for the pulp to be removed as it is too damaged. Sleep may be disturbed and over-the-counter painkillers are often taken in an attempt to provide relief, but are usually ineffective. Causes
Pulpitis may be caused by bacteria from dental caries that penetrate through the enamel and dentin to reach the pulp, or it may be mechanical, a result of trauma, such as physical damage to the tooth. Inflammation is commonly associated with a bacterial infection but can also be due to other insults such as repetitive trauma or in rare cases periodontitis. The inflammation of dental pulp is mainly caused by an opportunistic infection of the pulp by a commensal oral microorganism. To reach the pulp, the most common route of the microorganism is through dental caries as well as from trauma, dentinal cracks and exposed dentin. Exposed dentin gives the microorganisms access to the pulp of the tooth through the dentinal tubules. In the case of penetrating decay, the pulp chamber is no longer sealed off from the environment of the oral cavity.When the pulp becomes inflamed, pressure begins to build up in the pulp cavity, exerting pressure on the nerve of the tooth and the surrounding tissues. Pressure from inflammation can cause mild to extreme pain, depending upon the severity of the inflammation and the bodys response.
Using Marys serum as index, he found that the "missing" factor, which he labeled V (I–IV having been used in Morawitz model), had particular characteristics. Most investigations were performed during the Second World War, and while Owren published his results in Norway in 1944, he could not publish them internationally until the war was over. They appeared finally in The Lancet in 1947.The possibility of an extra coagulation factor was initially resisted on methodological grounds by Drs Armand Quick and Walter Seegers, both world authorities in coagulation. Confirmatory studies from other groups led to their final approval several years later.Owren initially felt that factor V (labile factor or proaccelerin) activated another factor, which he named VI. VI was the factor that accelerated the conversion from prothrombin to thrombin. It was later discovered that factor V was "converted" (activated) by thrombin itself, and later still that factor VI was simply the activated form of factor V.The complete amino acid sequence of the protein was published in 1987. In 1994 factor V Leiden, resistant to inactivation by protein C, was described; this abnormality is the most common genetic cause for thrombosis. Interactions
Factor V has been shown to interact with Protein S.

References
Further reading
External links
The Coagulation Factor V Protein
Overview of all the structural information available in the PDB for UniProt: P12259 (Coagulation factor V) at the PDBe-KB.