Pulpitis is defined as an inflammation of the dental pulp. Based on the symptoms, it is defined as being reversible or irreversible. The dental pulp does have greater regenerative and reparative abilities than previously thought however at some point if it cannot withstand the trauma, it will ultimately become necrotic. This may be smaller repeated trauma or one excessive trauma to it.
The main three causes of pulpitis are bacterial infection, thermal insult and physical injury.
It is known that the bacteria can penetrate the dentinal tubules before dental caries even reaches the dental pulp. The formation of tertiary dentine reduces the permeability of the dentine so acts to slow down bacterial/caries attacking it.
Normal dentine has 70% mineral and 30% organic content but tertiary dentine has an increased mineral content with the organic portion having 10% less water, making it more resistant to attack. Bacterial contamination of the dentine occurs through various means such as dental caries, tooth fracture lines, open filling or crown margins, and after a tooth has been prepared for a crown or filling.
Thermal injury to the pulp usually results as the side effect of dental treatment. A dental hand piece rotates many thousands of times during the tooth filling preparation and this generates heat. The heat is increased if the dentist uses burrs that are blunt, uses excessive force and inadequate water cooling. For this reason, it is extremely important to have a good suction system in place and a good nurse who can adequately get rid of the water in the patient’s mouth without the patient getting up every few minutes or choking. Some dentists will turn down the water supply which generates more heat to the pulp’s detriment. Your handpieces should be of a good construction which focus water directly onto the burr tips.
The pulpitis initially will be localised but if the injury or stimulus continues, it will spread throughout and eventually lead to irreversible pulpitis.
Pulpitis has been described as a strangulation of the pulp due to inflammatory oedema raising the intra-pulpal pressure. After pulp necrosis, bacteria invade the pulp space. There are no WBCs from the pulp and no hydrostatic pressure from the dentinal fluid.
The bacteria and toxins can only be contained for so long inside the pulp but then eventually this causes an inflammatory reaction to the periodontal ligament at the apex of the tooth. This is known as periapical periodontitis.