Repair Of Pulp Inflammation

By Dr. Vishaal Bhat on Tuesday 10 June 2008 with 0 comments

Decreasing residual dentin thickness. Increasing pulp exposure. Point where dentin becomes so thin, you’ve exposed the pulp and you can see the pulp tissue. In shallow cavities, there is still about half a mm of dentin between pulp and the cavity. Shallow deep and very deep. very deep is less then a quarter mm. tertiary secretion is minimal in shallow cavities, survival rate is good. Maximum of reactionary dentin, odontoblast try to produce a lot of tertiary dentin to get rid of the stimulus and to reduce influx of bacteria or other substances through dentin. There is minimal reactionary dentin in very deep cavities, only a few odontoblasts survive. On the verge of having an exposed pulp. No survival of odontoblasts under lesion, no reactionary dentin. If the pulp survives body recruits odontoblast like cells, line up along the dentin abnd become new odontobpasts. Dentin that they reproduce is not as good as the dentin produced by primary odontoblast, full of holes. Difference between reactionary dentin, still have live odontoblasts and reparative that comes up after reqruitment of new cells. Reactionary dentin is formed by surviving odontoblasts.

Cavity cut in cervical area of tooth. See that the odontoblasts have tried to crate thick layer of tertiary dentin to create thicker dentin wall between the cavity and the odontoblasts.

Tertiary dentin leads to calcification of the pulp. Cant see any root canal at on on x-ray. Histologically still fine thin root canal but you can’t treat it any more. Complete obliteration of root canals. Also, how long has the pulp been exposed, chance of survival or if you can initiate root canal treatment. Partially necrotic after 8 days and completely after 14 days. Size of pulp exposure is important, tiny opening then prognosis is better than if it’s a huge opening where margin can be difficult to seal off. Chance of having leaking spot in filling is much higher. Contamination, has there been saliva or infected dentin chips through opening. Was pulp capping agent put without pressure or with. MTA used mostly, and calcium hydroxide.

Outcome is influenced by extent or amount of bacteria that have entered the rot canal. Peri apical tissue reflected by size of lesion. In a large lesion, infection has been more severe.

Theory that hasn’t been proven, anachoresis, through the general blood stream. In sepsis, bacteria in blood stream can be transported into tooth. some say no such thing.

Host defence. Met arterioles dilate. Because pulp is in hard tissue, no way it can swell. If pulp is injured, no way it can swell, that’s what makes it so vulnerable.

Proteolytic enzymes cause liquefied dead tissue causing pus.

When bacterial components enter root canal system first healthy periapex, assoon as there is contact with pulp dentin interface, endotoxins and exotoxins released (part of cell wall) secreted by microorganisms. Pulp becomes necrotic.

Category: Endodontics Notes



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