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Etiology of Pulpal Inflammation We are all know about Pulpa, but how about the etiology?

So Pulpal inflammation: microbial, traumatic, iatrogenic (dentist caused) idiopathic (dont know why it happened). Juveniles, teeth develop from outside to inside, start with thin walls and large pulp, no root tip, then slowly the walls become thicker and the pulp becomes narrower. (Sandra, 2009) First stage is reversible pulpitis, pulp can still go to healthy state if you remove caries. Prophylaxis, hygien, fluoride application. Trauma prophylaxes in sports (mouth guard). If pulpitis occurs for longer period of time, stimulant is not removed, it becomes irreversible. (Sandra, 2009) Early stage of irreversible pulptiis, means still vital and sterile tissue in root canal, but some infection in coronal portion of pulp, in pulp chamber. Strategies to keep tooth vital is pulpotomy, cutting off healthy tissue at orifice of root canal. Later stage continuously bacterial front advances into root canals and the only way to treat the tooth is total pulpectomy. (Hargreaves, 2002) If no treatment is done, the tooth becomes totally infected and we have apical radiolucecy, dark area around root tip on radiograph, body has rremoved bone, a vulnerable tissue, body removes it and replaces bone by granulation tissue. We dont have a lot of bacteria in apical granuloma, thick wall of immune competent cells that wall off the body against the exit out of the root canal system. (Hargreaves,2002) Different causes for pulpal inflammation. (Sandra, 2002) 1. Microbial causes, mainly caries. 2. Tiniest gaps between dentin and filling are enough to allow bacteria to infect 3. Periodontitis, infection of periodontium. 4. Trauma: parafunction, deep overbite 5. Iatrogenic, dentist inflicted trauma. During cavity prep, without enough water coolant, prep too close to pulp etc. Resorption, odontoblasts turn into dentinoclasts, eat away the walls of the tooth, remove dentin and cavity in tooth appears on radiograph. Typically tissue

coronal to resporption is decrotic, and below it is still vital, because vital cells are removing dentin. External resporption. Differentiate between internal and external resportpion, can see contour of root canal as opposted to no contour (internal). (Hargreaves,2002) And the pulpa histology. See dentin and light layer is secondary dentin that odontoblasts have put down. Probably a cavity opposed to inner surface of dentin, and odontoblast are lined on inside of the tooth. Connective tissue has reticular and collagen fibers. Rest of pulp is gorund ubsance, hyaluronic acid etc. (Micahelson,2002) Needs nutreitnsa nd oxygen, so there is blood supply. The microcirculation is that three to four arterioles are right under odontoblasts, run from apical to coronal direction, and venules are much higher than arterioles, more centrally located, one main central venule important in inflammation, drains excess fluid and blood out of the pulp, has protecteive function, same for lymphatic vessesl. Pain heat redness and loss of function, main signs of inflammation. Acute and chronic inflammation. Trauma, an injury to living tissue caused by extrinsic agent. Surgical or caused by accident. Bacteria, rod shaped. Dentin wiall if you have infected tooth under fluorescent microscolpe. (Michaelson, 2002) Localized death of living tissue. Pulp necrosis, indicates that dental pulp has died, doenst react to sensitivity testing. If pus collects then its an abcess. Pulp abcess or facial abcess in patient. Perirediculaar space is part of periodontium. In periodontal abcess, through food impaction, inflamed pocket with abcess. Rapid onset of pain etc. Pulp is vital. Inflammation doenst have to do with root canal system. Acute periredicualr also rapid onset but the pulp is pulpitic, already become necrotic. In vital pulp if you put cold stim on tooth thats vital, cold stim goes away immedittley, with pulpitis, if you do cold testing, pain will linger, for minutes tooth is still hurting from cold. No reaction, pulp tissue is dead. (Sandra, 2002) Chronic perirediucalr abcess, four kidns of abcesses. If no treatment is undertaine, pulptiis exists for longer period of tiem. Situation becomes chornic,

reaction to pulp necrosis. Onset is gradua, in most cases dont know there is a lesion there. (Hargreaves,2002) Acute is a state of inflammation. Location of inflammation. Intrareducular, inside root canal, and extra radicular. Also foreng body reactions like irrigating and rinsing root canals then drying them with paper points. Paper point through apex, cellulose, in periapical space will cause foreign body reaction. (Hargreaves,2002) Intraredicular infection, bacteria inside the root canal system. Bacteria contamination can happen, microorganism reaching pulp space through breeches in pulp space. Bone level has gone down, horizontal bone loss in distal area of tooth, crown margin doenst fit too well. Interesting, not necessary for bacteria to reach pulp space, before bacteria enter pulp, severe inflammation, bacteria shed parts of cell wall, lipopolsacc that can reach pulp through dentinal tubules, initiate inflammation. Main source of contamination is carious. (Michaelson, 2002) Carious is a slow lesion, chronic, takes time to reach the pulp. Protective mechanisms is that axons of odontoblasts processes shed minerals trying to occlude the tubules, make htem less permeable for fluids and bacteria. Posisiton of materials is one way to protect pulp from invading microorganisms. (Sandra, 2002) And about the longitudinal cross section through the tooth. Dont obturate the tooth right away, use extra disinfecting agents, to disinfect dentin walls and that takes some time. Bacteria to depth of 300 microns. Can be through and through contamination. And that was the mechanism how can pulpal inflammation happened. (Sandra, 2002) Reference : Michaelson PL, Holland GR. 2002. Is pulpitis painful?. International Endodontic Journal.p.35:82932. Sandra,"Pulpitis". The Aberdeen. 17 September 2003. pp. 3. Retrieved 4 September 2009 Hargreaves, KM. Goodis, HE.2002. Seltzer and Benders Dental Pulp. Quintessence.