69101542 Lecture 5 Disorders of the Dental Pulp Slide
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Transcript of 69101542 Lecture 5 Disorders of the Dental Pulp Slide
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Disorders of the Dental Pulp
Dr. Rima SafadiFrom Dr. Huda Hammad lectures
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Pulpitis
Inflammation of the pulpal tissue regardless of infective agent– Acute or chronic– Reversible or irreversible– With or without sypmtoms
We have to decide:– To restore the tooth– To remove the pulp– To remove the entire tooth
So: we have to decide if the process is reversible or irreversible
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Causes of PulpitisBacterial: Caries Cracks Periodontal pockets Malformed teethTraumatic: Crown fractures Root fractures Partial avulsion Bruxism Abrasion
Iatrogenic: Heat generation Deep preperations Pulp exposure Filling materials Toxic disinfictants
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Reversible pulpitis: Irritated pulp Mildest forms of inflammatory response
– Vasodilatation– Some transudation– Slight infiltrate of lymphocytes
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Reversible pulpitis
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Irreversible Wide spectrum of acute and chronic
inflammatory changes– Treatment removal of the pulp
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Acute irreversible pulpitis
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Pain Symptoms
Reversible: Elicited Sharp 10-15 minutes Unaffected by posture Easily localized
Irreversible: Spontaneous Dull >20 minutes Affected by body posture Difficult to localize
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Pulp is contained within a solid champer Has limited blood supply through apical
foramen Inflammation mechanism gets destructive
– Inflammation: dilatation of blood vessels– Leakage of fluid from blood vessels– Migration of cells
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Pulpal Necrosis: Untreated irreversible pulpitis (infected with bacteria):
– Lose acute and chronic symptoms– Degeneration of nerve fibers– Autolysis– Irritation to the periodontal membrane– Extensive pain (limited area), extrusion of tooth
Non infected pulpal necrosis:– No symptoms for months– Change in color of the tooth
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Histopathology of Pulpal Disease
It is difficult to correlate clinical signs and symptoms with the degree of pulpal inflammation
Spectrum of histologic changes between normal and necrotic
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Histopathology of Pulpal Disease
Overview:
Low caries level: mildest response:– Diffuse infiltration of lymphocytes and
macrophages– No exudate formation
Bacterial entrance: dilated and congested blood vessels– Exudate formation– Compression of blood vessels– Ischemia and necrosis---- pulp abscess
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Acute Pulpitis May be confined to one horn of dental pulp (focal
acute pulpitis) or involve the whole pulp ( total acute pulpitis)
Cause: 1. Rapid bacterial invasion of dentinal tubules2. Overheating to the extent of ruptured blood
vessels Mainly in children and adolescents No possibility of drainage
– Build up of pressure
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Acute Pulpitis
Pulp Abscess: Core: (exudate): PMN cells, fibrin, necrotic
cells, debris and RBC Zone of granulation tissue: newly formed
blood vessels, young fibroblasts plasma cells and lymphocytes
No outer surrounding capsule– Pus quickly spread reach PDL
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Chronic Pulpitis When there is little or no penetration into the
pulp by large numbers of virulent types of bacteria.– Older teeth
• Scelrotic dentin• Reparative dentin formation
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Chronic Pulpitis
Microscopically: Loose connective tissue, Dense Bundles of collagen Reduction in size and number of blood vessels and
nerves Diffuse infiltrate of lymphocytes and plasma cells
– Known as pulp fibrosis Focal and diffuse calcifications may occur
– Pulp stones: spherical calcifications– Dystrophic calcifications: linear calcifications
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Pulp Calcification Pulp stones (denticles): organic core
– True pulp stones: contain tubules– False pulp stones: concentric layers of calcified
material– Free, adherent, interstitial
Dystrophic calcifications: granular material scattered along collagen fibers or in larger masses– Mainly in root canals
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Chronic Hyperplastic Pulpitis
1. Opened occlusal cavity
2. Good blood supply through a widely opened apical foramen
3. Regenerative capacity of young pulpal tissue– Stimulation of pulp to proliferate– Excessive overgrowth– Fibrotic– Deficient in nerves– May be epithelialized
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