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8/3/2019 lecture 5, Disorders of the Dental Pulp (slide)
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Disorders of the Dental Pulp
Dr. Rima SafadiFrom Dr. Huda Hammad lectures
8/3/2019 lecture 5, Disorders of the Dental Pulp (slide)
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Pulpitis
Inflammation of the pulpal tissue regardless of infectiveagent
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 Pulpitis
Bacterial:
Caries
Cracks
Periodontal pockets Malformed teeth
Traumatic:
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 chronicinflammatory 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 bodyposture
Difficult to localize
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Pulp is contained within a solid champer
Has limited blood supply through apicalforamen
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 andsymptoms with the degree of pulpalinflammation
Spectrum of histologic changes betweennormal and necrotic
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Histopathology of Pulpal Disease
Overview:
Low caries level: mildest response:
Diffuse infiltration of lymphocytes andmacrophages
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 (focalacute pulpitis) or involve the whole pulp ( totalacute pulpitis)
Cause:1. Rapid bacterial invasion of dentinal tubules
2. Overheating to the extent of ruptured bloodvessels
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, necroticcells, debris and RBC
Zone of granulation tissue: newly formedblood vessels, young fibroblasts plasma cellsand lymphocytes
No outer surrounding capsule Pus quickly spread reach PDL
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Chronic Pulpitis
When there is little or no penetration into thepulp by large numbers of virulent types ofbacteria.
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 andnerves
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 materialscattered along collagen fibers or in largermasses
Mainly in root canals
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Chronic Hyperplastic Pulpitis
1. Opened occlusal cavity
2. Good blood supply through a widely openedapical 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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