Disorders of the Dental Pulp

Dr. Rima Safadi

From Dr. Huda Hammad lectures

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

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

Reversible pulpitis: Irritated pulp Mildest forms of inflammatory response

Vasodilatation Some transudation Slight infiltrate of lymphocytes

Reversible pulpitis

Irreversible Wide spectrum of acute and chronic inflammatory changes

Treatment removal of the pulp

Acute irreversible pulpitis

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

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

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

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

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

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 tubules 2. Overheating to the extent of ruptured blood vessels Mainly in children and adolescents No possibility of drainage
Build up of pressure

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

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

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

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

Chronic Hyperplastic Pulpitis

1.

2.

3.

Opened occlusal cavity Good blood supply through a widely opened apical foramen Regenerative capacity of young pulpal tissue
Stimulation of pulp to proliferate Excessive overgrowth Fibrotic Deficient in nerves May be epithelialized

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