69101542 Lecture 5 Disorders of the Dental Pulp Slide

Disorders of the Dental Pulp

Dr. Rima SafadiFrom 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 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

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 tubules2. 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. 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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