Preclinics of Conservative Dental Medicine · MU Sofia

51. Inflammatory pulp diseases – etiology, pathogenesis, classification, diagnostic methods, acute and chronic symptoms.

Explains how caries bacteria and mechanical, iatrogenic and chemical irritants cause pulp inflammation, and why the low-compliance pulp chamber drives progression to necrosis from crown to apex. Sets out the AAE clinical classification in a table linking each diagnosis to its treatment, then the traditional acute and chronic pulpitis forms. Covers history, inspection, percussion, cold and electric pulp tests, and radiographs, with their pitfalls.

Inside: 5 sections · 1 labelled picture · 1 table · 17 flashcards · 7 min

Topic 51 of 53 in the MU Sofia syllabus for Preclinics of Conservative Dental Medicine (Dental Medicine, Year 3). The free AceMed note covers it in 5 sections, about 873 words (7 min of reading), with 17 flashcards.

In this note

  1. Introduction
  2. Etiology and pathogenesis
  3. Classification
  4. Diagnostic methods
  5. Key points

Introduction

Pulpitis is inflammation of the dental pulp, almost always a reaction to caries bacteria. This note covers its causes, why it so easily ends in necrosis, its classification and diagnosis. The diagnosis decides the treatment: keep the pulp or remove it.

Etiology and pathogenesis

Etiology

  • Bacterial – by far the commonest: caries, cracks, microleakage under restorations. Bacterial toxins reach the pulp through the dentinal tubules before the bacteria do; inflammation becomes marked once bacteria are within about 0.5 mm of the pulp. Rarely retrograde, from a deep periodontal pocket.
  • Mechanical and iatrogenic – trauma; cutting without water cooling (a pulpal rise of 5.5 °C irreversibly damaged about 15% of pulps experimentally); over-drying of dentin, which draws odontoblasts into the tubules; very deep preparations.
  • Chemical – acid etching, resin monomers, disinfectants or irritating cements on thin dentin without a liner.

Pathogenesis

The pulp is loose connective tissue enclosed in rigid dentin – a low-compliance chamber that cannot swell – supplied only through the narrow apical foramen, with practically no collateral circulation.

  1. Vasodilation and leaky vessels: exudate collects and the local tissue pressure rises.
  2. The pressure compresses the thin-walled venules: blood stagnates and the tissue becomes hypoxic (failure of the microcirculation).
  3. Cells next to the irritant die and a microabscess forms (partial necrosis); the rest of the pulp is still vital and inflamed.
  4. Lymphatics and arteriovenous shunts relieve the neighbouring tissue, so necrosis spreads compartment by compartment, from the coronal pulp towards the apex, to total necrosis; bacteria then colonise the canal (topics 52–53).

Inflammation in a closed, low-compliance chamber raises the local pressure, stops the microcirculation and leads to necrosis that advances step by step from crown to apex.

A-δ fibres give sharp, short, provoked pain (reversible stage); C fibres give dull, throbbing, lingering, poorly localised pain (irreversible stage) and survive hypoxia, so a partly necrotic pulp can still ache. Symptoms correlate poorly with histology; a pulp can also die painlessly.

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