Pulp Necrosis

Pulp necrosis is death of the dental pulp, with loss of blood supply and nerve function. It can occur without symptoms and is the usual route to apical periodontitis and abscess.

Causes are untreated caries, trauma (including concussion, luxation and avulsion), deep restorations, cracks, periodontal disease reaching the apex, and orthodontic or thermal injury. It may be infected or, rarely, sterile.

Pathophysiology. Progressive or sudden loss of pulpal blood supply leads to coagulative or liquefactive necrosis. Bacteria colonise the necrotic canal system and reach the periapical tissue, causing apical periodontitis.

After trauma to an immature tooth, loss of vascularity stops root development and leaves thin dentine walls and an open apex.

Often asymptomatic. A grey, brown or yellow crown after trauma, a history of severe past toothache that stopped, tenderness on biting, a draining sinus, a bad taste, or swelling in flare up.

The tooth does not respond to cold or electric tests and may not be tender. Look for a deep restoration, caries, cracks and trauma. Fever, facial swelling and trismus indicate abscess and spread.

• Negative cold and electric pulp tests (consider false negatives after recent trauma, in calcified canals and in young teeth where sensibility returns late), compared with controls on other teeth.
• Percussion and palpation: tenderness when apical periodontitis is present.
• Periapical radiograph: normal appearance in early disease, then periapical radiolucency and loss of the lamina dura. Cone beam CT for unclear cases.
• Crown discolouration and, in immature teeth, a wide open apex and thin walls.
• Laser Doppler flowmetry or pulse oximetry where available to show absent perfusion.

Differential diagnosis.

• Irreversible pulpitis
• Pulp canal obliteration after trauma (with delayed or absent response)
• Chronic apical periodontitis and acute apical abscess
• Internal and external root resorption
• Cracked tooth and vertical root fracture
• Periodontal abscess and endo perio lesion
• Intrinsic staining from tetracyclines or fluorosis

• Mature teeth: root canal treatment with irrigation using sodium hypochlorite 1 to 5.25% and 17% EDTA, intracanal calcium hydroxide dressing for 1 to 4 weeks when symptoms or exudate persist, and a root filling with a good coronal seal. Success is about 85 to 90% for primary treatment. Extract an unrestorable tooth.
• Immature teeth with open apices:
  • Regenerative endodontics: irrigation with sodium hypochlorite 1.5% and 17% EDTA, calcium hydroxide dressing for 2 to 4 weeks, then induction of bleeding into the canal and a calcium silicate seal over the blood clot. Use calcium hydroxide rather than minocycline containing antibiotic paste to avoid crown discolouration.
  • Apexification with a 4 to 5 mm apical plug of calcium silicate cement, followed by a root filling.
• Internal bleaching of a discoloured, root filled tooth with sodium perborate or hydrogen peroxide 35% paste, placed over a sealed barrier on the root filling at the level of the cemento enamel junction and replaced every 3 to 7 days for 2 to 3 visits. Use the lowest effective concentration to limit the risk of cervical resorption.
• Antibiotics only for spreading infection or systemic upset: amoxicillin 500 mg orally three times daily for 5 days (reduce to 500 mg every 12 hours at eGFR 10 to 30), with metronidazole 400 mg three times daily if severe, or clindamycin 300 mg four times daily in penicillin allergy.
• Analgesia: ibuprofen 400 mg every 8 hours with food and paracetamol 1 g every 6 hours (maximum 4 g daily), for a short course.

Monitoring. Review at 6 and 12 months, then annually for up to 4 years, with periapical radiographs. For regenerative treatment, assess for continued root development, apical closure and resolution of the lesion at 6, 12 and 24 months.

Referral and escalation. Refer to an endodontist for immature teeth, complex anatomy, retreatment or a suspected fracture. Emergency referral for spreading infection, trismus or sepsis.