Regenerative Endodontics
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Direct answer
Regenerative endodontics aims to replace a necrotic pulp with living, vascularised tissue so that an immature permanent tooth thickens its walls, lengthens its root and closes its apex — the triad of tissue engineering applied chairside: stem cells from the apical papilla surviving beneath the infection, a scaffold (the induced blood clot, with its growth factors), and effective disinfection. The protocol is two visits: chemomechanical disinfection without aggressive instrumentation, dressing with an antibiotic paste or calcium hydroxide, then at a second visit deliberate over-instrumentation past the apex to provoke bleeding, sealing the clot with a tricalcium silicate barrier and composite. Apexification remains the alternative for the same teeth — an MTA apical plug seals quickly and well, but the walls stay thin forever, which is exactly the disadvantage regeneration exists to erase.
What you must remember
- Case selection: immature permanent teeth with necrotic pulp and open, divergent apices — typically traumatic necrosis of young incisors; a sinus tract or apical radiolucency is compatible, absent acute symptoms.
- The triad: stem cells (SCAP — stem cells of the apical papilla — and dental pulp stem cells), scaffold (blood clot, collagen), growth factors (released from dentine matrix by EDTA).
- First visit: access, minimal or no mechanical instrumentation, irrigation with low-concentration sodium hypochlorite (about 1.5-3 per cent) and saline, dressing with triple antibiotic paste (ciprofloxacin, metronidazole, minocycline), double antibiotic paste or calcium hydroxide, sealed one to four weeks.
- Minocycline discolours crowns: the double antibiotic paste or cefaclor substitution exists to prevent it, and coronal barriers (for example, a collagen plug or dentine-bonded layer) keep MTA grey from showing through.
- Second visit: on resolution of symptoms, irrigate and finish with 17 per cent EDTA (avoiding residual hypochlorite, which is cytotoxic to stem cells), induce bleeding two millimetres past the apex with a K-file, allow the clot to form level with the cementoenamel junction, and place a 3-4 mm tricalcium silicate (MTA or Biodentine) barrier, sealed with composite.
- Expected outcomes, in order of frequency: apical healing with resolution of lesions (most predictable), continued root thickening and lengthening, apical closure, and — least reliably — positive vitality responses.
- Apexification contrast: one-visit MTA apical plugs of 4-5 mm or classical long-term calcium hydroxide (months of changes) produce a barrier but no wall thickening, and long calcium hydroxide dressing itself embrittles thin roots.
- Histologically the regenerated tissue is commonly pulp-like with cementum or bone components — "revitalised", not a faithful pulp, a distinction examiners increasingly probe.
Treating a blunderbuss necrotic incisor
A nine-year-old's upper left central incisor, traumatised two years earlier, is discoloured, tender to percussion, with a periapical radiolucency and a wide-open divergent apex. First visit: isolate with rubber dam and remove necrotic debris with copious gentle 1.5-3 per cent hypochlorite irrigation without rotary shaping — these canals will be repopulated, not filled. Dry the canal and place a creamy antibiotic paste (double paste, avoiding minocycline in a front tooth), sealed with a cotton pellet and temporary cement for two weeks. Second visit, symptoms resolved: irrigate with saline, and finish with 17 per cent EDTA for several minutes to chelate the smear layer and liberate dentine growth factors. Bleed the canal deliberately: pass a K-file two millimetres beyond the apex until blood wells, and let it clot at the coronal level. Lay a collagen barrier, then 3-4 mm of white MTA or Biodentine over the clot, and close with bonded composite. Recall with radiographs: expect lesion resolution first, then measurable wall thickening and apical maturation.
Where students slip
Three answers decide this viva. "Which component of the triple paste is dropped and why?" — minocycline, for crown discolouration; candidates who do not know the substitution have not engaged with the protocol's complications. "Why EDTA last?" — because it releases growth factors from dentine matrix and because residual hypochlorite is cytotoxic to the very stem cells the technique depends on. "What actually forms inside?" — a pulp-like, vascularised tissue often containing cementum or bone, not identical native pulp; "new pulp, same as before" is the naive answer examiners set as bait.
Frequently asked questions
What is the tissue engineering triad in regenerative endodontics?
Stem cells (chiefly of the apical papilla), a scaffold (the induced blood clot), and signalling molecules — growth factors released from dentine by EDTA.
Why is minocycline often dropped from the triple antibiotic paste?
It discolours crowns; the double paste or cefaclor substitution keeps antimicrobial cover without staining.
Why is 17 per cent EDTA the final irrigant?
It removes the smear layer, liberates dentine growth factors and washes out hypochlorite residues toxic to apical cells.
How is the scaffold created?
Over-instrumentation two millimetres past the apex induces bleeding; the clot forms to the cementoenamel junction beneath the MTA barrier.
How do outcomes differ from apexification?
Regeneration pursues wall thickening and root lengthening with apical closure; apexification seals the apex but leaves walls thin.
What tissue actually regrows?
A vascularised pulp-like tissue often containing cementum or bone — revitalisation, not histologically native pulp.