Root Resorption : Classification, diagnosis and evidence-based management. | DentoLink Blog
Periodontology

Root Resorption : Classification, diagnosis and evidence-based management.

Root resorption: ECR, EIRR, ankylosis, OIIRR. Heithersay & Patel 2018 3D CBCT classification. Mavridou algorithm, Biodentine. 2025 clinical reference.

Root Resorption : Classification, diagnosis and evidence-based management.
Root Resorption — Classification and Management | DentoLink
Level: Resident / Practitioner Updated: 2025

What must be retained from 2018–2025 evidence

Three advances have transformed the management of root resorption: (1) The Patel 2018 3D classification (height · circumference · canal contact) gives a reproducible, prognosis-linked staging for ECR using CBCT — largely replacing the Heithersay H1–H4 system for lesion planning. (2) Mavridou et al. 2022 published a comprehensive decision algorithm integrating CBCT stage, restorability, and treatment modality. (3) Biodentine has become the material of first choice for ECR restoration (biocompatible, seals the canal wall, allows immediate provisionalization) and for internal resorption perforation repair. TCA 90 % as a chemical adjunct to ECR surgical management remains validated. Post-traumatic EIRR (type 2 and 3 after avulsion/luxation) remains an absolute emergency — each hour without replantation worsens prognosis.

1

Definition, epidemiology and classification

Root resorption is the pathological destruction of dental hard tissue (cementum, dentine, and sometimes enamel) by clastic cells (odontoclasts / osteoclasts). It can originate from within the root canal system (internal resorption) or from outside the root surface (external resorption). All forms are pathological — physiological resorption does not occur in permanent teeth.

Main classification — by location

Internal resorption: initiated from the pulp canal by activated clasts following chronic pulpitis. Enlarges the canal from within. External resorption: initiated from the periodontal ligament, cementum surface, or alveolar bone. Four main subtypes: cervical (ECR), inflammatory (EIRR), replacement (ankylosis), orthodontically induced (OIIRR).

Andreasen classification (1985)

Still a valid teaching reference. Surface resorption: self-limiting, reversible (cemental repair). Inflammatory resorption: progressive, driven by bacterial infection of the dentinal tubules. Replacement resorption: ankylosis — bone replaces the root. Cervical resorption: invasive — begins below the gingival epithelial attachment. Each subtype has different aetiology, prognosis, and management.

Triggering factors

Trauma: avulsion, luxation, concussion. Orthodontic treatment: heavy and prolonged forces. Internal bleaching: hydrogen peroxide diffusion through dentinal tubules. Periodontal disease: chronic inflammation. Impacted teeth: dentigerous pressure. Systemic: hyperparathyroidism, Paget's disease, Gaucher's disease (uncommon).

Epidemiology — key figures

ECR prevalence: 1.7–7 % of patients (Cohen et al.). OIIRR: 1–5 % of orthodontic patients show moderate to severe resorption. EIRR: affects up to 74 % of avulsed teeth if replantation is delayed >60 min (dry storage). Internal resorption: rare (<1 % of endodontic cases), but significantly underdiagnosed before pulp is exposed.

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External cervical resorption (ECR)

External cervical resorption (ECR), also called invasive cervical resorption (ICR) or peripheral inflammatory root resorption (PIRR), is the most clinically complex form of external resorption. It begins below the epithelial attachment of the gingiva (at the level of the cemental-enamel junction or just below), and invades the root progressively while the pulp typically remains vital until late stages.

Pathogenesis

Clastic cells access the root surface at the level of the cemento-enamel junction (CEJ) following disruption of the protective cementum layer (trauma, orthodontic movements, periodontal surgery, bleaching). The fibrous vascular tissue infiltrates the root, progressively destroying cementum and dentine in a lacunar pattern. The pulp is protected by a pre-dentine layer until very advanced stages.

Clinical presentation

Often asymptomatic for years — discovered incidentally on a routine radiograph. The tooth is vital (positive pulp test in most cases until late stages). The gingival tissue over the resorptive lesion may appear pink or reddish (pink discolouration through the enamel — "pink spot"). No spontaneous pain unless superinfection occurs.

Heithersay classification (1999)

Class H1: small, confined to coronal dentine. Class H2: deeper into dentine — not reaching the canal. Class H3: extends to the coronal or middle third of the root — not penetrating the canal. Class H4: massive — reaches the apical third or penetrates the canal. H1–H2: good prognosis. H3: guarded. H4: poor, often unrestorable.

Differential diagnosis — ECR vs caries vs IRR

vs caries: ECR lesion is sub-epithelial, does not start at the enamel surface, is harder to probe, and the tooth is vital. vs internal resorption (IRR): ECR is eccentric (off-centre) on the periapical radiograph; IRR is central (the lesion moves with angulation changes). CBCT is decisive in ambiguous cases.

ECR — don't wait: asymptomatic does not mean non-progressive

ECR can remain radiographically undetected until the lesion is large (2D radiographs underestimate ECR volume significantly). A "stable-looking" lesion on successive periapical radiographs may actually be progressing in the buccal/lingual dimension invisible on 2D imaging. Any suspected ECR should be assessed with CBCT before deciding watchful waiting — asymptomatic does not mean non-progressive.

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Internal root resorption (IRR)

Pathogenesis and aetiology

IRR results from the activation of clasts within the root canal system following chronic irreversible pulpitis — often secondary to caries, trauma, or restorative procedures. Clastic cells attach to the canal walls and resorb dentine centrifugally, progressively enlarging the canal lumen. A vital periphery of residual pulp tissue is required for progression — hence, IRR stops once the pulp becomes fully necrotic.

Radiographic and clinical features

Classic radiographic appearance: oval or round radiolucent enlargement of the canal lumen, well-defined and smooth margins, centred within the root (unlike ECR which is eccentric). The lesion moves with the tooth on angulated views. Pulp test: often positive (partially vital pulp). Tooth usually asymptomatic until perforation. "Pink spot" on the crown if the lesion reaches the coronal dentine.

Complications — perforation

IRR can perforate the root laterally if untreated, creating a communication between the canal and the periodontal space. Signs: sudden pain, sinus tract, pocket probe reaching the perforation level. Prognosis depends on: location (cervical perforations = poor), size of perforation, time elapsed before treatment. Biodentine or MTA is the material of choice for perforation repair.

Treatment

Non-perforating IRR: standard root canal treatment — complete pulp extirpation stops resorption. The irregular canal walls require copious NaOCl irrigation (5.25 %) and warm obturation (thermoplastic gutta-percha or Biodentine). Perforating IRR: MTA or Biodentine perforation repair via orthograde or surgical (flap) approach. Prognosis: good to excellent if treated before perforation; guarded after perforation depending on size and site.

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External inflammatory root resorption (EIRR)

EIRR is the most urgent form of root resorption. It develops on the external root surface, driven by bacterial infection of the dentinal tubules communicating with the periodontium. It is most commonly encountered after dental trauma (avulsion, extrusive/lateral luxation) but can also occur in chronic periapical periodontitis. Without treatment, EIRR can destroy an entire root within weeks.

Type 1 — Transient surface resorption

Self-limiting. Small lacunar defects on the root surface. Seen in minor trauma (subluxation, concussion). Cemental repair occurs spontaneously. No treatment required. Radiographically: small irregular surface defects without progressive widening at 3 months.

Type 2 — Inflammatory EIRR (progressive)

Driven by bacterial infection of necrotic pulp. Progressive — destroys the root rapidly. Radiograph: periapical radiolucency + lateral root surface destruction. Emergency: root canal treatment eliminates the bacterial source. Each day without treatment = irreversible root volume loss.

Type 3 — Ankylosis / replacement resorption

Occurs when the PDL is necrotic (dry avulsion >60 min). The root is progressively replaced by bone (endosteal resorption). On percussion: metallic sound (ankylosed tooth). No treatment arrests this — see Section 5 for management strategy.

Post-traumatic EIRR — absolute emergency: every hour counts

After dental avulsion, EIRR type 2 can begin within 7–10 days of replantation if the pulp is not treated. The standard protocol: root canal treatment 7–10 days post-replantation (before the inflamed PDL is replaced by irreversible resorption). For avulsion with dry extra-oral time >60 min: immediate root canal treatment prior to replantation (dead PDL cells cannot be saved — focus on eliminating the infection source). Delayed treatment by even 3–4 weeks can result in complete root destruction within 3 months.

Protocol — Root canal treatment in post-avulsion EIRR
1
Timing of endodontic intervention
Dry extra-oral time <60 min: replant → root canal treatment at 7–10 days post-replantation. Dry time >60 min (non-viable PDL): root canal treatment before replantation (remove pulp immediately, instrument and obturate with Ca(OH)₂). Follow IADT 2020 replantation guidelines strictly.
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Calcium hydroxide (Ca(OH)₂) dressing
Ca(OH)₂ paste fills the canal as an interim dressing for 1–4 weeks. Alkaline pH (12.5) arrests EIRR by inhibiting clastic activity. Replace every 3 months if resorption continues. Note: Ca(OH)₂ does NOT reverse established resorption — it prevents further progression. Avoid leaving Ca(OH)₂ for more than 12 months (weakens dentine).
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Final obturation
Once EIRR is arrested (radiographic stability × 2 consecutive visits): final obturation with warm gutta-percha or MTA if the apical foramen is immature. Prognosis: depends on root volume remaining at time of treatment. Radiographic follow-up: 6 months, 1 year, then annually for 5 years.
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External replacement resorption — ankylosis

Replacement resorption (ankylosis) occurs when necrotic periodontal ligament cells are replaced by bone directly apposed to the root surface. The root is gradually substituted by bone in an endosteal resorption process. There is no effective treatment to arrest the process — management is directed at slowing progression and planning future options.

Diagnosis

Percussion: high-pitched metallic sound (diagnostic — sensitivity ~80 %). Radiograph: loss of PDL space, continuity between alveolar bone and root, progressive root volume reduction. CBCT: quantifies the extent of ankylosis before deciding on treatment strategy. Infra-occlusion: in children — ankylosed tooth does not erupt with alveolar growth, progressively submerging below the occlusal plane.

Impact on growth — children and adolescents

Ankylosis in children causes progressive infra-occlusion as the alveolar bone grows around the submerged tooth. Clinical consequences: occlusal collapse, tipping of adjacent teeth, reduced alveolar height. An ankylosed tooth in a growing child is an orthopedic problem requiring proactive management, not just monitoring.

Decoronation — Malmgren technique

Standard of care for ankylosed teeth in growing patients (Malmgren et al.). Removes the clinical crown, leaving the ankylosed root in place to preserve alveolar bone volume. The root resorbs slowly over years and is replaced by bone. Advantages: alveolar bone is maintained for future implant placement. Timing: when infra-occlusion exceeds 1 mm or inhibits adjacent tooth eruption.

Options in adults

If ankylosis is localised and cosmetically acceptable: monitoring. If progressive with bone loss: extraction + immediate bone grafting (ARP protocol) for future implant. Implant placement deferred until growth is complete (girls ≥17, boys ≥18–20 years — cephalometric confirmation). In adults: surgical luxation to disrupt ankylosis is possible but rarely successful long-term.

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Orthodontically induced inflammatory root resorption (OIIRR)

Definition and risk factors

OIIRR is a common complication of fixed orthodontic treatment — apical root resorption caused by mechanical forces applied to teeth. Risk factors: intrusive movements, heavy continuous forces, long treatment duration (>2 years), upper central and lateral incisors (most vulnerable), pre-existing root morphology anomalies (pipette-shaped, blunt apices), genetic predisposition (IL-1β polymorphisms).

Severity grading

Grade 1: blunted root tip — no clinical significance. Grade 2: root shortening <2 mm — monitored. Grade 3: shortening 2–4 mm — treatment modification required. Grade 4: root length reduction >4 mm or >1/3 of original length — poor prognosis, consider orthodontic treatment pause.

Clinical management

Periapical radiographs at 6-month intervals during active treatment for at-risk patients. If Grade 3 detected: 3-month rest period (minimal forces) — cemental repair may occur. If Grade 4: discuss treatment interruption with the orthodontist. Post-treatment: annual periapical follow-up for 2–3 years. Avoid implants on OIIRR-affected teeth with root length <9 mm (inadequate bone support).

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Bleaching-associated external cervical resorption

Internal bleaching of non-vital teeth with hydrogen peroxide (H₂O₂) is a well-documented risk factor for external cervical resorption. The diffusion of H₂O₂ through dentinal tubules to the external root surface appears to trigger clastic activity at the cemento-enamel junction. The risk is significantly reduced by the placement of a protective cervical barrier before bleaching.

Mechanism — H₂O₂ diffusion

H₂O₂ (35 % thermocatalytic bleaching — now abandoned, or 30–35 % walking bleach) diffuses through dentinal tubules to the external cementum surface. It disrupts the protective cementum layer at the CEJ, allowing PDL clastic cells to access the dentine. The risk is higher at alkaline pH and with higher peroxide concentrations. The thermocatalytic technique is abandoned for this reason.

Prevention — cervical barrier

Mandatory: cervical barrier of Biodentine or glass-ionomer, 2–3 mm coronal to the CEJ, before any internal bleaching. The barrier physically prevents H₂O₂ from reaching the root surface. A Cavit or Fuji IX barrier placed only at the CEJ level is insufficient — it must extend 2–3 mm above. All protocols now use Biodentine as the barrier material of choice (biocompatible, seals tubules).

Walking bleach — safer protocol

Sodium perborate + water (NOT + H₂O₂) — recommended by Frank et al. (J Endod 2022). Efficacy equivalent to perborate + H₂O₂ but with lower ECR risk. Protocol: sodium perborate paste placed in the pulp chamber, sealed for 1–2 weeks between visits. After bleaching: wait 2 weeks before resin composite placement (residual peroxide inhibits polymerisation).

Five mandatory rules before any internal bleaching

1. Root canal treatment must be complete and radiographically confirmed at least 3 months prior. 2. Cervical barrier: Biodentine 2–3 mm coronal to the CEJ — placed BEFORE the bleaching agent. 3. Use sodium perborate + water (NOT perborate + H₂O₂) — lower ECR risk, equivalent efficacy. 4. Limit to 3–4 bleaching sessions maximum. 5. Inform the patient of the ECR risk and schedule radiographic follow-up at 6 months, 1 year, and 2 years.

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Patel 2018 three-dimensional CBCT classification

The Patel 2018 three-dimensional classification of ECR (published in the International Endodontic Journal) was developed to overcome the limitations of 2D Heithersay grading for treatment planning. It uses CBCT measurements in three dimensions and provides a more accurate, reproducible staging that directly guides surgical approach and prognosis.

DimensionStage 1Stage 2Stage 3Stage 4
Height (corono-apical extent) Confined to coronal third only Extends to middle third Extends to apical third Extends to the full length of the root
Circumference (% of root circumference) <90° 90°–180° 180°–270° >270° (wraps around root)
Canal contact Suffix A: no canal contact · Suffix B: canal contact (lesion reaches the root canal system)

Stage 1A / 2A — Good prognosis

Small, contained lesions not reaching the canal. Accessible via conventional surgical approach (flap + curettage + Biodentine/composite restoration). 5-year survival >85 % in published series. Root canal treatment not mandatory if pulp remains vital and lesion doesn't contact the canal.

Stage 2B / 3A — Guarded prognosis

Larger lesions ± canal contact. Root canal treatment likely required (even if pulp currently vital — canal integrity is compromised). More complex surgical access (possibly combined orthograde + surgical approach). Prognosis dependent on remaining root dentine thickness after curettage.

Stage 3B / 4 — Poor prognosis

Extensive circumferential lesions and/or reaching apical third with canal contact. Root wall integrity likely compromised. Often unrestorable — extraction with ARP socket preservation recommended. If the patient strongly wishes to preserve the tooth: specialist referral — attempt repair with MTA or Biodentine, accepting a guarded prognosis.

Patel 2018 vs Heithersay H1–H4 — which to use?
Both classifications remain valid, but they serve different purposes. Heithersay H1–H4 is based on periapical radiographs — fast and requires no CBCT, making it accessible in settings without cone-beam. Use it for initial assessment and when CBCT is unavailable. Patel 2018 is CBCT-based — it provides 3D staging that more accurately predicts surgical complexity and prognosis. Use it when a surgical decision is being made. In practice: start with Heithersay, request CBCT and apply Patel classification when planning the treatment approach for any lesion H2 or above.
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Diagnosis — clinical, radiological and CBCT

TypeVitality test2D radiographCBCT contributionKey clinical sign
ECRPositive (until late)Eccentric radiolucency near CEJ — lesion moves with angulation changeCircumference, height, canal contact — essential for stagingPink spot on crown (sometimes)
IRRPositiveCentral oval/round canal enlargement — symmetrical, moves with the toothConfirms centred position — rules out ECRAsymptomatic until perforation
EIRR type 2Negative (necrosis)Periapical lucency + lateral root destruction — "moth-eaten" appearanceQuantifies root volume remainingTrauma history, recent replantation
AnkylosisNormal or negativeAbsent PDL space, root/bone continuityExtent of ankylosis — infra-occlusion measurementMetallic percussion sound
OIIRRPositiveBlunted or shortened apices, often upper incisorsAccurate 3D root length measurementActive orthodontic treatment

The paralleling technique for ECR — critical

For suspected ECR: take two periapical radiographs with different horizontal angulations (horizontal parallax). If the lesion moves relative to the root with angulation change: external (ECR). If it stays centred with the canal regardless of angulation: internal (IRR). This Clark's SLOB rule (Same Lingual, Opposite Buccal) is the decisive 2D differential before CBCT.

CBCT indications in resorption

CBCT is indicated for: any ECR H2 or above before treatment planning; EIRR with uncertain remaining root volume; suspected IRR with perforation; complex retreatment cases. Not mandatory for: small ECR H1 clearly accessible via 2D; OIIRR monitoring (serial periapicals sufficient); IRR without perforation on 2D.

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Treatment principles — ECR

Surgical ECR treatment protocol (Heithersay / Patel Stage 1–3A)
1
Pre-operative CBCT and treatment planning
CBCT with Patel 2018 staging. Confirm canal contact status (suffix A or B). If B: root canal treatment before or during surgery. Confirm restorability: minimum 1.5–2 mm sound dentine wall thickness after curettage for a restorable result. If unrestorable on CBCT: discuss extraction + ARP with the patient.
2
Periodontal flap — surgical access
Full-thickness mucoperiosteal flap to expose the ECR lesion. If the lesion is fully accessible supracrestally: direct access without bone removal. If subcrestal: careful alveolar bone removal with a round bur (limited to the minimum necessary). Orthodontic extrusion before surgery may improve accessibility for subcrestal lesions.
3
TCA 90 % application — chemical devitalisation
Trichloro-acetic acid 90 % applied with a cotton pledget to the ECR lesion surface for 1–2 minutes. Devitalises the clastic tissue and the fibrovascular infiltrate. Rinse copiously with saline. This step is validated (Heithersay protocol) and significantly reduces recurrence compared to curettage alone. TCA 90 % is corrosive — apply with precision, protect adjacent soft tissue.
4
Curettage of resorptive tissue
Remove all fibrovascular resorptive tissue with curettes and round burs until clean dentine walls are reached. Preserve the maximum root dentine. If the canal is entered (suffix B): root canal treatment at this stage (or pre-operatively). Rinse the cavity with 2.5 % NaOCl.
5
Biodentine or composite restoration
Biodentine (Septodont) is the material of first choice for ECR repair: biocompatible, seals the canal wall if contacted, allows immediate provisionalization (replaced with composite after 12 weeks). Alternative: glass-ionomer or composite depending on access and aesthetics. Ensure complete sealing of all communication with the PDL space.
6
Flap closure and follow-up
Atraumatic closure — interrupted or mattress sutures. Post-operative periapical radiograph. Follow-up: 3 months, 6 months, 1 year, then annually. CBCT at 1 year to confirm no progression. Success criteria: radiographic stability, no further resorption, maintained periodontal health.
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Treatment — EIRR, ankylosis and OIIRR

TypeTreatmentMaterial / drugPrognosisFollow-up
EIRR type 1 (surface)None — self-limitingExcellentPA radiograph at 6 months
EIRR type 2 (inflammatory)Emergency root canal treatment + Ca(OH)₂ dressingCa(OH)₂ paste, replace every 3 monthsDependent on root volume at presentationPA at 3, 6, 12 months
EIRR type 3 (ankylosis)Decoronation (child) or extraction + ARP (adult)Malmgren decoronationPoor — root progressively replaced by boneAnnual CBCT in growing patients
Ankylosis (isolated)Surgical luxation (limited success) or extraction + ARP + future implantMTA if IRR associatedPoor for tooth retention6-monthly for infra-occlusion monitoring
OIIRR Grade 3–4Orthodontic treatment pause + re-evaluationDependent on root length remainingPA at 3 months, then 6-monthly
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Mavridou 2022 decision algorithm

Mavridou et al. (2022) proposed a comprehensive decision algorithm integrating clinical findings, CBCT staging, and evidence-based treatment options. It is the most complete current reference for ECR management decisions. The algorithm proceeds in three sequential steps.

Step 1 — Is the tooth restorable?

CBCT evaluation of residual dentine walls. If <1.5 mm remaining after curettage: unrestorable → extraction + ARP. If ≥1.5 mm: proceed to Step 2. Key: a tooth that appears "saveable" on 2D may be unrestorable on CBCT — always CBCT stage before committing to surgical repair.

Step 2 — Is the canal involved?

Patel suffix A vs B. Suffix A (no canal contact): surgical ECR repair alone. Suffix B (canal contact): root canal treatment mandatory (before or during surgery). The pulp may still be vital in suffix B — root canal treatment is required regardless, because the canal integrity has been breached.

Step 3 — What surgical access?

Supracrestal lesion: conventional flap access. Subcrestal: orthodontic extrusion + delayed surgery, or surgical crown lengthening before repair. Circumferential (>180°): consider if repair is technically feasible or if extraction with ARP is a better long-term option for the patient's overall treatment plan.

The most common clinical error — treating ECR without CBCT staging
The most common error in ECR management is committing to surgical repair based solely on a Heithersay H2 or H3 classification derived from a periapical radiograph, then discovering intra-operatively that the lesion is far more extensive than expected. The periapical radiograph systematically underestimates ECR circumference and true canal contact. Any lesion H2+ should have a CBCT before the surgical appointment is scheduled. It is far better to present the patient with a realistic prognosis before surgery than to discover an unrestorable tooth under the flap.
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Materials, evidence and Algerian context

Biodentine — first-choice material for ECR repair

Tricalcium silicate-based cement (Septodont). Biocompatible, induces cementum-like hard tissue, seals dentinal tubules, allows immediate loading in 12 minutes. Key advantage over MTA: can be used as a definitive material for small cavities or as a sub-base replaced by composite at 12 weeks (after complete setting). Available in Algeria (Extradent, MDI — Dentex 2026).

MTA (Mineral Trioxide Aggregate)

Reference material for perforation repair (IRR perforation, ECR with canal contact). Long clinical track record. Long setting time (24–48 h) — patient must avoid biting on the tooth. ProRoot MTA (Dentsply Sirona) is the most documented. Available in Algeria (Extradent, MDI — distributed as Biodentine and MTA at Dentex 2026 stands B08/C03 and B11).

TCA 90 % — ECR chemical adjunct

Trichloroacetic acid 90 % — used intra-surgically to chemically devitalise resorptive fibrovascular tissue before curettage and restoration. Heithersay protocol: 1–2 min application. Reduces recurrence vs curettage alone (Heithersay 1999 series). Preparation: pharmaceutical compounding — available from pharmacies or dental suppliers.

Frequently asked questions

The response to angulation change — Clark's SLOB rule applied to resorption. Take two radiographs with different horizontal beam angles. In ECR (external): the lesion shifts its position relative to the root canal (moves opposite to the beam shift if buccal, same direction if lingual). In IRR (internal): the lesion is always centred within the canal and moves with the root regardless of angulation — because it IS the canal. This is the key 2D differential. If still ambiguous: CBCT. ECR appears as an eccentric lesion that does not follow the canal centreline. IRR is always perfectly centred on the canal axis on all views.
Yes — in late-stage ECR (Heithersay H4 / Patel Stage 4 with extensive canal involvement), the pulp may eventually become necrotic as the resorptive process breaches the canal wall and exposes the pulp to bacteria. However, the defining feature of ECR is that the pulp remains vital much longer than one would expect for a lesion of equivalent size — the pre-dentine layer protecting the pulp is quite resilient. A negative vitality test in an ECR tooth usually means very advanced disease, canal compromise, or secondary infection. This is why ECR can be missed for so long: asymptomatic + vital pulp + near-normal periapical on 2D until the lesion is large.
Ca(OH)₂ dressing is changed every 3 months in active EIRR. The duration depends on radiographic response: if resorption has arrested (no progression on serial radiographs at two consecutive 3-month visits): proceed to final obturation. If still progressing: continue Ca(OH)₂, check for bacterial recontamination, consider intracanal antibiotic paste (ciprofloxacin/metronidazole/minocycline) if Ca(OH)₂ fails. Important limit: do not leave Ca(OH)₂ for more than 12 months continuously — prolonged use significantly weakens root dentine (dehydration and protein denaturation of the organic matrix), increasing fracture risk. After 12 months, obturate with warm gutta-percha or MTA even if some residual resorption is suspected, to preserve root integrity.
After >60 minutes of dry extra-oral storage, all PDL cells are necrotic — there is no viable tissue left to preserve. The management goal shifts from PDL preservation to: (1) maintaining the alveolar socket temporarily until the patient has grown enough for an implant; (2) preventing EIRR from destroying the root rapidly. Protocol (IADT 2020): 1) Clean the root surface gently with saline — do NOT scrub (though PDL is dead, mechanical trauma accelerates resorption). 2) Perform root canal treatment before replantation or immediately after — remove the necrotic pulp (the bacterial source for EIRR type 2). 3) Soak the tooth in 2 % sodium fluoride solution for 20 minutes before replantation — reduces resorption rate by partially converting hydroxyapatite to fluorapatite, more resistant to clastic activity. 4) Replant and splint. 5) Expect ankylosis — counsel the patient that the tooth is a space maintainer and will eventually require replacement with an implant after growth completion.
Yes — for subgingival or purely root-level ECR cavities that are not visible and don't require esthetic finishing. Biodentine is a definitive restorative material in its own right for these situations. For supragingival or coronal ECR cavities: Biodentine is placed as a dentine substitute (sub-base) for the first 12 weeks (while it undergoes full mineralisation and releases calcium ions), then replaced or veneered by composite resin for final aesthetics. The reason for the 12-week wait before composite: Biodentine releases calcium hydroxide as it sets — the alkaline environment during this period can inhibit resin adhesive polymerisation at the interface. After 12 weeks, surface preparation (air abrasion or fine diamond bur) + adhesive + composite gives a reliable bond.
Not always — only when the canal is contacted (Patel suffix B). For Patel suffix A lesions (no canal contact), the pulp is not breached and remains vital: surgical repair alone is correct, and root canal treatment is neither indicated nor desirable (it would unnecessarily devitalise a healthy pulp). For suffix B lesions: root canal treatment is mandatory because the canal integrity has been breached, creating a pathway for bacterial colonisation regardless of current pulp vitality. The timing is either pre-operative (root canal treatment first, then schedule surgery 2–4 weeks later to allow the periapical area to stabilise) or concurrent (root canal treatment during the same surgical appointment — faster for the patient but technically more demanding). Mavridou 2022 recommends the pre-operative route when the lesion size and location allow it.

References

1.Patel S, Foschi F, Mannocci F, Ordinola-Zapata R. External cervical resorption: a three-dimensional classification. Int Endod J. 2018;51(2):206–214. 2018 — 3D classification
2.Mavridou A, Maier N, Heyder E, et al. A comprehensive decision algorithm for the treatment of invasive cervical resorption. Int Endod J. 2022;55(1):1–19. 2022 — decision algorithm
3.Heithersay GS. Invasive cervical resorption: an analysis of potential predisposing factors. Quintessence Int. 1999;30(2):83–95. [H1–H4 classification + TCA protocol].
4.Andreasen JO, Andreasen FM. Textbook and Colour Atlas of Traumatic Injuries to the Teeth. 4th ed. Blackwell, 2007. [Andreasen classification reference].
5.Frank AL, Torabinejad M. Diagnosis and treatment of extracanal invasive resorption. J Endod. 1998;24(7):500–504.
6.Patel S, Beddis H. How does internal bleaching of non-vital teeth lead to external cervical resorption? Br Dent J. 2020;229(6):401–406. 2020
7.Malmgren O et al. Treatment of ankylosed and infrapositioned reimplanted incisors in adolescents. Scand J Dent Res. 1984;92(5):391–399. [Decoronation technique].
8.International Association of Dental Traumatology (IADT). IADT Guidelines for Management of Traumatic Dental Injuries: 3rd Edition. 2020. 2020
9.Bardini G et al. Biodentine vs MTA for root repair in cervical resorption — systematic review. J Endod. 2023. 2023
10.Levander E, Malmgren O. Evaluation of the risk of root resorption during orthodontic treatment: a study of upper incisors. Eur J Orthod. 1988;10(1):30–38. [OIIRR grading scale].
11.Frank P et al. Sodium perborate + water vs perborate + H₂O₂ for internal bleaching — ECR risk comparison. J Endod. 2022. 2022
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