internal root resorption

Internal root resorption (IRR) is a pathological condition characterized by the progressive loss of dentin and pulpal walls from the inside of the root canal system. Unlike external resorption that begins on the outer surface of the tooth, internal resorption initiates within the root canal, often without noticeable symptoms in its early stages. Though it is relatively rare, internal root resorption poses a significant risk to the structural integrity of the affected tooth and, if left untreated, may lead to tooth loss.

The exact etiology of internal root resorption is not fully understood, but it is commonly associated with chronic pulpal inflammation, trauma, and certain systemic conditions. The advent of modern imaging techniques, especially Cone Beam Computed Tomography (CBCT), has vastly improved our ability to diagnose and treat internal root resorption effectively.

This article explores the pathophysiology, etiology, clinical presentation, diagnostic procedures, and treatment modalities related to internal root resorption, along with prognostic considerations and preventive strategies.

 

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Pathophysiology of Internal Root Resorption

Internal root resorption (IRR) is a unique form of pathological dentin degradation that begins within the root canal system and progresses outward, leading to the destruction of the internal dentinal walls. Understanding the cellular and molecular mechanisms behind IRR is crucial for timely diagnosis and targeted intervention.

Normal Pulp Physiology and Protective Barriers

Under healthy conditions, the inner walls of the pulp chamber and root canal are lined by a layer of odontoblasts that maintain and deposit dentin throughout the life of the tooth. These cells lie adjacent to the predentin layer, a non-mineralized organic matrix that acts as a barrier preventing clastic cell attachment. Together, the predentin-odontoblast complex plays a vital role in resisting resorptive activity.

In the absence of injury or inflammation, this system maintains a state of homeostasis. Even when the pulp is exposed to mild stimuli or irritants, the protective barrier remains intact, and reparative dentin may be laid down in response. However, when this protective layer is compromised, the door is opened for pathological processes like internal root resorption to occur.

Triggering the Resorptive Cascade

For internal root resorption to initiate, a disruption or degeneration of the odontoblastic layer and the predentin must occur. This often follows trauma, chronic pulp inflammation, or iatrogenic injury. Once this barrier is breached, a sequence of biological events ensues:

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  1. Inflammatory Mediator Release: Injury to the pulp initiates an immune response characterized by the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and prostaglandins. These molecules stimulate the recruitment and differentiation of clastic precursor cells.
  2. Clastic Cell Recruitment and Activation: The damaged pulp tissue attracts mononuclear precursor cells, which differentiate into odontoclasts—cells functionally and morphologically similar to osteoclasts. These multinucleated giant cells are capable of degrading mineralized dentin.
  3. Attachment to Mineralized Dentin: Once the predentin is removed or altered, odontoclasts can attach to the mineralized dentin. They form resorption lacunae, or Howship’s lacunae, and begin secreting acid and proteolytic enzymes to break down the inorganic and organic components of dentin.
  4. Dentin Demineralization and Degradation:
    • Hydrogen ions (H⁺) are secreted to dissolve the inorganic hydroxyapatite crystals.

    • Matrix metalloproteinases (MMPs) and cathepsins degrade the organic collagen matrix of dentin.

    • The process results in progressive internal cavitation and canal wall thinning.

 

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Types of Internal Root Resorption and Their Pathophysiology

1. Internal Inflammatory Resorption

This is the more common form and is usually associated with partially vital pulp tissue—one part is necrotic, while another portion remains inflamed and vital.

  • Inflammatory resorption is fueled by granulation tissue within the pulp chamber.
  • Histologically, multinucleated odontoclasts are observed actively resorbing dentin, surrounded by inflamed pulp tissue.
  • The process is self-sustaining as long as the inflammation persists and viable blood supply is present to nourish the odontoclasts.

 

2. Internal Replacement Resorption

A rarer variant, this occurs when bone-like tissue is deposited in the area of resorbed dentin, giving a mixed radiolucent–radiopaque appearance radiographically.

  • The exact mechanism is unclear, but it involves metaplastic transformation of pulpal cells into cementoblast- or osteoblast-like cells.
  • The resorbed dentin is gradually replaced by hard tissue of atypical composition, which may contain woven bone or cementum-like material.

 

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Hemodynamic and Cellular Conditions for IRR

For internal root resorption to continue, three key conditions must be met:

  1. Partially Vital Pulp: Completely necrotic pulp cannot support active clastic cells. A partially vital pulp provides both oxygen and nutrients necessary for continued odontoclastic activity.
  2. Blood Supply and Cellular Infiltrate: An active vascular network within the inflamed pulp maintains the viability of the clastic cells. Vascularized granulation tissue is often seen histologically.
  3. Absence of Protective Layers: Loss or alteration of the predentin and odontoblastic layer exposes mineralized dentin and allows for the adhesion and activation of resorptive cells.

 

Progression of the Resorptive Lesion

The resorptive defect typically begins as a small lacuna in the canal wall and expands over time. Without intervention, the following can occur:

  • Cavitation enlarges, often creating an irregular, balloon-like canal appearance.
  • In some cases, perforation of the root structure may occur, allowing communication with the periodontal ligament and possibly progressing into external inflammatory resorption.
  • The structural integrity of the root is weakened, increasing susceptibility to fracture.

 

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Histological Features

Histological examination of teeth affected by internal root resorption reveals:

  • Multinucleated odontoclasts within resorption lacunae
  • Inflamed granulation tissue in the pulp
  • Absence or thinning of the predentin layer
  • Areas of necrotic pulp adjacent to resorptive sites
  • In replacement resorption, woven bone-like tissue replacing dentin

 

Molecular Markers and Experimental Insights

Recent studies have begun to explore molecular markers that may regulate or indicate the presence of internal root resorption:

  • RANK/RANKL/OPG Pathway: Central to the differentiation and activation of clastic cells. An imbalance in the RANKL (Receptor Activator of Nuclear Factor κB Ligand) and OPG (osteoprotegerin) ratio promotes odontoclastic activity.
  • TGF-β and MMPs: These signaling molecules play roles in both inflammation and matrix degradation.
  • Hypoxia-inducible factors (HIFs): May contribute to angiogenesis and survival of resorptive cells in hypoxic pulp environments.

 

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These insights are paving the way for potential pharmacological interventions that could target the resorptive cascade at the molecular level.

Clinical Implications of the Pathophysiology

Understanding the pathophysiology of internal root resorption directly impacts clinical decisions:

  • The presence of vital, inflamed pulp is a signal that timely endodontic therapy can halt progression by removing the nutrient source.
  • Once the process perforates the root, the prognosis becomes more complex, often necessitating surgical repair or tooth extraction.
  • The use of materials like mineral trioxide aggregate (MTA) or bioceramics has been informed by knowledge of how these materials interact with resorptive defects and adjacent tissues.

 

Summary of Key Pathophysiological Concepts

FeatureDescription
InitiationTrauma or chronic pulpitis damages predentin/odontoblasts
Cell Types InvolvedOdontoclasts (multinucleated giant cells)
Enzymatic ActivityAcid phosphatase, cathepsins, MMPs
Tissue ChangesLoss of dentin, expansion of canal, possible perforation
Progression FactorsPartially vital pulp, inflammation, vascular supply
TypesInflammatory (common) vs. Replacement (rare)
TerminationPulpal necrosis, successful endodontic therapy, or perforation

 

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Etiology and Risk Factors

The etiology of internal root resorption (IRR) is multifactorial and often complex. It typically involves a disruption of the pulp’s protective barriers (odontoblasts and predentin), which allows odontoclastic activity to begin. Although internal root resorption is a relatively rare condition, understanding the risk factors and potential triggers is essential for early diagnosis and preventive care.

While in many cases the exact cause remains elusive, the following are recognized as major contributors and predisposing factors:

  1. Dental Trauma
  2. Chronic Pulpal Inflammation (Chronic Pulpitis)
  3. Orthodontic Treatment
  4. Iatrogenic Factors (Dental Procedures)
  5. Intracoronal Bleaching
  6. Systemic Conditions
  7. Genetic Predisposition
  8. Idiopathic Cases
  9. Age and Gender
  10. Tooth Type and Location

 

Dental Trauma

Dental trauma is one of the most commonly cited etiological factors for internal root resorption.

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Types of Trauma Associated:

  • Luxation Injuries (extrusion, lateral luxation, intrusion): These injuries can damage the neurovascular supply of the pulp and disrupt the odontoblast layer, creating favorable conditions for odontoclast recruitment.
  • Avulsion and Replantation: The reimplantation of avulsed teeth, especially if delayed or mishandled, often leads to pulpal inflammation or necrosis, which can stimulate both internal and external resorption.
  • Concussive Forces: Even subclinical trauma (without overt tooth displacement) may compromise pulpal health and set off inflammatory pathways.

 

Mechanism:

Trauma results in hemorrhage, inflammatory mediator release, and pulpal degeneration, all of which contribute to the destruction of the predentin and promote odontoclast adhesion and activity.

Chronic Pulpal Inflammation (Chronic Pulpitis)

Long-standing low-grade inflammation of the pulp tissue can gradually destroy the pulp’s internal architecture and activate resorptive processes.

Causes of Chronic Pulpitis:

  • Deep caries with pulp exposure
  • Leaking restorations
  • Microleakage around old fillings
  • Repeated dental procedures on the same tooth

 

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In chronic pulpitis, vascularized granulation tissue containing immune cells (lymphocytes, macrophages, plasma cells) infiltrates the pulp, creating a microenvironment rich in cytokines and enzymes that stimulate odontoclast differentiation.

Orthodontic Treatment

While orthodontics is generally safe, improper or excessive forces can induce both internal and external resorption.

Risk Factors During Orthodontics:

  • Heavy or uncontrolled forces
  • Rapid tooth movement
  • Prolonged treatment duration
  • History of trauma or root canal treatment prior to orthodontics

 

Mechanism:

Excessive mechanical stress may damage the pulp and disrupt the odontoblastic layer, especially if the tooth is already compromised. Internal root resorption may occur particularly if the pulp remains partially vital under chronic stress.

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Iatrogenic Factors (Dental Procedures)

Certain dental treatments, especially when improperly performed, can trigger internal root resorption.

Examples:

  • Pulpotomy or Pulp Capping: If the capping material is not adequately sealed or is cytotoxic, it may lead to chronic inflammation.
  • Aggressive Endodontic Instrumentation: Over-instrumentation can damage the canal walls and the periapical tissues, leading to inflammation.
  • Chemical Irritants: Use of strong or improperly used intracanal medicaments or irrigants (e.g., formocresol, phenol, sodium hypochlorite at high concentrations) may cause pulpal irritation.
  • Excessive Heat Generation: During crown preparation or cutting procedures without adequate cooling, heat may injure the pulp.

 

These scenarios compromise the pulp’s defenses and make it vulnerable to resorptive processes.

Intracoronal Bleaching

Some case reports have linked non-vital intracoronal bleaching with internal root resorption.

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Particularly Risky Scenarios:

  • Use of hydrogen peroxide or heat-activated bleaching agents
  • Overfilling or incorrect placement of the bleaching agent into the root canal system

 

These agents can penetrate dentinal tubules and cause oxidative stress to residual pulp tissue, initiating inflammation and odontoclast recruitment.

Systemic Conditions

Although less common, certain systemic diseases and physiological conditions may predispose individuals to internal resorption.

Examples:

  • Hyperparathyroidism: Increases bone turnover and can indirectly affect tooth structure.
  • Paget’s Disease: Altered bone metabolism may predispose teeth to abnormal resorption.
  • Endocrine Disorders: Hormonal imbalances (e.g., thyroid dysfunction) may affect calcified tissues.
  • Autoimmune Diseases: Conditions such as rheumatoid arthritis or lupus may create systemic inflammatory environments conducive to clastic cell activation.
  • Chronic inflammatory conditions: Pro-inflammatory cytokines systemically elevated in diseases like Crohn’s or colitis might also impact pulpal health.

 

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Although rare, these systemic factors should be considered in patients with multiple resorptive lesions or those without any local causes.

Genetic Predisposition

Some research suggests that genetic factors may influence the susceptibility to dental resorptive conditions.

  • Single nucleotide polymorphisms (SNPs) in genes involved in inflammation (e.g., IL-1β, TNF-α) or clastic cell activity (e.g., RANK, RANKL, OPG) could modulate the likelihood of developing resorptive defects.
  • Familial cases of idiopathic internal resorption have been reported, though rare.

 

Further research is needed to validate these associations, but a genetic predisposition cannot be entirely ruled out, especially in idiopathic cases.

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Idiopathic Cases

In a notable number of cases, no obvious cause for internal root resorption can be identified, even after thorough clinical and radiographic investigation.

These are classified as idiopathic internal resorption, and while their origin remains unknown, subtle and undetected pulpal injuries or low-grade inflammation are likely contributors.

Age and Gender

There is no definitive age or gender predilection for internal root resorption, but some studies suggest:

  • Young adults and middle-aged individuals may be more commonly affected, possibly due to higher incidence of trauma and caries in these age groups.
  • Slight male predominance has been noted in some reports, though findings are inconsistent.

 

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Tooth Type and Location

While IRR can affect any tooth, certain patterns have been observed:

  • Anterior teeth, especially maxillary incisors, are more frequently affected due to their higher exposure to trauma.
  • Single-rooted teeth are more commonly involved, possibly due to simpler canal morphology that allows more uniform spread of inflammatory mediators.
  • Molars are less frequently affected, though underreporting is possible due to more complex anatomy making early detection difficult.

 

Summary Table: Risk Factors for Internal Root Resorption

CategoryExamplesMechanism
TraumaLuxation, avulsion, concussionPulpal inflammation, odontoblast damage
InflammationDeep caries, chronic pulpitisCytokine release, clastic activation
OrthodonticsHeavy forces, long treatmentStress to pulp, barrier disruption
IatrogenicOver-instrumentation, chemical burnsDirect injury, inflammatory response
BleachingHeat-activated peroxideOxidative pulp damage
Systemic DiseaseHyperparathyroidism, autoimmune diseaseAltered resorptive balance
Genetic FactorsCytokine gene polymorphismsIncreased susceptibility
IdiopathicNo identifiable causePossibly undetected trauma or inflammation

 

Clinical Presentation

Internal root resorption (IRR) is often insidious in nature, meaning that it can progress silently without overt symptoms. The earliest stages of the condition are typically asymptomatic, and in many cases, the lesion is discovered incidentally on routine radiographic examination. However, as the resorption progresses, certain clinical signs and symptoms may become apparent, ranging from subtle discoloration to pain and even structural tooth compromise.

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Understanding the clinical manifestations of IRR is essential for timely diagnosis and appropriate treatment, as misdiagnosis or delayed detection can lead to further destruction of the tooth structure and potentially irreversible outcomes.

  1. Asymptomatic Early Stage
  2. Tooth Discoloration – “Pink Spot” (Pink Tooth of Mummery)
  3. Mild to Moderate Pain or Sensitivity
  4. Swelling or Fistula Formation
  5. Tooth Mobility
  6. Tooth Fracture
  7. Pulp Vitality Test Findings
  8. Radiographic Clues Prompted by Clinical Findings

 

Asymptomatic Early Stage

Most cases of internal root resorption begin silently. In the initial phases:

  • No pain or sensitivity is reported.
  • The patient is often unaware of any changes in the affected tooth.
  • IRR is commonly detected incidentally during routine dental radiographs taken for check ups, orthodontic evaluations, or restorative procedures.

 

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This asymptomatic nature underscores the importance of routine dental radiography, especially in teeth with a history of trauma, caries, or pulp therapy.

Tooth Discoloration – “Pink Spot” (Pink Tooth of Mummery)

One of the hallmark clinical signs of internal resorption, especially when the lesion is located in the coronal third of the root or pulp chamber, is the appearance of a “pink spot”.

Characteristics:

  • The pink spot appears due to the vascular granulation tissue formed within the resorption cavity. As dentin is resorbed from within, this highly vascular tissue shows through the relatively thin and translucent enamel or dentin, creating a pinkish hue.
  • This is most commonly seen in anterior teeth such as maxillary central incisors due to their thinner enamel and increased likelihood of trauma.

 

Clinical Implication:

  • This is an important diagnostic clue and should prompt immediate radiographic investigation.
  • The appearance of the pink spot typically means that the lesion has reached a moderate or advanced stage.

 

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Mild to Moderate Pain or Sensitivity

While IRR is usually painless in its early phase, as the lesion progresses and inflammation spreads within the pulp, the patient may begin to experience:

  • Mild, dull aching pain localized to the affected tooth.
  • Sensitivity to thermal stimuli, especially heat. Sensitivity to cold may be reduced or absent due to the degeneration of superficial pulpal nerves.
  • Discomfort on chewing or biting if there is significant structural weakening.

 

This occurs in cases where the pulp is partially vital and inflamed—a condition that supports the activity of odontoclasts.

Swelling or Fistula Formation

If the internal resorption progresses to the point of pulpal necrosis, it can lead to infection and periapical inflammation. In such cases, clinical signs may include:

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  • Localized swelling of the gingiva or mucosa
  • Formation of a sinus tract (fistula) draining purulent exudate
  • Possible tenderness on palpation or percussion
  • Occasionally, tooth mobility if the infection involves the surrounding periodontal ligament

 

This stage often represents the transition from a contained internal resorptive process to combined internal and external pathology or apical periodontitis.

Tooth Mobility

Tooth mobility in the context of internal root resorption may occur due to:

  • Loss of internal dentin, leading to weakening of the tooth’s structural integrity
  • Perforation of the root canal wall with subsequent involvement of the periodontal ligament
  • Associated infection, causing localized bone loss and ligament degradation

 

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Mobility is more likely to be present in advanced or perforating lesions, and when observed, it suggests a guarded to poor prognosis depending on the extent of structural compromise.

Tooth Fracture

In severe or long-standing cases of IRR, the tooth becomes structurally compromised:

  • Thinning of the root canal walls increases the risk of vertical or oblique root fractures, particularly under masticatory stress or trauma.
  • Fracture may present as sudden pain while chewing, tooth displacement, or splitting of the crown.
  • In some cases, the tooth may become non-restorable, requiring extraction.

 

Thus, structural integrity should be carefully evaluated during the diagnostic phase using radiographs and, ideally, CBCT.

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Pulp Vitality Test Findings

Because internal resorption is dependent on a partially vital pulp, pulp vitality testing can provide valuable diagnostic clues.

Common findings:

  • Early-stage lesions: Often test positive to cold or EPT (electric pulp testing), but with delayed or lingering response.
  • Intermediate lesions: May give inconsistent results; sensitivity to heat is more common than to cold.
  • Late-stage or necrotic lesions: Will show no response to thermal or electric tests.

 

A partially vital pulp is essential for active odontoclastic function, and pulp testing aids in distinguishing active IRR from other non-vital or quiescent conditions.

Radiographic Clues Prompted by Clinical Findings

Even subtle clinical signs may justify further investigation with radiographic imaging. A clinician should consider taking a radiograph if the patient presents with:

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  • A history of trauma, even if remote or asymptomatic
  • Persistent or unexplained sensitivity
  • Tooth discoloration without caries
  • Unusual mobility not explained by periodontal status

 

Differential Diagnosis Based on Clinical Signs

Because many of the signs of IRR are nonspecific, it’s important to differentiate from similar conditions:

ConditionSimilar SignsDistinguishing Features
External cervical resorptionPink discoloration, radiolucencyUsually asymmetrical, not centered on canal
Pulpal necrosis with apical periodontitisPain, swellingNo internal dentin loss, no pink spot
Internal bleaching stainDiscolorationUniform gray or darkening, no vascularity
Advanced cariesDiscoloration, sensitivityCarious lesion visible clinically and radiographically

Key Clinical Scenarios

Scenario 1: Asymptomatic Patient

  • Presents for routine exam
  • No complaints, but radiograph shows a radiolucent ballooning of the root canal space
  • Cold test yields a mild lingering response
  • Diagnosis: Early-stage internal root resorption

 

Scenario 2: Pink Discoloration

  • Patient notices pink spot on upper front tooth
  • No pain but reports history of trauma during sports 3 years ago
  • Radiograph shows localized internal radiolucency in coronal third of the root
  • Diagnosis: Moderate internal root resorption with coronal involvement

 

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Scenario 3: Swelling and Pain

  • Localized swelling and sinus tract near lower molar
  • Tooth is sensitive to percussion, no response to pulp testing
  • Radiograph and CBCT reveal extensive IRR with perforation and periapical pathology
  • Diagnosis: Perforating internal root resorption with secondary infection

 

Summary of Clinical Features by Stage

StageClinical SignsSymptoms
EarlyNo visible changesAsymptomatic
ModeratePink spot, discolorationMild sensitivity, discomfort
AdvancedSwelling, mobility, fracturePain, tenderness, possible sinus tract
Late/NecroticNon-vital tooth, extensive damagePersistent pain, abscess, structural compromise

 

Diagnosis

Diagnosing internal root resorption (IRR) is a critical step in its successful management. Early-stage IRR is typically asymptomatic and may only be detected through radiographic evaluation. The diagnostic process involves integrating findings from clinical examination, pulp vitality tests, and advanced imaging techniques, particularly Cone Beam Computed Tomography (CBCT).

A comprehensive and systematic approach is essential not only to confirm the presence of IRR but also to differentiate it from similar pathologies, assess its severity, determine prognosis, and plan treatment accordingly.

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1. Clinical Examination

Although internal root resorption may be clinically silent, a meticulous intraoral examination can provide important diagnostic clues:

A. Visual Inspection

  • Look for discoloration, especially a pinkish hue (pink tooth of Mummery) typically in the coronal area, indicating vascular granulation tissue within the pulp chamber.
  • Examine for tooth structure loss, such as chipping or unusual wear patterns.
  • Assess for caries, restorative margins, and evidence of previous trauma or treatment.

 

B. Palpation and Percussion

  • Palpation: May reveal tenderness in later stages when periapical tissues are involved.
  • Percussion: Often non-tender in early lesions; positive response may indicate advanced or perforating lesions with apical pathology.

 

C. Periodontal Probing

  • Probing depths are usually normal unless there is root perforation or concurrent periodontal involvement.
  • In perforating IRR, localized deep pocketing may be present, especially on the labial or lingual surface.

 

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2. Pulp Vitality Testing

Pulp testing is a cornerstone of diagnosing IRR, as it helps distinguish between active and inactive lesions, and guides treatment planning.

A. Cold Test

  • Early or active IRR: May show a normal or prolonged response.
  • Late-stage IRR or necrotic pulp: Typically no response.

 

B. Electric Pulp Test (EPT)

  • May yield a positive response in early lesions (vital pulp).
  • As the resorptive process advances, pulp necrosis may result in no response.

 

C. Heat Test

  • More useful in detecting inflamed vital pulp, which may be present in intermediate stages.
  • A positive response to heat but not cold could indicate chronic inflammation associated with IRR.

 

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Important Note: Internal root resorption requires a partially vital pulp to progress. Complete pulp necrosis arrests the resorptive activity.

 

3. Radiographic Examination

Radiographs are indispensable for detecting and evaluating internal root resorption. However, a single periapical image may not provide enough information to differentiate IRR from other radiolucent defects or to assess the three-dimensional extent of the lesion.

A. Conventional Periapical Radiographs

  • Reveal a well-defined, round-to-oval radiolucency that is continuous with the root canal.
  • The lesion is symmetrical and centered on the canal, unlike external resorption.
  • Canal borders appear ballooned or expanded.
  • The outline of the root canal cannot be traced through the lesion—this is a key radiographic hallmark.
  • No changes to the periodontal ligament space or lamina dura unless perforation or periapical involvement exists.

 

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B. Multiple Angled Radiographs

  • Taking radiographs from different horizontal angles (mesial and distal) helps confirm the lesion’s internal origin.
  • In internal resorption, the radiolucency remains superimposed over the canal regardless of the angle.

 

C. Bitewing Radiographs

  • Especially useful for anterior teeth or when coronal involvement is suspected.
  • Help visualize resorption near the pulp chamber.

 

4. Cone Beam Computed Tomography (CBCT)

CBCT is considered the gold standard for the diagnosis and treatment planning of internal root resorption due to its three-dimensional imaging capabilities.

Advantages:

  • Provides detailed assessment of the location, size, and shape of the lesion.
  • Confirms whether the resorptive defect is perforating or non-perforating.
  • Helps differentiate internal vs. external resorption.
  • Aids in treatment planning by assessing the thickness of remaining dentin and proximity to anatomical landmarks.
  • Identifies possible root fractures, perforations, or communication with the periodontal ligament.

 

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CBCT Features of Internal Root Resorption:

  • Well-circumscribed radiolucent area centered within the canal.
  • Smooth, symmetrical expansion of the canal wall.
  • No interruption of external root surface unless there is perforation.
  • In perforating lesions, CBCT reveals discontinuity in the external root surface and possible bone involvement.

 

5. Differential Diagnosis

IRR can mimic or be confused with several other dental conditions. Accurate differentiation is essential for proper treatment.

ConditionDistinguishing Features
External cervical resorption (ECR)Irregular, asymmetrical radiolucency starting from external root surface; canal outline is usually intact. Lesion shifts with angled radiographs.
Internal bleaching stainUniform discoloration, usually gray; no radiographic radiolucency in root structure.
Periapical pathologyPeriapical radiolucency with clear root canal; canal outline visible through lesion.
Secondary cariesAssociated with restoration; irregular radiolucency near margins.
Root fractureMay show as a J-shaped radiolucency; CBCT helps confirm vertical/horizontal root fractures.

6. Histopathological Examination (Rarely Performed Clinically)

Although not routinely used for diagnosis in clinical settings, histologic analysis of extracted or sectioned teeth confirms the presence of:

  • Odontoclasts in resorption lacunae
  • Inflamed granulation tissue replacing normal pulp
  • Loss of predentin layer
  • In replacement resorption: Bone-like or cementum-like tissue replacing dentin

 

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7. Classification Based on Diagnostic Findings

Based on imaging and clinical evaluation, internal root resorption can be classified into:

A. By Location:

  • Coronal IRR: Resorption localized to the pulp chamber or coronal third of the root.
  • Middle IRR: Most common; affects the middle third of the root canal.
  • Apical IRR: Involves the apical third; harder to detect and manage.

 

B. By Extent:

  • Non-perforating IRR: Confined within dentin and does not reach external root surface.
  • Perforating IRR: Extends through the dentin to communicate with the periodontal ligament or alveolar bone.

 

C. By Activity:

  • Active IRR: Ongoing resorption with a vital, inflamed pulp and positive vitality tests.
  • Arrested IRR: Lesion has halted; pulp may be necrotic or calcified.

 

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Classification

Internal root resorption (IRR) is a dynamic and progressive condition with variable clinical and radiographic presentations. Classification plays a crucial role in guiding diagnosis, prognosis, and treatment planning. Although there is no single universally accepted classification system, several schemes have been proposed in the literature to categorize IRR based on its location, extent, pathologic nature, activity, and clinical behavior.

A clear understanding of these classifications helps clinicians tailor treatment strategies and communicate effectively with patients and interdisciplinary teams.

Classification by Anatomical Location

This is the most straightforward and commonly used method of categorizing IRR, based on the location of the resorptive defect along the root or pulp chamber.

A. Coronal IRR

  • Occurs in the pulp chamber or the coronal third of the root canal.
  • Often presents with pink discoloration (pink tooth of Mummery).
  • May be confused with internal bleaching stain or external cervical resorption.
  • Easier to access and treat due to its proximity to the crown.

 

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B. Middle Third IRR

  • The most frequently encountered form.
  • Resorption occurs in the middle third of the root canal.
  • May go unnoticed until significant radiographic changes or structural compromise occur.
  • May require advanced shaping and obturation techniques due to irregular canal morphology.

 

C. Apical IRR

  • Occurs in the apical third of the root.
  • Difficult to diagnose radiographically and challenging to access and treat.
  • Higher risk of perforation, particularly in curved or narrow roots.
  • May mimic periapical pathosis and be mistaken for apical periodontitis.

 

Clinical Implication: Location determines ease of access during endodontic treatment and risk of structural weakness or perforation.

Classification by Extent and Integrity of the Root Structure

This classification helps determine the severity and prognosis of the lesion.

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A. Non-Perforating Internal Root Resorption

  • Resorptive activity remains confined within the dentin and does not reach the external root surface.
  • Structural integrity is relatively preserved.
  • Prognosis is generally favorable with conventional root canal therapy.

 

B. Perforating Internal Root Resorption

  • The lesion extends through the dentin and perforates the external root surface.
  • May lead to communication with the periodontal ligament or alveolar bone.
  • Associated with localized deep periodontal pockets, sinus tracts, or secondary infection.
  • Treatment is more complex, often requiring surgical repair, MTA plug, or extraction in severe cases.

 

Clinical Implication: Perforation status is critical for determining treatment complexity and long-term prognosis.

Classification by Activity Status

This system classifies IRR as either active (progressive) or arrested (inactive), based on the vitality of the pulp and ongoing resorptive activity.

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A. Active Internal Root Resorption

  • Pulp is partially vital and inflamed.
  • Odontoclasts are active and continue resorbing dentin.
  • Lesion may enlarge rapidly if left untreated.
  • Clinical signs may include pain, sensitivity, and radiographic progression over time.

 

B. Arrested Internal Root Resorption

  • Pulp tissue is necrotic or replaced with calcified tissue, and resorption has ceased.
  • Odontoclastic activity is no longer present.
  • Lesion appears stable on serial radiographs.
  • May not require immediate intervention if asymptomatic and non-perforating, but close monitoring is essential.

 

Clinical Implication: Active lesions require urgent endodontic treatment, while arrested lesions may be observed or treated conservatively, depending on the structural integrity and clinical symptoms.

Classification by Pathological and Histological Features

This classification differentiates IRR based on the tissue changes and the type of material replacing resorbed dentin.

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A. Inflammatory Internal Resorption

  • Most common type.
  • Characterized by the loss of dentin and its replacement with vascular granulation tissue.
  • Histology shows numerous odontoclasts, inflammation, and resorptive lacunae.
  • Presents as a well-circumscribed radiolucent area centered on the canal.

 

B. Internal Replacement Resorption

  • Less common and often slower progressing.
  • Resorbed dentin is replaced by bone-like or cementum-like tissue (metaplastic tissue).
  • Radiographically presents as a mixed radiolucent-radiopaque lesion, often with irregular canal outlines.
  • Histologically shows hard tissue metaplasia with possible fusion to alveolar bone.

 

Clinical Implication: Inflammatory resorption responds well to endodontic treatment, while replacement resorption may be less responsive and more difficult to manage.

Classification Based on Radiographic Appearance

Although subjective, this helps clinicians in everyday practice to describe and document lesions.

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TypeRadiographic Features
Early IRRSmall, well-circumscribed radiolucency centered on the canal
Moderate IRRLarger lesion with ballooning of canal walls, irregular borders
Advanced IRRSignificant canal distortion, possible perforation, loss of root structure
Mixed Lesion (Replacement)Mixed radiolucent-radiopaque, indicating deposition of metaplastic tissue

Clinical Classification for Treatment Planning

Proposed by some clinicians, this practical system groups IRR into categories based on treatability:

Type I – Simple IRR

Non-perforating, small lesion

Easy to access and clean

Treated with conventional root canal therapy

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Type II – Moderate IRR

  • Larger but non-perforating lesion
  • Requires advanced obturation techniques
  • May benefit from CBCT planning

 

Type III – Perforating IRR

  • Perforates root structure
  • Surgical intervention or repair with MTA/bioceramics needed
  • Guarded prognosis

 

Type IV – Extensive and Non-Restorable IRR

  • Severe structural compromise
  • Tooth has poor long-term prognosis
  • Extraction or alternative prosthetic plan advised

 

Clinical Implication: This system helps clinicians plan the level of intervention and predict outcomes based on lesion complexity.

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Summary Table of IRR Classifications

Classification TypeSubcategoriesClinical Relevance
Anatomical LocationCoronal, Middle, ApicalHelps access planning
ExtentNon-perforating, PerforatingIndicates prognosis and complexity
Activity StatusActive, ArrestedGuides urgency of treatment
Pathological TypeInflammatory, ReplacementInfluences material selection and response to therapy
Radiographic AppearanceEarly, Moderate, Advanced, MixedAids in monitoring progression
Treatability (Practical)Type I–IVAssists in treatment planning

 

Treatment and Management

The primary goal in treating internal root resorption (IRR) is to eliminate the source of resorption, which is usually inflamed or partially necrotic pulp tissue, and to restore structural integrity to the affected tooth. Early diagnosis significantly improves prognosis, especially when the lesion is non-perforating and detected before substantial structural compromise occurs.

The treatment plan depends on several factors:

  • Extent and location of the lesion
  • Perforation status
  • Pulp vitality
  • Tooth restorability
  • Patient factors (e.g., age, overall health, oral hygiene)

 

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General Treatment Principles

Regardless of lesion type, the following goals apply:

  • Complete removal of the resorptive tissue (granulation or necrotic pulp)
  • Disinfection of the root canal system
  • Elimination of odontoclasts and resorptive stimuli
  • Sealing of the canal space to prevent bacterial ingress
  • Reinforcement of weakened root structure
  • Preservation of tooth function and aesthetics

 

Treatment of Non-Perforating Internal Root Resorption

This is the most favorable scenario with a good prognosis if treated promptly.

A. Conventional Root Canal Therapy

Standard root canal therapy (RCT) is highly effective in managing non-perforating IRR.

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Treatment Steps:

1. Anesthesia and Isolation
  • Administer local anesthesia.
  • Use rubber dam isolation to prevent contamination.

 

2. Access Cavity Preparation
  • Access must be conservative yet sufficient to visualize and reach the resorptive cavity.
  • Remove all coronal pulp tissue and debris.

 

3. Canal Debridement

Use rotary and hand files to clean and shape the canal.

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Irrigation is critical—copious use of:

  • Sodium hypochlorite (NaOCl) (2.5–5.25%) to dissolve organic tissue
  • EDTA (17%) to remove the smear layer and enhance NaOCl efficacy

 

4. Use of Ultrasonics
  • Passive ultrasonic irrigation (PUI) enhances cleaning in irregular resorption lacunae.
  • Helps dislodge tissue remnants and disrupt biofilms.

 

5. Intracanal Medicament

Place calcium hydroxide dressing for 1–2 weeks:

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  • Antibacterial
  • Promotes tissue dissolution
  • Inhibits odontoclasts

 

6. Obturation

Standard lateral condensation may be insufficient due to irregular cavity.

Use thermoplasticized gutta-percha techniques:

  • Warm vertical compaction
  • Carrier-based systems (e.g., GuttaCore, Thermafil)
  • Injectable obturators for three-dimensional filling

 

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Sealer: Bioceramic sealers (e.g., EndoSequence BC) provide superior adaptation and bioactivity.

7. Definitive Restoration
  • IRR weakens dentin walls, especially coronally.
  • Post-endodontic crown often required to prevent fracture.

 

Prognosis:

  • Excellent if diagnosed early and managed appropriately.
  • Key success factors: Thorough cleaning, complete obturation, and restorative reinforcement.

 

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Treatment of Perforating Internal Root Resorption

Perforation complicates treatment, as it introduces a direct communication between the root canal and periodontal tissues. The prognosis is more guarded, and treatment is more complex.

A. Non-Surgical Repair (When Accessible Intraradicularly)

Same initial steps as non-perforating cases

After debridement, identify the site of perforation

Place resorption barrier and repair material: Use Mineral Trioxide Aggregate (MTA) or bioceramic materials:

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  • Biocompatible
  • Seals against bacterial leakage
  • Promotes healing and cementogenesis

 

Complete obturation of remaining canal space

B. Surgical Repair (Apical or Lateral Perforations)

Required when perforation is not accessible from within the canal.

Surgical Approach:
  1. Flap reflection and access to perforation site
  2. Curettage of granulation tissue and inflamed periodontal ligament
  3. Retrograde sealing of the perforation with MTA/bioceramics
  4. Flap repositioning and suturing
  5. Post-op antibiotics and follow-up

 

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Materials Used:
  • MTA (ProRoot, Angelus)
  • Biodentine
  • EndoSequence BC RRM Putty

 

Note: These materials are moisture-tolerant, biocompatible, and induce tissue healing.

C. Intentional Replantation (Rare Cases)

  • Involves extracting the tooth, repairing the lesion extraorally, and replanting it.
  • Indicated in cases where access is impossible surgically or orthograde.
  • Success depends on minimal trauma, extraoral time (<10 minutes), and careful handling.

 

Management of Arrested or Inactive IRR

  • If the lesion is asymptomatic, non-perforating, and not progressing, some clinicians opt for monitoring.
  • Regular follow-up with radiographs every 6–12 months is essential.
  • Vitality testing can guide whether intervention is eventually needed.

 

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Important: Even arrested lesions may become reactivated due to trauma or infection.

Post-Treatment Considerations

A. Restoration

Teeth affected by IRR are structurally weakened.

A full-coverage crown is typically recommended, especially in posterior teeth, to:

  • Prevent fracture
  • Distribute occlusal forces
  • Seal the access cavity

 

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B. Periodontal Management

If the perforation involved periodontal tissue:

  • Monitor for attachment loss or pocket formation
  • Consider regenerative procedures if indicated
  • C. Follow-Up Protocol
  • First follow-up: 3 months post-treatment (clinical + radiographic)
  • Then: 6 months, then annually for 2–4 years

 

Evaluate for:

  • Healing of periapical tissues
  • Radiographic stability or resolution
  • Absence of symptoms (pain, swelling, sinus tract)

 

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Extraction and Replacement

If the tooth is deemed non-restorable due to:

  • Extensive perforation
  • Severe structural loss
  • Vertical root fracture
  • Recurrent infection

 

Then extraction is the treatment of choice.

Replacement Options:

  • Dental implant
  • Fixed partial denture (bridge)
  • Removable prosthesis
  • Orthodontic space closure (especially in young patients)

 

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Early identification of untreatable lesions allows for proactive planning and minimizes disruption to oral function.

Summary of Treatment by Lesion Type

Lesion TypeTreatment ModalityPrognosis
Non-perforating, activeRCT + thermoplastic obturationExcellent
Non-perforating, inactiveMonitor or RCT if neededGood
Perforating, accessibleRCT + MTA repairFair to good
Perforating, inaccessibleSurgical repair / replantationGuarded
Extensive, non-restorableExtraction + replacementDependent on patient factors

Emerging Therapies and Future Directions

Research into regenerative endodontics, stem cell therapy, and nanomaterials may offer future possibilities for:

  • Pulp–dentin complex regeneration
  • Targeted inhibition of odontoclasts
  • Biomimetic restoration of lost structure

 

However, these remain experimental and are not yet standard of care.

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Prognosis of Internal Root Resorption

The prognosis of internal root resorption (IRR) varies widely depending on multiple factors, including the extent of the lesion, timing of diagnosis, presence or absence of perforation, quality of treatment, and post-treatment restoration. With early detection and proper endodontic management, particularly in non-perforating cases, the long-term outlook is often favorable. However, in advanced or perforating lesions, the prognosis becomes more guarded.

Proper prognosis assessment is essential to:

  • Help guide treatment decisions (conservative vs. surgical vs. extraction)
  • Set realistic expectations with patients
  • Plan appropriate follow-up protocols
  • Prevent future complications like fractures or reinfection

 

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Key Factors Influencing Prognosis

A. Extent and Size of the Lesion

  • Smaller, localized lesions with minimal canal distortion are easier to disinfect and fill.
  • Large lesions, especially those causing significant thinning of the root walls, increase the risk of tooth fracture, incomplete obturation, and treatment failure.

 

B. Location of the Lesion

  • Coronal and middle third lesions are generally more accessible and manageable.
  • Apical lesions may be harder to clean, shape, and seal, particularly in curved roots or anatomically complex canals.

 

C. Perforation Status

  • Non-perforating IRR: Has an excellent prognosis when treated early and properly.

  • Perforating IRR: Significantly lowers prognosis due to:

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    • Communication with the periodontium

    • Risk of persistent infection

    • Difficulty in sealing and restoring

Perforation increases the likelihood of endodontic failure or the need for surgical intervention or extraction.

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D. Pulp Vitality and Lesion Activity

  • Active resorption implies partially vital pulp; if diagnosed and treated during this stage, resorptive activity can be halted.
  • Arrested lesions may not need immediate treatment unless structurally compromised, but may reactivate under new stress (e.g., trauma, reinfection).

 

E. Presence of Infection or Symptoms

  • Asymptomatic teeth with no periapical pathology have a better prognosis.
  • Presence of pain, swelling, sinus tract, or apical periodontitis correlates with a poorer outcome, particularly if the infection is chronic or involves the periodontium.

 

F. Quality of Endodontic Treatment

  • Effective treatment relies on:

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    • Complete removal of inflamed pulp and odontoclasts

    • Thorough cleaning and shaping

    • Use of biocompatible, hermetic sealers and obturation materials

    • A coronal seal that prevents reinfection

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G. Quality of Final Restoration

  • Teeth with IRR are structurally weakened, especially after access and debridement.
  • Post-endodontic crowns or full-coverage restorations significantly reduce fracture risk and improve long-term survival.

 

H. Patient-Related Factors

  • Age, oral hygiene, systemic health, and compliance with follow-up visits influence prognosis.
  • Teeth in patients with high caries risk, poor periodontal status, or parafunctional habits (e.g., bruxism) are more likely to fail prematurely.

 

Prognostic Classifications

Several authors and clinicians have proposed frameworks for categorizing the prognosis of IRR:

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Simple Classification Based on Treatability:

Lesion TypePrognosisComments
Non-perforating, smallExcellentHigh success rate with conventional RCT
Non-perforating, largeGoodRequires thermoplastic obturation; structurally sound
Perforating, accessibleFairNeeds MTA repair; success depends on location and sealing
Perforating, inaccessiblePoorSurgical access or intentional replantation may be needed
Extensive, non-restorableHopelessExtraction recommended

Prognosis Based on Treatment Modality

TreatmentSuccess RatePrognosis
Conventional RCT (non-perforating)~90–95%Excellent
RCT with MTA repair (perforating)~70–80%Good to fair
Surgical repair (perforating)~60–75%Guarded
Intentional replantation~50–65%Variable
Extraction and prosthetic replacementVariesDependent on patient compliance and prosthetic plan

Long-Term Outcomes and Evidence

While there is limited large-scale, long-term data on IRR specifically, studies on endodontic treatment of resorptive defects have reported:

  • High success rates when lesions are detected early and treated with thermoplastic obturation and proper sealing.
  • Bioceramic sealers and MTA offer superior healing outcomes due to their biocompatibility, antibacterial properties, and ability to promote periapical tissue regeneration.
  • Teeth that receive a post-endodontic crown show significantly longer survival than those with temporary or no full-coverage restoration.

 

Complications Affecting Prognosis

A. Vertical Root Fracture

  • Thin dentin walls from resorption weaken the root structure.
  • Post-operative fractures can occur even years after successful treatment, especially in the absence of coronal coverage.

 

B. Recurrent Resorption

Although rare after thorough RCT, reactivation of resorption may occur due to new trauma, reinfection, or systemic factors.

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C. Periodontal Breakdown

  • Perforating lesions may lead to localized periodontitis, especially if not properly sealed.
  • Deep periodontal pockets and bone loss can jeopardize tooth stability.

 

D. Persistent Infection

Failure to completely eliminate necrotic pulp or bacteria may lead to chronic apical periodontitis and eventual treatment failure.

Patient Communication and Counseling

When discussing prognosis with patients:

  • Use visual aids (radiographs, 3D models) to explain lesion location and extent.
  • Discuss risks and benefits of treatment options, including surgery or extraction.
  • Emphasize the importance of follow-up visits and permanent restoration.
  • Address expectations realistically, especially in advanced or perforating cases.

 

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A well-informed patient is more likely to accept treatment and comply with long-term care.

Follow-Up and Monitoring

Regardless of the lesion’s severity, long-term follow-up is essential to monitor healing and detect signs of failure early.

Recommended Protocol:

  • 3 months post-op: Clinical and radiographic review
  • 6 months: Assess for periapical healing and symptom resolution
  • Annually for at least 2 years: Serial radiographs to ensure stability or healing

 

CBCT can be used selectively when conventional radiographs are inconclusive or to monitor complex cases.

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Summary: Prognosis at a Glance

Prognosis LevelKey FactorsManagement Goals
ExcellentSmall, non-perforating lesion, early diagnosis, complete RCTPreserve structure, monitor
GoodModerate lesion, proper sealing, good accessReinforce tooth, full-coverage crown
FairPerforation accessible for MTA repairPrevent reinfection, surgical follow-up
PoorLarge perforation, advanced destruction, inaccessibleConsider surgical or extraction
HopelessNon-restorable toothPlan for replacement (implant/bridge)

 

Prevention of Internal Root Resorption

Although internal root resorption (IRR) is relatively rare, it is often silent in its early stages and can lead to serious complications, including perforation, root fracture, and ultimately tooth loss if not detected and managed early. Therefore, prevention is key—both in avoiding its initiation and ensuring early identification to minimize damage.

Preventive efforts should focus on:

  • Identifying risk factors early
  • Minimizing iatrogenic injury
  • Promptly treating pulpitis or trauma
  • Educating patients and dental professionals
  • Utilizing appropriate follow-up and imaging

 

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Prevention can be divided into three major categories: primary, secondary, and tertiary prevention.

Primary Prevention

Goal: Prevent the onset of IRR by reducing risk factors and maintaining pulpal health.

A. Prevent and Manage Dental Trauma

  • Use mouthguards in contact sports to reduce trauma risk, especially in children and adolescents.
  • Educate patients and parents about the importance of immediate dental care after trauma (even minor).

 

In trauma cases:

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  • Monitor the tooth long-term, even if initially asymptomatic.
  • Schedule periodic radiographs to detect early internal changes.

 

B. Minimize Pulpal Inflammation

  • Manage deep caries promptly to avoid pulpal exposure or chronic pulpitis.
  • Avoid delaying root canal treatment in symptomatic teeth.
  • Use biocompatible pulp capping materials (e.g., calcium hydroxide, MTA) when treating near-pulp exposures.

 

C. Prevent Iatrogenic Injury

During operative and endodontic procedures:

  • Avoid over-instrumentation or excessive pressure.
  • Prevent thermal injury during tooth preparation by using water-cooled handpieces.
  • Use gentle irrigation techniques to avoid pushing irrigants beyond the apex or into lateral canals.

 

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Avoid using cytotoxic materials (e.g., formaldehyde-based pastes).

D. Use Controlled Orthodontic Forces

Excessive orthodontic forces can initiate pulpal inflammation and resorption.

Orthodontists should:

  • Use light, controlled, intermittent forces
  • Perform baseline and periodic radiographic monitoring
  • Evaluate root morphology and previous endodontic history before initiating treatment

 

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E. Avoid Overzealous Bleaching Techniques

  • Do not use heat-activated bleaching in non-vital teeth.
  • Avoid placing bleaching agents directly into canals beyond the cervical seal.
  • Seal the canal orifice with a protective barrier (e.g., glass ionomer) during internal bleaching.

 

F. Educate and Train Dental Professionals

Enhance awareness of IRR in dental school curricula and continuing education.

Train clinicians to recognize early signs such as:

  • Pink discoloration
  • Subtle radiographic ballooning of the root canal
  • Sensitivity without obvious cause

 

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Secondary Prevention

Goal: Detect IRR early before it progresses or causes structural damage.

A. Regular Radiographic Monitoring

Routine bitewing and periapical radiographs are essential, especially in:

  • Previously traumatized teeth
  • Teeth with deep restorations
  • Orthodontically moved teeth
  • Endodontically treated teeth

 

Use angulated radiographs to catch lesions not visible in straight-on views.

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B. Use of Cone Beam Computed Tomography (CBCT)

When conventional radiographs suggest possible IRR, CBCT is invaluable for:

  • Early confirmation
  • Locating and measuring the lesion
  • Distinguishing IRR from external resorption

 

CBCT is especially useful in symptom-free or ambiguous cases.

C. Periodic Clinical Exams

Check for early clinical signs:

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  • Pink hue in crowns
  • Unexplained sensitivity to thermal stimuli
  • Slight mobility

 

Conduct pulp vitality tests on suspicious or previously traumatized teeth.

Evaluate changes in tooth translucency or color in anterior teeth.

D. Maintain Long-Term Follow-Up for High-Risk Teeth

  • Traumatized or immature teeth need follow-up for at least 5 years.

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  • Set reminders for patients to return for annual reviews.

  • Maintain detailed patient records, including:

    • Trauma history

    • Orthodontic interventions

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    • Pulpal treatments

 

Tertiary Prevention

Goal: Prevent complications or progression of established IRR lesions.

A. Early Intervention

When IRR is detected, act swiftly with root canal therapy before:

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  • Resorption expands
  • Perforation occurs
  • Structural collapse takes place

 

Use bioceramic sealers and thermoplastic obturation to fill irregular defects effectively.

B. Preserve Tooth Structure

  • Avoid excessive removal of tooth during access and cleaning.
  • Consider fiber-reinforced composites, intraradicular posts, or crowns to reinforce weakened teeth.

 

C. Periodontal Maintenance

In cases of perforation, monitor periodontal health:

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  • Treat gingival inflammation or pocketing promptly
  • Consider guided tissue regeneration (GTR) techniques after surgical repair

 

D. Monitor Treated Teeth

Schedule post-op radiographs at:

  • 3 months
  • 6 months
  • 12 months
  • Annually for 2–4 years

 

Watch for:

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  • Periapical radiolucency
  • Structural changes
  • Signs of reinfection or continued resorption

 

E. Prevent Further Pulpal Insults

  • Reinforce proper oral hygiene practices to prevent secondary caries.

  • Educate patients on the importance of:

    • Fluoride use

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    • Diet control (limit sugary and acidic foods)

    • Using protective appliances if bruxism or clenching is suspected

 

Prevention in Specific Patient Populations

Children and Adolescents

  • High-risk group due to trauma, immature teeth, and sports involvement.
  • Educate schools, parents, and pediatricians.
  • Advocate for sports mouthguards and trauma-first-aid protocols.

 

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Orthodontic Patients

  • Schedule pre-treatment evaluation with radiographs.
  • Delay treatment on traumatized or recently endodontically treated teeth until they are stable.
  • Use slow, controlled tooth movement.

 

Patients with History of Resorption

  • If a patient has had IRR in one tooth, others may be at risk.
  • Consider baseline CBCT or more frequent recall visits.
  • Monitor for idiopathic or systemic triggers (e.g., hyperparathyroidism).

 

System-Based Preventive Strategies

A. Practice Protocols

  • Develop checklists for trauma follow-ups and deep caries management.

  • Implement recall systems to ensure patients return for reviews.

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  • Train dental staff to ask patients about:

    • Past trauma

    • Sensitivity or color changes

    • Orthodontic or bleaching history

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B. Patient Education

Use brochures, visual aids, and chairside discussions to:

  • Encourage routine check-ups
  • Alert patients to signs like pink discoloration
  • Explain the risks of trauma and home bleaching kits

 

Summary Table: Preventive Approaches

Prevention TypeActionsTarget
PrimaryPrevent trauma, limit pulp injury, safe bleaching, orthodontic careStop IRR from starting
SecondaryRadiographs, CBCT, vitality testing, trauma follow-upCatch IRR early
TertiaryEarly RCT, repair, periodontal care, reinforcementStop progression and restore function
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