Pathological Root Resorption: Causes, Types, Diagnosis, and Treatment

Root resorption refers to the breakdown of hard dental structures caused by multinucleated giant cells, such as osteoclasts and odontoclasts. This phenomenon can be categorized as either physiological or pathological and may affect both primary and permanent teeth. Physiological resorption plays a natural role in the shedding of primary teeth, whereas pathological resorption is typically linked to dental trauma, carious lesions, or iatrogenic factors, often complicating treatment and prognosis. 

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In dental practice, accurate treatment planning and prognosis assessment require a solid grasp of pathological processes, including root resorption. Although commonly encountered, its impact on clinical outcomes is frequently overlooked. Root resorption leads to the gradual degradation of mineralized dental tissues and surrounding alveolar bone due to the activity of resorptive cells. While physiological resorption is essential for the normal exfoliation of primary teeth, pathological resorption in permanent teeth is considered abnormal, as protective structures—precementum from cementoblasts and predentin from odontoblasts—ordinarily inhibit the attachment of resorptive cells. When these protective barriers are compromised, external factors can trigger and sustain the resorption process unless properly addressed.

Classification of Root Resorption 

Currently, there is no universally accepted classification of pathological root resorption. However, root resorption can be categorized based on its progression, location, depth of tissue involvement, and underlying etiology.

1. Classification by Progression:

• Transient resorption: Self-limiting and reversible.
• Progressive resorption: Continuous destruction of mineralized tissues, often requiring intervention.

1. Classification by Location:

• Internal Resorption: Occurs within the pulp chamber or root canal, often due to chronic pulp inflammation or infection.
• External Resorption: Initiates from the root surface and progresses inward, further categorized as:
  • Apical Resorption: Affects the root apex, often seen after trauma or orthodontic treatment.
  • Mid-Root Resorption: Affects the central portion of the root, commonly due to pressure from adjacent structures.

Cervical Resorption: Occurs near the cementoenamel junction (CEJ), often idiopathic or associated with trauma and bleaching procedures.

        3. Classification by Etiology:

• Inflammatory apical resorption: Associated with chronic periapical inflammation.
• Inflammatory lateral resorption: Linked to post-traumatic pulp necrosis.
• Cervical (idiopathic) resorption: Often of unknown origin.
• Ankylosis and replacement resorption: Occurs due to fusion between root surfaces and alveolar bone.
• Resorption secondary to systemic conditions: Includes cases associated with endocrine disorders or metabolic diseases.
• Resorption caused by mechanical trauma: Induced by orthodontic treatment, excessive occlusal forces, or dental prosthetics.

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Pathophysiology of Root Resorption 

The initiation of resorption involves localized tissue damage, leading to the recruitment of resorptive cells such as osteoclasts, cementoclasts, and odontoclasts. These cells share ultrastructural and histochemical similarities and are activated under pathological conditions. The resorption process occurs extracellularly along the osteoclast membrane-bone interface, involving:

1. Demineralization via dissolution of the inorganic matrix due to localized pH reduction.
2. Enzymatic degradation of the organic matrix by proteolytic enzymes such as cysteine proteases and matrix metalloproteinases (MMPs).

Diagnostic Approaches of Root Resorption 

Early diagnosis of root resorption is critical for successful management. Diagnostic tools include:

• Radiographic Techniques: Periapical radiographs, cone-beam computed tomography (CBCT), and panoramic imaging are commonly used.
• Pulp Vitality Testing: Electrical pulp testing (EPT) and thermal sensitivity tests help differentiate between vital and necrotic pulp states.
• Histological Analysis: In select cases, biopsy and histopathological examination provide insights into the nature of resorptive lesions.

Treatment of Pathological Root Resorption

The choice of treatment depends on resorption type and severity:

• Endodontic Therapy: Internal resorption is managed by root canal therapy using calcium hydroxide or bioceramic sealers to halt resorptive activity.
• Surgical Management: External cervical resorption may require surgical debridement and restoration with glass ionomer cement or mineral trioxide aggregate (MTA).
• Regenerative Approaches: Severe cases involving ankylosis may necessitate ridge preservation or orthodontic space closure to maintain function.

Preventive Strategies: Monitoring orthodontic forces, controlling occlusal trauma, and managing systemic conditions reduce resorption risk.

Treatment of Different Types of Root Resorption

1. Trauma-Induced Root Resorption

This category includes pathological resorption of dental tissues resulting from acute or chronic trauma (such as excessive pressure). It involves damage to the cement-periodontal complex, leading to the activation of osteoclasts. Notably, these resorption processes occur without infection. 

• Surface Resorption

Surface resorption occurs as a result of mild dental trauma. It is nearly impossible to detect radiographically and is considered the least problematic form of resorption. Clinically, it remains limited to the cementum, and over time, the defect undergoes natural repair. No treatment is necessary, surface resorption is self-limiting as long as the initiating factor (e.g., trauma) is removed. Histologically, this process involves small lacunae filled with new cementum.

• Transient Apical Internal Resorption

First described by J. Andreasen in 1986, this form of trauma-induced resorption can arise from incomplete tooth luxation, lateral luxation, orthodontic treatment, or continuous occlusal trauma. It is associated with the phenomenon of transient apical breakdown, appearing radiographically as a localized radiolucency in the apical region of the tooth root.

Clinically, the tooth may exhibit discoloration, and responses to thermal tests can be either positive or negative. In most cases, the pulp remains vital. If the damaging factor is removed, spontaneous resolution is likely within a few months due to the good blood supply to the apical region and the pulp’s reparative capacity. In cases of pulpal necrosis, endodontic treatment should be initiated.

Treatment: A watchful waiting approach is recommended. If the condition does not resolve within six months or symptoms of periodontitis appear, endodontic treatment with root canal obturation is necessary.

• Pressure-Induced and Orthodontic Resorption

This broad category includes resorption due to prolonged mechanical pressure, such as from an impacted tooth, neoplasms, or incorrect orthodontic treatment. It is characterized by the loss of hard dental tissues at the site of pressure application.

Studies indicate that root resorption from orthodontic treatment occurs more frequently in adults than in adolescents, and more often in women than in men. Additionally, resorption progresses more slowly in patients who have undergone prior orthodontic treatment compared to those receiving it for the first time. Some studies suggest that adolescents are more susceptible due to their higher cellular activity. However, adults may show more severe resorption when it occurs because of their slower reparative response. Excessive force is the primary cause, and progression halts upon removal of the orthodontic appliance. While cementum regeneration occurs in an intact periodontium, the apical structure of the root does not regenerate. However, some degree of repair may happen if the damage is limited to the cementum and does not extend deeply into dentin.

Treatment: Eliminating the mechanical pressure effectively stops the resorption process.

• Replacement Resorption (Ankylosis)

This is the most severe form of trauma-induced, non-inflammatory resorption. It results from periodontal cell death and precementum damage, often due to trauma or improper handling during tooth replantation.

In this process, dental tissues are slowly replaced by alveolar bone through a remodeling mechanism typical of bone tissue. Ankylosis occurs more rapidly in younger patients due to their high bone turnover rate. Clinically, it presents as loss of physiological tooth mobility, sometimes with a high percussion sound. Radiographically, the periodontal ligament space disappears, but the process is otherwise asymptomatic.

Treatment: Endodontic therapy does not halt this type of resorption. However, replacement resorption progresses slowly, and complete replacement of the tooth by alveolar bone can take years. A wait-and-see approach is recommended. However, if ankylosis is confirmed in a growing patient, intervention (such as decoronation) should be planned to preserve alveolar ridge development for future implant placement.

        2. Inflammation-Induced Root Resorption

Inflammatory resorption occurs as a reaction of the dentino-alveolar complex to infection. It involves the destruction of hard dental tissues and may originate from endodontic infections or be secondary to trauma-induced resorption. These resorptive processes can occur internally within the root system, externally on the cementum surface, or in a combined manner.

Despite variations in severity, inflammatory resorption generally has a favorable prognosis if the infectious agent is removed.

• Internal Inflammatory Resorption

This destructive process occurs exclusively within the root canal system or pulp chamber, characterized by dentin loss due to osteoclastic activity.

• Apical Internal Inflammatory Resorption

Recent studies suggest that this form of resorption is more prevalent in teeth with periapical inflammatory conditions than previously thought.

Treatment: Two approaches exist for managing this condition:

1. Instrumentation of the root canal up to the level of resorption, with the expectation that removing microorganisms will allow for tissue healing.
2. Expanding and preparing the apical portion of the root, including the resorbed area, followed by filling to the apex of the root canal.

Currently, no comparative studies have evaluated the long-term success of these two approaches. The key factor in success is thorough disinfection rather than simply choosing one approach over another.

• Intra-Canal Inflammatory Resorption

This process has two phases: an initial trauma-induced phase and a subsequent infection-driven phase. Trauma, such as excessive heat from improper tooth preparation, can lead to intra-pulpal bleeding. The resulting hematoma is replaced by granulation tissue, which, in turn, exerts pressure on dentin walls. Ongoing infection sustains osteoclastic differentiation and further resorption.

Clinical Features: This process is often painless, with possible positive or negative responses to vitality tests. Radiographically, an internal radiolucency is observed, though conventional two-dimensional radiography is limited in early diagnosis. Cone-beam computed tomography (CBCT) is the preferred diagnostic tool.

Treatment: Complete removal of both vital and necrotic pulp tissue is necessary to halt resorption. Standard endodontic procedures, including thorough sodium hypochlorite irrigation and temporary calcium hydroxide dressing, are recommended. The canal should be obturated using a combination of lateral condensation and warm gutta-percha techniques.

• External Inflammatory Resorption

This aggressive resorptive process typically results from an infection superimposed on trauma, such as following tooth replantation or luxation.

External inflammatory resorption is triggered by infection on the root surface, leading to osteoclastic activation and subsequent tissue destruction. However, the rate of resorption is influenced by the severity of injury to the precementum rather than just the presence of bacteria. The process is often asymptomatic but can be identified radiographically as bowl-shaped defects in the root and adjacent bone.

Endodontic pathology can also induce external resorption, requiring:

• Damage to the predentin, precementum, and cementum, compromising dentinal tubule sealing.
• Complete pulp necrosis with infection spreading into the root system.

Bacterial toxins from dentinal tubules can reach the periodontium, triggering an inflammatory response that sustains osteoclastic activity and leads to concurrent resorption of both the tooth and surrounding bone. This mechanism is particularly aggressive in young teeth due to their larger dentinal tubule diameters.

Treatment: The primary goal is eliminating the infectious agent responsible for sustaining resorption.

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Prognosis and Prevention

The prognosis depends on the extent of resorption and the effectiveness of intervention. Internal resorption treated early with root canal therapy has a favorable prognosis, while advanced external resorption may lead to tooth loss. Preventive measures, such as timely diagnosis, reducing excessive orthodontic forces, and addressing systemic risk factors, are key to preserving dental integrity.

In conclusion, root resorption remains a significant challenge in endodontic and periodontal practice. Timely diagnosis, differentiation between external and internal resorption, and the use of advanced imaging techniques such as CBCT are critical for successful treatment outcomes. When feasible, high-quality endodontic therapy should be prioritized to preserve the affected tooth. However, in cases of severe external resorption or extensive defects, extraction and subsequent ridge preservation may be necessary. Further research into the underlying molecular mechanisms of root resorption and improved biomaterials for defect restoration will enhance future treatment strategies.