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Tooth resorption

Tooth resorption is a physiological or pathological process involving the loss of dental hard tissues, such as dentin and cementum, and occasionally bone, mediated by odontoclastic activity and distinct from caries, restorative procedures, or trauma-induced fractures.^[1] Pathological resorption is relatively uncommon in permanent teeth, affecting approximately 1-5% in the general population but up to 90% in cases of dental trauma or orthodontics, with external forms being more prevalent than internal.^[2]^[3] This condition can affect both primary and permanent teeth, with physiological resorption occurring naturally during the shedding of deciduous teeth, while pathological resorption represents an abnormal, often progressive destruction that may lead to tooth loss if untreated. It is classified primarily as internal root resorption (originating from the pulp chamber or root canal) or external root resorption (originating from the periodontal ligament or external tooth surface), each with subtypes that influence diagnosis and management.^[4] Internal resorption typically arises from inflammatory processes within the pulp, such as following trauma or pulp necrosis, leading to a radiolucent enlargement of the pulp canal visible on radiographs and sometimes presenting clinically as a pinkish hue through the crown due to vascular granulation tissue.^[1] External resorption encompasses several forms, including inflammatory (associated with chronic infection or apical periodontitis), replacement (where resorbed tooth structure is substituted by bone, often post-trauma leading to ankylosis), surface (mild, self-limiting resorption of cementum), and invasive cervical (a more aggressive, idiopathic or trauma-related erosion at the cementoenamel junction).^[2] Other variants include pressure resorption from orthodontic forces or adjacent tumors, and idiopathic forms without clear etiology.^[4] The etiology of pathological tooth resorption is multifactorial, commonly involving dental trauma (e.g., luxation or avulsion injuries activating clastic cells), microbial invasion from untreated caries or failed endodontics, excessive orthodontic pressures exceeding physiological limits, or systemic factors like hypoparathyroidism in rare cases.^[1] Many cases remain asymptomatic until advanced stages, when symptoms such as tooth mobility, pain on percussion, or sinus tract formation may emerge, underscoring the importance of routine radiographic monitoring for early detection.^[2] Diagnosis relies on clinical examination combined with imaging modalities like periapical radiographs or cone-beam computed tomography (CBCT) to delineate the extent and type of resorption.^[4] Treatment strategies are tailored to the resorption type, location, and severity; for instance, non-surgical root canal therapy with calcium hydroxide or bioceramic materials can arrest inflammatory internal resorption if the pulp is non-vital and perforation is absent, while external cervical resorption often requires surgical intervention using trichloroacetic acid to devitalize resorptive tissue followed by restoration.^[1] Replacement resorption generally lacks direct treatment and may necessitate decoronation to manage infraocclusion in growing patients, whereas mild surface or pressure resorption can resolve upon removal of the causative factor, such as orthodontic appliance adjustment.^[2] In severe or untreatable cases, extraction is indicated to prevent complications like infection spread or functional impairment, highlighting the need for multidisciplinary dental care to preserve tooth vitality and oral health.^[4]

Overview and Epidemiology

Definition

Tooth resorption is defined as the physiologic or pathologic loss of dentin, cementum, and/or bone, not immediately attributable to caries or trauma, mediated by the activity of odontoclasts or osteoclast-like cells that produce resorption lacunae on dental hard tissues.^[1]^[5] These multinucleated cells, analogous to osteoclasts but typically smaller with fewer nuclei, attach to mineralized tooth surfaces and resorb structure through acidic and enzymatic mechanisms.^[5] In permanent teeth, this process is invariably pathological and progressive, potentially leading to tooth weakening or loss if unchecked.^[6] Unlike the normal exfoliation of primary teeth, where resorption is a controlled physiological event facilitating eruption of permanent successors, pathological tooth resorption in permanent dentition represents an aberrant breakdown without restorative intent.^[1] Physiological resorption in deciduous teeth involves coordinated odontoclastic activity triggered by inflammatory signals from the erupting permanent tooth, culminating in root dissolution and shedding, whereas in permanent teeth, it disrupts structural integrity without such programmed resolution.^[4] Tooth resorption was first described in the early 19th century by Thomas Bell, who identified absorptive defects in tooth structure in his 1829 treatise on dental anatomy and diseases.^[7] Modern understanding of the condition, particularly the central role of odontoclast activity in resorptive mechanisms, emerged in the 1970s through advances in histologic and radiographic studies that differentiated clastic cell involvement from earlier vague notions of "absorption."^[7] Tooth resorption may occur internally within the root canal system or externally along the root surface, though detailed classification follows separate considerations.^[1]

Prevalence and Risk Factors

Tooth resorption exhibits variable prevalence depending on the type and detection method, with external forms generally more common than internal resorption. Radiographic studies, particularly those using cone-beam computed tomography (CBCT), report external resorption in up to 20-30% of cases examined, reflecting higher detection rates for subtle lesions compared to traditional periapical radiographs.^[8] In contrast, internal root resorption is rarer, with prevalence estimates ranging from 0.1% to 2% in clinical and radiographic assessments of permanent teeth.^[6] Specific subtypes like external cervical resorption show even lower rates, typically 0.02% to 0.08% in population-based epidemiological studies.^[9] Prevalence varies by region and detection method, with higher rates reported in some clinical settings.^[8] Demographic patterns indicate that tooth resorption is more frequently observed in adults aged 36 to 55 years, accounting for approximately 51% of detected cases in some radiographic surveys.^[10] Gender differences are minimal across broader cohorts, with some studies showing no significant association.^[6] Prevalence increases notably in orthodontic patients, where mild resorption can affect up to 45% of individuals undergoing treatment.^[11] General risk factors include age-related progression, with incidence rising gradually over time due to cumulative exposures.^[12] Genetic predispositions contribute in some cases, evidenced by familial patterns and associations with specific polymorphisms that heighten susceptibility, particularly to orthodontic-induced resorption.^[13] Systemic conditions like hypoparathyroidism are also linked, potentially through disruptions in calcium metabolism that promote resorptive activity.^[2]

Causes

Trauma to the teeth, particularly in permanent dentition, serves as a primary initiator of root resorption by mechanically disrupting the protective barriers surrounding the root structure. Acute dental injuries such as luxation and avulsion damage the periodontal ligament (PDL) and pulp, exposing the underlying dentin to clastic cells like osteoclasts, which are activated through inflammatory mediators including interleukin-1α (IL-1α) and tumor necrosis factor-α (TNF-α).^[14] This exposure triggers the RANKL/RANK/OPG signaling pathway, promoting osteoclast differentiation and subsequent resorption of root tissues.^[14] In severe cases, the loss of PDL integrity allows direct contact between resorptive cells and the root surface, leading to progressive breakdown if not arrested.^[14] Luxation injuries, involving displacement of the tooth within its socket, frequently result in external inflammatory root resorption due to combined damage to the cementum and pulp vitality, with the disrupted PDL facilitating bacterial invasion and sustained inflammation.^[14] For instance, intrusive luxation exhibits the highest association, with external resorption observed in up to 92.8% of cases among permanent teeth.^[15] Avulsion, the complete displacement of the tooth from its socket, heightens the risk even further, particularly following replantation, where the inflammatory response to damaged tissues and prolonged extraoral time can lead to replacement resorption in over 50% of instances, and up to 87.2% in some cohorts.^[14]^[15] Replantation exacerbates this by inducing an immune-mediated inflammatory cascade that replaces resorbed root dentin with bone-like tissue, often progressing without intervention.^[14] Chronic low-grade trauma, such as that from bruxism or habitual clenching, contributes to resorption through sustained excessive occlusal forces that induce microtrauma to the PDL and cementum, gradually exposing root surfaces to resorptive processes. This ongoing pressure disrupts the balance of bone remodeling, activating osteoclasts in a manner akin to acute injury but over an extended period, with studies linking it to progressive external root resorption in affected teeth. Overall prevalence of resorption following any dental trauma in permanent teeth ranges from 2.3% in adolescent populations to higher rates in severe injuries, underscoring the role of trauma severity in disease progression.^[14] These mechanisms intersect with broader inflammatory pathways, where initial mechanical damage amplifies immune responses leading to sustained resorption.^[14]

Infection and Inflammation

Infection and inflammation play a central role in driving tooth resorption through microbial invasion of the dental pulp or periodontal tissues, leading to the activation of resorptive processes. Pulpal necrosis, often resulting from untreated caries, creates an environment where bacteria proliferate within the root canal, triggering an inflammatory response in the adjacent periodontal ligament. Similarly, periodontal infections associated with periodontitis allow bacterial pathogens to invade the root surface, initiating localized inflammation. These infections stimulate the release of pro-inflammatory cytokines, such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α), from immune and stromal cells, which in turn upregulate receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). This cytokine-mediated signaling promotes the differentiation and activation of odontoclastic cells, which resorb dentin and cementum at the affected sites.^[16]^[17]^[18] Apical periodontitis, a common sequela of pulpal infection, is particularly linked to inflammatory root resorption, accounting for approximately 13.7% of identified resorption cases in cone-beam computed tomography scans of patients with periapical lesions. Chronic inflammation arising from failed endodontic treatments exacerbates this risk, with resorption observed in 43.1% of previously treated teeth compared to only 3.7% of untreated ones, due to persistent bacterial colonization and ongoing inflammatory mediator release. These conditions highlight how unresolved infections sustain the resorptive environment, distinguishing inflammatory resorption from other forms.^[8] If left untreated, such infections lead to progressive and persistent odontoclastic activity, particularly at the root apex, where blunting or widening of the apical foramen occurs as resorptive cells continue to degrade hard tissues under the influence of prolonged cytokine signaling. This unchecked process can result in extensive root loss and potential tooth perforation, underscoring the need for timely intervention to halt the inflammatory cascade. The underlying cellular and molecular mechanisms, including RANKL-RANK interactions, are explored in greater detail in the Pathophysiology section.^[16]^[8]

Iatrogenic Factors

Iatrogenic factors in tooth resorption refer to resorptive processes induced by dental interventions, where procedural techniques or materials inadvertently trigger odontoclastic activity. These cases often involve mechanical stress, chemical irritation, or thermal damage to the periodontal ligament, cementum, or pulp, leading to external or internal resorption subtypes. Unlike idiopathic or trauma-related causes, iatrogenic resorption is directly linked to treatment errors or inherent risks in procedures such as orthodontics, endodontics, and bleaching.^[19] Orthodontic treatment is a primary iatrogenic contributor, primarily through orthodontically induced external root resorption (OIRR), where applied forces cause compression of the periodontal ligament and subsequent hyaline degeneration, initiating pressure resorption. This affects the apical region most commonly, with nearly 80% of patients experiencing some degree of OIRR, though severe cases (exceeding 2 mm or one-third of root length) occur in 1-5% of patients. Incidence rises with heavy intermittent forces, prolonged treatment duration exceeding 12 months, and specific tooth movements like intrusion of maxillary incisors. Risk is further elevated in patients with predisposing factors such as short root form or prior trauma, prompting guidelines for radiographic monitoring every 6 months during active treatment.^[20]^[19]^[21] Endodontic procedures can provoke internal root resorption through pulp irritation or mechanical injury, such as over-instrumentation causing pulp necrosis or perforation, which allows clastic cells access to dentin. This iatrogenic internal resorption typically begins multilocularly near the pulp canal and progresses slowly if untreated, often asymptomatic until advanced. Overfilling or inadequate obturation may also contribute by inducing chronic inflammation, with case reports highlighting its occurrence post-root canal therapy in non-vital teeth.^[22]^[23]^[24] Bleaching agents, particularly in non-vital internal bleaching, pose risks for external cervical root resorption due to chemical diffusion through dentinal tubules, especially when combined with heat application in thermo-catalytic methods. Hydrogen peroxide at concentrations above 30% can weaken cementum and trigger inflammatory resorption at the cervical third, with historical incidence linked to over 20 cases in early reports, though modern walking bleach techniques reduce this risk. This complication is more prevalent in anterior teeth with prior endodontic treatment, emphasizing the need for barriers like glass ionomer seals during procedures.^[25]^[26]^[27] Restorative procedures, including deep cavity preparations or ill-fitting crowns, may irritate the pulp via thermal or bacterial ingress, fostering conditions for internal resorption in vital teeth. Such iatrogenic events are less common but documented in cases of excessive heat during crown fabrication without adequate cooling, leading to pulp hyperemia and resorptive defects.^[23]^[22]

Idiopathic and Systemic Causes

Idiopathic tooth resorption refers to pathological resorption of dental hard tissues without an identifiable local or systemic trigger. This condition is relatively uncommon, with prevalence rates for specific subtypes such as idiopathic external cervical root resorption estimated at 0.02% to 2.3% in population studies.^[28] Cases often involve multiple teeth and progress insidiously, potentially leading to significant root loss if undetected. Genetic predisposition plays a role in many instances, with familial aggregation observed in external apical root resorption and heritability estimates indicating a genetic contribution of up to 64% in orthodontic contexts.^[29] Polymorphisms in genes like IL1B, IL6, and P2RX7 have been associated with heightened susceptibility to resorption, influencing inflammatory and osteoclastic pathways.^[30] Systemic diseases can precipitate tooth resorption through dysregulated mineral metabolism or immune responses affecting periodontal structures. Endocrine disorders, including hypoparathyroidism and hyperparathyroidism, disrupt calcium homeostasis and have been linked to external root resorption in affected individuals.^[31] Paget's disease of bone, marked by aberrant osteoclast activity and excessive remodeling, is another established systemic cause, resulting in irregular resorption patterns around tooth roots.^[32] Hormonal imbalances, such as estrogen deficiency following menopause, exacerbate root resorption risk by elevating RANKL/OPG ratios and promoting inflammatory osteoclastogenesis, particularly in orthodontically stressed teeth.^[33] Rare associations exist with autoimmune conditions like systemic sclerosis (scleroderma), where multiple invasive cervical resorptions may occur due to fibrotic and immune-mediated damage to cementum and dentin.^[34] Other systemic links include Gaucher's disease and Turner's syndrome, both involving altered bone turnover that extends to dental structures.^[32] Overall, resorption tied to these systemic factors is infrequent, comprising less than 1% of diagnosed cases and primarily documented through case reports rather than epidemiological data.^[35]

Pathophysiology

Resorptive Processes

Tooth resorption initiates when protective layers of the tooth, such as the cementum on the root surface or the predentin and odontoblast layer internally, are damaged, exposing the underlying mineralized dentin to odontoclastic activity.^[5] This exposure occurs due to various insults, allowing multinucleated odontoclasts—derived from hematopoietic precursors—to attach to the denuded surface via integrin receptors and arginine-glycine-aspartic acid (RGD) motifs in the extracellular matrix.^[36] Upon attachment, these cells form initial resorption lacunae, marking the onset of tissue breakdown at the tissue level.^[5] The progression of resorption involves odontoclasts actively dissolving mineralized tissues through a combination of acidic and enzymatic mechanisms. These cells create localized acidic microenvironments via proton pumps, secreting hydrochloric acid to demineralize hydroxyapatite, while enzymes such as tartrate-resistant acid phosphatase (TRAP), cathepsin K, and matrix metalloproteinases (MMPs) degrade the organic matrix.^[36] This results in characteristic Howship's lacunae—pitted resorption bays on the tooth surface—contrasting with the smoother demineralization fronts observed in dental caries.^[36] The process advances as odontoclasts migrate along the exposed surface, progressively eroding dentin and cementum until repair mechanisms, such as cementum deposition, may intervene.^[5] Unlike dental caries, which is driven by bacterial demineralization and biofilm formation, true tooth resorption is typically a sterile, odontoclast-mediated process without direct microbial involvement.^[36] While secondary infection can complicate some cases, the core resorptive sequence relies on host cellular responses to injury rather than pathogenic invasion.^[5]

Cellular and Molecular Mechanisms

Tooth resorption is primarily driven by odontoclasts, specialized multinucleated cells derived from hematopoietic precursors such as circulating TRAP-positive monocytes, which differentiate and fuse to form giant resorptive cells capable of degrading mineralized dental tissues. Unlike osteoclasts, which resorb bone and form larger Howship's lacunae, odontoclasts are typically smaller, possess fewer nuclei (often 2-10 compared to 10-20 in osteoclasts), and generate more superficial, smaller resorption pits on root dentin surfaces. This distinction arises from their adaptation to the unique composition of dental hard tissues, including higher mineral content and lack of vascularity, though both cell types share a common monocyte-macrophage lineage and express similar markers like tartrate-resistant acid phosphatase (TRAP) and cathepsin K. The core molecular regulation of odontoclast formation and activation occurs via the RANKL/RANK/OPG signaling pathway, where receptor activator of nuclear factor kappa-B ligand (RANKL), secreted by periodontal ligament (PDL) fibroblasts, odontoblasts, and cementoblasts, binds to RANK receptors on odontoclastic precursors to trigger proliferation, fusion into multinucleated forms, and enhanced resorptive enzyme production. Osteoprotegerin (OPG), a decoy receptor produced by the same stromal cells, counteracts this by sequestering RANKL, thereby inhibiting odontoclastogenesis and maintaining homeostasis in dental tissues. In response to inflammatory stimuli, cytokines such as interleukin-1 (IL-1α and IL-1β) and tumor necrosis factor-alpha (TNF-α) from inflamed PDL tissues amplify the pathway by upregulating RANKL expression while suppressing OPG, leading to increased odontoclast recruitment and activity at resorption sites. The resorption process is self-limiting when the inciting stimulus is removed, as OPG induction triggers apoptosis in mature odontoclasts via caspase activation and detachment from the resorption surface, effectively halting further tissue breakdown.

Classification

Internal Root Resorption

Internal root resorption originates from the pulpal surface within the tooth structure, primarily affecting the walls of the root canal and leading to progressive loss of dentin.^[37] This process begins in the pulpal space due to chronic inflammation, involving damage to the odontoblastic layer, predentin, and organic sheath, which exposes the dentin to resorptive cells.^[37] It is typically asymptomatic in its early stages, often remaining undetected until advanced, when it may present as a pinkish hue on the crown—known as the "pink tooth of Mummery"—caused by vascular granulation tissue filling the enlarged pulp chamber and visible through thinned dentin or enamel.^[38] The condition is classified into two main subtypes based on the underlying mechanism and tissue response. Inflammatory internal root resorption is linked to pulp necrosis, where bacterial by-products from the coronal pulp stimulate odontoclastic activity, resulting in persistent resorption unless interrupted by treatment.^[39] In contrast, replacement internal root resorption involves a reparative process, where low-grade irritation leads to deposition of bone-like or cementum-like tissue in the resorbed areas, potentially stabilizing the defect if inflammation is minimal.^[38] Unlike external resorption, which initiates from the tooth's surface, internal resorption is confined to the endodontic space until potential perforation.^[37] The prevalence of internal root resorption in permanent teeth is relatively low, estimated at 0.01% to 1% in the general population, though it may be higher in cases of prior pulpitis or necrosis, and it is often underdiagnosed due to its insidious onset.^[38] A 2025 study introduced a novel classification system to stage the extent of internal resorption, dividing it into three levels: coronal (affecting the pulp chamber), cervical (at the neck of the tooth), and root (further subdivided into coronal, middle, and apical thirds).^[37] This classification also considers the depth of involvement, ranging from dentin-only resorption to perforating lesions extending through enamel or cementum, aiding in better prognostic assessment and management planning.^[37]

External Inflammatory Root Resorption

External inflammatory root resorption (EIRR) is a pathological condition characterized by the progressive loss of tooth root structure due to odontoclastic activity on the external root surface, primarily driven by inflammatory processes associated with bacterial infection.^[36] It typically manifests as radiolucent areas at the root apex on radiographs, reflecting the destruction of cementum and dentin, and is often linked to pulp necrosis following dental trauma such as luxation injuries.^[1] If left untreated, EIRR progresses rapidly, potentially leading to significant root loss and tooth mobility.^[40] The condition arises from a combination of injury to the root cementum and subsequent pulp necrosis, allowing bacterial invasion through the periodontal ligament and dentinal tubules.^[36] Bacterial toxins stimulate the recruitment and activation of odontoclasts, mediated by pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which perpetuate the resorptive process.^[36] This differs from internal root resorption, which originates from within the pulp chamber, as EIRR involves external periodontal inflammation and is typically more aggressive due to ongoing infection.^[1] EIRR is particularly prevalent following severe traumatic injuries, with studies reporting an incidence of approximately 23% after avulsion and replantation of permanent teeth.^[41] It is often subclinical in early apical stages, associated with chronic apical periodontitis, but can become symptomatic with pain and swelling as inflammation intensifies.^[40] In contrast to external surface resorption, which is superficial and self-limiting, EIRR penetrates deeper into the root due to persistent inflammatory stimuli and lacks the reparative potential seen in transient forms.^[1]

External Surface Root Resorption

External surface root resorption is a superficial, noninflammatory form of external root resorption characterized by shallow, saucer-shaped pits or defects limited to the cementum and superficial dentin layers of the root surface. These lesions are typically asymptomatic and subclinical, often detected incidentally through radiographic imaging rather than clinical symptoms. Unlike more aggressive forms, the resorption does not extend deeply into the root or involve the pulp, and it remains confined to localized areas without widespread progression.^[42] This condition frequently arises following orthodontic tooth movement or dental trauma, such as luxation injuries, where mechanical forces compress the periodontal ligament and disrupt the root's protective precementum layer. In orthodontic patients, mild external surface resorption is common, with prevalence rates of approximately 20-30% reported in studies evaluating post-treatment radiographs, particularly affecting anterior teeth under intrusive or torque forces. Following trauma, it manifests as a transient response to localized injury but is less prevalent unless combined with ongoing pressure from adjacent structures.^[43]^[44] The underlying mechanism is primarily pressure-induced, involving transient activation of odontoclasts due to mechanical stress on the root surface, leading to localized breakdown of cementum without bacterial infection or significant inflammatory mediator release. This differs from external inflammatory root resorption, which involves deeper tissue invasion and persistent inflammation; here, the process lacks chronic odontoclastic activity and rarely progresses to ankylosis, as the periodontal ligament typically remains viable for repair.^[42] In most instances, external surface root resorption is self-limiting and repairable, with the resorptive activity arresting spontaneously after 2-3 weeks once the initiating pressure is alleviated, allowing cementoblasts from adjacent intact areas to deposit reparative cellular cementum and restore periodontal attachment. Self-arrest occurs in 50-70% of cases without further intervention, underscoring its benign prognosis and distinction from progressive subtypes.^[43]

External Cervical Root Resorption

External cervical root resorption (ECR) is a localized form of external root resorption that originates on the external surface of the tooth root in the cervical region, typically near the cemento-enamel junction (CEJ), and involves the progressive loss of cementum, dentin, and sometimes enamel through odontoclastic activity.^[45] This defect is often insidious in its early stages, presenting as a radiolucency or mottled area on radiographs, and may manifest clinically as a "pink spot" due to thin overlying enamel or gingival cavitation in more advanced cases.^[46] Unlike milder forms of surface resorption, ECR tends to be more aggressive and localized, potentially leading to significant structural compromise if undetected.^[45] The etiology of ECR remains incompletely understood but is frequently idiopathic or associated with predisposing factors such as dental trauma, orthodontic treatment, or surgical interventions that disrupt the protective cementum layer and periodontal ligament.^[47] Hypoxia within the periodontal tissues has been proposed as a contributing mechanism, potentially triggering inflammatory responses that facilitate clastic cell invasion.^[45] Predisposing elements like intracoronal restorations or viral infections (e.g., hepatitis B) have also been linked in some cases, though no single factor consistently explains all occurrences.^[47] Prevalence of ECR is generally low in the general population, estimated at 0.02-0.08% based on early radiographic surveys, but it is notably higher among patients seeking endodontic care, where rates range from 0.5% to 1.35%, with a twofold increase observed in certain cohorts.^[48] It affects a broad age range (mean around 41 years) and shows a slight male predominance (54.6%), with maxillary central incisors (21.4%) and mandibular first molars (10.2%) most commonly involved.^[46] Multiple lesions occur in approximately 7.7-20% of affected individuals, particularly in cases of multiple cervical root resorption (MCRR).^[46] Histopathologically, ECR progresses through distinct phases: initiation with cementum breakdown, followed by invasive resorption of dentin by multinucleated osteoclast-like cells within fibrovascular granulation tissue comprising blood vessels, fibroblasts, endothelial cells, and inflammatory leukocytes.^[47] This tissue penetrates via multiple channels, extending circumferentially or toward the pulp, and may enter a reparative phase with fibro-osseous deposition in advanced stages, though progression often remains unchecked without intervention.^[45] The process is typically detected in the resorptive phase (70.2% of cases), with symptoms like pulpitis arising from proximity to the pulp rather than lesion size alone.^[46] According to the European Society of Endodontology (ESE) 2023 position statement, ECR is classified as a progressive subtype of external resorption, emphasizing the need for early diagnosis via cone-beam computed tomography (CBCT) and prompt intervention to halt advancement and preserve tooth vitality.^[45] The Heithersay (I-IV) or Patel classifications guide assessment based on lesion extent, with smaller, superficial defects (e.g., Patel height 1, spread A) offering better manageability through excavation and restoration.^[45] In MCRR, involving three or more teeth, systemic factors may warrant further investigation, though the condition's aggressive nature underscores the importance of regular monitoring in at-risk patients.^[47]

External Replacement Root Resorption

External replacement root resorption, also referred to as replacement resorption or ankylosis-related resorption, is characterized by the progressive resorption of root cementum and dentin followed by their substitution with bone-like tissue, resulting in direct fusion between the tooth root and alveolar bone, a condition known as ankylosis. This form of resorption typically arises after severe trauma to the periodontal ligament (PDL) and root surface, such as in cases of tooth avulsion, intrusion, or lateral luxation, where the protective layers of precementum and cementoblasts are damaged, exposing the underlying dentin.^[49] The process is initiated by odontoclasts, multinucleated cells derived from hematopoietic precursors, which attach to the denuded root surface and resorb tooth structure through the secretion of lysosomal enzymes and acids, leading to the breakdown of mineralized tissues. Following this resorptive phase, osteoblasts from the surrounding bone marrow deposit new bone matrix in the defect areas, gradually replacing the lost root components with lamellar bone that integrates the tooth into the alveolar process. This ankylotic union causes the affected tooth to become immobile relative to the jaw, as the normal PDL is absent, and the tooth behaves as an integral part of the bone. Such replacement is particularly common after tooth replantation, affecting approximately 51% of avulsed and replanted permanent teeth, particularly with extraoral dry times or improper storage.^[50]^[14] The prognosis for external replacement root resorption is generally unfavorable due to its self-perpetuating nature, with the resorbed root progressively substituted by bone over time, often culminating in tooth loss through fracture or spontaneous exfoliation. Most progression occurs within the first 2-3 years post-trauma, though active resorption can continue for 5-10 years in some instances, particularly in younger patients where bone remodeling is more rapid. Unlike inflammatory types, this resorption lacks an infectious trigger and resists conventional interventions, emphasizing the importance of preventive measures like immediate replantation in milk or saline to minimize PDL damage.^[14]^[51]

Diagnosis

Clinical Features

Tooth resorption is frequently asymptomatic during its initial phases, particularly for internal and external surface types, and is often detected incidentally during routine dental examinations rather than through patient complaints.^[2] In early internal root resorption, the pulp typically remains vital, allowing the process to progress without immediate discomfort, though a characteristic "pink spot" may appear on the crown due to vascular granulation tissue replacing dentin and becoming visible through the thinned enamel. Pulp vitality testing is essential to assess for internal resorption, where the pulp often remains vital in early stages.^[52] As resorption advances, especially in inflammatory or replacement variants, patients may experience intermittent pain, swelling, or sensitivity, often linked to secondary pulpitis or periapical involvement.^[2] Clinical signs vary by type and extent but commonly include tooth discoloration, ranging from pink hues in internal cases to yellowish or brownish tones in external inflammatory resorption due to pulp necrosis and exposure.^[52] Tenderness to percussion or palpation can emerge in progressing lesions, particularly with external inflammatory root resorption, signaling involvement of the periodontal ligament. Advanced inflammatory external resorption may manifest as increased tooth mobility due to loss of supporting periodontal structures, while in replacement resorption, involvement of more than 20% of the root surface can lead to ankylosis and reduced mobility; external cervical resorption often presents with detectable probing defects—firm, irregular areas on the cervical region that may bleed profusely upon exploration due to their vascular nature.^[52] Patient history plays a crucial role in identifying at-risk cases, with trauma—such as luxation, avulsion, or intrusion—being a primary predisposing factor that can initiate both internal and external resorption through disruption of the protective cementum or predentin layers.^[2] Orthodontic treatment is another common association, particularly for external surface or inflammatory root resorption, where mechanical forces exacerbate resorption in previously traumatized teeth.^[52] These historical elements, combined with the absence of early symptoms, underscore the importance of thorough anamnesis in susceptible individuals.^[53]

Imaging and Diagnostic Techniques

Conventional radiography, particularly periapical radiographs, serves as the initial imaging modality for detecting tooth resorption. These two-dimensional images can identify characteristic features such as radiolucencies along the root surface for external resorption, elliptical radiolucencies within the pulp canal for internal resorption, root shortening, or apical blunting.^[39] However, their limitations include superimposition of structures, which often underestimates the extent of resorption and hinders early detection, especially for small or superficial lesions.^[54] Parallax techniques using multiple angled views may help localize external defects but remain insufficient for precise staging or differentiation between resorption types.^[39] Cone-beam computed tomography (CBCT) has emerged as the advanced standard for comprehensive diagnosis, offering three-dimensional multiplanar reconstructions that accurately delineate the location, size, and progression of resorptive lesions. CBCT is recommended for complex cases involving suspected perforation, invasive resorption, or unclear boundaries, enabling superior visualization of the resorption's proximity to vital structures like the periodontal ligament or neurovascular bundle.^[39] Compared to conventional radiography, CBCT demonstrates significantly higher detection rates for root resorption lesions and provides quantitative assessment for staging severity.^[55] Its use adheres to the ALARA principle to minimize radiation exposure, with small field-of-view protocols preferred for endodontic applications.^[56] CBCT also facilitates differential diagnosis by distinguishing resorption from mimics such as caries, which typically show demineralization patterns confined to enamel-dentin junctions, or periapical pathology, characterized by well-defined radiolucent areas at the apex without root contour alterations. The European Society of Endodontology (ESE) 2019 position statement emphasizes CBCT for confirming resorption types and guiding surgical planning, particularly when conventional images are inconclusive.^[39] In practice, initial clinical features like pulp vitality changes may prompt radiographic evaluation, but CBCT refines the diagnostic accuracy for treatment decisions.^[54]

Management and Treatment

Conservative Approaches

Conservative approaches to tooth resorption emphasize non-invasive or minimally interventional strategies for early-stage or stable lesions, particularly in cases of external surface resorption and arrested inflammatory root resorption, where the goal is to preserve tooth structure without immediate operative intervention. These methods are suitable when the resorption is asymptomatic, the pulp remains vital, and there is no evidence of progression or associated pathology. Monitoring forms the cornerstone of conservative management for stable resorption types. Regular clinical examinations combined with radiographic imaging, such as periapical radiographs or cone-beam computed tomography (CBCT), are recommended at intervals of 6-12 months to assess lesion stability, extent of hard tissue loss, and periodontal ligament integrity. For external surface resorption, which typically heals spontaneously once the inciting factor (e.g., orthodontic pressure) is removed, no treatment is necessary if radiographs show reestablishment of the lamina dura and no ongoing activity. Similarly, arrested inflammatory root resorption, often following trauma, requires vigilant surveillance to detect any reactivation, with intervention deferred as long as the process remains inactive and the tooth is functional. Pharmacological options are limited and primarily experimental, focusing on anti-resorptive agents to modulate osteoclast activity in idiopathic or slowly progressive cases. Low-dose bisphosphonates, such as alendronate or zoledronate, have shown potential in animal models to reduce root resorption by inhibiting bone remodeling, but human applications remain investigational with sparse clinical data, often guided by serial pulp vitality testing to monitor tooth response. These agents are not routinely recommended due to risks like osteonecrosis of the jaw and lack of large-scale trials confirming efficacy in non-traumatic resorption. Endodontic interventions provide a targeted conservative treatment for internal root resorption and apical inflammatory types by addressing pulpal stimuli without surgical access. Root canal therapy (RCT) is performed to eliminate infected or inflamed pulp tissue, thereby halting the resorptive process and allowing potential repair of the root structure. Per International Association of Dental Traumatology (IADT) guidelines for traumatic dental injuries, calcium hydroxide is applied as an interim intracanal medicament for 1-4 weeks post-instrumentation to create an alkaline environment that neutralizes clastic activity and promotes hard tissue deposition before final obturation. This approach yields favorable outcomes in vital or necrotic cases amenable to disinfection, with success rates exceeding 80% in arresting progression when initiated early.

Surgical Treatments

Surgical treatments for tooth resorption are indicated when conservative approaches fail or when resorption defects are advanced, localized, and accessible via operative intervention, particularly in cases of external cervical resorption or post-traumatic scenarios involving immature teeth. These procedures typically involve raising a mucoperiosteal flap to expose the defect, thorough debridement of resorptive tissue, hemostasis, and restoration of the root structure to prevent further progression and promote healing. Success depends on early detection, complete removal of granulation tissue, and biocompatible sealing materials, with overall survival rates reported around 71-95% over 2-5 years depending on lesion severity.^[57]^[58] Flap surgery is a primary surgical method for managing external cervical root resorption (ECRR), especially in Heithersay class II and III lesions where the defect is supragingival or at the cemento-enamel junction. The procedure begins with local anesthesia and elevation of a full-thickness mucoperiosteal flap to visualize the resorptive site, followed by careful curettage to excise fibrovascular granulation tissue while preserving healthy root structure. Hemostasis is achieved, and the defect is restored using mineral trioxide aggregate (MTA) or glass ionomer cement (GIC) due to their biocompatibility, sealing ability, and promotion of cementum-like repair. Clinical studies report success rates of 80-90% for MTA-sealed defects, with radiographic evidence of arrest in resorption and minimal periapical pathology at 1-2 year follow-ups, though outcomes are poorer for deeper class IV lesions extending subgingivally.^[59]^[60]^[58] Decoagulation using trichloroacetic acid (TCA) is often integrated into flap surgery for invasive resorption defects to devitalize and halt resorptive cellular activity. A 90% aqueous TCA solution is applied via a soaked cotton pellet to the curetted cavity for 1-2 minutes, inducing coagulation necrosis in the granulation tissue, rendering it avascular, and inactivating odontoclastic cells without significantly affecting adjacent dentin. This step facilitates complete debridement and is particularly effective for vascular lesions prone to bleeding, allowing subsequent grafting with materials like MTA or bioactive cements to fill irregular defects and support hard tissue deposition. Clinical studies confirm TCA's efficacy in achieving hemostasis and resorption arrest, with no adverse effects on bond strength of calcium silicate sealers when used judiciously.^[61]^[58]^[62] In post-traumatic cases involving immature permanent teeth with root resorption, revascularization procedures align with the International Association of Dental Traumatology (IADT) 2020 guidelines to emphasize regenerative endodontics for necrotic pulps following luxation or avulsion injuries. After accessing the root canal via a surgical or non-surgical approach, the canal is irrigated with sodium hypochlorite, medicated with triple antibiotic paste, and sealed to induce blood clot formation, promoting stem cell ingress from the periapical tissues for pulp-like regeneration and continued root development. This technique has shown high success in arresting inflammatory resorption, with meta-analyses reporting over 90% radiographic healing in immature teeth up to 25 years post-trauma, though long-term apical closure varies.^[63]^[64]^[65]

Prognosis

The prognosis of tooth resorption varies significantly by type, extent, and timeliness of intervention, with early detection generally improving tooth survival and functional outcomes. Overall, approximately 60-70% of affected teeth can be salvaged if diagnosed and treated promptly, though advanced cases often necessitate extraction followed by prosthetic replacement such as dental implants or bridges. Factors influencing prognosis include the lesion's location, patient's age, and associated trauma or infection, with pediatric cases showing higher risks due to ongoing root development.^[52]^[28] For internal root resorption, endodontic treatment such as root canal therapy (RCT) yields favorable outcomes, with survival rates of 88-95% reported over a mean 2-year follow-up period when resorption is arrested early. Success depends on complete removal of resorptive tissue and sealing of the defect, preventing progression in most cases.^[28] External inflammatory root resorption responds well to RCT aimed at eliminating pulpal infection, achieving high success rates (up to 96%) in arresting progression when treated before extensive root loss occurs. In adults, outcomes are more predictable than in children, where wider dentinal tubules facilitate faster advancement if untreated.^[66]^[52] External surface root resorption typically has a good prognosis, as it is often self-limiting and reversible upon removal of the initiating factor (e.g., orthodontic pressure), with vital pulp allowing natural repair of cementum in minor cases. However, persistent stimuli can lead to progression into more severe forms.^[52] External cervical root resorption carries a guarded prognosis, particularly in advanced lesions, with success rates varying by Heithersay classification: 100% for classes 1 and 2 (minor defects), 78% for class 3 (mid-level involvement), and as low as 12.5% for class 4 (severe, circumferential). Failure rates reach 70% in posterior teeth over 10 years versus under 30% in anterior teeth, often due to incomplete resection or recurrence despite surgical repair. Internal repair techniques show 78-80% survival, outperforming external approaches at 50-62%.^[67]^[28]^[68] External replacement root resorption portends a poorer outlook, especially if more than 20% of the root surface is involved, frequently resulting in ankylosis and progressive tooth loss. In avulsion cases, 24% of affected teeth are lost over a mean 5.4-year period, with overall survival around 65% when combined with other complications. Extraction is common in extensive cases, as bone replacement of root structure compromises long-term stability.^[52]^[69]

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