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Journal of Conservative Dentistry and Endodontics logoLink to Journal of Conservative Dentistry and Endodontics
. 2025 Aug 1;28(8):714–726. doi: 10.4103/JCDE.JCDE_407_25

Indian Association of Conservative Dentistry and Endodontics consensus statement on deep caries management

Deepak Kumar Sharma 1, R S Mohan Kumar 1, Shishir Singh 2, Suparna Ganguly Saha 3, Meenal Nithin Gulve 4, Dipali Y Shah 5, Sathish Abraham 6, Shruthi Nagaraja 7, Raksha Bhat 8,
PMCID: PMC12377675  PMID: 40860391

Abstract

Dental caries remains one of the most ubiquitous chronic diseases worldwide, affecting people across geographic, socioeconomic, and demographic boundaries. In response to this pervasive burden, the consensus statement; developed by a panel of experts in cariology, restorative dentistry and endodontics during the Symposium on Deep Caries Management Symposium at the 39th Indian Association of Conservative Dentistry and Endodontics National Conference, Jio Convention Centre, Mumbai, November 29, to December 3, 2024, synthesises contemporary understanding of carious pathogenesis with evidence-based clinical strategies. It is intended for dental practitioners managing deep caries in vital permanent teeth of all age groups, from adolescents to older adults. Recommendations are grounded in systematic reviews, high-quality clinical trials, and structured expert consensus, charting the paradigmatic evolution from traditional, invasive endodontic approaches toward biologically informed, minimally invasive care that prioritises tissue preservation and harnesses natural reparative processes. The guideline outlines diagnostic thresholds, risk-assessment tools, and operative protocols – such as selective caries excavation and vital pulp therapy – that optimise long-term outcomes while reducing adverse events. This consensus statement has been formulated according to the AGREE guidelines for reporting consensus-based recommendations, ensuring methodological rigour and transparency in development. It elucidates the complex interplay between microbiological, biochemical, and structural factors governing caries initiation and progression, while establishing evidence-based protocols for conservative management that optimize long-term therapeutic outcomes.

Keywords: Dental caries, dental pulp, pulpitis, vital pulp therapy

INTRODUCTION AND GLOBAL EPIDEMIOLOGICAL PERSPECTIVES

Dental caries, etymologically derived from the Latin terminology signifying decay or putrefaction, constitutes a localized, posteruptive pathological process characterized by progressive demineralization of dental hard tissues initiated by microbial metabolic activity and culminating in cavitation and structural compromise.[1] The disease entity has maintained its position as the most prevalent chronic condition affecting human populations throughout recorded history, with archaeological evidence documenting carious lesions in skeletal remains dating approximately seven millennia.[2] Contemporary epidemiological surveillance demonstrates that dental caries affects approximately 2.3 billion individuals worldwide in permanent dentition, while an additional 532 million children experience carious involvement of primary teeth.[3] The global burden of dental caries exhibits remarkable persistence across the human lifespan, with prevalence rates demonstrating significant variability influenced by geographical distribution, socioeconomic determinants, dietary patterns, and access to preventive interventions.[4]

The epidemiological landscape of dental caries in developed nations has undergone substantial transformation over the past five decades, primarily attributable to widespread fluoride exposure through multiple delivery mechanisms, enhanced oral hygiene practices, and improved access to preventive dental care.[5] Nevertheless, the disease continues to demonstrate disproportionate impact on socioeconomically disadvantaged populations, creating persistent health disparities that reflect broader systemic inequities in healthcare access and health literacy.[6] Among adult populations, caries prevalence demonstrates progressive increase with advancing age, approaching nearly universal occurrence in elderly demographics where root surface caries becomes particularly problematic due to physiological gingival recession and medication-induced xerostomia.[7] The epidemiological data underscores the critical importance of developing comprehensive, evidence-based management strategies that address both the immediate therapeutic needs and long-term prevention of carious disease across diverse population groups. This consensus statement is intended for a broad range of dental professionals including general dentists, endodontists, restorative and paediatric dental specialists, dental educators, and policymakers involved in defining standards for caries management.

THEORETICAL FRAMEWORKS AND CLASSIFICATION SYSTEMS

Evolution of cariological theories

The theoretical understanding of dental caries has undergone substantial evolution through multiple paradigmatic shifts, each contributing essential components to contemporary comprehensive models of disease pathogenesis. The acidogenic theory, originally formulated by Miller in the late nineteenth century, established the fundamental concept that dental caries results from organic acid production through bacterial fermentation of dietary carbohydrates.[8] This theoretical framework proposed that pathogenic microorganisms metabolize fermentable substrates, primarily simple sugars, to produce organic acids including lactic, acetic, and propionic acids, which subsequently demineralize tooth structure through direct chemical dissolution processes. The acidogenic theory provided the foundational basis for modern preventive strategies emphasizing dietary modification, fluoride supplementation, and antimicrobial interventions.

The proteolytic theory emerged as an alternative explanatory framework, proposing that bacterial enzymes directly attack the organic matrix components of dental tissues, particularly collagen fibers within dentin, independent of acid-mediated demineralization.[9] Proponents of this theoretical model argued that proteolytic enzymes could solubilize organic components of tooth structure, creating pathways for subsequent mineral loss and facilitating progressive tissue destruction. This concept gained particular relevance in understanding root surface caries, where organic content comprises a proportionally higher percentage of tissue composition compared to enamel. The proteolytic-chelation theory represents a synthesis of previous theoretical frameworks, proposing that caries development involves simultaneous proteolytic enzyme activity and chelation-mediated mineral removal.[10] This integrated model suggests that bacterial enzymes degrade organic matrices while chelating agents sequester metallic ions, facilitating comprehensive tissue destruction through multiple coordinated mechanisms.

Contemporary understanding has largely validated the acidogenic theory while incorporating elements from alternative theoretical frameworks, recognizing that caries pathogenesis involves complex, multifactorial processes that cannot be adequately explained by any single mechanism.[11] Modern research emphasizes the critical role of biofilm ecology and metabolic interactions between different bacterial species in determining cariogenic potential. The ecological plaque hypothesis proposes that environmental changes within dental biofilms, particularly pH fluctuations and nutrient availability, drive selective pressures that favor shifts in microbial composition toward increasingly pathogenic communities.[12] This ecological perspective recognizes that caries development results from dysbiotic alterations in biofilm ecosystems rather than simple colonization by specific pathogenic organisms.

Contemporary classification systems

Modern classification systems for dental caries have undergone substantial refinement parallel to advances in understanding disease pathogenesis, incorporating multiple parameters including anatomical location, histopathological characteristics, activity status, and etiological factors. The International Caries Detection and Assessment System (ICDAS) represents a paradigmatic advancement in standardized caries assessment, providing reproducible criteria for lesion detection, characterization, and monitoring.[13] This comprehensive system employs a numerical scoring methodology ranging from zero, indicating sound tooth surfaces, to six, representing extensive cavitation with visible dentin involvement. The ICDAS framework facilitates consistent clinical evaluation across diverse practice settings and enables standardized research methodology for comparative studies and epidemiological surveillance.

The Caries Assessment Spectrum and Treatment index represents an innovative approach that combines elements of ICDAS with the Pulp, Ulcer, Fistula, and Abscess system, addressing both early lesion detection and advanced caries complications.[14] This integrated classification system incorporates staging for both incipient lesions amenable to non-invasive interventions and severe caries levels requiring complex therapeutic approaches. The CAST index provides comprehensive assessment capabilities that span the entire spectrum of carious disease, from initial subsurface demineralization to extensive pulpal involvement with associated complications.

Activity-based classification systems represent a fundamental conceptual shift toward understanding caries as a dynamic process rather than a static pathological condition.[15] This approach distinguishes between active lesions characterized by ongoing demineralization, surface roughness, and progressive tissue loss, and arrested lesions that exhibit signs of remineralization, surface hardness, and cessation of progressive destruction. The activity-based assessment enables clinicians to implement appropriate interventional strategies based on lesion dynamics rather than relying solely on morphological characteristics or extent of tissue involvement.

MULTIFACTORIAL ETIOLOGY AND BIOFILM DYNAMICS

The expanded four-factor etiological model

Contemporary understanding of caries etiology has evolved from Keyes’ original triad to incorporate temporal considerations and recognize the complex interactions between host susceptibility, microbial pathogenicity, environmental factors, and time-dependent processes.[16] The host factor encompasses multiple components including tooth structure composition, morphological characteristics, and the surrounding oral environment including salivary function and acquired pellicle formation. Tooth composition demonstrates significant variability between individuals and even within individual teeth, with fluoride incorporation during odontogenesis enhancing acid resistance through fluorapatite formation and improved crystalline structure.[17] The highly organized hydroxyapatite arrangement within enamel provides inherent resistance to acid dissolution, though this resistance can be compromised by developmental defects, acquired damage, or environmental challenges.

Salivary factors represent critical host determinants of caries susceptibility, serving multiple protective functions including mechanical cleansing, buffering capacity, antimicrobial activity, and provision of ions for remineralization processes.[18] The buffering capacity of saliva determines the rate of pH recovery following acidogenic challenges, while salivary flow rate affects clearance of fermentable substrates and bacterial metabolites from oral surfaces. Quantitative and qualitative alterations in salivary function, whether resulting from medications, systemic diseases, or genetic factors, substantially increase caries risk and modify disease progression patterns.

Microbial factors involve the complex ecosystem of oral biofilms, with specific bacterial species playing distinct roles in caries initiation, progression, and potential arrest.[19] Streptococcus mutans serves as a primary colonizer, producing surface adhesins that facilitate initial biofilm formation and glucosyltransferases that synthesize extracellular polysaccharides from sucrose. These polysaccharides create a protective matrix that enhances bacterial survival under environmental stress and provides structural stability to developing biofilms. Lactobacillus species contribute to caries progression through efficient acid production in low pH environments, demonstrating remarkable acid tolerance that enables continued metabolic activity under conditions that inhibit other bacterial species.[20]

Dietary substrate availability determines the metabolic activity and pathogenic potential of cariogenic biofilms.[21] Fermentable carbohydrates, particularly sucrose, provide readily metabolizable substrates for rapid acid production and extracellular polysaccharide synthesis. The frequency and duration of substrate exposure influence the cumulative acid challenge to tooth surfaces, with repeated exposures overwhelming natural protective mechanisms and leading to net mineral loss. The physical properties of foods affect retention time and clearance patterns, with adhesive foods prolonging substrate availability and extending periods of acid production.

Biofilm formation and ecological succession

Dental biofilm formation represents a highly orchestrated process involving sequential bacterial colonization, extracellular matrix development, and ecological succession toward increasingly complex microbial communities.[22] Initial biofilm development begins with adsorption of salivary proteins and glycoproteins onto clean tooth surfaces, creating the acquired pellicle that provides specific binding sites for pioneer bacterial species. Streptococci possess surface adhesins with high affinity for pellicle components, enabling initial attachment and establishment of primary colonization.[23]

Primary colonizers establish the foundation for subsequent biofilm development through cell-to-cell adhesion mechanisms and production of extracellular polymeric substances that provide structural support and create favorable microenvironments for secondary colonizers.[24] These early colonizers modify local environmental conditions through oxygen consumption, creating reducing conditions that facilitate anaerobic bacterial growth and enable establishment of nutritional cross-feeding relationships where metabolic byproducts of some species serve as essential nutrients for others.

Biofilm maturation involves increasing structural complexity and functional specialization, with extracellular polysaccharides forming a protective matrix that provides mechanical stability and creates concentration gradients of nutrients, metabolites, and antimicrobial agents.[25] Water channels develop within mature biofilms, facilitating nutrient transport and waste removal while enabling communication between different regions of the biofilm community. Spatial organization becomes increasingly sophisticated, with different bacterial species occupying specific ecological niches based on oxygen availability, pH conditions, nutrient access, and metabolic requirements.

The ecological dynamics within dental biofilms determine their pathogenic potential and response to environmental perturbations.[26] Frequent sugar exposure drives selective pressures that favor acid-producing and acid-tolerant bacterial species, leading to ecological shifts termed dysbiosis that transform relatively harmless microbial communities into highly cariogenic ecosystems. This concept of ecological succession explains how repeated acidogenic challenges progressively select for increasingly pathogenic bacterial communities that demonstrate enhanced capacity for sustained acid production and survival under extreme environmental conditions.

HISTOPATHOLOGICAL PROGRESSION AND TISSUE RESPONSES

Enamel caries development and zonation

The histopathological progression of enamel caries follows predictable patterns determined by the unique structural characteristics and mineral composition of enamel tissue.[27] Enamel caries initiation occurs subsurface, beneath a relatively intact surface layer, due to the protective effects of salivary buffering and fluoride incorporation that enhance remineralization of surface zones. The initial lesion manifests as a zone of increased porosity extending along enamel prisms, with progressive mineral loss creating microscopic voids between hydroxyapatite crystallites and disrupting the highly organized crystalline structure.

Advanced enamel lesions demonstrate four distinct histological zones reflecting different stages of the demineralization-remineralization process.[28] The surface zone maintains relatively high mineral content due to ongoing remineralization from salivary ions and fluoride, creating a protective barrier that may temporarily slow lesion progression. The body of the lesion represents the area of maximum porosity and mineral loss, appearing characteristically translucent under polarized light microscopy due to extensive crystalline disruption and void formation.

The dark zone represents an area of active remineralization where mineral precipitation has partially restored crystalline structure, indicating the dynamic nature of the carious process and the potential for lesion arrest under favorable conditions.[29] The translucent zone, also termed the advancing front, demonstrates the earliest detectable changes with approximately 1%–5% mineral loss and represents the active edge of lesion progression where ongoing demineralization extends into previously sound enamel structure.

Dentin caries characteristics and clinical implications

Dentinal caries presents distinct histopathological features that reflect the unique tubular architecture and organic composition of dentin tissue.[30] The presence of dentinal tubules influences bacterial invasion patterns and acid diffusion pathways, creating characteristic zones that have critical implications for clinical decision-making regarding tissue removal and preservation strategies. Infected dentin exhibits extensive bacterial colonization within dentinal tubules, accompanied by complete collagen destruction and total loss of mineral content that renders this tissue unsuitable for remineralization or structural support.

The affected dentin zone demonstrates demineralization without significant bacterial invasion, characterized by intact but demineralized collagen fibrils that retain structural integrity and possess potential for remineralization under appropriate conditions.[31] This tissue maintains firm consistency and demonstrates resistance to instrumental penetration, contrasting sharply with the soft, easily excavated characteristics of infected dentin. The preservation of affected dentin aligns with contemporary minimally invasive principles that recognize the tooth’s inherent capacity for repair and the importance of maintaining pulpal vitality.

The distinction between infected and affected dentin represents a crucial concept in conservative dentistry that directly influences clinical decision-making regarding extent of tissue removal and treatment success.[32] Infected dentin appears soft, wet, and easily excavated with hand instruments, exhibiting dark brown or black coloration due to bacterial pigments and organic degradation products. The microbiological composition includes diverse bacterial species with high concentrations of acidogenic and proteolytic organisms that have irreversibly compromised tissue integrity.

Affected dentin maintains lighter coloration ranging from light brown to yellowish, demonstrates firm, leathery consistency, and shows minimal bacterial invasion with demineralization primarily resulting from acid diffusion rather than direct bacterial colonization.[33] The collagen matrix remains structurally intact and capable of serving as a template for remineralization when environmental conditions become favorable through elimination of bacterial activity and restoration of physiological pH levels.

CONTEMPORARY DIAGNOSTIC FRAMEWORK AND ASSESSMENT PROTOCOLS

Standardized pulpal diagnosis and classification

Contemporary pulpal diagnosis has evolved beyond traditional binary classifications to incorporate nuanced understanding of inflammatory processes and their potential reversibility.[34] The revised pulpitis classification system proposed by Wolters et al. recognizes that pulpal inflammation exists along a continuum rather than discrete categories, with important implications for treatment selection and prognosis. Initial pulpitis presents as heightened but transient response to thermal stimuli, indicating localized inflammatory activity that can be effectively managed through causative factor removal and preventive interventions.[34]

Mild pulpitis demonstrates heightened and prolonged response to cold stimuli lasting up to 20 s with spontaneous pain resolution, suggesting limited local inflammation confined to coronal pulp regions that may respond favorably to indirect pulp capping procedures or stimulus elimination.[35] The inflammatory process remains localized and demonstrates potential for resolution when appropriate therapeutic interventions eliminate ongoing irritation and promote healing responses.

Moderate pulpitis exhibits strong, heightened, and prolonged response to cold stimuli lasting several minutes, often accompanied by dull spontaneous pain that can be controlled with analgesic medications and potential percussion sensitivity.[36] This classification indicates extensive coronal pulp inflammation that may require partial or complete pulpotomy procedures to remove irreversibly damaged tissue while preserving healthy radicular pulp with regenerative potential.

Severe pulpitis presents with intense pain sensation, marked reaction to warm stimuli, limited response to analgesic medications, and characteristic worsening of symptoms when recumbent.[37] Teeth demonstrate extreme sensitivity to palpation and percussion, indicating extensive coronal pulp inflammation that may extend into radicular pulp tissues to varying degrees. Complete coronal pulpotomy represents the recommended vital pulp therapy approach when adequate hemostasis can be achieved at canal orifices, suggesting viable radicular pulp tissue capable of maintaining vitality and function.

Integrated diagnostic protocol development

Comprehensive caries diagnosis for vital pulp therapy requires systematic integration of clinical examination findings, radiographic assessment, and pulpal status evaluation to enable accurate treatment planning and prognostic assessment.[38] Visual examination utilizing appropriate illumination and magnification forms the foundation of diagnostic assessment, with particular attention to lesion characteristics including depth, extent, activity status, and relationship to pulpal tissues. The traditional use of sharp explorers for initial caries detection has been superseded by gentle probing techniques using ball-ended instruments that assess lesion depth and activity without causing iatrogenic damage to remineralizable tissue.

Digital radiographic examination provides essential supplementary information regarding lesion extent, pulpal proximity, and periapical tissue status.[39] Standardized paralleling techniques utilizing appropriate positioning devices ensure geometric accuracy and enable reliable assessment of caries depth and pulpal involvement. The radiographic appearance of carious lesions consistently underestimates actual histological extent, as radiolucency becomes visible only after approximately 40% demineralization has occurred, emphasizing the importance of integrating clinical and radiographic findings for accurate diagnosis.

Pulp sensibility testing provides valuable information regarding pulpal innervation and vascular status, though interpretation requires careful consideration of testing limitations and potential confounding factors.[40] Cold testing utilizing refrigerant sprays or carbon dioxide demonstrates superior reliability compared to electric pulp testing, particularly in young patients with immature root development where electric pulp testing shows reduced accuracy. Negative responses to cold testing provide greater diagnostic reliability for pulp necrosis compared to electric pulp testing, though positive responses must be interpreted in conjunction with other clinical findings.

Intraoperative diagnostic assessment through direct pulp visualization represents the most reliable method for determining tissue viability and treatment suitability.[41] Microscopic examination of exposed pulp tissue enables assessment of bleeding characteristics, tissue color, consistency, and hemostatic response that provide critical information for treatment decision-making. The ability to achieve hemostasis within 5 min using appropriate antimicrobial irrigation represents a key prognostic indicator for vital pulp therapy success.

EVIDENCE-BASED CARIES EXCAVATION STRATEGIES

Comparative analysis of excavation methodologies

Contemporary caries excavation strategies represent a fundamental departure from traditional complete removal approaches, embracing biologically-guided techniques that prioritize tissue preservation and optimize healing potential.[42] Selective caries removal represents a single-visit technique that involves complete removal of carious tissue at cavity peripheries to hard dentin while limiting pulpal removal to soft or firm dentin, preserving remineralizable tissue and minimizing pulpal exposure risk. This approach emphasizes the critical importance of establishing an effective peripheral seal to prevent continued bacterial activity and enable arrested caries formation.

Systematic reviews and meta-analyses demonstrate that selective caries removal exhibits superior clinical success rates compared to alternative approaches, with studies reporting 14%–19% higher success rates than stepwise or non-selective techniques, particularly in follow-up periods exceeding 36 months.[43] The reduced pulpal exposure risk associated with selective caries removal, demonstrated as an 83% lower exposure rate compared to stepwise excavation, represents a significant clinical advantage that enables preservation of pulpal vitality and reduces treatment complexity.

Stepwise excavation employs a two-stage technique involving initial removal to soft dentin followed by temporary restoration placement and subsequent re-entry after 6 to 12 months for additional tissue removal and permanent restoration.[44] This approach enables pulpal healing, tertiary dentin formation, and progressive bacterial inactivation during the interval between procedures. However, clinical evidence indicates higher pulpal exposure rates during the second procedure compared to single-visit selective removal techniques.

Non-selective caries removal, involving complete excavation of all carious tissue regardless of anatomical location or tissue characteristics, demonstrates consistently higher incidence of pulpal exposure, increased postoperative symptoms, and elevated long-term failure rates.[45] This approach is currently considered clinically obsolete for deep carious lesions due to unnecessary tissue removal and increased treatment-related complications.

Clinical decision-making framework

The selection of appropriate excavation techniques requires systematic evaluation of multiple clinical factors including lesion depth and radiographic characteristics, pulpal status assessment, biofilm presence and activity, patient age and healing capacity, and anatomical considerations.[46] Radiographic assessment of lesion depth provides initial guidance for treatment planning, though clinical evaluation during excavation enables real-time modification of approach based on actual tissue characteristics encountered.

Pulpal status evaluation through comprehensive history, clinical examination, and sensibility testing influences excavation strategy selection and establishes baseline parameters for postoperative monitoring.[47] Teeth demonstrating signs of irreversible pulpitis may still be candidates for selective removal techniques when combined with appropriate vital pulp therapy procedures, challenging traditional approaches that mandated complete pulpal extirpation in such cases.

The assessment of dentin texture and bacterial contamination levels during excavation provides critical information for determining appropriate endpoints and predicting treatment success.[48] Soft, wet, heavily contaminated dentin requires complete removal to eliminate bacterial reservoirs and prevent continued infection, while firm, leather-like dentin with minimal bacterial invasion can be preserved and demonstrates potential for remineralization under appropriate conditions.

STANDARDIZED CLINICAL PROTOCOL IMPLEMENTATION

Operative environment and isolation protocols

Successful deep caries management requires meticulous attention to operative environment control and contamination prevention throughout all procedural phases.[49] Rubber dam isolation represents an absolute clinical requirement that must be supplemented with additional barrier materials including teflon tape and liquid dam applications to ensure complete separation from oral fluids and prevent bacterial contamination of the operative field. The isolation protocol extends beyond simple moisture control to create a sterile working environment that enables optimal healing responses and minimizes infection risk.

Comprehensive disinfection of the operative field using antimicrobial agents represents a critical preparatory step that significantly influences treatment outcomes.[50] Sodium hypochlorite solutions at concentrations ranging from 0.5% to 5.25% demonstrate broad-spectrum antimicrobial activity and tissue dissolution properties that facilitate bacterial elimination and debris removal. Alternative disinfection protocols utilizing povidone-iodine solutions provide effective antimicrobial activity with reduced tissue toxicity, particularly beneficial in cases requiring direct pulpal contact.

The utilization of appropriate magnification, preferably through surgical loupes providing eight to ten times magnification or operating microscopes, represents an essential component of contemporary practice that enables accurate tissue assessment and precise instrumentation.[51] Enhanced visualization facilitates discrimination between infected and affected dentin based on color consistency, surface texture, moisture content, and instrumental resistance, enabling informed decisions regarding tissue preservation or removal.

Instrumentation selection and technique refinement

Instrumentation selection plays a critical role in successful deep caries management, with specific instruments demonstrating distinct advantages for different aspects of the excavation procedure.[52] Diamond rotary instruments are contraindicated for deep caries removal due to their aggressive cutting characteristics that increase risks of inadvertent pulpal exposure, thermal damage, and excessive tissue removal. The high cutting efficiency and heat generation associated with diamond instruments can cause irreversible pulpal damage even when direct exposure does not occur.

Tungsten carbide burs represent the preferred instrumentation for controlled caries removal, providing efficient cutting action with superior tactile feedback that enables discrimination between tissue types during excavation.[53] The blade design and cutting characteristics of carbide burs facilitate selective tissue removal while minimizing risks of overextension or iatrogenic damage to sound tooth structure.

Ceramic burs manufactured from zirconia demonstrate equivalent efficacy to traditional metal instruments while providing enhanced tactile feedback and reduced thermal generation during operation.[54] The unique cutting characteristics of ceramic instruments enable selective removal of demineralized tissue while preserving sound dentin, contributing to improved treatment outcomes and reduced procedural complications.

Polymer burs specifically designed for caries removal demonstrate hardness characteristics intermediate between sound and carious dentin, enabling selective removal of demineralized tissue while automatically stopping on sound tooth structure.[55] Although these instruments demonstrate reduced cutting efficiency compared to traditional burs, their selective cutting action provides additional safety margins and reduces risks of excessive tissue removal.

VITAL PULP THERAPY: CONTEMPORARY EVIDENCE AND CLINICAL PROTOCOLS

Biological foundations and paradigm evolution

Vital pulp therapy has undergone fundamental conceptual evolution from traditional pulp capping procedures to become a comprehensive strategy for preserving and revitalizing pulp tissue, fundamentally challenging conventional approaches that mandated complete pulpal extirpation in cases of irreversible pulpitis.[56] The contemporary paradigm recognizes that infection consistently associates with inflammation, but inflammatory processes do not necessarily indicate bacterial infection or irreversible tissue damage. Inflammation often represents the initial phase of wound healing, providing essential cellular and molecular components including stem cells, extracellular matrix scaffolds, growth factors, cytokines, chemokines, and macrophages required for tissue repair and regeneration.

The biological foundation for vital pulp therapy draws upon landmark research demonstrating that pulpal responses to injury depend critically on bacterial exposure and environmental contamination.[57] Studies in germ-free laboratory animals revealed that pulpal exposures in sterile environments consistently resulted in vital tissue maintenance and calcific bridge formation, while identical exposures in conventional laboratory environments led to pulpal necrosis and inflammatory complications. These findings established the critical importance of bacterial control and aseptic technique in determining treatment outcomes.

Contemporary understanding recognizes that clinical diagnoses of irreversible pulpitis frequently overestimate the extent of pulpal damage and may not accurately reflect tissue viability or regenerative potential.[58] Histopathological studies comparing clinical diagnoses with actual tissue conditions revealed that a significant percentage of teeth clinically diagnosed with irreversible pulpitis demonstrated only localized inflammation with extensive areas of normal pulpal architecture, suggesting that root canal treatment may represent overtreatment in carefully selected cases.

Professional guidelines and evidence synthesis

The European Society of Endodontology position statement acknowledges that carious exposures presenting with symptoms traditionally associated with irreversible pulpitis can be successfully treated with complete pulpotomy procedures when performed under strict aseptic conditions with effective hemostasis achievement following coronal pulp amputation.[59] This position represents a significant departure from traditional endodontic teaching that considered irreversible pulpitis an absolute indication for complete pulpal extirpation.

The American Association of Endodontists position statement similarly recommends direct visualization of exposed pulp tissue and subsequent hemostasis achievement to provide additional diagnostic information for determining pulpotomy suitability in teeth presenting with irreversible symptomatic pulps.[60] Both professional organizations emphasize that calcium silicate-based cements represent the current gold standard for pulp coverage materials, with immediate coronal restoration being essential for optimal treatment outcomes.

Clinical research supporting vital pulp therapy in mature permanent teeth has demonstrated success rates that compare favorably with conventional endodontic treatment while offering significant advantages including preservation of tooth vitality, maintenance of proprioceptive function, and reduced treatment complexity.[61] Long-term follow-up studies report clinical success rates exceeding 90% at 3-year intervals, with radiographic success rates consistently above 85% in appropriately selected cases.

Treatment modality selection and clinical decision-making

Direct pulp capping procedures are classified into distinct categories based on clinical circumstances surrounding pulpal exposure and expected tissue responses.[62] Class I exposures occur in teeth with healthy surrounding tissues where exposure results from traumatic injury or iatrogenic causes during cavity preparation, representing ideal conditions for conservative pulp capping with excellent prognosis for successful outcomes.

Class II exposures involve preoperative presence of deep or extremely deep carious lesions with pulpal exposure occurring through zones of bacterial contamination, requiring more aggressive tissue management and careful assessment of pulpal viability.[63] The clinical expectation of underlying pulpal inflammation in Class II exposures necessitates thorough debridement and may require partial tissue removal to achieve optimal treatment results.

Partial pulpotomy procedures involve controlled removal of superficial pulp tissue, typically limited to 2 mm depth for single exposures or horizontal connection of multiple exposures with underlying tissue removal.[64] This conservative approach preserves the cell-rich coronal pulp and minimizes destruction of primary odontoblasts, theoretically enabling continued tertiary dentinogenesis and enhanced healing potential. Clinical studies demonstrate that partial pulpotomy results in higher percentages of dentin bridge formation and lower incidence of root canal calcification compared to complete pulpotomy procedures.

Complete pulpotomy involves removal of entire coronal pulp tissue while preserving radicular pulp vitality and function.[65] This approach demonstrates higher primary success rates compared to partial pulpotomy, potentially attributed to more complete removal of inflamed tissue and elimination of potential bacterial reservoirs. However, complete pulpotomy results in loss of pulpal sensibility and eliminates the potential for continued coronal pulp function.

BIOMATERIAL SELECTION AND RESTORATIVE CONSIDERATIONS

Advanced biomaterials and tissue responses

Contemporary vital pulp therapy success depends critically on appropriate selection and application of bioactive materials that promote healing responses while providing effective sealing against bacterial contamination.[66] Calcium hydroxide has served as the traditional gold standard for pulp capping applications, demonstrating consistent ability to induce calcific barrier formation when applied directly to exposed pulp tissue. However, the barriers formed by calcium hydroxide demonstrate significant limitations including non-uniform thickness, lack of structural bonding to surrounding dentin walls, and susceptibility to dissolution and bacterial penetration over time.

Mineral trioxide aggregate (MTA) represents a significant advancement in pulp capping materials, demonstrating superior sealing ability, enhanced biocompatibility, and improved long-term stability compared to traditional calcium hydroxide formulations.[67] The unique setting chemistry of MTA creates a highly alkaline environment that promotes antimicrobial activity while stimulating cellular differentiation and matrix formation. Clinical studies consistently demonstrate superior success rates with MTA compared to calcium hydroxide in both direct pulp capping and pulpotomy applications.

Biodentine and other newer calcium silicate-based materials have been developed to address specific limitations of traditional MTA while maintaining the biological advantages of calcium silicate chemistry.[68] These materials demonstrate significantly reduced setting times, improved handling characteristics, and enhanced aesthetic properties while promoting comparable biological responses including mineralization induction and cellular differentiation. The rapid setting characteristics enable single-visit treatment protocols while maintaining optimal sealing properties and biological activity.

Substrate management and adhesive protocols

The establishment of reliable adhesive interfaces with caries-affected dentin presents significant technical challenges due to altered substrate characteristics and compromised bonding potential.[69] Research consistently demonstrates that bond strength to caries-affected dentin is reduced by approximately 33% compared to bonding to sound dentin, while bonding to caries-infected dentin shows dramatic reductions of 78% compared to healthy tissue substrates.

The compromised bonding characteristics of caries-affected dentin result from mineral deposition within dentinal tubules, altered collagen fiber architecture, and modified surface chemistry that affects etching patterns and resin penetration.[70] Consequently, cavity preparation should ensure that peripheral margins consist entirely of sound, hard dentin with recommendations for minimum widths of 1–2 mm of healthy dentin around restoration margins to ensure reliable bonding and long-term restoration integrity.

Acetone-based etch-and-rinse adhesive systems demonstrate superior bonding performance to caries-affected dentin compared to ethanol-based formulations, primarily due to enhanced penetration characteristics and improved polymer infiltration into partially demineralized substrates.[71] Two-step self-etch adhesive systems show favorable bond strength characteristics compared to etch-and-rinse techniques when applied to caries-affected substrates, attributed to preservation of collagen fibril integrity and reduced technique sensitivity.

High-viscosity glass ionomer cements offer significant advantages for restoration of deep carious lesions, including excellent biocompatibility, chemical bonding to dental tissues, sustained fluoride release, and protection against secondary caries development.[72] These materials demonstrate equivalent bond strength to both normal and caries-affected dentin substrates, while resin-based systems show significantly compromised performance on affected dentin compared to sound tooth structure.

LONG-TERM OUTCOMES AND SUCCESS EVALUATION

Comprehensive assessment protocols

The evaluation of long-term success following vital pulp therapy requires systematic assessment protocols implemented at specific intervals to ensure optimal outcomes and enable early detection of potential complications.[73] Initial postoperative assessment should occur within 24–48 h to monitor immediate healing responses and identify acute complications requiring intervention. Short-term follow-up at 7 days enables assessment of initial healing progress and patient comfort levels.

Critical evaluation periods occur at 6 months and 1 year postoperatively, representing essential timepoints for determining treatment success and long-term viability.[74] These assessments should encompass comprehensive clinical examination including symptom evaluation, palpation and percussion testing, and assessment of restoration integrity. Radiographic evaluation at these intervals enables detection of healing responses, calcific barrier formation, and potential complications including internal resorption or periapical pathology development.

Long-term success evaluation requires annual assessment for a minimum period of 4 years to establish definitive treatment outcomes and enable comparison with alternative treatment modalities.[75] The assessment protocol should include standardized clinical parameters and radiographic criteria to ensure consistent evaluation and enable accurate success rate determination.

Success criteria and prognostic factors

Clinical success is definitively established through demonstrated absence of symptoms combined with maintenance of pulp vitality for minimum periods of 1 year posttreatment.[76] Patient-centered outcomes including complete absence of pain, swelling, sinus tract formation, or pathological mobility represent primary success indicators that directly impact quality of life and treatment satisfaction.

Clinician-centered parameters include positive response to pulp sensibility testing within normal physiological limits, though interpretation must consider potential limitations in older patients, teeth with extensive restorations, and cases involving complete pulpotomy where sensibility loss is anticipated.[77] Radiographic success requires absence of periapical pathology development, internal root resorption, or other pathological changes that might indicate treatment failure or complications.

Contemporary clinical studies report success rates for vital pulp therapy that consistently exceed 90% for appropriately selected cases when modern materials and techniques are employed.[78] These outcomes compare favorably with conventional endodontic treatment while offering significant advantages including preservation of tooth vitality, maintenance of proprioceptive function, and reduced treatment complexity and cost.

COMPLICATIONS, RISK MANAGEMENT, AND CLINICAL CONSIDERATIONS

Potential complications and their management

Pulp canal obliteration represents one of the most frequently encountered complications following vital pulp therapy procedures, occurring as a consequence of excessive calcific deposition within the root canal system that may complicate future endodontic intervention if required.[56] This complication manifests radiographically as progressive narrowing or complete obliteration of canal spaces, typically developing gradually over months to years following treatment. While pulp canal obliteration does not necessarily indicate treatment failure, as the pulp may remain vital and functional, it creates significant challenges for conventional endodontic access and instrumentation should future treatment become necessary.

Internal root resorption may develop as an inflammatory response to vital pulp therapy procedures, potentially compromising long-term tooth structure integrity and function.[60] This complication typically manifests as progressive resorption of dentin from within the pulp chamber or root canals, creating characteristic radiographic appearances that may progress to perforation and structural compromise. Early detection through regular radiographic monitoring enables intervention before significant structural damage occurs, though advanced cases may require complex restorative procedures or extraction.

Tooth discoloration represents an aesthetic complication that can result from various factors including material selection, residual sodium hypochlorite interactions with bismuth oxide components, or pulpal hemorrhage during treatment procedures.[77] Gray discoloration particularly affects anterior teeth where aesthetic considerations are paramount, potentially requiring complex whitening procedures, veneer placement, or complete restoration replacement to achieve acceptable aesthetic outcomes.

Diagnostic limitations and clinical adaptations

Pulp sensibility testing demonstrates significantly reduced reliability in teeth that have received vital pulp therapy, complicating future diagnostic assessments and treatment planning.[40] The absence of response to cold testing and electric pulp testing does not accurately reflect the true histological status of pulp tissue following treatment procedures, particularly in cases involving complete pulpotomy where coronal nerve supply has been eliminated. Clinicians must rely on comprehensive clinical and radiographic assessment rather than sensibility testing alone when evaluating treatment outcomes and diagnosing potential complications.

Age-related factors influence treatment outcomes and must be considered in treatment planning and prognostic assessment.[5] While contemporary evidence indicates that chronological age alone should not preclude vital pulp therapy, physiological factors including reduced pulpal blood supply, decreased cellular activity, and compromised healing responses in older patients may influence success rates and treatment selection. However, successful outcomes have been documented across all age groups when appropriate case selection criteria are applied.

Systemic health conditions and medications may influence healing responses and treatment outcomes, though specific contraindications remain poorly defined in current literature.[73] Patients with compromised immune function, diabetes mellitus, or those receiving immunosuppressive medications may demonstrate altered healing responses that could affect treatment success. However, absolute contraindications based on systemic conditions have not been established, and treatment decisions should be individualized based on comprehensive risk-benefit analysis.

FUTURE DIRECTIONS AND EMERGING TECHNOLOGIES

Advanced diagnostic technologies

Molecular biomarker research represents one of the most promising areas for advancing diagnostic accuracy in vital pulp therapy.[38] Current research has identified multiple inflammatory markers including matrix metalloproteinases, cytokines, and neuropeptides that demonstrate significant correlations with pulpal inflammation status and treatment outcomes. Particular attention has focused on matrix metalloproteinase-9 levels in pulpal tissues, which show strong correlations with inflammatory status and may predict treatment success rates.

The development of chairside diagnostic tests capable of rapidly assessing molecular biomarkers could revolutionize treatment planning and case selection for vital pulp therapy.[38] These technologies would enable real-time assessment of pulpal inflammation levels and healing potential, moving beyond subjective clinical assessment toward objective, evidence-based treatment selection. However, significant technical challenges remain in developing reliable, cost-effective chairside testing systems suitable for routine clinical application.

Artificial intelligence applications in dental radiography and clinical diagnosis show considerable promise for improving diagnostic accuracy and consistency.[4] Machine learning algorithms trained on large datasets of radiographic images and clinical outcomes demonstrate capability for automated caries detection, depth assessment, and treatment recommendation. These technologies could provide valuable decision support tools for clinicians, particularly in complex cases where traditional diagnostic methods show limitations.

Therapeutic innovation and regenerative approaches

Tissue engineering approaches represent an emerging frontier in vital pulp therapy, with potential for enhancing healing responses and promoting more complete pulpal regeneration.[56] Research focuses on developing biomimetic scaffolds that can guide cellular organization and differentiation while providing sustained release of growth factors and bioactive molecules. These advanced materials could potentially restore normal pulpal architecture and function rather than simply inducing calcific barrier formation.

Stem cell-based therapies offer theoretical advantages for pulpal regeneration, with multiple cell sources including dental pulp stem cells, stem cells from human exfoliated deciduous teeth, and mesenchymal stem cells demonstrating regenerative potential.[56] However, significant regulatory, technical, and economic challenges must be addressed before these approaches become clinically viable for routine application.

Gene therapy approaches targeting specific cellular pathways involved in pulpal healing and regeneration represent long-term research directions with potential for revolutionary advances.[56] However, these approaches remain largely experimental and face substantial regulatory hurdles before clinical application becomes feasible.

Global health perspectives and access considerations

The development of simplified, cost-effective vital pulp therapy protocols suitable for implementation in resource-limited settings represents an important global health priority.[5] Many regions lack access to sophisticated diagnostic equipment and advanced biomaterials, necessitating adaptation of treatment protocols to local resources and capabilities while maintaining acceptable success rates.

Training and education programs for healthcare providers in developing regions could significantly expand access to vital pulp therapy and reduce reliance on tooth extraction as the primary treatment for deep caries.[3] However, these programs must address not only technical skills but also broader issues including supply chain management, quality assurance, and continuing education requirements.

Economic analysis of vital pulp therapy compared to alternative treatments including extraction and replacement demonstrates favorable cost-effectiveness ratios, particularly when long-term outcomes and quality of life factors are considered.[6] However, initial treatment costs and access to specialized materials may create barriers to implementation in resource-constrained environments.

CONCLUSION

The contemporary evolution of dental caries management represents a fundamental paradigmatic transformation from traditional mechanistic approaches toward sophisticated, biologically-informed therapeutic strategies that prioritize tissue preservation while optimizing natural healing mechanisms. This comprehensive review has synthesized current understanding of carious pathogenesis, diagnostic methodologies, and evidence-based treatment protocols to establish a framework for conservative management that challenges conventional assumptions regarding irreversible pulpal pathology and the necessity for complete tissue extirpation.

The integration of advanced molecular biological insights into pulpal pathophysiology has revolutionized understanding of inflammatory processes, revealing that tissue responses previously considered irreversible may demonstrate significant regenerative potential when appropriate therapeutic interventions are implemented under optimal conditions. Contemporary evidence demonstrates that vital pulp therapy can achieve success rates exceeding 90% in appropriately selected cases, representing outcomes that compare favorably with conventional endodontic treatment while offering substantial advantages including preservation of tooth vitality, maintenance of proprioceptive function, and reduced treatment complexity.

The systematic approach to caries excavation has evolved from complete tissue removal to selective preservation strategies that recognize the biological potential of affected dentin and the importance of maintaining adequate dentin thickness for continued pulpal health. Evidence-based protocols emphasizing selective caries removal demonstrate superior clinical outcomes compared to traditional approaches, with significantly reduced pulpal exposure rates and improved long-term success. The development of standardized clinical protocols incorporating appropriate isolation, disinfection, instrumentation selection, and material application has established reproducible methodologies that optimize treatment outcomes across diverse clinical settings.

The advancement of bioactive materials, particularly calcium silicate-based cements, has provided clinicians with tools that actively promote healing responses while ensuring effective sealing against bacterial contamination. These materials demonstrate superior biological properties compared to traditional options, enabling predictable outcomes in cases that would previously have required more invasive interventions. The continued development of rapid-setting formulations and improved handling characteristics has facilitated single-visit treatment protocols while maintaining optimal biological activity.

Future directions in vital pulp therapy encompass multiple promising areas including molecular diagnostic technologies, regenerative therapeutic approaches, and global health applications that could further expand treatment accessibility and success rates. The development of chairside biomarker testing could enable objective assessment of pulpal status and treatment potential, moving beyond subjective clinical judgment toward evidence-based case selection. Advanced biomaterials incorporating sustained-release drug delivery systems and tissue engineering principles offer potential for enhanced healing responses and more complete pulpal regeneration.

The implications of this paradigmatic shift extend beyond individual treatment decisions to encompass broader healthcare policy considerations including training requirements, material availability, and economic factors that influence treatment accessibility. The demonstration that conservative approaches can achieve excellent outcomes while preserving natural tooth structure supports the development of preventive strategies and early intervention protocols that prioritize tissue preservation throughout the disease management continuum.

In conclusion, the contemporary approach to deep caries management represents a synthesis of advanced scientific understanding, evidence-based clinical protocols, and innovative biomaterial technologies that collectively enable preservation of natural dental architecture while ensuring optimal patient outcomes. The continued evolution of this field promises further improvements in diagnostic accuracy, therapeutic effectiveness, and global accessibility that will benefit patients worldwide through enhanced preservation of natural tooth structure and function across the human lifespan.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.

REFERENCES

  • 1.Fejerskov O, Nyvad B, Kidd E. Dental Caries: The Disease and Its Clinical Management. 3rd ed. Oxford: Wiley-Blackwell; 2015. [Google Scholar]
  • 2.Hillson S. Dental pathology. In: Katzenberg MA, Saunders SR, editors. Biological Anthropology of the Human Skeleton. New York: Wiley-Liss; 2008. pp. 249–86. [Google Scholar]
  • 3.Kassebaum NJ, Smith AG, Bernabé E, Fleming TD, Reynolds AE, Vos T, et al. Global, regional, and national prevalence, incidence, and disability-adjusted life years for oral conditions for 195 countries, 1990-2015: A systematic analysis for the global burden of diseases, injuries, and risk factors. J Dent Res. 2017;96:380–7. doi: 10.1177/0022034517693566. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Marwaha J, Singla M, Nath A, Arya A. Revolutionizing the diagnosis of dental caries using artificial intelligence-based methods. J Conserv Dent Endod. 2025;28:401–5. doi: 10.4103/JCDE.JCDE_172_25. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Griffin SO, Jones JA, Brunson D, Griffin PM, Bailey WD. Burden of oral disease among older adults and implications for public health priorities. Am J Public Health. 2012;102:411–8. doi: 10.2105/AJPH.2011.300362. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Schwendicke F, Dörfer CE, Schlattmann P, Foster Page L, Thomson WM, Paris S. Socioeconomic inequality and caries: A systematic review and meta-analysis. J Dent Res. 2015;94:10–8. doi: 10.1177/0022034514557546. [DOI] [PubMed] [Google Scholar]
  • 7.Salem A, Aouididi R, Delatorre Bronzato J, Al-Waeli H, Abufadalah M, Shaikh S, et al. Perspective and practice of root caries management: A multicountry study –Part II: A deeper dive into risk factors. J Conserv Dent. 2021;24:163–8. doi: 10.4103/jcd.jcd_20_21. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Miller WD. The Microorganisms of the Human Mouth. Philadelphia: SS White Dental Manufacturing Company; 1890. [Google Scholar]
  • 9.Gottlieb B, Diamond M, Applebaum E. The demonstration of acid-proof bacteria in carious dentine. Br Dent J. 1946;81:423–8. [Google Scholar]
  • 10.Schatz A, Martin JJ, Schatz V. Chelation as a biological weathering factor in pedogenesis. Proc PA Acad Sci. 1957;31:246–51. [Google Scholar]
  • 11.Philip N, Suneja B. The revolutionary evolution in carious lesion management. J Conserv Dent. 2023;26:249–57. doi: 10.4103/jcd.jcd_54_23. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology (Reading) 2003;149:279–94. doi: 10.1099/mic.0.26082-0. [DOI] [PubMed] [Google Scholar]
  • 13.Shaalan OO. DIAGNOdent versus international caries detection and assessment system in detection of incipient carious lesions: A diagnostic accuracy study. J Conserv Dent. 2023;26:199–206. doi: 10.4103/jcd.jcd_575_22. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Frencken JE, de Amorim RG, Faber J, Leal SC. The caries assessment spectrum and treatment (CAST) index: Rational and development. Int Dent J. 2011;61:117–23. doi: 10.1111/j.1875-595X.2011.00022.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Nyvad B, Machiulskiene V, Baelum V. Reliability of a new caries diagnostic system differentiating between active and inactive caries lesions. Caries Res. 1999;33:252–60. doi: 10.1159/000016526. [DOI] [PubMed] [Google Scholar]
  • 16.Keyes PH. The infectious and transmissible nature of experimental dental caries. Findings and implications. Arch Oral Biol. 1960;1:304–20. doi: 10.1016/0003-9969(60)90091-1. [DOI] [PubMed] [Google Scholar]
  • 17.Robinson C, Shore RC, Brookes SJ, Strafford S, Wood SR, Kirkham J. The chemistry of enamel caries. Crit Rev Oral Biol Med. 2000;11:481–95. doi: 10.1177/10454411000110040601. [DOI] [PubMed] [Google Scholar]
  • 18.Humphrey SP, Williamson RT. A review of saliva: Normal composition, flow, and function. J Prosthet Dent. 2001;85:162–9. doi: 10.1067/mpr.2001.113778. [DOI] [PubMed] [Google Scholar]
  • 19.Praveen T, Kotrashetti VS, Nayak RS, Naik SS, Bhat K, Kugaji MS. Polymerase chain reaction-based identification of various serotypes of Streptococcus mutans in adults with and without dental caries. J Conserv Dent Endod. 2024;27:315–20. doi: 10.4103/JCDE.JCDE_312_23. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Marsh PD, Head DA, Devine DA. Ecological approaches to oral biofilms: Control without killing. Caries Res. 2015;49(Suppl 1):46–54. doi: 10.1159/000377732. [DOI] [PubMed] [Google Scholar]
  • 21.Touger-Decker R, van Loveren C. Sugars and dental caries. Am J Clin Nutr. 2003;78:881S–92S. doi: 10.1093/ajcn/78.4.881S. [DOI] [PubMed] [Google Scholar]
  • 22.Kolenbrander PE, Palmer RJ, Jr, Periasamy S, Jakubovics NS. Oral multispecies biofilm development and the key role of cell-cell distance. Nat Rev Microbiol. 2010;8:471–80. doi: 10.1038/nrmicro2381. [DOI] [PubMed] [Google Scholar]
  • 23.Banas JA, Vickerman MM. Glucan-binding proteins of the oral streptococci. Crit Rev Oral Biol Med. 2003;14:89–99. doi: 10.1177/154411130301400203. [DOI] [PubMed] [Google Scholar]
  • 24.Flemming HC, Wingender J. The biofilm matrix. Nat Rev Microbiol. 2010;8:623–33. doi: 10.1038/nrmicro2415. [DOI] [PubMed] [Google Scholar]
  • 25.Stewart PS, Franklin MJ. Physiological heterogeneity in biofilms. Nat Rev Microbiol. 2008;6:199–210. doi: 10.1038/nrmicro1838. [DOI] [PubMed] [Google Scholar]
  • 26.Takahashi N, Nyvad B. Caries ecology revisited: Microbial dynamics and the caries process. Caries Res. 2008;42:409–18. doi: 10.1159/000159604. [DOI] [PubMed] [Google Scholar]
  • 27.Silverstone LM. Structure of carious enamel, including the early lesion. Oral Sci Rev. 1973;3:100–60. [PubMed] [Google Scholar]
  • 28.ten Cate JM, Featherstone JD. Mechanistic aspects of the interactions between fluoride and dental enamel. Crit Rev Oral Biol Med. 1991;2:283–96. doi: 10.1177/10454411910020030101. [DOI] [PubMed] [Google Scholar]
  • 29.Featherstone JD. The continuum of dental caries – Evidence for a dynamic disease process. J Dent Res. 2004;83(Spec No C):C39–42. doi: 10.1177/154405910408301s08. [DOI] [PubMed] [Google Scholar]
  • 30.Fusayama T. Two layers of carious dentin;diagnosis and treatment. Oper Dent. 1979;4:63–70. [PubMed] [Google Scholar]
  • 31.Bjørndal L, Larsen T, Thylstrup A. A clinical and microbiological study of deep carious lesions during stepwise excavation using long treatment intervals. Caries Res. 1997;31:411–7. doi: 10.1159/000262431. [DOI] [PubMed] [Google Scholar]
  • 32.Kidd EA. How 'clean'must a cavity be before restoration? Caries Res. 2004;38:305–13. doi: 10.1159/000077770. [DOI] [PubMed] [Google Scholar]
  • 33.Maltz M, de Oliveira EF, Fontanella V, Bianchi R. A clinical, microbiologic, and radiographic study of deep caries lesions after incomplete caries removal. Quintessence Int. 2002;33:151–9. [PubMed] [Google Scholar]
  • 34.Wolters WJ, Duncan HF, Tomson PL, Karim IE, McKenna G, Dorri M, et al. Minimally invasive endodontics: A new diagnostic system for assessing pulpitis and subsequent treatment needs. Int Endod J. 2017;50:825–9. doi: 10.1111/iej.12793. [DOI] [PubMed] [Google Scholar]
  • 35.Hashem D, Mannocci F, Patel S, Manoharan A, Brown JE, Watson TF, et al. Clinical and radiographic assessment of the efficacy of calcium silicate indirect pulp capping: A randomized controlled clinical trial. J Dent Res. 2015;94:562–8. doi: 10.1177/0022034515571415. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.European Society of Endodontology (ESE) developed by. Duncan HF, Galler KM, Tomson PL, Simon S, El-Karim I, et al. European society of endodontology position statement: Management of deep caries and the exposed pulp. Int Endod J. 2019;52:923–34. doi: 10.1111/iej.13080. [DOI] [PubMed] [Google Scholar]
  • 37.Li W, Yang B, Shi J. Efficacy of pulpotomy for permanent teeth with carious pulp exposure: A systematic review and meta-analysis of randomized controlled trials. PLoS One. 2024;19:e0305218. doi: 10.1371/journal.pone.0305218. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38.Rechenberg DK, Galicia JC, Peters OA. Biological markers for pulpal inflammation: A systematic review. PLoS One. 2016;11:e0167289. doi: 10.1371/journal.pone.0167289. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Wenzel A. Radiographic modalities for diagnosis of caries in a historical perspective: From film to machine-intelligence supported systems. Dentomaxillofac Radiol. 2021;50:20210010. doi: 10.1259/dmfr.20210010. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Chen E, Abbott PV. Dental pulp testing: A review. Int J Dent 2009. 2009:365785. doi: 10.1155/2009/365785. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Glickman GN. AAE consensus conference on diagnostic terminology: Background and perspectives. J Endod. 2009;35:1619–20. doi: 10.1016/j.joen.2009.09.029. [DOI] [PubMed] [Google Scholar]
  • 42.Schwendicke F, Frencken JE, Bjørndal L, Maltz M, Manton DJ, Ricketts D, et al. Managing carious lesions: Consensus recommendations on carious tissue removal. Adv Dent Res. 2016;28:58–67. doi: 10.1177/0022034516639271. [DOI] [PubMed] [Google Scholar]
  • 43.Barros MM, De Queiroz Rodrigues MI, Muniz FW, Rodrigues LK. Selective, stepwise, or nonselective removal of carious tissue: Which technique offers lower risk for the treatment of dental caries in permanent teeth? A systematic review and meta-analysis. Clin Oral Investig. 2020;24:521–32. doi: 10.1007/s00784-019-03114-5. [DOI] [PubMed] [Google Scholar]
  • 44.Bjørndal L, Reit C, Bruun G, Markvart M, Kjaeldgaard M, Näsman P, et al. Treatment of deep caries lesions in adults: Randomized clinical trials comparing stepwise versus direct complete excavation, and direct pulp capping versus partial pulpotomy. Eur J Oral Sci. 2010;118:290–7. doi: 10.1111/j.1600-0722.2010.00731.x. [DOI] [PubMed] [Google Scholar]
  • 45.Li T, Zhai X, Song F, Zhu H. Selective versus non-selective removal for dental caries: A systematic review and meta-analysis. Acta Odontol Scand. 2018;76:135–40. doi: 10.1080/00016357.2017.1392602. [DOI] [PubMed] [Google Scholar]
  • 46.Lim ZE, Duncan HF, Moorthy A, McReynolds D. Minimally invasive selective caries removal: A clinical guide. Br Dent J. 2023;234:233–40. doi: 10.1038/s41415-023-5515-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47.Galicia JC, Peters OA. Proposal for a new diagnostic terminology to describe the status of the dental pulp. Int Endod J. 2021;54:1415–6. doi: 10.1111/iej.13545. [DOI] [PubMed] [Google Scholar]
  • 48.Innes NP, Frencken JE, Bjørndal L, Maltz M, Manton DJ, Ricketts D, et al. Managing carious lesions: Consensus recommendations on terminology. Adv Dent Res. 2016;28:49–57. doi: 10.1177/0022034516639276. [DOI] [PubMed] [Google Scholar]
  • 49.European Society of Endodontology. Quality guidelines for endodontic treatment: Consensus report of the European Society of Endodontology. Int Endod J. 2006;39:921–30. doi: 10.1111/j.1365-2591.2006.01180.x. [DOI] [PubMed] [Google Scholar]
  • 50.Mente J, Hufnagel S, Leo M, Michel A, Gehrig H, Panagidis D, et al. Treatment outcome of mineral trioxide aggregate or calcium hydroxide direct pulp capping: Long-term results. J Endod. 2014;40:1746–51. doi: 10.1016/j.joen.2014.07.019. [DOI] [PubMed] [Google Scholar]
  • 51.Zehnder M, Söderling E, Salonen J, Waltimo T. Preliminary evaluation of bioactive glass S53P4 as an endodontic medication in vitro. J Endod. 2004;30:220–4. doi: 10.1097/00004770-200404000-00009. [DOI] [PubMed] [Google Scholar]
  • 52.Dammaschke T, Leidinger J, Schäfer E. Long-term evaluation of direct pulp capping--treatment outcomes over an average period of 6.1 years. Clin Oral Investig. 2010;14:559–67. doi: 10.1007/s00784-009-0326-9. [DOI] [PubMed] [Google Scholar]
  • 53.Kundzina R, Stangvaltaite L, Eriksen HM, Kerosuo E. Capping carious exposures in adults: A randomized controlled trial investigating mineral trioxide aggregate versus calcium hydroxide. Int Endod J. 2017;50:924–32. doi: 10.1111/iej.12719. [DOI] [PubMed] [Google Scholar]
  • 54.Harms CS, Schäfer E, Dammaschke T. Clinical evaluation of direct pulp capping using a calcium silicate cement-treatment outcomes over an average period of 2.3 years. Clin Oral Investig. 2019;23:3491–9. doi: 10.1007/s00784-018-2767-5. [DOI] [PubMed] [Google Scholar]
  • 55.Parirokh M, Torabinejad M. Mineral trioxide aggregate: A comprehensive literature review--Part I: Chemical, physical, and antibacterial properties. J Endod. 2010;36:16–27. doi: 10.1016/j.joen.2009.09.006. [DOI] [PubMed] [Google Scholar]
  • 56.Duncan HF. Present status and future directions-vital pulp treatment and pulp preservation strategies. Int Endod J. 2022;55(Suppl 3):497–511. doi: 10.1111/iej.13688. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol. 1965;20:340–9. doi: 10.1016/0030-4220(65)90166-0. [DOI] [PubMed] [Google Scholar]
  • 58.Ricucci D, Loghin S, Siqueira JF., Jr Correlation between clinical and histologic pulp diagnoses. J Endod. 2014;40:1932–9. doi: 10.1016/j.joen.2014.08.010. [DOI] [PubMed] [Google Scholar]
  • 59.Al-Hiyasat AS, Al-Hammouri K, Abu-Hantash RO, Hattar S, Al-Omari WM. Success rate of direct pulp capping on permanent teeth using bioactive materials: A systematic review and meta-analysis of randomized clinical trials. Restor Dent Endod. 2024;49:e34. doi: 10.5395/rde.2024.49.e34. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60.AAE Position Statement on Vital Pulp Therapy. J Endod. 2021;47:1340–4. doi: 10.1016/j.joen.2021.07.015. [DOI] [PubMed] [Google Scholar]
  • 61.Taha NA, Ahmad MB, Ghanim A. Assessment of mineral trioxide aggregate pulpotomy in mature permanent teeth with carious exposures. Int Endod J. 2017;50:117–25. doi: 10.1111/iej.12605. [DOI] [PubMed] [Google Scholar]
  • 62.Barthel CR, Rosenkranz B, Leuenberg A, Roulet JF. Pulp capping of carious exposures: Treatment outcome after 5 and 10 years: A retrospective study. J Endod. 2000;26:525–8. doi: 10.1097/00004770-200009000-00010. [DOI] [PubMed] [Google Scholar]
  • 63.Aguilar P, Linsuwanont P. Vital pulp therapy in vital permanent teeth with cariously exposed pulp: A systematic review. J Endod. 2011;37:581–7. doi: 10.1016/j.joen.2010.12.004. [DOI] [PubMed] [Google Scholar]
  • 64.Barrangizan M, Asgary S, Nosrat A. Partial pulpotomy as an alternative treatment for cariously exposed mature permanent molars: A case series. J Endod. 2019;45:1062–7. [Google Scholar]
  • 65.Asgary S, Ahmadyar M. Vital pulp therapy using calcium-enriched mixture: An evidence-based review. J Conserv Dent. 2013;16:92–8. doi: 10.4103/0972-0707.108173. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 66.Parirokh M, Torabinejad M. Mineral trioxide aggregate: A comprehensive literature review--Part III: Clinical applications, drawbacks, and mechanism of action. J Endod. 2010;36:400–13. doi: 10.1016/j.joen.2009.09.009. [DOI] [PubMed] [Google Scholar]
  • 67.Roberts HW, Toth JM, Berzins DW, Charlton DG. Mineral trioxide aggregate material use in endodontic treatment: A review of the literature. Dent Mater. 2008;24:149–64. doi: 10.1016/j.dental.2007.04.007. [DOI] [PubMed] [Google Scholar]
  • 68.Grech L, Mallia B, Camilleri J. Characterization of set intermediate restorative material, biodentine, bioaggregate and a prototype calcium silicate cement for use as root-end filling materials. Int Endod J. 2013;46:632–41. doi: 10.1111/iej.12039. [DOI] [PubMed] [Google Scholar]
  • 69.Peumans M, De Munck J, Van Landuyt KL, Poitevin A, Lambrechts P, Van Meerbeek B. Eight-year clinical evaluation of a 2-step self-etch adhesive with and without selective enamel etching. Dent Mater. 2010;26:1176–84. doi: 10.1016/j.dental.2010.08.190. [DOI] [PubMed] [Google Scholar]
  • 70.Nakajima M, Sano H, Burrow MF, Tagami J, Yoshiyama M, Ebisu S, et al. Tensile bond strength and SEM evaluation of caries-affected dentin using dentin adhesives. J Dent Res. 1995;74:1679–88. doi: 10.1177/00220345950740100901. [DOI] [PubMed] [Google Scholar]
  • 71.Yoshiyama M, Tay FR, Doi J, Nishitani Y, Yamada T, Itou K, et al. Bonding of self-etch and total-etch adhesives to carious dentin. J Dent Res. 2002;81:556–60. doi: 10.1177/154405910208100811. [DOI] [PubMed] [Google Scholar]
  • 72.Mount GJ, Ngo HC. Minimal intervention: Early lesions. Quintessence Int. 2000;31:535–46. [PubMed] [Google Scholar]
  • 73.Cushley S, Duncan HF, Lappin MJ, Chua P, Elamin AD, Clarke M, et al. Efficacy of direct pulp capping for management of cariously exposed pulps in permanent teeth: A systematic review and meta-analysis. Int Endod J. 2021;54:556–71. doi: 10.1111/iej.13449. [DOI] [PubMed] [Google Scholar]
  • 74.Zander HA, Glass RL. The healing of phenolized pulp exposures. Oral Surg Oral Med Oral Pathol. 1949;2:803–10. doi: 10.1016/0030-4220(49)90116-4. [DOI] [PubMed] [Google Scholar]
  • 75.Matsuo T, Nakanishi T, Shimizu H, Ebisu S. A clinical study of direct pulp capping applied to carious-exposed pulps. J Endod. 1996;22:551–6. doi: 10.1016/S0099-2399(96)80017-3. [DOI] [PubMed] [Google Scholar]
  • 76.Asgary S, Eghbal MJ, Parirokh M, Ghanavati F, Rahimi H. A comparative study of histologic response to different pulp capping materials and a novel endodontic cement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;106:609–14. doi: 10.1016/j.tripleo.2008.06.006. [DOI] [PubMed] [Google Scholar]
  • 77.Nowicka A, Lipski M, Parafiniuk M, Sporniak-Tutak K, Lichota D, Kosierkiewicz A, et al. Response of human dental pulp capped with biodentine and mineral trioxide aggregate. J Endod. 2013;39:743–7. doi: 10.1016/j.joen.2013.01.005. [DOI] [PubMed] [Google Scholar]
  • 78.Hilton TJ, Ferracane JL, Mancl L Northwest Practice-based Research Collaborative in Evidence-based Dentistry (NWP) Comparison of CaOH with MTA for direct pulp capping: A PBRN randomized clinical trial. J Dent Res. 2013;92:16S–22S. doi: 10.1177/0022034513484336. [DOI] [PMC free article] [PubMed] [Google Scholar]

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