Chapter 1 presents a detailed overview of laboratory techniques for preparing teeth and periradicular tissues for light microscopy. It distinguishes between clinical diagnostic and research-focused histological processing, emphasizing the greater precision allowed in research settings. The chapter thoroughly explains key steps such as fixation, decalcification, paraffin embedding, sectioning, and staining, with particular focus on preserving the dental pulp and reducing artifacts. It addresses the challenges of adequately fixing pulp tissue encased in hard structures and describes solutions to improve fixative penetration. Special emphasis is given to staining methods, notably the Taylor-modified Brown and Brenn technique for bacterial detection, and to differentiating true pathological changes from artifacts introduced during specimen handling.

Chapter 2 provides a detailed examination of the normal dentin-pulp complex and associated periradicular tissues. It describes the structure and function of the normal dental pulp, including its cellular composition (odontoblasts, fibroblasts, immune cells) and specialized zones (odontoblast layer, cell-free zone, cell-rich zone, and pulp proper). The chapter also explains pulp vascularization and innervation, highlighting how the pulp is highly vascularized yet vulnerable to inflammation due to its encasement in hard tissue. Additionally, it discusses common features like pulp calcifications (e.g., pulp stones) and their clinical significance. Finally, it covers the anatomy and physiology of the periodontal ligament, cementum, and alveolar bone, emphasizing their roles in tooth support, remodeling, and immune responses.

Chapter 3 explores the response of the dentin-pulp complex to carious lesions, beginning with the latest insights into early non-cavitated lesions and progressing through moderate and deep caries to the point of bacterial pulp invasion. It highlights the pulp’s defense mechanisms, including tertiary dentin formation and increasingly complex immune-inflammatory responses. The chapter outlines the histological changes that mark the threshold between reversible and irreversible pulp inflammation. It also details the progression of pulpal degeneration following bacterial ingress and demonstrates how early periapical changes can be detected histologically, even when necrosis remains confined to the pulp chamber.

Chapter 4 delves into the principles and controversies surrounding vital pulp therapy (VPT), advocating for treatments that preserve pulp vitality in cases of deep caries. It critically evaluates the debate between selective and non-selective caries excavation, ultimately challenging the biological safety of leaving infected dentin beneath restorations. Histological evidence shows that "firm" or "leathery" dentin left during selective excavation invariably contains viable bacteria capable of provoking chronic pulp inflammation, even in asymptomatic teeth. The chapter presents multiple case studies comparing outcomes of selective versus complete caries removal, demonstrating that long-term pulpal health correlates with total bacterial elimination. It concludes that preserving pulp vitality requires both biological understanding and meticulous clinical execution, with an emphasis on thorough caries removal and well-sealed restorations to prevent persistent infection.

Chapter 5 provides a structured overview of the clinical principles, indications, and operative protocols for direct pulp capping, indirect pulp capping, partial pulpotomy, and full pulpotomy. Each procedure is discussed with a strong focus on its biological rationale, clinical judgment, and the technical factors that impact outcomes. The chapter also highlights the critical role of material selection, emphasizing the need for biocompatible agents that promote pulp healing and regeneration. By combining biological insight, modern materials, and precise clinical execution, this chapter offers a comprehensive, evidence-based guide for achieving predictable success in vital pulp therapy.

Chapter 6 emphasizes the critical role of restorative procedures as an essential extension of vital pulp therapy (VPT). It highlights that even the most carefully executed pulp therapy can fail if the overlying restoration permits bacterial leakage, thermal stress, or mechanical failure. The chapter reviews contemporary restorative materials, such as resin composites, glass ionomer cements, and adhesives, through the lens of their biocompatibility and sealing ability, stressing that pulp health depends primarily on preventing microbial ingress. Histological evidence from clinical cases demonstrates how restoration quality directly influences pulpal outcomes, showing that leakage, not symptoms, often predicts inflammation or necrosis.

Chapter 7 examines the etiopathogenesis of apical periodontitis as a consequence of pulp inflammation resulting from bacterial invasion. It presents the histological classification of apical lesions—abscesses, granulomas, and cysts—based on their morphological features and predominant inflammatory cell types. The chapter distinguishes between true cysts and bay (pocket) cysts, and highlights the rare occurrence of respiratory epithelium in apical cysts, typically associated with proximity to the maxillary sinus. It also explores the potential presence of bacteria within apical lesions and underscores the limitations of radiographic diagnosis in differentiating lesion types. Finally, it discusses the prevalence, histopathological characteristics, and clinical significance of root resorption, emphasizing its frequent underdetection on radiographs.

Chapter 8 presents a thorough exploration of apical periodontitis as a biofilm-mediated infectious disease that originates from microbial colonization of the root canal system. It describes the various pathways of infection, including caries, cracks, trauma, and periodontal communication, and emphasizes the role of structured bacterial biofilms in disease persistence and resistance to treatment. Histological and microbiological evidence shows that biofilms are found not only within the root canal but also on external root surfaces, especially in persistent or post-treatment cases. The chapter highlights the polymicrobial nature of endodontic infections, dominated by anaerobic species, and explains how extraradicular infections like actinomycosis or calcified biofilms may require surgical intervention. Effective management depends on recognizing, disrupting, and removing these biofilms from all anatomical areas they occupy.

Chapter 9 explores the etiopathogenesis and morphological features of both internal and external root resorption. It presents new evidence that questions the traditionally held belief in the protective role of predentin, suggesting that internal resorption may not always require prior damage to the odontoblast layer and predentin. The chapter also re-examines the conventional classification of internal resorption into “inflammatory” and “replacement” types, proposing a more nuanced interpretation based on recent findings. Various presentations of invasive cervical external resorption are illustrated, with particular attention to cases showing bone proliferation within the resorptive area. The chapter concludes with a discussion of diagnostic criteria and treatment strategies.

Chapter 10 redefines endodontic success through a biological lens, prioritizing infection control, tissue preservation, and long-term healing over technical execution alone. Treatment approaches are guided by the pulp’s status—vital or necrotic—with the former requiring conservation strategies and the latter demanding comprehensive disinfection. Emphasis is placed on asepsis, thorough caries removal, and restorative planning to create biologically favorable conditions. Through numerous clinical cases, the chapter offers practical guidance on pre-endodontic preparation, access cavity design, working length determination, intracanal medication, and obturation, all aligned with biological objectives. It also addresses the management of separated instruments and provides a balanced discussion on retreatment versus apical microsurgery for persistent cases.

This chapter provides an in-depth analysis of tooth cracks and vertical root fractures, covering their etiology, clinical presentation, diagnostic challenges, histopathology, and management strategies. Cracks may be asymptomatic or cause vague, difficult-to-localize pain, and can lead to pulpal inflammation, necrosis, and periradicular disease if they serve as conduits for bacterial infiltration. Diagnosis requires a multifactorial approach, incorporating magnification, transillumination, dyes, bite tests, radiographs, and sometimes surgical exploration. Treatment decisions depend on pulp vitality, crack extent, and periodontal involvement, with options ranging from conservative monitoring to endodontic therapy and full-coverage restorations. Vertical root fractures, particularly in previously treated teeth, often have a poor prognosis, highlighting the importance of early detection, occlusal management, and patient education on the risks of fracture progression.

This chapter provides a comprehensive overview of how periradicular tissues heal following endodontic therapy. Healing is influenced by pulp status, infection control, and procedural precision, with biologically respectful approaches leading to more favorable outcomes. The healing process involves predictable biological phases—hemostasis, inflammation, proliferation, and remodeling—and is shaped by host responses, the extent of injury, and the presence or absence of microorganisms. Histological studies show that healing is more predictable when instrumentation and obturation remain within the root canal, and that small amounts of extruded materials are generally well tolerated if infection is absent. Ultimately, successful periradicular healing depends less on the radiographic appearance of root fillings and more on microbial elimination, aseptic technique, and maintenance of an effective coronal seal.

This chapter critically examines the anatomy, pathology, and clinical significance of lateral canals and apical ramifications, clarifying misconceptions around the need to fill them. While these anatomical structures can act as conduits for bacterial migration and may contribute to lateral periodontitis, their involvement in treatment failure depends on size, patency, and microbial load. Histological evidence shows that filling materials rarely seal or disinfect these spaces effectively, and their presence in radiographs does not guarantee successful treatment. The chapter emphasizes that infection control, rather than obturation of ramifications, is key to healing, and that calcium hydroxide may help, though its efficacy is limited. Ultimately, disinfection—not filling—is the biologically meaningful goal in managing ramifications during root canal therapy.

This chapter presents recent research that updates the classification of root canal treatment failure causes. While persistent bacterial infection in anatomically complex areas of the root canal system remains the primary reason for failure, new evidence highlights the role of coronal leakage in compromising long-term outcomes. The chapter also discusses biofilms on external apical surfaces, sometimes forming calculus-like deposits, and actinomycotic colonies within periapical lesions, both of which are resistant to conventional disinfection. The potential role of true cysts as a cause of treatment failure is critically examined through histological analysis. Finally, the chapter evaluates factors influencing healing after apical surgery, with a focus on the biological performance of various biomaterials.

This chapter explores the complex anatomical and pathological connections between the dental pulp and periodontium, emphasizing that communication through apical, lateral, and furcal canals allows the bidirectional spread of bacteria and inflammation. While endodontic infections often affect the periodontium, advanced periodontal disease rarely causes significant pulpal changes unless biofilms reach the apical foramen or enter through exposed dentin and lateral canals. Histological studies confirm that the pulp typically remains healthy despite severe periodontal destruction, though isolated cases show that bacteria can invade pulpal vessels even before apical involvement. The chapter also classifies endodontic-periodontal lesions based on their origin and progression—primary endodontic, primary periodontal, and true combined lesions—and discusses clinical diagnosis and treatment strategies accordingly. Finally, it addresses root changes, root caries, and the effects of periodontal treatment on pulp vitality, concluding that most pulps withstand periodontal insults unless anatomical barriers are compromised.

This chapter presents a unique, 38-year longitudinal record of endodontically treated teeth that were eventually extracted, revealing patterns of failure rooted in structural, restorative, caries-related, or periodontal causes. Structural fatigue, particularly vertical root fractures due to occlusal stress, accounted for the largest portion of tooth loss, while secondary caries and periodontal breakdown were also common contributors. The data emphasize the importance of coronal seal integrity, occlusal balance, and maintenance over time, noting that longevity does not always equate to success. Observations show that teeth often fail not due to endodontic reinfection but as a culmination of biomechanical aging and restorative decline. Ultimately, the chapter reframes failure as part of a tooth’s natural life cycle, shaped by biological and functional forces across decades.