Diagnosis and Management of Apical Fenestrations Associated with Endodontic Diseases: A Literature Review.

Apical fenestration describes a window-like opening of the alveolar bone that involves the root apex of the associated tooth. Mucosal fenestration is a similar defect of the overlying mucosa and, when presented with a concomitant apical fenestration, may expose the root apex to the oral environment. A fenestration may arise from physiological and pathological processes. Although its presence does not necessitate treatment per se, these lesions have significant clinical implications when associated with endodontic diseases. Apical fenestrations associated with endodontic infections are relatively uncommon and can easily be overlooked or misdiagnosed. A thorough understanding of these lesions is key for timely diagnosis and successful management. The aim of this study was to review the epidemiology, aetiological factors, characteristics, management methods and potential outcomes of apical fenestrations associated with endodontic diseases. A search of online databases for relevant studies was conducted. With the inclusion of hand searched articles, 20 articles, consisting of case reports and series, were identified, and the key characteristics of each case were summarised. Apical fenestrations were found to be most commonly associated with maxillary teeth and almost always occur on the buccal aspect of the alveolar bone. Clinicians may consider the possibility of an apical fenestration with concurrent endodontic pathology when patients present with non-healing sinus tracts, exposed tooth apices and/or persistent pain after endodontic treatment, particularly on palpation and mastication. Clinical signs and symptoms can vary, hence cone-beam computed tomography is an important tool for diagnosis. The management involves surgically restoring a favourable anatomical configuration of the root apex in relation to the alveolar bony housing and may be combined with guided tissue regeneration and/or grafting procedures. Sloughing, reopening and infection are potential complications. The literature on apical fenestrations associated with endodontic diseases is limited, thus further research is needed to develop evidence-based guidelines for the diagnosis and management of these lesions.

Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology.

Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.

Pulp canal obliteration after traumatic injuries in permanent teeth - scientific fact or fiction?

Pulp canal obliteration (PCO) is a frequent finding associated with pulpal revascularization after luxation injuries of young permanent teeth. The underlying mechanisms of PCO are still unclear, and no experimental scientific evidence is available, except the results of a single histopathological study. The lack of sound knowledge concerning this process gives rise to controversies, including the most suitable denomination. More than a mere semantic question, the denomination is an important issue, because it reflects the nature of this process, and directly impacts the treatment plan decision. The hypothesis that accelerated dentin deposition is related to the loss of neural control over odontoblastic secretory activity is well accepted, but demands further supportive studies. PCO is seen radiographically as a rapid narrowing of pulp canal space, whereas common clinical features are yellow crown discoloration and a lower or non-response to sensibility tests. Late development of pulp necrosis and periapical disease are rare complications after PCO, rendering prophylactic endodontic intervention useless. Indeed, yellowish or gray crown discoloration may pose a challenge to clinicians, and may demand endodontic intervention to help restore aesthetics. This literature review was conducted to discuss currently available information concerning PCO after traumatic dental injuries (TDI), and was gathered according to three topics: I) physiopathology of PCO after TDI; II) frequency and predictors of pulpal healing induced by PCO; and III) clinical findings related to PCO. Review articles, original studies and case reports were included aiming to support clinical decisions during the follow-up of teeth with PCO, and highlight future research strategies.

Association of S100 calcium-binding protein A12, receptor for advanced glycation endproducts, and nuclear factor-κB expression with inflammation in pulp tissues from tooth caries.

AIM: S100 calcium-binding protein A1 (S100A12) is a pro-inflammatory molecule which is secreted during inflammation and induces chemotaxis and the production of pro-inflammatory cytokines via interaction with receptor for advanced glycation endproducts (RAGE) and subsequent, activation of nuclear factor-κB (NF-κB). The present study was designed to determine the expression levels of S100A12, RAGE, and NF-κB in the inflamed pulp of carried teeth. METHODS: In the present study, mRNA from 50 inflamed pulp and 50 healthy pulp were used for expression studies using real-time polymerase chain reaction. The expression levels of S100A12, RAGE, and NF-κB were compared between inflamed and healthy tissues. RESULTS: The results revealed that the expression of S100A12, but not of RAGE or NF-κB, was significantly decreased in inflamed pulp when compared to healthy pulp. mRNA levels of RAGE were also increased in the inflamed pulp taken from men when compared with women. CONCLUSION: The results suggest that S100A12 does not participate in the induction of inflammation in dental pulp. However, RAGE can participate in the inflammation in the pulp of males.

Pulp canal obliteration after traumatic injuries in permanent teeth - scientific fact or fiction?

Abstract: Pulp canal obliteration (PCO) is a frequent finding associated with pulpal revascularization after luxation injuries of young permanent teeth. The underlying mechanisms of PCO are still unclear, and no experimental scientific evidence is available, except the results of a single histopathological study. The lack of sound knowledge concerning this process gives rise to controversies, including the most suitable denomination. More than a mere semantic question, the denomination is an important issue, because it reflects the nature of this process, and directly impacts the treatment plan decision. The hypothesis that accelerated dentin deposition is related to the loss of neural control over odontoblastic secretory activity is well accepted, but demands further supportive studies. PCO is seen radiographically as a rapid narrowing of pulp canal space, whereas common clinical features are yellow crown discoloration and a lower or non-response to sensibility tests. Late development of pulp necrosis and periapical disease are rare complications after PCO, rendering prophylactic endodontic intervention useless. Indeed, yellowish or gray crown discoloration may pose a challenge to clinicians, and may demand endodontic intervention to help restore aesthetics. This literature review was conducted to discuss currently available information concerning PCO after traumatic dental injuries (TDI), and was gathered according to three topics: I) physiopathology of PCO after TDI; II) frequency and predictors of pulpal healing induced by PCO; and III) clinical findings related to PCO. Review articles, original studies and case reports were included aiming to support clinical decisions during the follow-up of teeth with PCO, and highlight future research strategies.

Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology

Abstract: Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.

Axin2-expressing cells differentiate into reparative odontoblasts via autocrine Wnt/ß-catenin signaling in response to tooth damage.

In non-growing teeth, such as mouse and human molars, primary odontoblasts are long-lived post-mitotic cells that secrete dentine throughout the life of the tooth. New odontoblast-like cells are only produced in response to a damage or trauma. Little is known about the molecular events that initiate mesenchymal stem cells to proliferate and differentiate into odontoblast-like cells in response to dentine damage. The reparative and regenerative capacity of multiple mammalian tissues depends on the activation of Wnt/ß-catenin signaling pathway. In this study, we investigated the molecular role of Wnt/ß-catenin signaling pathway in reparative dentinogenesis using an in vivo mouse tooth damage model. We found that Axin2 is rapidly upregulated in response to tooth damage and that these Axin2-expressing cells differentiate into new odontoblast-like cells that secrete reparative dentine. In addition, the Axin2-expressing cells produce a source of Wnt that acts in an autocrine manner to modulate reparative dentinogenesis.

Pulp and apical tissue response to deep caries in immature teeth: A histologic and histobacteriologic study.

Descriptions of the pathologic changes in the pulp and associated apical structures of human immature teeth in response to deep caries are lacking in the literature. OBJECTIVES: This article describes the histologic events associated with the radicular pulp and the apical tissues of human immature teeth following pulp inflammation and necrosis. METHODS: Twelve immature teeth with destructive caries lesions were obtained from 8 patients. Two intact immature teeth served as controls. Teeth were extracted for reasons not related to this study and immediately processed for histopathologic and histobacteriologic analyses. Serial sections were examined for the pulp conditions and classified as reversible or irreversible pulp inflammation, or pulp necrosis. Other histologic parameters were also evaluated. RESULTS: In the 3 cases with reversible pulp inflammation, tissue in the pulp chamber showed mild to moderate inflammation and tertiary dentin formation related to tubules involved in the caries process. Overall, the radicular pulp tissue, apical papilla and Hertwig's epithelial root sheath (HERS) exhibited characteristics of normality. In the 3 cases with irreversible pulp inflammation, the pulps were exposed and severe inflammation occurred in the pulp chamber, with minor areas of necrosis and infection. Large areas of the canal walls were free from odontoblasts and lined by an atubular mineralized tissue. The apical papilla showed extremely reduced cellularity or lack of cells and HERS was discontinuous or absent. In the 6 cases with pulp necrosis, the coronal and radicular pulp tissue was necrotic and colonized by bacterial biofilms. The apical papilla could not be discerned, except for one case. HERS was absent in the necrotic cases. CONCLUSION: While immature teeth with reversible pulpitis showed histologic features almost similar to normal teeth in the canal and in the apical region, those with irreversible pulpitis and necrosis exhibited significant alterations not only in the radicular pulp but also in the apical tissues, including the apical papilla and HERS. CLINICAL SIGNIFICANCE: Alterations in the radicular pulp and apical tissues help explain the outcome of current regenerative/reparative therapies and should be taken into account when devising more predictable therapeutic protocols for teeth with incomplete root formation.

[The importance of pulp therapy in deciduous teeth]. / Importance des traitements pulpaires en denture de lait.

Preserving primary teeth is crucial for maintaining the maxillary growth, aesthetics, mastication, and speech and for preventing from abnormal habits. Given the peculiar anatomy of the primary tooth, caries grow faster and more frequently to the pulp. In pediatric dentistry, new methods and enhanced material have been recently released on the market and broadened the field of treatments. In this paper, we review the pulp diseases affecting children and focus on the current root canal therapies that favour the physiological primary tooth loss.

Conserver les dents de lait est essentiel pour assurer la croissance des maxillaires, l'esthétique, la mastication et la phonation ainsi que pour prévenir l'apparition de dysfonctions. Vu les particularités anatomiques des dents de lait, la carie progresse toujours plus rapidement et plus fréquemment jusqu'à la pulpe. L'avènement de nouvelles techniques et de nouveaux matériaux en dentisterie pédiatrique a élargi nos possibilités thérapeutiques. De même, l'interdiction d'utilisation de certains produits a conduit le pédodontiste à devoir trouver des alternatives de traitement. Le but de cet article est de faire le point sur les pathologies pulpaires chez l'enfant et sur les thérapeutiques endocanalaires actuelles.

The expression of hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1) and HCN2 in the rat trigeminal ganglion, sensory root, and dental pulp.

Hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1) and 2 (HCN2) are abundantly expressed in primary sensory neurons and contribute to neuronal excitability and pathological pain. We studied the expression of HCN1 and HCN2 in the rat trigeminal ganglion (TG) neurons and axons in the dental pulp, and the changes in their expression following inflammation, using light- and electron-microscopic immunocytochemistry and quantitative analysis. HCN1 and HCN2 were expressed predominantly in large-sized, neurofilament 200-immunopositive (+) or parvalbumin+ soma in the TG whereas they were expressed mostly in unmyelinated and small myelinated axons in the sensory root. The expression was particularly strong along the plasma membrane in the soma. In the dental pulp, majority of HCN1+ and HCN2+ axons coexpressed calcitonin gene-related peptide. They were expressed mainly in the peripheral pulp and pulp horn where the axons branch extensively in the dental pulp. The expression of HCN1 and HCN2 in TG neurons increased significantly in rats with experimentally induced inflammation of the dental pulp. Our findings support the notion that HCN1 and HCN2 are expressed mainly by both the soma of mechanosensitive neurons in the TG and peripheral axons of nociceptive neurons in the sensory root, and may play a role in the mechanisms of inflammatory pain from the dental pulp.

Estimates of sensitivity and specificity of electric pulp testing depend on pulp disease spectrum: a modelling study.

AIM: To demonstrate how the spectrum of diseased pulps may influence sensitivity and specificity in diagnostic studies on pulp status. METHODOLOGY: An original sample from a previous study consisting of 59 teeth scheduled for root canal treatment was used where the relationship between the response to electric pulp testing and the visual status of the pulp was evaluated. To alter the spectrum of diseased pulps, a hypothetical sample of asymptomatic teeth with deep caries lesions was added to the original sample. Sensitivity and specificity were then compared for the two samples. RESULTS: In the original sample of 59 teeth, sensitivity was 72% and specificity 90%. When the spectrum of diseased pulps was altered, sensitivity decreased to 67% and specificity increased to 97%. The change in disease spectrum also decreased the prevalence of necrotic pulps. CONCLUSIONS: The spectrum of diseased pulps included in a diagnostic study on the accuracy of electric pulp testing, and indirectly also disease prevalence (here pulp necrosis), influences estimates of sensitivity and specificity. This implies that estimates of diagnostic accuracy from one study with a particular tooth population spectrum may not apply to another tooth population with a different disease spectrum.

Histopathological condition of the remaining tissues after endodontic infection of rat immature teeth.

INTRODUCTION: Recently, case reports have shown that immature teeth diagnosed with necrotic pulp and periapical periodontitis can be repaired through a regenerative endodontic procedure. True regeneration depends on the presence of stem cells in the remaining vital tissues. The aim of this study was to evaluate the histologic condition of the pulp tissue, root apical papilla, and periapical tissues after inducing endodontic infection in immature rat teeth for different periods. METHODS: This study evaluated 18 first upper rat molars (36 roots). Periapical lesions were induced and were confirmed radiographically, and the animals were divided into 3 groups according to the days of pulp exposure for endodontic infection induction: 30, 60, and 90 days. Histologic analysis was performed in 5 different areas (ie, cervical, middle, and apical root canal thirds; the apical papilla; and the periapex surrounding the apical papilla). RESULTS: At 30 days, one third of the specimens still showed vital but intensely inflamed pulp tissue in the apical third and vital apical papilla with varying degrees of inflammation. After 60 days, the results were similar with respect to the apical pulp tissue and apical papilla. Completely necrotic pulp tissue in the space canal and vital apical papilla were observed in about 67% of the cases after 90 days. CONCLUSIONS: Vital pulp tissue was observed in the apical third until 60 days and in the vital apical papilla until 90 days of infection in a rat model.

Development of an ex vivo coculture system to model pulpal infection by Streptococcus anginosus group bacteria.

INTRODUCTION: Streptococcus anginosus group (SAG) bacteria are opportunistic pathogens and a major cause of pulpal infection and subsequent abscess formation. Understanding of the processes involved in SAG oral infections has been limited by the lack of an appropriate model system. METHODS: Cocultures of SAG bacteria and mammalian tooth slices were maintained using a combination of Dulbecco modified eagle medium and brain-heart infusion broth at 60 rpm, 37°C, 5% CO(2) for 4, 8, or 24 hours before histologic examination or staining with acridine orange/ethidium bromide. Tooth slices were also incubated as described with SAG bacteria stained with fluorescein diacetate. Pulps were extirpated from infected and sterile cultured tooth slices, messenger RNA was extracted and converted to complementary DNA, and polymerase chain reaction were performed for genes encoding tumor necrosis factor α, interleukin 1ß, and interleukin-6. RESULTS: SAG bacteria were able to adhere directly to the central region of the pulpal matrix in small foci that were associated with a localized matrix breakdown. Acridine orange-ethidium bromide staining and cell counts indicated a decrease in mammalian cell viability with increasing incubation times in the presence of SAG bacteria. The increased expression of tumor necrosis factor α and interleukin 1ß was detected in infected tooth slices. CONCLUSIONS: A novel ex vivo model system has been developed that allows coculture of SAG bacteria with a 3-dimensional organotypic tooth slice. The model allows observation of bacterial growth patterns and subsequent responses from host tissues. Therefore, it may be of future use in testing the efficacy of both antimicrobial and anti-inflammatory treatments for use in endodontic therapy.

Microscopic aspects of pulpal changes in patients with chronic marginal periodontitis.

Chronic periodontitis is one of the most frequent and severe diseases involving the tooth. Untreated, they can lead to tooth loss. Our study involved 67 patients with chronic marginal periodontitis who underwent tooth extraction, of which 29 had moderate periodontal lesions and 38 severe periodontal lesions. The microscopic study of the dental pulp revealed significant changes in all patients. In patients with moderate periodontitis the pulp tissue was found to be the site of an enhanced process of collagenous fibrosis associated with a moderate inflammatory infiltrate, dystrophic mineralization, reduced blood vascularization and arteriolosclerosis. The dental pulp of patients with severe periodontitis showed an abundant chronic inflammatory infiltrate associated with pulpal necrosis, vascular congestion, microhemorrhages, dentin demineralization and odontoblast impairment.

Comprehensive analysis of secondary dental root canal infections: a combination of culture and culture-independent approaches reveals new insights.

Persistence of microorganisms or reinfections are the main reasons for failure of root canal therapy. Very few studies to date have included culture-independent methods to assess the microbiota, including non-cultivable microorganisms. The aim of this study was to combine culture methods with culture-independent cloning methods to analyze the microbial flora of root-filled teeth with periradicular lesions. Twenty-one samples from previously root-filled teeth were collected from patients with periradicular lesions. Microorganisms were cultivated, isolated and biochemically identified. In addition, ribosomal DNA of bacteria, fungi and archaea derived from the same samples was amplified and the PCR products were used to construct clone libraries. DNA of selected clones was sequenced and microbial species were identified, comparing the sequences with public databases. Microorganisms were found in 12 samples with culture-dependent and -independent methods combined. The number of bacterial species ranged from 1 to 12 in one sample. The majority of the 26 taxa belonged to the phylum Firmicutes (14 taxa), followed by Actinobacteria, Proteobacteria and Bacteroidetes. One sample was positive for fungi, and archaea could not be detected. The results obtained with both methods differed. The cloning technique detected several as-yet-uncultivated taxa. Using a combination of both methods 13 taxa were detected that had not been found in root-filled teeth so far. Enterococcus faecalis was only detected in two samples using culture methods. Combining the culture-dependent and -independent approaches revealed new candidate endodontic pathogens and a high diversity of the microbial flora in root-filled teeth with periradicular lesions. Both methods yielded differing results, emphasizing the benefit of combined methods for the detection of the actual microbial diversity in apical periodontitis.

External radicular resorption: selected cases and review of the literature.

External radicular resorption is a pathological process that generates the loss of cementum, dentin and bone, almost irreversibly, involving vital and pulpless teeth. The early stage is asymptomatic and might be diagnosed by a routine radiograph or a clinical examination. Radicular resorption appears because of cementoclastic, dentinoclastic or/and osteoclastic activity. The process of resorption is associated with a damage of the periodontal ligament as a result of injury and necrosis, macrophages are the first cells that are detected, followed by multinucleated cells, odontoclasts, which affect the cementum and dentin.

Bases morfofisiopatológicas de la respuesta inflamatoria aguda pulpar / Morphophysiopathological bases of pulpar acute inflammatory response

Teniendo en cuenta el desconocimiento existente sobre las bases morfofisiopatológicas que caracterizan la respuesta inflamatoria aguda pulpar; conocimiento este que resulta imprescindible para tomar decisiones según se trate de enfermedades pulpares reversibles o irreversibles, tratables o intratables, tejidos para el recubrimiento y su conservación o pulpas que deben ser extraídas, se decidió describir las mencionadas bases en el presente artículo, con la finalidad de que se reflexione acerca de ello y se debatan los aspectos de mayor interés en relación con el tema.

Given the lack of knowledge on morphophysiopathological bases characterizing pulpar acute inflammatory response, which becomes essential knowledge to make decisions depending on reversible or irreversible and treatable or untreatable pulpar diseases, tissues for covering and preservation or pulps to be extracted, it was decided to describe the bases mentioned in this article in order to reflect on this and to discuss the aspects of greatest significance in relation to the topic.

[An index for untreated severe caries]. / Een index voor onbehandelde ernstige cariës.

Hardly any data are available on the clinical consequences of untreated severe caries, because there is no method to quantify the prevalence of oral conditions resulting from untreated caries. In the Philippines, an index was developed which records for (the location of) each tooth whether caries has reached the dental pulp, whether ulceration is present in the surrounding soft tissues due to sharp edges of fragments of a tooth lost due to caries, or whether a fistula or abscess is present. By adding the index to the existing Decayed Missing Filled Tooth index, insight is provided on the extent and the consequences of untreated caries and research may be carried out on its possible impact on the general health and wellbeing of national populations.

Dental caries and pulpal disease.

This article reviews the diagnostic process, from the first clinically evident stages of the caries process to development of pulpal pathosis. The caries diagnostic process includes 4 interconnected components-staging caries lesion severity, assessing caries lesion activity, and risk assessments at the patient and tooth surface level - which modify treatment decisions for the patient. Pulpal pathosis is diagnosed as reversible pulpitis, irreversible pulpitis (asymptomatic), irreversible pulpitis (symptomatic), and pulp necrosis. Periapical disease is diagnosed as symptomatic apical periodontitis, asymptomatic apical periodontitis, acute apical abscess, and chronic apical abscess. Ultimately, the goal of any diagnosis should be to achieve better treatment decisions and health outcomes for the patient.

Validation of an algorithm for chronic periodontitis risk assessment and prognostication: analysis of an inflammatory reactivity test and selected risk predictors.

BACKGROUND: Patients with severe forms of chronic periodontitis present with varying degrees of decreased inflammatory reactivity. A previously reported algorithm for chronic periodontitis risk assessment and prognostication is based on the analysis of some 20 risk predictors. One of these predictors is a skin provocation test that assesses the individual patient's reactivity to a lipid A challenge. The aim of this report was to analyze results from validation data for the algorithm with respect to the contribution of results of the skin provocation test as a risk predictor for the progression of chronic periodontitis and to compare these results with the contribution from other predictors, namely smoking, angular bony destruction, furcation involvement, abutment teeth, and endodontic pathology. METHODS: Data from a previously reported clinical validation sample were used for the analysis, including the calculation of quality measures and explanatory values using different types of regression analysis and non-parametric testing. RESULTS: Smoking, endodontic pathology, abutment teeth, angular bony destruction, and furcation involvement presented with individual explanatory values for periodontitis progression between 4% and 13% and highly significant parameter estimates. Explanatory values for the results of the skin provocation test ranged between 2.6% and 5.1% depending on the disease severity group, with a positive predictive value of 82% for the identification of high-risk patients. CONCLUSION: The skin provocation test provided a clinically significant contribution to the quality of analysis with the periodontitis risk and prognostication algorithm, in particular in the selection of high-risk patients for in-depth individual tooth analysis.