The Dilemma Of Management Of Cystic Lesions; An Uncertain Way Forward: A Case Report.

Periapical diseases ranges from mild granulomatous lesions to large cystic ones, with the treatments corresponding to their respective pre-operative diagnoses. However, the determination of cause of periapical radiolucency is impossible on pre-operative clinical and radiographic examinations. We present a case highlighting the difficulties encountered in treating a periapical cyst using the current evidence in literature. It demonstrates the uncertainty involved in treating such lesions, owing to the impossible nature of determining the histopathological nature of the cyst, i.e., being either true cysts or pocket cysts. This case includes orthograde re-treatment; decompression of the cystic lesion, followed by peri-apical surgery of two teeth over a course of three years; and the uncertain outcomes encountered after each phase of the treatment.

Autophagy in tooth: Physiology, disease and therapeutic implication.

Autophagy is an evolutionarily conserved cellular process, in which damaged organelles and proteins are engulfed in autophagic vesicles and subsequently fuse with lysosomes for degradation. Autophagy is widely involved in different physiologic or pathologic processes in human. Accumulating evidence indicates that autophagy operates as a critical quality control mechanism to maintain pulp homeostasis and structural integrity of the dentin-pulp complex. Autophagy is activated during stresses and is involved in the pathogenesis of pulpitis and periapical infection. Recent discoveries have also provided intriguing insights into the roles of autophagy in tooth development, pulp aging and stress adaptation. In this review, we provide an update on the multifaceted functions of autophagy in physiology and pathophysiology of tooth. We also discuss the therapeutic implications of autophagy modulation in diseases and the regeneration of dentin-pulp complex.

Mesenchymal stem cell markers in periodontal tissues and periapical lesions.

INTRODUCTION: Mesenchymal stem cells (MSCs) are characterized by the potential to differentiate into multiple cell lineages, high proliferation rates, and self-renewal capacity, in addition to the ability to maintain their undifferentiated state. These cells have been identified in physiological oral tissues such as pulp tissue, dental follicle, apical papilla and periodontal ligament, as well as in pathological situations such as chronic periapical lesions (CPLs). The criteria used for the identification of MSCs include the positive expression of specific surface antigens, with CD73, CD90, CD105, CD44, CD146, STRO-1, CD166, NANOG and OCT4 being the most specific for these cells. AIM: The aim of this review was to explore the literature on markers able to identify MSCs as well as the presence of these cells in the healthy periodontal ligament and CPLs, highlighting their role in regenerative medicine and implications in the progression of these lesions. METHODS: Narrative literature review searching the PubMed and Medline databases. Articles published in English between 1974 and 2020 were retrieved. CONCLUSION: The included studies confirmed the presence of MSCs in the healthy periodontal ligament and in CPLs. Several surface markers are used for the characterization of these cells which, although not specific, are effective in cell recognition. Mesenchymal stem cells participate in tissue repair, exerting anti- inflammatory, immunosuppressive and proangiogenic effects, and are therefore involved in the progression and attenuation of CPLs or even in the persistence of these lesions.

Effect of Periapical Diseases in Development of MRONJ in Immunocompromised Mouse Model.

OBJECTIVES: This study aimed to assess the effect of zoledronic acid on an immunocompromised mice model with periapical disease. MATERIALS AND METHODS: Thirty C57BL/6N mice were randomly divided into three groups (N = 10). All animals were subjected to bilateral ovariectomy (OVX) and then treated with saline (Veh), zoledronic acid (ZA), or concomitant zoledronic acid and dexamethasone (ZA/Dx) for 12 weeks. Eight weeks after starting drug administration, pulpal exposure was conducted on the lower left first molar. Four weeks after pulpal exposure, all mice were sacrificed and the mandibles were collected for radiological and histological examinations. RESULTS: Microcomputed tomography (µ-CT) examination showed significantly reduced periapical bone resorption in the ZA/Dx group and decreased periodontal bone resorption in both ZA and ZA/Dx groups. Higher bone mineral density (BMD) and strengthened microstructure were found in ZA and ZA/Dx groups. More empty lacunae were found in ZA and ZA/Dx groups. CONCLUSIONS: Apical periodontitis aggravates MRONJ under immunocompromised circumstances. Concurrent use of ZA and steroids inhibits alveolar bone resorption but increases the risk of developing MRONJ.

Metformin Ameliorates Periapical Lesions through Suppression of Hypoxia-induced Apoptosis of Osteoblasts.

INTRODUCTION: Intramuscular injection of metformin has been shown to inhibit the progression of periapical lesions in rats by decreasing the number of receptor activator of nuclear factor-κß ligand- and tartrate-resistant acid phosphatase-positive cells. In this study, we investigated the effect of metformin on hypoxia-induced apoptosis of osteoblasts and the therapeutic activity of intracanal metformin in induced periapical lesions in rats. METHODS: The influence of metformin on hypoxia-induced mitochondrial superoxide production in human osteoblasts was examined by using MitoSOX (Invitrogen, Carlsbad, CA) fluorescence dye signaling. The release of cytochrome c from mitochondria and the cleavage of procaspase-9 and poly(adenosine diphosphate-ribose) polymerase were evaluated by Western blot analysis. Apoptotic cell fraction was assessed by DNA content flow cytometry. In a rat model of induced periapical lesions, the effect of intracanal metformin on disease progression was appraised by 2-dimensional radiography and micro-computed tomographic imaging. Oxidative lesions and apoptotic activity of osteoblasts in vivo were estimated, respectively, by 8-hydroxy-2'-deoxyguanosine staining and terminal deoxynucleotidyl transferase dUTP nick end labeling. RESULTS: Metformin inhibited hypoxia-enhanced mitochondrial superoxide production in osteoblasts. Metformin suppressed hypoxia-induced cytochrome c release from mitochondria and the cleavage of procaspase-9 and poly(adenosine diphosphate-ribose) polymerase. Metformin repressed hypoxia-augmented apoptotic cell fraction. In a rat model, intracanal metformin diminished the size of periapical lesions and the oxidative damage and apoptotic activity in osteoblasts. CONCLUSIONS: Hypoxia increased oxidative stress in osteoblasts and enhanced cell death through activation of the mitochondrial pathway of apoptosis. Metformin attenuated the oxidative and cytotoxic action of hypoxia. The therapeutic effect of metformin on periapical lesions is partially caused by its antioxidative activity.

The Expression of Interferon Regulatory Factor 8 in Human Periapical Lesions.

INTRODUCTION: Interferon regulatory factor 8 (IRF8) is a critical transcription factor in innate immune responses that regulates the development and function of myeloid cells. Human periapical lesions are caused by endodontic microbial infections. However, the presence of IRF8 in human periapical lesions remains elusive. This study aims to explore the expression of IRF8 in human periapical lesions and the possible association of IRF8 with macrophages, nuclear factor kappa B (NF-κB) signaling, and the autophagy process. METHODS: Thirty-nine human periapical tissues, including healthy control tissues (n = 15), radicular cysts (RCs, n = 11), and periapical granulomas (PG, n = 13), were examined. Tissues were fixed in paraformaldehyde and analyzed. The inflammatory infiltrates of lesions were evaluated by hematoxylin-eosin, and the expression of IRF8 was analyzed by immunohistochemistry. Double immunofluorescence assessment was performed to colocalize IRF8 with CD68, NF-κB p65, and LC3B. RESULTS: The expression of IRF8 was significantly higher in RCs and PGs than in the healthy control group, but no significant difference was found between RCs and PGs. There were significantly more IRF8-CD68 double-positive cells in RCs and PGs than in the healthy control group, but no significant difference was observed between RCs and PGs. Double-labeling analysis of IRF8 with NF-κB and LC3B indicated that IRF8 expression is associated with NF-κB signaling and the autophagy process during periapical lesions. CONCLUSIONS: IRF8 could be observed and might possibly be involved in macrophages in the development of periapical lesions.

Mucoepidermoid Carcinoma Mimicking a Lesion of Endodontic Origin.

Cancer of the oral cavity and pharynx ranks eighth among the top 10 cancer sites in all United States males. Salivary gland tumors (SGTs) are uncommon, and malignancies in SGT are even more uncommon than benign tumors. Intraoral minor SGTs are rare, and when they do occur, the tumor is often benign. The purpose of this report is to present a case of a malignant, intraoral minor SGT mimicking a lesion of endodontic origin. Histopathologic analysis determined the tumor to be a high-grade mucoepidermoid carcinoma. The patient was referred to oral and maxillofacial surgery where it was determined the patient would best be treated by partial maxillectomy. Recall examination at 5 years revealed no recurrent or new disease. Suspicious lesions require histopathological assessment.

Comparative Expression of CD34, Intercellular Adhesion Molecule-1, and Podoplanin and the Presence of Mast Cells in Periapical Granulomas, Cysts, and Residual Cysts.

INTRODUCTION: The aim of the present study was to compare the immunoexpression of CD34, intercellular adhesion molecule-1 (ICAM-1), and podoplanin and the presence of mast cells with clinical, demographic, radiologic, and histologic features from periapical granulomas, periapical cysts, and residual cysts. METHODS: Thirty-one lesions (5 granulomas, 15 periapical cysts, and 11 residual cysts) were selected. Histologic sections in silanized slides were used for the immunohistochemical reactions. The analysis of the images was performed by using an optical microscope, and data were analyzed with 5% significance (P < .05). RESULTS: Cysts presented atrophic and hyperplastic epithelium in 11 cases (35.5%) and 15 cases (48.8%), respectively (P > .05). The intensity of the inflammatory infiltrate was similar when comparing the 3 groups (P > .05). CD34 and podoplanin expression and the presence of mast cells were similar when comparing the 3 groups; ICAM-1 expression was more intense in granulomas than cysts (P < .05). There were no statistically significant differences associated with the expression of the evaluated markers according to the intensity of the inflammatory infiltrate. CONCLUSIONS: There were no differences in the expression of CD34 and podoplanin and in the presence of mast cells when the 3 groups were compared. ICAM-1 expression was more common in periapical granulomas.

Regenerative endodontics: a comprehensive review.

The European Society of Endodontology and the American Association for Endodontists have released position statements and clinical considerations for regenerative endodontics. There is increasing literature on this field since the initial reports of Iwaya et al. (Dental Traumatology, 17, 2001, 185) and Banchs & Trope (Journal of Endodontics, 30, 2004, 196). Endogenous stem cells from an induced periapical bleeding and scaffolds using blood clot, platelet rich plasma or platelet-rich fibrin have been utilized in regenerative endodontics. This approach has been described as a 'paradigm shift' and considered the first treatment option for immature teeth with pulp necrosis. There are three treatment outcomes of regenerative endodontics; (i) resolution of clinical signs and symptoms; (ii) further root maturation; and (iii) return of neurogenesis. It is known that results are variable for these objectives, and true regeneration of the pulp/dentine complex is not achieved. Repair derived primarily from the periodontal and osseous tissues has been shown histologically. It is hoped that with the concept of tissue engineering, namely stem cells, scaffolds and signalling molecules, that true pulp regeneration is an achievable goal. This review discusses current knowledge as well as future directions for regenerative endodontics. Patient-centred outcomes such as tooth discolouration and possibly more appointments with the potential for adverse effects needs to be discussed with patients and parents. Based on the classification of Cvek (Endodontics and Dental Traumatology, 8, 1992, 45), it is proposed that regenerative endodontics should be considered for teeth with incomplete root formation although teeth with near or complete root formation may be more suited for conventional endodontic therapy or MTA barrier techniques. However, much is still not known about clinical and biological aspects of regenerative endodontics.

Immunohistochemical Analysis of Galectins-1, -3, and -7 in Periapical Granulomas, Radicular Cysts, and Residual Radicular Cysts.

INTRODUCTION: Galectins play important roles in immunoinflammatory responses, but their participation in the development of periapical lesions remains unclear. This study aimed to evaluate the expressions of galectins-1, -3, and -7 in periapical lesions, correlating them with the intensity of the inflammatory infiltrate and the pattern of the cystic epithelium. METHODS: Twenty periapical granulomas (PGs), 20 radicular cysts (RCs), and 20 residual radicular cysts (RRCs) were submitted to immunohistochemistry using anti-galectin-1, -3, and -7 antibodies. The percentage of immunopositive cells in epithelial and connective tissues was determined. RESULTS: In connective tissue, PGs exhibited higher cytoplasmic/membrane expression of galectins-1 and -7 than RCs and RRCs (P < .05). There was higher nuclear expression of galectin-1 in PGs compared with RCs and RRCs (P < .05). The expression of galectins-1 and -7 in connective tissue was higher in lesions with grade III inflammation (P < .05). No significant differences in galectin-3 immunoexpression were observed for any of the parameters evaluated (P > .05). In the epithelial component, a higher nuclear expression of galectin-7 was detected in RRCs (P < .05), and a higher cytoplasmic/membrane expression of this protein was found in cysts with hyperplastic epithelium (P < .05). Positive correlations were observed between the nuclear and cytoplasmic/membrane expression of galectin-1 in connective tissue (P < .05) as well as between the nuclear and cytoplasmic/membrane expression of galectin-7 in epithelial tissue of cysts (P < .05). CONCLUSIONS: Galectins-1 and -7 may play important roles in the pathogenesis of PGs, RCs, and RRCs. On the other hand, the present results suggest only a minor involvement of galectin-3 in the development of these lesions.

SPHK1-S1PR1-RANKL Axis Regulates the Interactions Between Macrophages and BMSCs in Inflammatory Bone Loss.

Accumulating evidence indicates that the immune and skeletal systems interact with each other through various regulators during the osteoclastogenic process. Among these regulators, the bioactive lipid sphingosine-1-phosphate (S1P), which is synthesized by sphingosine kinase 1/2 (SPHK1/2), has recently been recognized to play a role in immunity and bone remodeling through its receptor sphingosine-1-phosphate receptor 1 (S1PR1). However, little is known regarding the potential role of S1PR1 signaling in inflammatory bone loss. We observed that SPHK1 and S1PR1 were upregulated in human apical periodontitis, accompanied by macrophage infiltration and enhanced expression of receptor activator of NF-κB ligand (RANKL, an indispensable factor in osteoclastogenesis and bone resorption) and increased numbers of S1PR1-RANKL double-positive cells in lesion tissues. Using an in vitro co-culture model of macrophages and bone marrow stromal cells (BMSCs), it was revealed that in the presence of lipopolysaccharide (LPS) stimulation, macrophages could significantly induce SPHK1 activity, which resulted in activated S1PR1 in BMSCs. The activated S1P-S1PR1 signaling was responsible for the increased RANKL production in BMSCs, as S1PR1-blockage abolished this effect. Applying a potent S1P-S1PR1 signaling modulator, Fingolimod (FTY720), in a Wistar rat apical periodontitis model effectively prevented bone lesions in vivo via downregulation of RANKL production, osteoclastogenesis, and bone resorption. Our data unveiled the regulatory role of SPHK1-S1PR1-RANKL axis in inflammatory bone lesions and proposed a potential therapeutic intervention by targeting this cell-signaling pathway to prevent bone loss. © 2018 American Society for Bone and Mineral Research.

Effects of Zoledronic Acid in Experimental Periapical Lesions in Rats: An Imaging and Histological Analysis.

The aim of this study was to assess the imaging and histological features of experimental periapical lesions, including the adjacent alveolar bone, in rats under zoledronic acid treatment. The study used 40 male Wistar rats distributed into 8 groups of 5 animals each: G1: induction of periapical lesion (PL) and weekly intraperitoneal administration (WIPA) of saline solution (0.9% NaCl) for 4 weeks; G2: PL induction and WIPA of zoledronic acid (0.15 mg/kg/week) for 4 weeks; G3: PL induction and WIPA of saline solution for 8 weeks; G4: PL induction and WIPA of zoledronic acid for 8 weeks; G5:WIPA of saline solution for 4 weeks and subsequent PL induction; G6: WIPA of zoledronic acid for 4 weeks and subsequent PL induction; G7: WIPA of saline solution for 8 weeks and subsequent PL induction; G8: WIPA of zoledronic acid for 8 weeks and subsequent PL induction. The administration of zoledronic acid or saline solution continued after PL induction until the euthanasia. Thus, cone beam computed tomography and histological analysis were performed. Statistical analyzes were performed by ANOVA and Kruskal-Wallis test. Groups treated with zoledronic acid showed significantly smaller size of PL than the groups treated with 0.9% NaCl (p<0.05). PLs were formed by chronic inflammation ranging from mild to moderate, with no difference between groups. In all specimens, no mandibular necrosis was observed. In conclusion, the presence of PLs apparently does not represent an important risk factor for the development of bisphosphonate-related osteonecrosis of the jaws.

Differentiating early stage florid osseous dysplasia from periapical endodontic lesions: a radiological-based diagnostic algorithm.

BACKGROUND: Osseous dysplasia (OD) is the most common fibro-osseous lesion of the jaw affecting the periapical region. Early stages of OD can resemble periapical radiolucencies, thus mimicking the radiological aspects of an endodontic pathology. Such radiolucent lesions affecting previously decayed or treated teeth are even more complex to interpret. CASE PRESENTATION: The aim of this paper is to report a case-series of representative clinical situations describing the radiological features and illustrating the diagnostic workup of patients with florid osseous dysplasia (FOD). Emphasis is given to the endodontic implications of such periapical bone disease and the complexity of accurate diagnosis in the context of endodontic retreatment. We then propose a practical radiological-based diagnostic algorithm to assist the clinician in the diagnostic of OD periapical lesions. CONCLUSION: Periapical lesions may be confused with bone diseases such as osseous dysplasia, especially in the radiolucent initial stage. Knowledge of clinical features associated with a careful reading of cone beam CT images, such as fine opacities within the hypodense periapical lesion, may help determine the right diagnostic.

Langerhans Cell Histiocytosis Mimicking Periapical Pathology in a 39-year-old Man.

Langerhans cell histiocytosis (LCH) is a clonal neoplastic proliferation of Langerhans-type dendritic cells, with more than 50% of cases of LCH seen in children younger than 15 years of age. The most common clinical presentation of LCH is solitary or multiple bony lesions. The jaws are affected in approximately 10%-20% of cases, with a strong predilection for the mandible. The maxilla is involved in only 1% of head and neck cases. When the jaws are involved, lesions of LCH may mimic periapical pathology as seen in patients requiring endodontic therapy or bone loss as seen in periodontal disease. We report the case of a 39-year-old man with LCH involving the posterior maxilla. This is a rare presentation of LCH with respect to both location and patient age. Clinicians should consider LCH when developing a differential diagnosis of an apical radiolucency of vital teeth or teeth that fail to respond to endodontic therapy and be aware of its clinical and radiographic mimics.

Effects of Zoledronic Acid in Experimental Periapical Lesions in Rats: An Imaging and Histological Analysis

Abstract The aim of this study was to assess the imaging and histological features of experimental periapical lesions, including the adjacent alveolar bone, in rats under zoledronic acid treatment. The study used 40 male Wistar rats distributed into 8 groups of 5 animals each: G1: induction of periapical lesion (PL) and weekly intraperitoneal administration (WIPA) of saline solution (0.9% NaCl) for 4 weeks; G2: PL induction and WIPA of zoledronic acid (0.15 mg/kg/week) for 4 weeks; G3: PL induction and WIPA of saline solution for 8 weeks; G4: PL induction and WIPA of zoledronic acid for 8 weeks; G5:WIPA of saline solution for 4 weeks and subsequent PL induction; G6: WIPA of zoledronic acid for 4 weeks and subsequent PL induction; G7: WIPA of saline solution for 8 weeks and subsequent PL induction; G8: WIPA of zoledronic acid for 8 weeks and subsequent PL induction. The administration of zoledronic acid or saline solution continued after PL induction until the euthanasia. Thus, cone beam computed tomography and histological analysis were performed. Statistical analyzes were performed by ANOVA and Kruskal-Wallis test. Groups treated with zoledronic acid showed significantly smaller size of PL than the groups treated with 0.9% NaCl (p<0.05). PLs were formed by chronic inflammation ranging from mild to moderate, with no difference between groups. In all specimens, no mandibular necrosis was observed. In conclusion, the presence of PLs apparently does not represent an important risk factor for the development of bisphosphonate-related osteonecrosis of the jaws.

Resumo O objetivo deste estudo foi avaliar as características histológicas e de imagem de lesões periapicais experimentais, incluindo o osso alveolar adjacente, em ratos sob tratamento com ácido zoledrônico. O estudo utilizou 40 ratos Wistar, machos, distribuídos em 8 grupos de animais cada: G1: indução de lesão periapical (LP) e administração intraperitoneal semanal (AIS) de solução salina (NaCl 0.9%) por 4 semanas; G2: indução de LP e AIS de ácido zoledrônico (0,15 mg/kg/week) por 4 semanas; G3: indução de LP e AIS de solução salina por 8 semanas; G4: indução de LP e AIS de ácido zoledrônico por 8 semanas; G5- AIS de solução salina por 4 semanas e subsequente indução de LP; G6- AIS de ácido zoledrônico por 4 semanas e subsequente indução de LP; G7: AIS de solução salina por 8 semanas e subsequente indução de LP; G8: AIS de ácido zoledrônico por 8 semanas e subsequente indução de LP. A administração de ácido zoledrônico ou solução salina continuou após indução de LP até a eutanásia. Após isso, tomografia computadorizada de feixe cônico e análise histológica foram realizadas. Análises estatísticas foram realizadas por ANOVA e teste de Kruskal-Wallis. Os grupos tratados com ácido zoledrônico mostraram LPs significativamente menores que os grupos tratados com NaCl 0.9% (p <0.05). LPs eram formadas por inflamação crônica variando de leve a moderada, sem diferença entre os grupos. Em todos os espécimes, necrose mandibular não foi observada. Em conclusão, a presença de LPs aparentemente não representa um fator de risco importante para o desenvolvimento de osteonecrose relacionada ao uso de bisfosfonatos.

20-year Follow-up of Recurrent Glandular Odontogenic Cyst Mimicking a Periapical Lesion.

Periapical lesions usually are caused by root canal infection; nevertheless, other pathologies may eventually involve the tooth apex, making the correct diagnosis more difficult. Glandular odontogenic cysts (GOCs) are uncommon and, despite their cystic nature, may present an aggressive behavior and a high recurrence rate. This report describes a recurrent GOC mimicking a periapical lesion that was followed up for 20 years. A 45-year-old woman described tooth discomfort for several years in the anterior region of the mandible that was not exacerbated during eating or occlusion. Clinical examination revealed no signs of swelling, redness, or inflammation in the gingival or surrounding soft tissue. Nevertheless, periapical radiography showed a well-defined large radiolucent lesion in the periapical region of teeth #22, #23, #24, and #25. The pulp test confirmed that all these teeth were vital. An incisional biopsy was performed, and with the histopathological diagnosis of an odontogenic cyst, the lesion was enucleated surgically. After recurrence, the extensive periapical multilocular lesions were again surgically removed. Based on the microscopic findings, the final diagnosis was GOC. One year later, there were no signs of recurrence. GOCs associated with the root apex may mimic periapical inflammatory diseases. Clinical, radiographic, and histopathological findings are essential for the diagnosis of inconclusive radiolucent findings in the periapical region. Biopsy specimens should be sent to a specialized oral pathology laboratory.

Differential diagnosis and clinical management of periapical radiopaque/hyperdense jaw lesions.

Great attention has been given to the study of radiolucent periapical lesions to avert possible misdiagnosis of apical periodontitis associated with certain radiolucent non-endodontic lesions. However, there are a significant number of radiopaque lesions found in the periapical region, which could be equally relevant to endodontic practice. The diagnosis and management of these radiopaque/hyperdense lesions could be challenging to the endodontist. These bone alterations could be neoplastic, dysplastic or of metabolic origin. In the context of the more widespread use of cone-beam CT, a detailed review of radiopaque inflammatory and non-inflammatory lesions is timely and may aid clinicians perform a differential diagnosis of these lesions. Distinguishing between inflammatory and non-inflammatory lesions simplifies diagnosis and consequently aids in choosing the correct therapeutic regimen. This review discusses the literature regarding the clinical, radiographic, histological and management aspects of radiopaque/hyperdense lesions, and illustrates the differential diagnoses of these lesions.

Maxillary and Mandibular Non-Hodgkin Lymphoma with Concurrent Periapical Endodontic Disease: Diagnosis and Management.

Extranodal non-Hodgkin lymphoma (NHL) in the oral region can present similarly to diseases of odontogenic origin. The objective of this report was to describe a rare case of maxillary and mandibular NHL that presented similarly to and concurrently with lesions of odontogenic origin.A unique case of extranodal NHL, which presented at the apices of maxillary and mandibular teeth in conjunction with lesions of odontogenic origin in a 68-year-old white man, is described. The patient sought care because of a lesion in the right maxillary paranasal region that caused him paresthesia. Radiographically, periapical radiolucencies were present along teeth #5-8, #23 and 24, and #30 and 31. Biopsies of the right maxillary and anterior mandibular lesions were completed and led to a diagnosis of NHL at the apices of teeth #5-8 extending to the hard palate and granulation tissue at the apices of teeth #23 and 24. Two years later, the patient returned because of pressure and sensitivity associated with teeth #30 and 31. Vestibular swelling was noted clinically, and a multilocular periapical radiolucency was present radiographically. Via endodontic therapy and a positron emission tomographic scan, the lesion associated with teeth #30 and 31 was determined to be of both odontogenic and nonodontogenic origin because it possessed both a sinus tract associated with tooth #30 and NHL. Lesions of odontogenic and nonodontogenic origin possess diagnostic and treatment challenges because they may present similarly and/or concurrently. Thoughtful and conservative management of odontogenic lesions with associated NHL is imperative. Interprofessional collaboration and communication among providers must be thorough and clear to properly coordinate care and prevent delays in diagnosis and treatment when these entities occur together.

Characterisation of apical bone lesions: Comparison of MRI and CBCT with histological findings - a case series.

PURPOSE: The aim of this case series was to compare magnetic resonance imaging (MRI) with cone beam computed tomography (CBCT) in the representation of periapical osteolyses. Based on the histological findings, the potential of MRI for further lesion characterisation was investigated. MATERIALS AND METHODS: Thirteen patients (average age: 41 ±â€…27 years) with a total of 15 periapical lesions (five molars, five premolars, and five front teeth) were examined. Lesion characterisation was based on the homogeneity/heterogeneity of the lesions, the signal intensity within the lesion compared to the surrounding tissue and differences in the signal intensities between different MRI contrast weightings. Results were compared with CBCT and histological findings. RESULTS: Although all patients presented with dental restorations, such as fixed partial dentures and filling materials, all periapical lesions could be diagnosed with either imaging modality. Histologically, 13 cysts and two apical granuloma were confirmed. In CBCT, the similar appearance of all lesions did not allow any further characterisation. In MRI, radicular cysts and granuloma could be characterised by their appearance in the MRI images with different contrast weightings. The MRI-derived characterisations were consistent with the histological findings. CONCLUSIONS: The presented study shows that the application of multi-contrast MRI may lead to better characterisation of apical lesions, thus enabling an improved patient-specific selection of the optimal treatment option. Conflict-of-interest statement: MAG, ESS, and LKS do not report any potential conflict-of-interest; EH and JU are employees of Sirona Dental Systems; VR is receiving a research grant by Sirona Dental Systems.

High-mobility Group Box 1 Is Associated with the Inflammatory Infiltration and Alveolar Bone Destruction in Rats Experimental Periapical Lesions.

INTRODUCTION: This study was conducted to observe the immunohistochemical localization of high-mobility group box 1 (HMGB1) and its receptor, Toll-like receptor 4 (TRL4), in the development of periapical lesions induced in rats. The possible role of these molecules in the pathogenesis of periapical lesions was also explored. METHODS: Periapical lesions developed within 35 days after mandibular first molar pulp exposure in Wistar rats. The animals were randomly killed at 0, 7, 14, 21, 28, and 35 days after pulp exposure. The jaws that contained the first molar were obtained and prepared for histologic analysis, enzyme histochemistry, immunohistochemistry, and double immunofluorescence staining. RESULTS: From day 0 to 35, the areas of periapical bone loss increased and appeared to be stabilized on day 35. A few HMGB1-positive, TLR4-positive cells and osteoclasts could be observed on day 7. From day 7 to 28, the HMGB1 and TLR4 protein expression increased and subsequently remained stable. The number of osteoclasts multiplied from day 0 to 14 and then gradually decreased from day 14 to 35. Double immunofluorescence staining results showed HMGB1-positive, TLR4-positive cells around periapical lesions surrounding the apical foramen. CONCLUSIONS: Thus, HMGB1 and TLR4 may be associated with the pathogenesis of the periapical lesions.