Higher Expression of Galectin-3 and Galectin-9 in Periapical Granulomas than in Radicular Cysts and an Increased Toll-like Receptor-2 and Toll-like Receptor-4 Expression Are Associated with Reactivation of Periapical Inflammation

Introduction

Cysts and periapical granulomas are inflammatory reactions that develop in response to periapical infection by microbial species in dental root canal. It is known that toll-like receptors (TLRs) are pathogen recognition molecules and that galectins are lectins that can be associated with the inflammatory process, stimulating or inhibiting the immune system. The objective of this study was to evaluate the in situ expression of TLRs and galectins in radicular cysts and periapical granulomas.

Methods

We analyzed 62 cases (30 radicular cysts, 27 periapical granulomas, and 5 control cases). Indirect immunohistochemistry was used to evaluate the expression of TLRs (TRL-2 and TLR-4) and galectins (Gal-3 and Gal-9).

Results

The expression of Gal-3 and Gal-9 was significantly higher in periapical granulomas and radicular cysts than in the control group. Similarly, both Gal-3 and Gal-9 were expressed significantly more in periapical granulomas than in radicular cysts. The expression of TLR-2 was significantly higher in periapical granulomas and radicular cysts than in the control group, and it was also significantly higher in radicular cysts with sinus tract than in the cases without sinus tract. Furthermore, the expression of TLR-4 was significantly higher in the cases of periapical granulomas with sinus tract than in the cases without sinus tract.

Conclusions

Gal-3/Gal-9 and TLR-2/TLR-4 expression in the periapical granulomas and radicular cysts is associated with reactive periapical inflammation. Pathobiology of periapical disease is a very complex interplay of many bioactive molecules involved in immunoinflammatory responses. Up-regulation of these bioactive molecules might be an important modulator of inflammatory periapical lesions.     

Orthokeratinized Odontogenic Cysts Presenting as a Periapical Lesion: Report of a Case and Literature Review

Introduction

Inflammatory cysts, granulomas, abscesses, and fibrous scars represent most periapical radiolucencies. However, other less common lesions, such as orthokeratinized odontogenic cysts (OOCs), can be found at this region, and they deserve to be discussed because the prognosis for an OOC is different from that expected for the ordinary inflammatory periapical diseases.

Methods

An interesting case of OOC associated with a nonvital tooth in a 40-year-old woman is described. After a previous clinical diagnosis of a radicular cyst, the tooth was extracted, and the lesion was enucleated and submitted to microscopy examination.

Results

Because of the detection of an orthokeratinized epithelium lining, a diagnosis of OOC was concluded. After 2 years of periodic follow-up, no signs of recurrence were detected.

Conclusions

The presence of keratin in radicular lesions must be carefully evaluated to eliminate the diagnosis of lesions with more aggressive behavior, such as an OOC or even a keratocystic odontogenic tumor. Hence, histopathologic examination is mandatory to confirm the type of lesion and to differentiate other pathologic conditions, therefore establishing patients' prognoses precisely.     

Midkine expression in human periapical granulomas

Introduction

The expression of midkine (MK), a heparin-binding growth factor, is increased in various human tumors, making it a promising tumor marker and target for tumor therapy. MK is also related to the regulation of the development and etiology of chronic or autoimmune diseases; however, the involvement of MK in apical periodontitis has never been examined. This study compared the localization of MK-expressing cells and MK messenger RNA expression in periapical granulomas with healthy gingival tissues.

Methods

Periapical lesions were removed surgically from chronic apical periodontitis patients, and serial tissue sections were stained with hematoxylin-eosin. The lesions diagnosed as periapical granulomas pathologically were examined by immunohistochemistry using human MK monoclonal antibodies. MK messenger RNA expression was also detected using real-time polymerase chain reaction analysis. Healthy gingival tissues were analyzed in the same manner.

Results

MK was expressed by inflammatory cells, such as macrophages, lymphocytes, and neutrophils, as well as by endothelial cells in periapical granulomas but not in healthy gingival tissues. The MK-expressing inflammatory cells were seen adjacent to blood vessels, which contained MK-expressing endothelial cells, suggesting the interaction of MK among these cells during the process of inflammatory cell infiltration. Quantitative analysis of MK messenger RNA expression revealed that periapical granulomas expressed significantly more MK than healthy gingival tissues.

Conclusions

These findings suggest that MK is involved in the pathogenesis of periapical granulomas.     

Mesenchymal Stem Cells as Active Prohealing and Immunosuppressive Agents in Periapical Environment: Evidence from Human and Experimental Periapical Lesions

Introduction

Previous studies describe contrasting molecular profiles of active and inactive periapical granulomas characterized by distinct expression of cytokines, osteoclastogenic factors, and wound healing markers. Although the molecular mechanisms underlying such a dichotomy remain unknown, in this study we investigated the potential involvement of mesenchymal stem cells (MSCs) in determining human and murine periapical lesion activity and outcomes.

Methods

Periapical granulomas (n = 83) and control samples (n = 24) were comparatively assessed for the expression levels of 11 mesenchymal stem cell (MSC) markers using real-time polymerase chain reaction. Experimental periapical lesions induced in mice were evaluated for MSC marker expression and the effects of AMD3100 treatment on lesion outcomes.

Results

MCS marker expression was prevalent in periapical granulomas compared with that in controls, whereas CD29, CD73, CD90, CD146, CD166, NANOG, Stro-1, and CXCR4 expressions were higher in inactive than in active lesions. Experimental periapical lesion inactivity was also associated with an increased expression of MSC markers. The inhibition of MSC mobilization to the periapex by AMD3100 resulted in increased lesion sizes; decreased expression of MSCs and wound healing markers; and increased expression of interleukin 1 beta (IL-17β), interleukin 17 (IL-17), tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), and nuclear factor kappa-B ligand (RANKL).

Conclusions

Our results show that MSC markers are overexpressed in inactive human and experimental periapical lesions and that MSC mobilization results in the attenuation of experimental lesion progression associated with immunosuppressive and prohealing mechanisms.     

10-Year Follow-up of Calcifying Odontogenic Cyst in the Periapical Region of Vital Maxillary Central Incisor

Introduction

Radiographic images may lead to misinterpretations of lesions of endodontic and nonendodontic origin. This report describes a case of a 10-year follow-up of a calcifying odontogenic cyst (COC) in the periapical region of a vital maxillary central incisor in a 9-year-old boy.

Methods

The patient revealed a history of a swelling in the periapical area of tooth #9. The patient denied any dental trauma or history of pain. Clinical examination revealed no mobility, but there was discrete discomfort when horizontal pressure was applied. Pulp vitality was present in all maxillary anterior teeth. Radiographs revealed an oval radiolucent lesion in the periapical region of maxillary central incisor. The therapeutic option was enucleation of the periapical lesion and histologic examination of the specimen. Microscopic findings suggested the diagnosis of a COC.

Results

At a follow-up visit 10 years after surgery, panoramic and periapical radiographs showed new bone formation; the patient did not have any pain, and pulp vitality was maintained in all teeth in this area.

Conclusions

A COC should be part of the differential diagnosis of other jaw lesions, such as apical periodontitis. The definitive diagnosis of a COC can only be made after microscopic evaluation of the specimen. The follow-up is a helpful reference because it confirms the survival of pulp tissue and no recurrence of the COC.     

Receptor for advanced glycation end products (RAGE)-expressing endothelial cells co-express AGE and S100 in human periapical granulomas

Objective

The engagement of the receptor for advanced glycation end products (RAGE) by AGE or S100 perturbs homeostatic mechanisms and provides a basis for cellular dysfunction in pathological situations. To assess the mechanism of vascular immune reactions in chronic periapical periodontitis, we analysed co-expression of RAGE and AGE or S100 in periapical granulomas.

Methods

Surgically removed periapical lesions, which had been diagnosed as chronic periodontitis, were inspected histologically using paraffin-embedded sections stained with haematoxylin and eosin. Cryostat sections of the tissues, which were identified histologically as periapical granulomas, were then examined by double immunohistochemistry using polyclonal antibodies raised against human CD34 and monoclonal antibodies specific for human RAGE, AGE or S100. Dual-colour immunofluorescence image analysis was also performed to assess the co-expression of RAGE and AGE or RAGE and S100 by endothelial cells.

Results

Marked expression of RAGE, AGE, and S100 by CD34⁺ endothelial cells was noted. Dual-colour immunofluorescence image analysis revealed that the RAGE-expressing endothelial cells co-expressed AGE and S100; however, the number of RAGE-AGE-expressing endothelial cells was significantly higher than that of RAGE-S100-expressing endothelial cells.

Conclusions

Co-expression of RAGE and AGE by endothelial cells in periapical granulomas is more relevant than that of RAGE and S100. The possible engagement of RAGE and AGE may trigger cellular activation and mediate tissue injury.     

Expression of Heat Shock Proteins in Periapical Granulomas

Introduction

Cells from virtually all organisms respond to a variety of stresses by the rapid synthesis of a highly conserved set of polypeptides termed heat shock proteins (HSPs). HSPs protect cells under adverse conditions such as infection, inflammation, and disease. We hypothesize that endodontic infection might result in an imbalance in the expression of heat shock genes, accounting for different clinical outcomes in periapical lesions.

Methods

We analyzed the expression of 44 HSPs genes using a pathway-specific real-time polymerase chain reaction array in 93 human periapical granulomas and 24 healthy periodontal ligament tissues collected postoperatively. Observed variations in the expression of HSP genes were also analyzed based on the classification of periapical granulomas as active or inactive. In addition, U937 cells were differentiated into macrophages, infected with different concentrations of purified Escherichia coli lipopolysaccharide (LPS), and used as templates for the HSP gene array. Protein expression was assessed by immunohistochemistry.

Results

The expression of HSP genes was significantly increased in granulomas compared with healthy periodontal ligament (P < .00001). Among the 44 HSP genes, DNAJC3, HSPA4, HSPA6, and HSPB1 showed the highest expression levels in both granulomas and LPS-treated macrophages. DNAJC3, HSPA6, and HSPB1 were highly expressed in active lesions, whereas HSPA4 expression was higher in inactive lesions (P < .005). Higher concentrations of LPS led to increased HSP expression in macrophages (P < .0001). Immunocytochemistry confirmed the expression and colocalization of HSPB1 and HSPA6 proteins in the cytoplasm of LPS-infected macrophages.

Conclusions

The observed differential expression patterns of HSPs in periapical granulomas and LPS-infected macrophages suggest that HSP genes and proteins are involved in periapical lesion development and may account for different clinical outcomes. Understanding the role of the heat shock response might provide additional insights into the process of periapical lesion development.     

8-Year Follow-up of Central Giant Cell Lesion Mimicking Apical Periodontitis

Introduction

Lesions of nonendodontic origin may mimic apical periodontitis. Central giant cell lesions (CGCLs) are aggressive or nonaggressive benign idiopathic intraosseous lesions of the jaw. This report describes a case of a CGCL in the periapical region of teeth #21–#26 of a 17-year-old female who sought orthodontic care because of a change in the position of tooth #23.

Methods

Clinical examination revealed mild facial asymmetry caused by increased volume in the mental region and cortical bone expansion but no cortical disruption. A panoramic radiograph showed a well-defined radiolucent osteolytic lesion involving teeth #21–#26. The cortical bone was not affected, and there was no root resorption. Incisional biopsy was performed, and the diagnosis was a CGCL. The lesion was enucleated surgically. CGCLs should be included in the differential diagnosis of jaw lesions that mimic apical periodontitis.

Results

The patient subsequently underwent orthodontic treatment successfully.

Conclusions

The 8-year clinical and radiographic follow-up confirmed lesion remission, no recurrence, and pulp vitality of all teeth.     

Overlapping Protective and Destructive Regulatory Pathways in Apical Periodontitis

Introduction

Protective and destructive immunoreactions take place simultaneously in apical periodontitis. However, the same reactions defending the periapical area from infection-derived damage may also result in host tissue injury.

Methods

The inflammatory reaction of the periapical tissues is self-limited. Regeneration of the injured tooth-supporting structures may follow elimination of the causative microbial irritation.

Results

Recent experimental and clinical observations have identified important interplay between positive and negative regulatory pathways. A network of stimulatory and inhibitory feedback loops may influence the intensity of the defense and inflammatory responses and the balance between bone resorption and regeneration, resulting in lesion expansion or healing of apical periodontitis.

Conclusions

We critically discuss research data on regulatory mechanisms that control the activity of host effector cells and signaling molecules during interactions with pathogenic microbes.     

Immunoexpression of Interleukin 17 in Apical Periodontitis Lesions

Introduction

Interleukin (IL)-17 expression has been detected in apical periodontitis lesions, but its role in the disease process remains unclear. The present study compared the expression of IL-17 in periradicular cysts and granulomas and evaluated the association of this cytokine with clinical and radiographic findings.

Methods

Apical periodontitis lesions (18 cysts and 20 granulomas) were obtained from 38 patients subjected to periradicular surgery. Some clinical, radiographic, and cone-beam computed tomographic features were recorded. Silanized slides containing paraffin sections were used for the immunohistochemical reactions using anti–IL-17 antibody. Image analysis was performed using an optical microscope, and each sample was divided into 5 high-power fields, which were evaluated for the expression of IL-17 in the epithelium and connective tissues. Results were evaluated for correlations with the lesion size and the occurrence of symptoms and sinus tract.

Results

Expression of IL-17 was significantly higher in cysts than in granulomas (P = .02). Among the periradicular cysts, a thin epithelium showed significantly increased labeling for IL-17 when compared with a hyperplastic epithelium (P = .003). IL-17 expression was usually associated with focal accumulations of polymorphonuclear leukocytes. No association of IL-17 expression with symptoms, sinus tract, or lesion size was observed (P > .05).

Conclusions

The present study reinforces the notion that IL-17 may take part in the pathogenesis of apical periodontitis lesions. A role in the exacerbation of chronic inflammation and cyst formation is suspected. Further studies are required to shed light on the specific functions of IL-17 in periradicular inflammatory processes.     

Evaluation of the Reliability and Accuracy of Using Cone-beam Computed Tomography for Diagnosing Periapical Cysts from Granulomas

Introduction

The purpose of this study was to evaluate the reliability and accuracy of cone-beam computed tomographic (CBCT) imaging against the histopathologic diagnosis for the differential diagnosis of periapical cysts (cavitated lesions) from (solid) granulomas.

Methods

Thirty-six periapical lesions were imaged using CBCT scans. Apicoectomy surgeries were conducted for histopathological examination. Evaluator 1 examined each CBCT scan for the presence of 6 radiologic characteristics of a cyst (ie, location, periphery, shape, internal structure, effects on surrounding structure, and perforation of the cortical plate). Not every cyst showed all radiologic features (eg, not all cysts perforate the cortical plate). For the purpose of finding the minimum number of diagnostic criteria present in a scan to diagnose a lesion as a cyst, we conducted 6 receiver operating characteristic curve analyses comparing CBCT diagnoses with the histopathologic diagnosis. Two other independent evaluators examined the CBCT lesions. Statistical tests were conducted to examine the accuracy, inter-rater reliability, and intrarater reliability of CBCT images.

Results

Findings showed that a score of ≥4 positive findings was the optimal scoring system. The accuracies of differential diagnoses of 3 evaluators were moderate (area under the curve = 0.76, 0.70, and 0.69 for evaluators 1, 2, and 3, respectively). The inter-rater agreement of the 3 evaluators was excellent (α = 0.87). The intrarater agreement was good to excellent (κ = 0.71, 0.76, and 0.77).

Conclusions

CBCT images can provide a moderately accurate diagnosis between cysts and granulomas.     

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.     

The Dynamics of Periapical Lesions in Endodontically Treated Teeth That Are Left without Intervention: A Longitudinal Study

Introduction

The long-term dynamics of periapical lesions in endodontically treated teeth is not fully elucidated, thus presenting a clinical dilemma regarding the need for an intervention. The aim of the study was to retrospectively evaluate the long-term dynamics of periapical lesions that were left without intervention in endodontically treated teeth.

Methods

Periapical status surveys of patients treated in a public dental clinic were retrospectively evaluated for the presence of periapical lesions in endodontically treated coronally restored teeth. The dynamics of the included periapical lesions was evaluated based on the periapical index (PAI) score changes between 2 consecutive periapical surveys of at least a 4-year interval. The influence of various factors on lesion dynamics was statistically evaluated.

Results

The study cohort consisted of 74 patients with a total of 200 endodontically treated teeth having periapical lesions that fulfilled the inclusion criteria. Fifty-seven (28.5%) lesions remained unchanged, 103 (51.5%) lesions worsened (PAI score increased), and 40 (20%) lesions improved (PAI score decreased). Poor root canal filling and poor restoration were found to adversely affect the long-term dynamics of the periapical lesions (P < .05). Age, sex, and the presence of a post had no statistically significant influence on lesion dynamics (P > .05).

Conclusions

Poor root canal filling and poor restoration may adversely affect the long-term dynamics of periapical lesions that are left without intervention in endodontically treated teeth. Therefore, in cases of poor root canal filling or poor restoration, further intervention may be indicated.     

Repair of Extensive Apical Root Resorption Associated with Apical Periodontitis: Radiographic and Histologic Observations after 25 Years

Introduction

Root resorption is a frequent finding in teeth with apical periodontitis. In cases of severe apical periodontitis, root resorption may involve not only cementum but also dentin. Resorbed tooth structures can only be repaired with cementum because stem cells in the periradicular tissues are not capable of differentiating into odontoblasts. This article reports the repair of extensive apical root resorption associated with apical periodontitis 25 years after treatment.

Methods

A 51-year-old man presented with pulp necrosis and symptomatic apical periodontitis in tooth #7. The periapical radiograph showed a large radiolucent periradicular lesion and severe root resorption. Nonsurgical root canal therapy was performed. Twenty-five years after treatment, a crown fracture developed, and the tooth could not be restored. The periapical radiograph revealed complete healing of the previous apical periodontitis lesion and restoration of the resorbed root structure. The tooth was removed and examined histologically.

Results

The apical canal was almost completely filled with a cementumlike tissue with some strands of entrapped vital uninflamed connective tissue. Areas of cementum and dentin resorption in the apical third were repaired by a combination of cellular and acellular cementum to which periodontal ligament fibers were attached.

Conclusions

Root resorption caused by apical periodontitis can be restored almost to its normal structure after adequate nonsurgical root canal treatment that succeeded in controlling infection. The mechanisms behind this process are not clear but probably involve signaling pathways regulating root development, cell-cell and cell-matrix interaction, and morphogens.     

Expression and immunohistochemical localization of leptin in human periapical granulomas

Background

Leptin, initially described as an adipocyte-derived hormone to regulate weight control, is expressed in normal and inflamed human dental pulp, being up-regulated during pulp experimental inflammation. Leptin receptor (LER) has been identified in human periapical granulomas. The aim of this study was to analyze and characterize the expression of leptin in human periapical granulomas.

Material and Methods

Fifteen periapical inflammatory lesions were obtained from extracted human teeth and teeth which underwent periapical surgery. After their morphological categorization as periapical granulomas and gradation of the inflammatory infiltrate, they were examined by immunohistochemistry using human leptin policlonal antibodies. Leptin mRNA expression was also determined by quantitative real-time PCR (qRT-PCR) and the amount of leptin protein was analyzed by immunoblot.

Results

All periapical lesions exhibited the characteristic of chronic granulomatous inflammatory process with inflammatory infiltrate grade III. Leptin+ cells were detected in 13 periapical granulomas (86.6%). The median number of Leptin+ cells in periapical granulomas was 1.70 (0.00-7.4). Amongst the inflammatory cells in the periapical granulomas, only macrophages were reactive to leptin antibodies. Western blot analysis revealed the presence in all samples of a protein with apparent molecular weight of approximately 16 kDa, corresponding to the estimated molecular weights of leptin. The expression of leptin mRNA was confirmed by qRT-PCR analysis and the size of the amplified fragment (296 bp for leptin and 194 bp for cyclophilin) was assessed by agarose gel electrophoresis.

Conclusions

For the first time, it has been demonstrated that human periapical granuloma expresses the adipokine leptin. Key words: Apical granuloma, dental pulp, endodontics, leptin, leptin receptor, immune system, immunohistochemistry, periapical inflammatory response.     

Association of matrix metalloproteinase inducer (EMMPRIN) with the expression of matrix metalloproteinases-1, -2 and -9 during periapical lesion development

Objective

To evaluate the expression of matrix metalloproteinase inducer (EMMPRIN) and its correlation with the expression of matrix metalloproteinases (MMPs)-1, -2 and -9 during the development of periapical lesion in mice.

Methods

Periapical lesions were induced in the lower first molars of mice and after 7, 14, 21 and 42 days the mandibles were removed. The periapical lesions were measured by micro-computed tomography. The expression of EMMPRIN, MMPs-1, -2, and -9 genes were determined by real-time RT-PCR. The location and expression of EMMPRIN and MMPs were evaluated by immunohistochemistry.

Results

At 14 days, the periapical lesion area was higher than at 7 days. At 21 and 42 days no statistically significant bone loss was observed in comparison to 14 days. The control group showed discrete and occasional EMMPRIM, MMP-1, -2 and -9 immunostaining in the periodontal ligament fibroblasts. At 7, 14, 21 and 42 days intense immunoexpression was observed for EMMPRIN, MMPs-1, -2 and -9 in the region adjacent to the apical foramen. The EMMPRIN immunoexpression was higher at 7, 14, 21 and 42 days compared with the control. There was a positive correlation between gene expression of EMMPRIN and MMPs in the active phase of periapical lesion development.

Conclusion

There is a high expression of EMMPRIM mainly by the inflammatory infiltrate in the region adjacent to the apical foramen during periapical lesion development. Furthermore, the positive correlation with MMP-1, -2, and -9 during the first days after periapical lesion induction indicates that EMMPRIM may be involved in the active phase of periapical lesions development.     

Histologic Evaluation of the Effects of Emdogain Gel on Injured Root Apex in Rats

Introduction

This study investigated the effects of Emdogain gel (EMD) on the injured open apex within periapical lesions.

Methods

Periapical lesions were induced in rats by opening the pulp chambers of the mandibular first molars and filing the apical foramen through the distal root canal with #25 K-files to make an open apex. The teeth were exposed to the oral environment for 7 days. Then we irrigated the distal root canals and divided them into EMD-treated and propylene glycol alginate–treated groups. The rats were killed 7, 14, and 28 days after treatment and examined histochemically.

Results

In the EMD-treated rats, more cells expressed transforming growth factor-β1 or bone morphogenetic protein-2 at 7 days after treatment, and the regeneration of cementum and bone was observed around the root apex at 14 days after treatment. Conversely, in the propylene glycol alginate–treated group, few cells expressed transforming growth factor-β1 or bone morphogenetic protein-2, and apical periodontal tissue recovery was rarely seen within the periapical lesions throughout the experiment.

Conclusions

These results suggest that EMD does not irritate injured periapical tissue and may create a favorable environment that promotes the healing of destroyed periapical tissues.     

Nonendodontic Lesions Misdiagnosed as Apical Periodontitis Lesions: Series of Case Reports and Review of Literature

Introduction

This study aimed to analyze cases referred from a reference service in oral pathology that were initially misdiagnosed as periapical lesions of endodontic origin and to perform a review of the literature regarding lesions located in the apical area of teeth with a nonendodontic source.

Methods

A survey was made of clinical cases derived from the service of oral pathology from 2002 to 2012. The pertinent literature was also reviewed using ScienceDirect and PubMed databases. The lesions were grouped into benign lesions mimicking endodontic periapical lesions (BLMEPLs), malignant lesions mimicking endodontic periapical lesions (MLMEPLs), and Stafne bone cavities. The clinical presentations were divided into lesions with swelling without pain, lesions with swelling and pain, and lesions without swelling but presenting with pain.

Results

The results showed that 66% (37/56) of cases represented benign lesions, 29% (16/56) malignant lesions, and 5% (3/56) Stafne bone cavities. The most commonly reported BLMEPLs were ameloblastomas (21%) followed by nasopalatine duct cysts (13.5%). The most frequently cited MLMEPLs were metastatic injuries (31.5%) followed by carcinomas (25%). The main clinical presentation of BLMEPLs was pain, whereas that of MLMEPLs was swelling associated with pain; Stafne bone cavities displayed particular clinical findings.

Conclusions

Clinical and radiologic aspects as well as the analysis of the patients' medical history, pulp vitality tests, and aspiration are essential tools for developing a correct diagnosis of periapical lesions of endodontic origin. However, if the instruments mentioned earlier indicate a lesion of nonendodontic origin, a biopsy and subsequent histopathological analysis are mandatory.     

Mineral Trioxide Aggregate as Apical Plug in Teeth with Necrotic Pulp and Immature Apices: A 10-year Case Series

Introduction

This 10-year study evaluated the clinical and radiologic outcomes of teeth with necrotic pulp, immature apices, and periapical lesions treated with the mineral trioxide aggregate (MTA) apical plug technique.

Methods

Seventeen single-rooted immature teeth with necrotic pulp and periapical lesion from 17 patients treated between January 2001 and December 2001 were included in this study. Apical obturation on all teeth included in the study was completed in 2 visits: first using calcium hydroxide as an interappointment intracanal medication and a second visit for the creation of the artificial apical barrier with MTA. The outcome, based on clinical and radiographic criteria, was assessed by 2 calibrated investigators using the periapical index (PAI). The Friedman test was used to verify the differences between baseline and the 1-, 5-, and 10-year PAI scores.

Results

Of the 17 patients treated, 1 patient dropped out at 5 years. At the 10-year follow-up, 15 teeth were healed (PAI ≤2), and 1 tooth had been extracted because of the presence of a longitudinal root fracture. The PAI score exhibited a significant decrease between baseline and 1 year and between 1 and 5 years. The difference between 5 and 10 years was not significant.

Conclusions

The apical plug with MTA was a successful and effective technique for long-term management of this group of teeth with necrotic pulps with immature root development and periapical lesions.