Immunolocalization of matrix metalloproteinases-2 and -9 during apical periodontitis development

Objective

The objective of this study was to determine the expression of matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9) during apical periodontitis development.

Methods

Using an experimental design of induced periapical lesions in rats and immunohistochemistry assay as investigative tool, the MMP-2 and MMP-9 expression and distribution were evaluated at 3, 7, 14, 21, 30, 60 and 90 days after coronary access and pulp exposure of the first left mandibular molar to the oral environment. Two blind observers scored the immunoreactivity. A semi-quantitative analysis was performed.

Results

Except at day 3, MMP-2 and MMP-9 immunostaining was observed in all experimental periods. The MMP-2 (p = 0.004) and MMP-9 (p = 0.005) immunostaining was higher in the period between 7 and 21 days. They were mainly observed in cells surrounding the apical foramen and adjacent periapical areas. Cells into the hypercementosis areas were strongly stained while both osteoblasts and osteoclasts presented discrete staining along of this study. No staining was observed on epithelial walls. At 30, 60 and 90 days, the subjacent connective tissue presented intense MMP-2 and MMP-9 immunostaining in mononuclear cells (suggestive of fibroblasts, macrophages, infiltrating neutrophils and lymphocytes).

Conclusion

The results observed in this study suggest that MMP-2 and MMP-9 play a critical role in the development of inflammatory periapical lesions, probably involved in the extracellular matrix (ECM) degradation during the initial phase of the lesion development.     

Histochemical Localization of Dickkopf-1 in Induced Rat Periapical Lesions

Introduction

The purpose of this study was to evaluate the expression of Dickkopf-1 (DKK-1), a secreted antagonist of the Wnt (wingless)/beta-catenin signaling pathway, during the development of periapical lesions in rats.

Methods

Periapical lesions were induced in Wistar rats by occlusal exposure of the pulp of their mandibular first molars. The animals were sacrificed randomly at 0, 7, 14, 21, and 28 day after pulpal exposure. Jaws containing the first molar were obtained and routinely prepared for histologic, immunohistochemical, and enzyme histochemical double immunofluorescence analyses. Data were analyzed using 1-way analysis of variance and Pearson correlation test.

Results

The expansion of the area of periapical lesions was visible from days 7–21 and slowed down thereafter. A few DKK-1- and receptor activator of nuclear factor kappa B ligand (RANKL)-positive cells and osteoclasts were observed on day 7. All positive samples peaked in number on day 14. The expression levels of DKK-1 and RANKL and the number of osteoclasts decreased on days 21 and 28. DKK-1 expression was positively correlated with RANKL expression and osteoclast number from days 7–28.

Conclusions

DKK-1 expression was up-regulated during periapical lesion development. DKK-1 may be associated with the inflammatory response and bone resorption in periapical lesions.     

Imbalance of Interleukin-17+ T-cell and Foxp3+ Regulatory T-cell Dynamics in Rat Periapical Lesions

Introduction

Interleukin (IL)-17⁺ T-helper (Th17) cells and Foxp3⁺ regulatory T (Treg) cells are CD4⁺ T-helper cells with reciprocal functions in immunology and bone metabolism. The present study aimed to investigate the expression dynamics of Th17 and Treg cells in rat periapical lesions as well as their correlation with bone resorption.

Methods

Experimental pulp exposures were made in the lower first molars of 28 Wistar rats to induce periapical lesions. Rats were killed on days 0, 7, 21, and 35. Mandibles were prepared for micro–computed tomography scanning, histologic observation, immunohistochemistry, enzyme histochemistry, and double immunofluorescence analysis.

Results

Through 3-dimensional and 2-dimensional measurements, the volume and area of periapical lesions visibly increased from day 7 to day 21 and then expanded slowly between days 21 and 35. IL-17–positive cells markedly increased from day 7 to day 35. However, Foxp3-positive cells remained at low levels until day 21 and then dramatically increased by day 35. The IL-17⁺/Foxp3⁺ ratio and number of osteoclasts simultaneously increased from day 7 to day 21 and then decreased on day 35. Finally, the distinct distribution of CD4⁺/IL-17⁺ Th17 and CD4⁺/Foxp3⁺ Treg cells was observed on days 7 and 35.

Conclusions

Our findings imply the imbalance of IL-17⁺ T cell and Foxp3⁺ Treg cell dynamics in induced periapical lesions, which may play an important role in periapical lesion progression.     

MMP-7 and TIMP-1, New Targets in Predicting Poor Wound Healing in Apical Periodontitis

Introduction

Matrix metalloproteinases (MMPs) and the tissue inhibitors of metalloproteinases (TIMPs) are strongly associated with tissue destruction because of inflammation. In this study, we investigated the expression of MMPs and TIMPs messenger RNA and protein levels in apical periodontitis lesions.

Methods

Tissue samples from patients presenting clinical signs of chronic apical abscess (CAA) or asymptomatic apical periodontitis (AAP) were collected postoperatively and used for gene expression analysis of MMP-2, -3, -7, -9, -14, -16, and -25; TIMP-1; and TIMP-2 in real-time polymerase chain reaction. Immunohistochemistry was also performed to detect the expression of MMP-7 and TIMP-1 proteins. Lastly, U-937 cells were induced to terminal differentiation into macrophages, infected with purified Escherichia coli lipopolysaccharide, and assessed for the expression of MMP-7 and TIMP-1 using immunocytochemistry and confocal microscopy.

Results

Significantly higher messenger RNA levels were found for all genes in AAP and CAA samples when compared with healthy control samples (P < .001). AAP cases exhibited significantly higher TIMP-1 when compared with CAA cases, whereas CAA cases showed higher MMP-2, MMP-7, and MMP-9 messenger RNA levels (P < .05). We also detected positive the expression of MMP-7 and TIMP-1 proteins in the tissue samples. The expression of both MMP-7 and TIMP-1 were increased in lipopolysaccharide-stimulated cells compared with nonstimulated cells and appear to colocalize in the Golgi apparatus.

Conclusions

MMPs appear to have an influential role in CAA cases in which ongoing tissue destruction is observed. TIMPs are preferentially associated with AAP, perhaps as a subsequent defense mechanism against excessive destruction. Taken together, our findings implicate MMP and TIMP molecules in the dynamics of inflammatory periapical lesion development.     

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.     

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.     

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.     

The expression of MCP-1 and CCR2 in induced rats periapical lesions

Objective

Monocyte chemotatic protein-1 (MCP-1) has been found to promote chemotaxis, differentiation, and activation of osteoclasts. The aim of this study is to detect and localize the expressions of MCP-1 and its receptor CCR2 in a rat model of apical periodontitis.

Design

After exposing the pulp of the first mandibular molars, 25 Wistar rats were killed on days 0, 7, 14, 21, 28, and 35. Rat jaws containing the first molar were obtained and routinely prepared for histological analysis, immunohistochemistry, enzyme histochemistry and immunofluorescence staining.

Results

Lesions expanded from day 0 to day 28, and stabilized thereafter. Most of the MCP-1-positive cells were inflammatory cells, and their amount increased from day 7 to day 28. Aside from inflammatory cells, CCR2 was also detected in osteoclasts in the lesions. From day 7 to day 14, the number of osteoclasts increased. From day 21 to day 35, fewer osteoclasts could be observed, and the number of osteoclast was negatively correlated with positive MCP-1 expression.

Conclusion

These findings showed that MCP-1/CCR2 could be observed and might possibly be involved in the development of periapical lesions.     

The role of components of the extracellular matrix and inflammation on oral squamous cell carcinoma metastasis

Objectives

Oral squamous cell carcinoma (OSCC) accounts for about 90% of malignant oral lesions, and is identified as the most frequently occurring malignant tumour of oral structures. We aimed to investigate the genes and pathways related with metastasis on Turkish OSCC patients.

Materials and methods

We performed whole genome expression profiling array on an Illumina platform. A total of 24 samples with 12 OSCC and 12-paired controls that had no tumour were included in the study. Hierarchic clustering and heat map were used for data visualisation and p-values assessed to identify differentially expressed genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Ingenuity Pathway Systems (IPA) analysis were performed to consider biologic meaning of differential expression of the genes between tumour and control groups.

Results

We identified 790 probe sets, corresponding to 648 genes that were effective in separating invasive and metastatic OSCC. Consequently, we found statistically relevant expression results on extracellular matrix members on MMPs such as MMP3, MMP10, MMP1 and MMP9; on laminin such as LAMC2, LAMA3 and LAMB3; several genes in the collagen family; and also on chemokines from the inflammation process.

Conclusion

Statistically relevant expression changes for MMPs, laminins, collagens, and chemokines, which are components of the extracellular matrix and inflammation process, may be considered as a molecular biomarker for early prediction. Further studies are necessary to determine and understand the molecular mechanisms that underlie OSCC metastasis.     

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.     

Histochemical localization of neutral proteases released during development of rat periradicular lesion

Objective

The purpose of the present study was to examine the role of various neutral proteases released during the development of periradicular lesion.

Design

This lesion produced by pulpal exposure of mandibular first molar in rat. The histological and histometrical changes in periapical tissue examined. The presence of neutrophil elastase, cathepsin G, collagenase 2, gelatinase B, and secretory leukocyte protease inhibitor (SLPI) was immunohistochemically evaluated in the periapical tissue.

Results

After pulpal exposure, some inflammatory cells were present in the periapical tissue at 7 days, and periapical inflammation gradually increased. Alveolar bone resorption observed after 14 days and apical abscess found after 21 days. After 14 days, the area of periradicular lesion significantly increased compared from normal one (p < 0.05). Neutrophil elastase, cathepsin G, collagenase 2, and gelatinase B were detected around the root apex at 14 days, then these proteases increased gradually and demonstrated in and around the abscess at 21 and 28 days. Morphologically, these protease-expressing cells are almost polymorphic and polynuclear shaped after 14 days. These cells significantly increased after 14 days compared from normal one (p < 0.05). However, SLPI detected after 21 days around apical root. It significantly increased after 21 days (p < 0.05).

Conclusions

These results suggested that neutrophil elastase, cathepsin G, collagenase 2, and gelatinase B induce the destruction of periapical tissue. We demonstrated that these neutral proteases released play an important role in development of periradicular lesion.     

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.     

The inhibition effect of non-protein thiols on dentinal matrix metalloproteinase activity and HEMA cytotoxicity

Objectives

Phosphoric acid (PA) etching used in etch-and-rinse adhesives is known to activate host-derived dentinal matrix-metalloproteinases (MMPs) and increase dentinal permeability. These two phenomena will result, respectively; in degradation of dentine-adhesive bond and leaching of some monomers especially 2-hydroxyethyl methacrylate (HEMA) into the pulp that would negatively affect the viability of pulpal cells. This study is the first to investigate the inhibitory effect of non-protein thiols (NPSH); namely reduced glutathione (GSH) and N-acetylcysteine (NAC) on dentinal MMPs and compare their effects on HEMA cytotoxicity.

Methods

Dentine powder was prepared from human teeth, demineralized with 1% PA and then treated with 2% GSH, 2% NAC or 2% chlorhexidine (CHX). Zymographic analysis of extracted proteins was performed. To evaluate the effect of GSH, NAC and CHX on HEMA cytotoxicity, solutions of these compounds were prepared with or without HEMA and rat pulpal cells were treated with the tested solutions for (6 and 24 h). Cells viability was measured by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cytotoxicity data were analysed by one-way ANOVA and Tukey post hoc tests (p < 0.05).

Results

The inhibitory effect of GSH and NAC on dentinal MMPs was confirmed. GSH showed similar effectiveness to NAC regarding HEMA cytotoxicity inhibition.

Conclusion

NPSH were effective to inhibit dentinal MMPs and HEMA cytotoxicity.

Clinical significance

The tested properties of NPSH provide promising clinical use of these agents which would enhance dentine-bond durability and decrease post-operative sensitivity.     

Outcomes of Hospitalizations Attributed to Periapical Abscess from 2000 to 2008: A Longitudinal Trend Analysis

Introduction

Root canal therapy is a highly successful in-office treatment and preventive measure against periapical abscesses. Left untreated, periapical abscesses can have serious consequences that can lead to hospitalization. This study observes the trends of hospitalizations attributed to periapical abscesses.

Methods

A retrospective analysis of the Nationwide Inpatient Sample (years 2000–2008) was used; we selected cases with a primary diagnosis of a periapical abscess with/without sinus involvement. The demographic characteristics and outcomes were examined. Each individual hospitalization was the unit of analysis.

Results

During the 9-year study period, a total of 61,439 hospitalizations were primarily attributed to periapical abscesses in the United States. The average age was 37 years, and 89% of all hospitalizations occurred on an emergency/urgent basis. The mean length of stay was 2.96 days, and a total of 66 patients died in hospitals. Medicare, Medicaid, and private insurance plans paid for 18.7%, 25.2%, and 33.4% of hospitalizations, respectively. Uninsured patients accounted for 18.5% of hospitalizations. Significant predictors that influenced both hospital charges and length of stay included age, race, insurance status, a periapical abscess with sinus involvement, geographic region of country, the Charlson comorbidity index, and the year of study (P < .05).

Conclusions

The current study highlights the increasing burden of hospitalization of patients with periapical abscesses over a 9-year study period from 2000 to 2008. The high-risk groups likely to seek a hospital setting for the treatment of periapical abscesses were identified as were groups associated with higher hospital charges and a longer length of stay.     

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.     

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.     

Area and 3-dimensional Volumetric Changes of Periapical Lesions after Root Canal Treatments

Introduction

This study compared the changes in size of periapical lesions after root canal treatment as revealed by periapical radiography (PA) and cone-beam computed tomography (CBCT) imaging using area and 3-dimensional volumetric measurements and assessed the outcome of the treatments based on these parameters.

Methods

Both PA and CBCT scans were taken preoperatively and at recall. In total, 50 teeth (71 roots) with evidence of periapical bone loss on both PA and CBCT images were endodontically treated and followed for 10–37 months. The area and volume of periapical lesions were measured, and changes were presented in the following 4 categories: lesion undetected, lesion reduced in size, lesion unchanged, or lesion enlarged. The McNemar and chi-square tests were used to compare the lesion changes determined by CBCT imaging and PA.

Results

The 4-category diagnosis made using both methods were in agreement in 39 of 71 (54.9%) roots, whereas disagreement was observed in 32 of 71 (45.1%) roots (P < .001). At recall, lesion was absent in 11 of 71 (15.5%) roots on CBCT scans and 32 of 71 (45.1%) roots on PA (P < .001). When success was defined as the absence of a lesion or a reduction in size of a lesion, 55 (77.5%) roots on CBCT imaging showed success and 63 (88.7%) roots on PA (P = .073).

Conclusions

Changes in lesion size after root canal treatment determined with 3-dimensional volumetric CBCT data and 2-dimensional PA data are different. The outcome of root canal treatments determined with PA could be untrue.     

Distribution of Mast Cells and Macrophages and Expression of Interleukin-6 in Periapical Cysts

Introduction

Mast cells and macrophages are important components of the inflammatory infiltrate found in inflammatory periapical diseases. Several cytokines participate in the mechanisms of inflammation, tissue repair, and bone resorption associated with periapical cysts. The aim of the present study was to evaluate the distribution of mast cells and macrophages and the expression of interleukin-6 (IL-6) in periapical cysts.

Methods

Thirty periapical cysts were selected for the study, and clinical, demographic, and gross information from the cases was obtained from the laboratory records. Five-micrometer sections stained with hematoxylin-eosin were reviewed for analysis of the microscopic features of the cysts, and 3-μm sections on silanized slides were used for immunohistochemical reactions with anti-tryptase, anti-CD68, and anti–IL-6.

Results

There was no statistically significant difference in the mean number of mast cells and macrophages when comparing superficial and deep regions of the fibrous capsule of the cysts. Mean number of mast cells on the superficial region of the fibrous capsule was higher in cysts showing intense superficial inflammation and exocytosis. Macrophages were more commonly found in areas showing IL-6 expression, and IL-6 was less expressed in deep regions of the fibrous capsule in cysts showing greater gross volume.

Conclusions

The results reinforced the participation of mast cells and macrophages in the pathogenesis of periapical cysts and suggested that IL-6 is not the major bone resorption mediator in larger periapical cysts.     

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.     

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.