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.     

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.     

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.     

p38MAPK在大鼠实验性根尖病变中的作用研究

目的：观察大鼠根尖周病变过程中P-p38,RANKL和破骨细胞的表达及变化,探讨p38MAPK信号通路在根尖周炎症性骨吸收中的作用。方法：将24只SD大鼠开髓,分别于术后7,14,21,28d取下颌骨,制备组织切片,用免疫组织化学的方法测定P-p38和RANKL在大鼠根尖周炎中的表达,酶组织化学方法检测抗酒石酸酸性磷酸酶,观察破骨细胞。结果：在正常根尖周组织中偶见P-p38、RANKL阳性细胞和破骨细胞;术后7d根尖周有炎症细胞浸润,可见P-p38、RANKL阳性细胞和破骨细胞数量增多;术后14d,P-p38、RANKL阳性细胞和破骨细胞数量上升至最高值;术后21~28d,P-p38、RANKL阳性细胞和破骨细胞数量下降。从7d组到28d组,破骨细胞数量的变化与P-p38和RANKL阳性细胞数的变化呈现一致的趋势。结论：p38MAPK信号通路可能通过参与RANKL介导的信号转导途径,介导破骨细胞分化,参与根尖炎骨吸收的病理过程。     

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.     

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.     

Antiosteoclastogenic Activity of Silicate-based Materials Antagonizing Receptor Activator for Nuclear Factor KappaB Ligand–induced Osteoclast Differentiation of Murine Marcophages

Introduction

This study investigated whether calcium silicate cement extract exerted antiosteoclastogenic actions in murine RAW 264.7 macrophages cultured with receptor activator for nuclear factor kappaB (RANKL).

Methods

The RAW 264.7 macrophage cell was treated with RANKL to osteoclastogenesis. Then, cell viability, cell death, and cathepsin K expression were examined.

Results

The silicon (Si)-inhibited RANKL-induced formation of osteoclasts during the osteoclast differentiation process. It was also found that ≥4 mmol/L Si reduced RANKL-enhanced tartrate-resistant acid phosphatase (TRAP) activity in a dose-dependent manner. Furthermore, Si diminished the expression and secretion of cathepsin K elevated by RANKL and was concurrent with the inhibition of TRAF6 induction and nuclear factor kappaB activation.

Conclusions

The current report shows that silicate abrogated RANKL-induced osteoclastogenesis by retarding osteoclast differentiation. The Si can modulate every cell through dose-dependent in vitro RANKL-mediated osteoclastogenesis, such as the proliferation and fusion of preosteoclasts, and the function of osteoclasts. Therefore, silicate-based materials may be a potential therapeutic agent targeting osteoclast differentiation in bone defects.     

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.     

Incidence of Cholesterol in Periapical Biopsies among Adolescent and Elderly Patients

Introduction

Cholesterol clefts are common histologic findings in periapical biopsies; they have a reported incidence in periapical periodontitis of up to 44%. Cholesterol crystals are also recognized in advanced atherosclerotic plaques in humans. Male sex, genetic abnormalities, and age have been associated with advanced atherosclerotic lesions. Among these nonmodifiable risk factors, age is the most dominant. The aim of the study was to evaluate if age is also linked to cholesterol deposition in periapical periodontitis.

Methods

The database of biopsy reports obtained between 2006 and 2009 was searched for specimens diagnosed as radicular cysts or periapical granulomas. Only data relating to biopsies obtained from adolescent (13–21 years old) and elderly (over 60 years old) patients were selected. The biopsies were examined by a pathologist under a light microscope (Zeiss, Jena, Germany) at magnifications of 40×–200×. The available material was scanned for the presence of cholesterol clefts and foamy cells in radicular cysts and granulomas.

Results

A total of 41 specimens were collected in the adolescent group and 48 specimens in the elderly group over a 4-year period. A higher incidence of cholesterol was found in the elderly group compared with that in the adolescent group (odds ratio = 6.857).

Conclusions

The highly significant incidence of cholesterol deposits in periapical biopsies among elderly patients may be a possible cause for the lack of repair. The mechanism for cholesterol accumulation is probably similar to the process leading to atherosclerosis and coronary artery disease. Statin administration may be advantageous for the treatment of persistent lesions. A clinician should be aware of the risk for persistent lesions after endodontic treatment in elderly patients.     

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.     

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.     

Simultaneous analysis of T helper subsets (Th1, Th2, Th9, Th17, Th22, Tfh,Tr1 and Tregs) markers expression in periapical lesions reveals multiple cytokine clusters accountable for lesions activity and inactivity status

Previous studies demonstrate that the balance between pro- and anti-inflammatory mediators determines the stable or progressive nature of periapical granulomas by modulating the balance of the osteoclastogenic factor RANKL and its antagonist OPG. However, the cytokine networks operating in the development of periapical lesions are quite more complex than what the simple pro- versus anti-inflammatory mediators'' paradigm suggests. Here we simultaneously investigated the patterns of Th1, Th2, Th9, Th17, Th22, Thf, Tr1 and Tregs cytokines/markers expression in human periapical granulomas.

Methods

The expression of TNF-α, IFN-γ, IL-17A, IL23, IL21, IL-33, IL-10, IL-4, IL-9, IL-22, FOXp3 markers (via RealTimePCR array) was accessed in active/progressive (N=40) versus inactive/stable (N=70) periapical granulomas (as determined by RANKL/OPG expression ratio), and also to compare these samples with a panel of control specimens (N=26). A cluster analysis of 13 cytokine levels was performed to examine possible clustering between the cytokines in a total of 110 granulomas.

Results

The expression of all target cytokines was higher in the granulomas than in control samples. TNF-α, IFN-γ, IL-17A and IL-21 mRNA levels were significantly higher in active granulomas, while in inactive lesions the expression levels of IL-4, IL-9, IL-10, IL-22 and FOXp3 were higher than in active granulomas. Five clusters were identified in inactive lesion groups, being the variance in the expression levels of IL-17, IL-10, FOXp3, IFN-γ, IL-9, IL-33 and IL-4 statistically significant (KW p<0.05). Three clusters were identified in active lesions, being the variance in the expression levels of IL-22, IL-10, IFN-γ, IL-17, IL-33, FOXp3, IL-21 and RANKL statistically significant (KW p<0.05).

Conclusion

There is a clear dichotomy in the profile of cytokine expression in inactive and active periapical lesions. While the widespread cytokine expression seems to be a feature of chronic lesions, hierarchical cluster analysis demonstrates the association of TNF-α, IL-21, IL-17 and IFN-γ with lesions activity, and the association of FOXP3, IL-10, IL-9, IL-4 and IL-22 with lesions inactivity.     

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.     

Activation of p38 mitogen-activated protein kinase in rat periapical lesions

The purpose of this study was to investigate the activation of p38 mitogen-activated protein kinase (MAPK) during the development of periapical lesions in rats. Periapical lesions developed within 28 days after pulp exposure of mandibular first molars in Wistar rats. The animals were sacrificed randomly at 0, 7, 14, 21, and 28 days after pulpal exposure. The jaws that contained the first molar were obtained and routinely prepared for immunohistochemistry and enzyme histochemistry. A few phosphorylated p38 MAPK (P-p38)-positive cells and osteoclasts could be observed on day 7; both peaked in number on day 14. In the 21- and 28-day samples, the P-p38 MAPK expression decreased and fewer osteoclasts were observed. From day 7 to day 28, a significant positive correlation was found between P-p38 MAPK expression and osteoclasts. These findings showed that the activation of p38 MAPK might be associated with bone resorption in periapical lesions.     

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.     

Correlation between the expression of c-Fos and osteoclasts in induced periapical lesions in rats

The experiment was undertaken to observe the correlation between the expression of c-Fos and osteoclasts in experimental periapical lesions in rats. Apical periodontitis was induced in Wistar rats by occlusal exposure of the pulp of their mandibular first molars. After the exposure, 25 Wistar rats were killed on days 0, 7, 14, 21, and 28. The jaws that contained the first molar were obtained and routinely prepared for immunohistochemistry and enzyme histochemistry. A few c-Fos-positive cells and osteoclasts could be observed on day 7, and both climaxed on day 14. In the 21-day and 28-day samples, the expression of c-Fos decreased, and fewer osteoclasts could be observed. From day 7 to day 28, a significant positive correlation was found between the expression of c-Fos and osteoclasts. These findings demonstrated that c-Fos might be associated with the differentiation of osteoclasts in the periapical lesions.     

Correlation between platelet-derived growth factor B chain and bone resorption in rat periapical lesions

The purpose of this study was to examine the relationship between platelet-derived growth factor B chain (PDGF-B) and bone resorption in rat periapical lesions. Periapical lesions were induced in Sprague-Dawley rats by occlusal exposure of the pulp of their mandibular first molars. Animals were sacrificed randomly at 0, 7, 14, 21, and 28 days after the exposure, and frontal sections were prepared for immunohistochemistry and enzymehistochemistry. PDGF-B-positive cells and osteoclasts could be observed on day 7. From day 7 to day 14, the number of PDGF-B-positive cells and osteoclasts were ascending, and a significant correlation was found between them; from day 21 to day 28, more PDGF-B-positive cells and fewer osteoclasts could be observed, and the positive expression of PDGF-B was negatively correlated with osteoclasts. These findings showed that PDGF-B could be observed, which might be associated with the bone resorption of periapical lesions.     

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.