Vital pulp therapy of a dens evaginatus‒affected tooth with an immature apex and inflamed pulpal and periapical tissue: a case report.

Dens evaginatus (DE) is a developmental anomaly presenting as an enamel-covered tubercle on the occlusal surface of a premolar, particularly found in people of Asian descent. This case report describes partial pulpotomy in a mandibular premolar with a fractured evaginatus tubercle and endodontic infection. A 10.5-year-old girl of Asian descent was referred for endodontic evaluation and treatment because of local swelling and pain. Clinical examination suggested the presence of DE in a noncarious mandibular right second premolar with a diagnosis of symptomatic irreversible pulpitis and symptomatic apical periodontitis. On access, the pulp was hemorrhagic. A single-appointment mineral trioxide aggregate (MTA) pulpotomy and an immediate composite resin restoration were performed. Recall examinations at 3, 6, and 18 months verified periapical healing and root development without clinical symptoms. This case report suggests that MTA pulpotomy could be a viable alternative option for DE-affected immature teeth with pulpal and periapical inflammation.

Contemporary endodontic treatment choices for adult patients with dens evaginatus and apical periodontitis: a case report with a 2-year follow-up.

Dens evaginatus (DE) frequently leads to pulp exposure and subsequent pulpal inflammation, pulpal necrosis, and periapical inflammation. This case report describes the application of regenerative endodontic therapy and mineral trioxide aggregate (MTA) apexification in a 22-year-old man with mandibular second premolars affected by DE and apical periodontitis. Regenerative endodontic therapy was performed after thorough debridement and placement of calcium hydroxide in the root canal of the left premolar. In contrast, an apical plug of MTA was placed prior to gutta percha compaction in the root canal of the right premolar. Both teeth were restored with adhesive composite resin. A 2-year follow-up examination revealed complete periapical healing.

[Costimulatory molecule CD40 expression in thyroid tissue of Graves' disease patients and its immune pathogenetic significance].

OBJECTIVE: To explore the expression of costimulatory molecule CD40 in thyroid tissue of Graves' disease patients and understand its immune pathogenetic significance. METHODS: From January 2008 to December 2011, 8 patients undergoing partial thyroidectomy for Graves' disease (n = 3) or non-toxic goiter (n = 5) at Affiliated Suzhou Hospital of Nanjing Medical University and Third Affiliated Hospital of Soochow University were enrolled. Using the method of immunohistochemistry, the expression of CD40 was detected in their thyroid tissues. Variation in CD40 expression on thyroid follicular (TFC) in primary cultures was analyzed in the absence (no stimulation group) or presence of inflammatory cytokines including interleukin interferon-γ (IFN-γ) (IFN-γ stimulation group), interferon-6 (IL-6) (IL-6 stimulation group)and tumor necrosis factor (TNF)-α (TNF-α stimulation group) with flow cytometry. IFN-γ-stimulated TFC were cultured with agonist CD40 monoclonal antibody (5C11) (IFN-γ + CD40 group) or isotypic mouse IgG (mIgG) antibody (IFN-γ + mIgG group). And the proliferation of TFC was assessed by 3-(4,5)-dimethyl-thiazolyl-3,5-di-phenytetrazoliumromide (MTT) assays for each donor. The production of free triiodothyronine (FT3) and free thyroxine (FT4) and the release of thyroglobulin (Tg) were measured with radioimmunoassays. RESULTS: The expression of CD40 on infiltrated lymphocytes and TFC were detected in Graves' disease but not in non-toxic goiter patient tissues. Compared with no stimulation group (23.7% ± 7.3%), the expression of CD40 on TFC increased in IFN-γ stimulation group (86.4% ± 4.6%), IL-6 stimulation group (90.0% ± 4.2%) and TNF-α stimulation group (87.3% ± 4.2%). Compared with the IFN-γ + mIgG group (0.75 ± 0.06), the TFC proliferation of IFN-γ + CD40 group (1.14 ± 0.14) significantly increased (P < 0.01). The levels of FT3, FT4 and Tg secretion of IFN-γ + CD40 group were (1.10 ± 0.15) pmol/L, (0.80 ± 0.14) pmol/L and (30.23 ± 1.60) µg/L respectively. They were all significantly increased compared with the IFN-γ + mIgG group, of which the FT3, FT4 and Tg production were (0.76 ± 0.07) pmol/L, (0.63 ± 0.09) pmol/L and (21.37 ± 3.22) µg/L respectively (all P < 0.05). CONCLUSIONS: CD40 is abnormally expressed in thyroid tissue of Graves' disease patients. And its costimulatory signal may take part in the immunopathologic mechanism of Graves' disease.

A retrospective study of initial root canal treatment failure in maxillary premolars via using cone-beam computed tomography.

BACKGROUND: This case-series study examined canal morphology and common factors for endodontic failure in maxillary first and second premolars that were referred for retreatment owing to clinical symptoms or radiographic signs. METHODS: Records were retrospectively searched using Current Dental Terminology codes to identify maxillary first and second premolars with endodontic failure. Periapical and cone-beam computed tomographic images were examined to determine Vertucci classifications and suspected factors related to treatment failure. RESULTS: A total of 235 teeth from 213 patients were included for evaluation. The following Vertucci classification of canal configurations were observed for maxillary first and second premolars: type I (1-1) (4.6% and 32.0%, respectively), type II (2-1) (15.9% and 27.9%, respectively), type III (2-2) (76.1% and 36.1%, respectively), type IV (1-2) (0% and 2%, respectively), and type V (3) (3.4% and 2%, respectively). More treatment failures were noticed in maxillary second premolars than first premolars and in females than in males. The 4 most common factors related to failure were inadequate filling, restorative failure, vertical root fracture, and missed canals. Missed canals were more frequently identified in maxillary second premolars (21.8%) than first premolars (11.4%) (P = .044). CONCLUSIONS: Multiple factors are associated with primary root canal treatment failures in maxillary premolars. Variations in canal morphology appear to be underappreciated in maxillary second premolars. PRACTICAL IMPLICATIONS: Maxillary second premolars have more complicated canal configurations than first premolars. Besides adequate filling, clinicians should give extra attention to anatomic variability in second premolars owing to higher failure incidence.

Regulation of unfolded protein response modulator XBP1s by acetylation and deacetylation.

XBP1 (X-box-binding protein 1) is a key modulator of the UPR (unfolded protein response), which is involved in a wide range of pathological and physiological processes. The mRNA encoding the active spliced form of XBP1 (XBP1s) is generated from the unspliced form by IRE1 (inositol-requiring enzyme 1) during the UPR. However, the post-translational modulation of XBP1s remains largely unknown. In the present study, we demonstrate that XBP1s is a target of acetylation and deacetylation mediated by p300 and SIRT1 (sirtuin 1) respectively. p300 increases the acetylation and protein stability of XBP1s, and enhances its transcriptional activity, whereas SIRT1 deacetylates XBP1s and inhibits its transcriptional activity. Deficiency of SIRT1 enhances XBP1s-mediated luciferase reporter activity in HEK (human embryonic kidney)-293 cells and the up-regulation of XBP1s target gene expression under ER (endoplasmic reticulum) stress in MEFs (mouse embryonic fibroblasts). Consistent with XBP1s favouring cell survival under ER stress, Sirt1-/- MEFs display a greater resistance to ER-stress-induced apoptotic cell death compared with Sirt1+/+ MEFs. Taken together, these results suggest that acetylation/deacetylation constitutes an important post-translational mechanism in controlling protein levels, as well as the transcriptional activity, of XBP1s. The present study provides a novel insight into the molecular mechanisms by which SIRT1 regulates UPR signalling.

ß-Catenin and Rho GTPases as downstream targets of TGF-ß1 during pulp repair.

TGF-ß1 (transforming growth factor-ß1) plays a central role in regulating proliferation, migration and differentiation of dental pulp cells during the repair process after tooth injury. Our previous study showed that p38 mitogen-activated protein kinase may act downstream of TGF-ß1 signalling to effect the differentiation of dental pulp cells. However, the molecular mechanisms that trigger and regulate the process remain to be elucidated. TGF-ß1 interacts with signalling pathways such as Wnt/ß-catenin and Rho to induce diverse biological effects. TGF-ß1 activates ß-catenin signalling, increases ß-catenin nuclear translocation and interacts with LEF/TCF to regulate gene expression. Morphologic changes in response to TGF-ß1 are associated with activation of Rho GTPases, but are abrogated by inhibitors of Rho-associated kinase, a major downstream target of Rho. These results suggest that the Wnt/ß-catenin and Rho pathways may mediate the downstream events of TGF-ß1 signalling.

Roles of lysophosphatidic acid and the Rho-associated kinase pathway in the migration of dental pulp cells.

During the dental pulp repair process, dental pulp cells (DPCs) migrate to the site of injury and differentiate into odontoblasts or odontoblast-like cells. Although migration of DPCs is an important reparative process, the underlying mechanism remains unknown. The objective of this study was to determine the roles of lysophosphatidic acid (LPA) and the Rho-associated kinase (ROCK) pathway in the migration and morphology of dental pulp cells and alpha smooth muscle actin expression in vitro. We demonstrated that both LPA and ROCK inhibition enhanced cell motility and that their combined effects significantly increased migration rate. LPA induced fine cytoskeleton assembly and increased the level of alpha smooth muscle actin (alpha-SMA). ROCK inhibition by Y-27632 and ROCK-(1+2) small interfering RNA (siRNA) resulted in less actin cytoskeleton formation, a lower alpha-SMA level, a star-like cellular morphology and membrane ruffling. LPA and ROCK inhibition induced activation of another Rho GTPase, Rac, which may explain how LPA and ROCK inhibition increases cellmigration and lamellipodium formation.

[Risk factors for acute fulminant myocarditis in children].

OBJECTIVE: To investigate the risk factors for fulminant myocarditis by analyzing clinical symptoms/signs or laboratory findings in children with viral myocarditis. METHODS: The medical data of 71 children with acute viral myocarditis from March 2005 to September 2008 were retrospectively studied. They were classified into fulminant (n=16) and non-fulminant myocarditis groups (n=55). Chi-square and Student's t-test were used to analyze the clinical presentations, laboratory data, EEG and cardiac ultrasound findings on admission. The multiple regression analysis was used to identify the independent risk factors for fulminant myocarditis. RESULTS: Eight children (50%) died in the fulminant myocarditis group, but none in the non-fulminant group. The following factors were closely related to the fulminant course of myocarditis: lower blood pressure, higher serum CK-MB level, positive cTnI, complete atrioventricular block and left bundle branch block, ST segment alterations, prolonged QRS complex, and decreased left ventricular ejection fraction and short axis fractional shortening. Multiple regression analysis revealed that prolonged QRS complex (OR=1.139; CI=1.014-1.279, P<0.05) and decreased left ventricular ejection fraction (OR=0.711; CI=0.533-0.949, P<0.05) were independent risk factors for fulminant myocarditis. CONCLUSIONS: The mortality of fulminant myocarditis is high in children. Prolonged QRS complex and decreased left ventricular ejection fraction on admission are independent risk factors for fulminant myocarditis in children.

Resveratrol represses tumor necrosis factor α/c-Jun N-terminal kinase signaling via autophagy in human dental pulp stem cells.

OBJECTIVES: To study the effects of polyphenol resveratrol on TNFα-induced inflammatory signaling as well as the underlying mechanism in human dental pulp stem cells (DPSCs). MATERIALS AND METHODS: Human DPSCs were cultured and treated by TNFα in the presence or absence of resveratrol. NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways were analyzed by Western blotting and immunofluorescence staining. Interleukin 6 (IL6) and interleukin 8 (IL8) mRNA levels were analyzed by reverse transcription polymerase chain reaction. For the mechanistic study, autophagy was examined and further manipulated by gene silencing of Atg5 using siRNAs. Statistical analysis was performed by Student's t- test, and values of p < 0.05 were considered significant. RESULTS: Upon TNFα treatments, neither degradation of IκBα nor the phosphorylation and nuclear translocation of p65 NF-κB were inhibited by resveratrol at different concentrations. In contrast, resveratrol dramatically inhibited TNFα-induced phosphorylation of c-Jun N-terminal kinase (JNK) MAPK. Furthermore, resveratrol activated autophagy, as evidenced by the accumulated autophagic puncta formed by lipid bound LC3B in resveratrol-treated cells. Intriguingly, both resveratrol and JNK inhibitor SP600125 suppressed TNFα-induced IL6 and IL8 mRNA expression (P < 0.05). Silencing autophagy gene Atg5 led to the hyper-activation of JNK and augmented TNFα-induced IL6 and IL8 mRNA expression (P < 0.05). CONCLUSIONS: The results suggest that resveratrol suppresses TNFα-induced inflammatory cytokines expressed by DPSCs through regulating the inhibitory autophagy-JNK signaling cascade. Resveratrol might be beneficial to ameliorate pulpal damage during the acute phase of inflammation in vital pulp therapy.

Full-Genome Sequence of an Enterovirus 71 Strain Isolated from a Throat Swab from a Child with Severe Hand-Foot-and-Mouth Disease in Changzhou, China, in 2017.

The full-length genome sequence of a human enterovirus 71 (EV71) strain (EV71/CZTN01/CHN/2017) was isolated from a throat swab from a child in Changzhou, China, in 2017. According to the phylogenetic analyses, the full-genome sequence in this study belongs to sub-subgenotype C4a.

Growth factor independence 1 expression in myeloma cells enhances their growth, survival, and osteoclastogenesis.

BACKGROUND: In spite of major advances in treatment, multiple myeloma (MM) is currently an incurable malignancy due to the emergence of drug-resistant clones. We previously showed that MM cells upregulate the transcriptional repressor, growth factor independence 1 (Gfi1), in bone marrow stromal cells (BMSCs) that induces prolonged inhibition of osteoblast differentiation. However, the role of Gfi1 in MM cells is unknown. METHODS: Human primary CD138+ and BMSC were purified from normal donors and MM patients' bone marrow aspirates. Gfi1 knockdown and overexpressing cells were generated by lentiviral-mediated shRNA. Proliferation/apoptosis studies were done by flow cytometry, and protein levels were determined by Western blot and/or immunohistochemistry. An experimental MM mouse model was generated to investigate the effects of MM cells overexpressing Gfi1 on tumor burden and osteolysis in vivo. RESULTS: We found that Gfi1 expression is increased in patient's MM cells and MM cell lines and was further increased by co-culture with BMSC, IL-6, and sphingosine-1-phosphate. Modulation of Gfi1 in MM cells had major effects on their survival and growth. Knockdown of Gfi1 induced apoptosis in p53-wt, p53-mutant, and p53-deficient MM cells, while Gfi1 overexpression enhanced MM cell growth and protected MM cells from bortezomib-induced cell death. Gfi1 enhanced cell survival of p53-wt MM cells by binding to p53, thereby blocking binding to the promoters of the pro-apoptotic BAX and NOXA genes. Further, Gfi1-p53 binding could be blocked by HDAC inhibitors. Importantly, inoculation of MM cells overexpressing Gfi1 in mice induced increased bone destruction, increased osteoclast number and size, and enhanced tumor growth. CONCLUSIONS: These results support that Gfi1 plays a key role in MM tumor growth, survival, and bone destruction and contributes to bortezomib resistance, suggesting that Gfi1 may be a novel therapeutic target for MM.

A novel anti-human syndecan-1 (CD138) monoclonal antibody 4B3: characterization and application.

Syndecan-1 (CD138), a member of integral membrane heparin sulfate proteoglycans, is an essential matrix receptor for maintaining the normal morphological phenotypes. In this study, we generated a specific mouse anti-human syndecan-1 monoclonal antibody (mAb) 4B3 and identified it by competition assay with the available syndecan-1 mAb (BB4). Stained by 4B3, the expression of syndecan-1 was detected on tumor cell lines, such as 8226, U266, XG-1, XG-2, Daudi and Jurkat. The expression was also found on neuron stem cells. It was established that 4B3 mAb could inhibit XG-1 and XG-2 proliferation. The data not only determined that 4B3 mAb was a functional anti-human syndecan-1 mAb, but also indicated that syndecan-1 might be a valuable surface antigen and play an important role in regulation of tumor pathology and differentiation of neural stem cells. This novel antibody 4B3 may be value of study of tumor proliferation/survival mechanism and contributes to diagnosis and treatment of diverse diseases.

[Importance of colonoscopy combined with biopsy in the diagnosis of colonic Crohn's disease].

OBJECTIVE: An attempt was made to provide a better insight into endoscopic and histological features and/or problems encountered when establishing a diagnosis of colonic Crohn's disease (Crohn's colitis). METHODS: As presented in our 27 cases with Crohn's colitis, the endoscopic findings and histological changes of biopsy specimens were summarized. As collated with correspondent results of biopsy and surgical specimens, the diagnostic accuracy of endoscopy was evaluated. RESULTS: twenty-six involvements of the large intestine (combined with other sites of the intestine) was found (96.3%). However, involvement limited to the colon alone was seen in only 4 cases (14.8%). Endoscopically, overlapped lesions with multistaged-segmental distributed and multi-sited diverse patterns (destructive and proliferative/regenerative) of inflammatory changes were observed. Endoscopic accuracy was 66.7%. The characteristic features of mucosal biopsy include focal distribution of the lesions, a thickened and edematous submucosa, deep fissuring ulcers, lymphoid aggregate, and hyperplasia, fibrosis and granulomas (detected in 30% of the group), etc. CONCLUSIONS: Colonic involvement of Crohn's disease is common. Colonoscopy may be valuable in establishing the diagnosis and in assessing the extent and severity of colonic involvement, and CDEIS was value in the follow up of patients. Colonoscopic biopsies are helpful for verification of the diagnosis in difficult cases. Colonoscopy has replaced radiology as the initial test of choice in many clinical situations.

[Study on enzymatically released human dental pulp cells with collagenase I in vitro].

OBJECTIVE: To investigate the alkaline phosphatase activity of enzymatically released human dental pulp cells with collagenase I in vitro. METHODS: We cultivated human dental pulp cells from connective tissue explants digested with collagenase I. Immunocytochemical staining was performed for characterization. When the subcultured cells grew in multilayers, the activity of alkaline phosphatase was examined by enzyme histochemical staining,and the ability of mineralization was detected. RESULTS: Cultures of human primary dental pulp cells became confluent after 15-20 days. Subcultured cells proliferated to multilayers in long-term cultures, and the staining of alkaline phosphatase was noted to be regional on culture slides. The pulp cells cultured in the presence of beta-glycerophosphate and L-ascorbic acid formed mineralization nodules. CONCLUSION: These results suggest that human dental pulp cells can be cultivated preferably from tissue explants digested with collagenase I in vitro. Enzyme histochemistry is useful for studying the biological behavior of dental pulp cells.

Clinical features and management of Crohn's disease in Chinese patients.

BACKGROUND: An increasing incidence of Crohn's disease has been found in China in recent years. Our study has been focused on evaluating the diversity of the clinical manifestations of Crohn's disease in order to improve early diagnostic accuracy and therapeutic efficacy. METHODS: Thirty patients with active Crohn's disease were enrolled and their clinical data, including diagnostic and therapeutic results, were analyzed. Endoscopy combined with histological examination of biopsy specimens provided characteristic features of the disease. Transabdominal bowel sonography (TABS) was used for detecting intestinal complications. Nutritional supportive therapy was given to 20 subjects with active cases of the disease. RESULTS: Most patients were young adults with a higher proportion of females to males (ratio: 1.14:1). The disease affects any segment or a combination of segments along with the alimentary tract (from the mouth to the anus). In this study, the colon and small bowel were the major sites involved. Recurrent episodes of abdominal pain in the right lower quadrant and watery diarrhea were the most common symptoms. Granulomas were identifiable in nearly one-third (30.8%) of all biopsy specimens. In moderate cases of the disease, remission was achieved more quickly through the use of oral prednisone therapy than with SASP or 5-ASA. Beneficial effects on the host's nutritional status were observed. Immunosuppressives were used on an individual basis and showed variable therapeutic effects. Sixteen patients had surgery due to intestinal obstruction or failure to respond to drug therapies. Rapid improvement after surgery was reported. CONCLUSION: Endoscopy (with biopsy) and TABS were both crucial procedures for diagnosis. SASP (or 5-ASA) and prednisone were effective as inductive therapies. Azathioprine has demonstrable benefits after induction therapy with prednisone. Surgery, as an alternative treatment, provided another effective choice in selected patients.

TBK1 mediates critical effects of measles virus nucleocapsid protein (MVNP) on pagetic osteoclast formation.

Paget's disease of bone (PDB) is characterized by abnormal osteoclasts with unique characteristics that include increased sensitivity of osteoclast progenitors to 1,25(OH)2 D3 , receptor activator of NF-κB ligand (RANKL), and TNF-α; increased osteoclast numbers; and increased expression of IL-6 and several transcription factors. We recently reported that measles virus nucleocapsid protein (MVNP) plays a key role in the development of these abnormal osteoclasts. MVNP can induce the pagetic osteoclast phenotype in vitro and in vivo in TRAP-MVNP transgenic mice. However, the molecular mechanisms by which MVNP generates pagetic osteoclasts have not been determined. TANK-binding kinase 1 (TBK1) and IκB kinase-ϵ (IKKϵ) are IKK family members that complex with MVNP and activate both IRF3 and NF-κB pathways. MVNP increases the amount of TBK1 protein in bone marrow monocytes (BMM). Interestingly, we found that RANKL increased TBK1 and IKKϵ early in osteoclast differentiation, suggesting a possible role in normal osteoclastogenesis. However, only TBK1 is further increased in osteoclasts formed by TRAP-MVNP BMM owing to increased TBK1 protein stability. TBK1 overexpression induced IL6 promoter reporter activity, and elevated endogenous IL6 mRNA and p65 NF-κB, TAF12, and ATF7 proteins in several cell lines. Overexpression of TBK1 was insufficient to induce pagetic osteoclasts from WT BMM but synergized with MVNP to increase pagetic osteoclast formation from TRAP-MVNP BMM. BX795 inhibition of TBK1 impaired MVNP-induced IL-6 expression in both NIH3T3 cells and BMM, and shRNA knockdown of Tbk1 in NIH3T3 cells impaired IL-6 secretion induced by MVNP and decreased TAF12 and ATF7, factors involved in 1,25(OH)2 D3 hypersensitivity of pagetic osteoclasts. Similarly, Tbk1 knockdown in BMM from TRAP-MVNP and WT mice specifically impaired development of the MVNP-induced osteoclast pagetic phenotype. These results demonstrate that TBK1 plays a critical role in mediating the effects of MVNP on osteoclast differentiation and on the expression of IL-6, a key contributor to the pagetic osteoclast phenotype.

Measles virus nucleocapsid protein, a key contributor to Paget's disease, increases IL-6 expression via down-regulation of FoxO3/Sirt1 signaling.

Measles virus plays an important role as an environmental factor in the pathogenesis of Paget's disease (PD). Previous studies have shown that IL-6 is increased in the bone marrow of Paget's patients and that measles virus nucleocapsid protein (MVNP) induces IL-6 secretion by pagetic osteoclasts. Further, IL-6 plays a critical role in the development of pagetic osteoclasts and bone lesions induced by PD, but the mechanisms regulating IL-6 production by MVNP remain unclear. Our current studies revealed that MVNP expression in osteoclast precursors down-regulated Sirt1 mRNA and protein, a negative regulator of NF-κB activity, which is a key factor for IL-6 expression. MVNP expression in NIH3T3 cells also elevated Il-6 transcription and impaired the expression of Sirt1 mRNA both under basal conditions and upon activation of the Sirt1 upstream regulator FoxO3 by LY294002 (a PI3K/AKT inhibitor). Luciferase activity assays showed that constitutively active FoxO3 abolished the repressive effect of MVNP on reporters driven by either FoxO3 response elements or the Sirt1 promoter. Further, protein stability assays revealed that FoxO3 was degraded more rapidly in MVNP-expressing cells than in control cells following the addition of cycloheximide. Similarly, co-transfection of MVNP and FoxO3 into HEK293 cells demonstrated that MVNP decreased the protein levels of over-expressed FoxO3 in a dose-dependent manner. Treatment with the proteasome inhibitor, MG132, blocked the MVNP-triggered decrease of FoxO3, and the treatment with the serine/threonine phosphatase inhibitor, calyculin A, revealed that MVNP increased phosphorylation of FoxO3. Further, over-expression of Sirt1 or treatment with the Sirt1 activator resveratrol blocked the increase in Il-6 transcription by MVNP. Finally, resveratrol reduced the numbers of TRAP positive multi-nuclear cells in bone marrow cultures from TRAP-MVNP transgenic mice to wild type levels. These results indicate that MVNP decreases FoxO3/Sirt1 signaling to enhance the levels of IL-6, which in part mediate MVNP's contribution to the development of Paget's disease.

Acute appendicitis in patients with end-stage renal disease.

BACKGROUND: Acute appendicitis in patients with end-stage renal disease (ESRD) poses a diagnostic challenge. Delayed surgery can contribute to higher morbidity and mortality rates. However, few studies have evaluated this disease among ESRD patients. Our study focused on the lack of data on the incidence and risk factors of acute appendicitis among ESRD patients and compared the outcomes in patients who underwent different dialysis modalities. METHODS: This national survey was conducted between 1997 and 2005 and included ESRD patients identified from the Taiwan National Health Insurance database. The incidence rate of acute appendicitis in ESRD patients was compared with that in randomly selected age-, sex-, and Charlson comorbidity score-matched non-dialysis controls. A Cox regression hazard model was used to identify risk factors. RESULTS: Among 59,781 incident ESRD patients, matched one-to-one with controls, there were 328 events of acute appendicitis. The incidence rate of 16.9 per 10,000 person-years in the ESRD cohort was higher than that in the control cohort (p = 0.003). The independent risk factors were atrial fibrillation (hazard ratio [HR], 2.08), severe liver disease (HR, 1.74), diabetes mellitus (HR, 1.58), and hemodialysis (HR, 1.74). Compared with the control cohort, subsequent perforation and mortality rates of acute appendicitis were also higher in the ESRD cohorts. There was no effect of dialysis modality on the patient outcomes. CONCLUSIONS: ESRD patients had a higher risk for acute appendicitis and poorer outcomes than non-dialysis populations. A careful examination of ESRD patients presenting with atypical abdominal pain to avoid misdiagnosis is extremely important to prevent delayed surgery.