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Background: Synovial chondromatosis, or osteochondromatosis, is a rare benign disorder that occurs in joints, tendon sheaths, or bursae, characterized by cartilage proliferations of varying sizes and shapes, often with ossifications. In this study the prevalence, sensitivity, gender predominance, differential diagnoses, and primary localization of synovial chondromatosis are analyzed within the Histopathological Arthritis Registry of the German Society for Orthopedic Rheumatology., Methods: All cases of patients diagnosed with "synovial chondromatosis" from the Histopathological Arthritis Registry of the German Society for Orthopedic Rheumatology were retrospectively examined, covering the period from 1 January 2018, to 31 December 2022., Results: Between 1 January 2018, and 31 December 2022, there were 14 cases of synovial chondromatosis out of a total of 13,222 cases in the Histopathological Arthritis Register of the German Society for Orthopedic Rheumatology. The available data include primary localization, and age and gender of the patients. Among the 13,222 cases in the Histopathological Arthritis Register of the German Society for Orthopedic Rheumatology, 14 were histopathologically confirmed as synovial chondromatosis. This resulted in a prevalence of 0.1% or 1.13 per 1,000 cases. The correct clinical presumptive diagnosis was made in 5 cases, yielding a sensitivity of 35.7%, 95% confidence interval (CI) 12.8% to 64.9%., Discussion: Differential diagnoses for this condition include pigmented villonodular synovitis, tenosynovial giant cell tumor, and chondrosarcoma. Synovial chondromatosis frequently occurs in large joints such as the knee, hip, and the temporomandibular joint. A peak incidence is described in the fifth decade of life. However, the disorder can also occur in children. For the first time, the study was able to provide data for Germany based on a large sample. Additionally, initial statements regarding the prevalence and sensitivity of synovial chondromatosis could be made. The aim of this work is to raise awareness of this very rare disease to enable faster and more efficient diagnosis. The study also highlights the importance of histopathology in the diagnosis of synovial chondromatosis., Competing Interests: Einhaltung ethischer Richtlinien. Interessenkonflikt: S. Kriegsmann, V. Krenn und M. Liebisch geben an, dass kein Interessenkonflikt besteht. In dieser Studie werden prospektiv keine Interventionen an Menschen oder Tieren durchgeführt. Die Daten sind vollständig anonymisiert, werden nur für wissenschaftliche Zwecke verwendet und retrospektiv erhoben. Positives Votum der Ethikkommission der Sigmund Freud PrivatUniversität: Es liegt ein positives Ethikvotum aus der Sitzung der Ethikkommission der Sigmund Freud PrivatUniversität vom 06.11.2023 für diese Arbeit vor. Vorsitzende der Sitzung war Prim. Univ. Prof. Mag. Mag. Dr. Dr. med. Univ. Barbara Maier. Die Nummer des Ethikvotums für die vorliegende Masterarbeit lautet: Antrags-Nr. 882-2023. Positives Ethikvotum der Landesärztekammer Rheinland-Pfalz, Mainz: Es liegt ein positives Ethikvotum aus der Sitzung der Ethikkommission vom 19.07.2019 der Landesärztekammer Rheinland-Pfalz, Mainz, Deutschland vor. Die Bearbeitungsnummer bzw. Kennzeichnungsnummer des Votums lautet: 2019-14353., (© 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Background: Diabetic kidney disease (DKD) is a global health issue. Epigenetic changes play an important role in the pathogenesis of this disease., Summary: DKD is currently the leading cause of kidney failure worldwide. Although much is known about the pathophysiology of DKD, the research field of epigenetics is relatively new. Several recent studies have demonstrated that diabetes-induced dysregulation of epigenetic mechanisms alters the expression of pathological genes in kidney cells. If these changes persist for a long time, the so-called "metabolic memory" could be established. In this review, we highlight diabetes-induced epigenetic modifications associated with DKD. While there is a substantial amount of literature on epigenetic changes, only a few studies describe the underlying molecular mechanisms. Detailed analyses have shown that epigenetic changes play an important role in known pathological features of DKD, such as podocyte injury, fibrosis, accumulation of extracellular matrix, or oxidative injury, all of which contribute to the pathophysiology of disease. The transforming growth factor-β plays a key role as it is involved in all-mentioned epigenetic types of regulation., Key Messages: Epigenetic is crucial for the development and progression of DKD, but the detailed molecular mechanisms have to be further analyzed more in detail., Competing Interests: The authors have no conflicts of interest to declare., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

Preanaesthesia consultation is performed to assess and optimise patient-specific risk factors before surgery, to inform patients about anaesthesia techniques and to obtain consent. Aside from face-to-face visits, telephone consultation is increasingly being used clinically. Concentration on the content and avoidance of confounding factors could lead to improved patient preparation. We hypothesised that patients receiving a telemedical intervention have less anxiety. Patients scheduled for elective surgery were randomised into two groups according to the consultation performed face-to-face (FTF) or via telephone (TEL). Before consultation (< 48 h) and 1-2 h prior to surgery, both groups had to fill in the State-Trait Anxiety Inventory (STAI). A total of 271 patients were randomised and 130 were analysed. There were no significant intergroup differences in mean state anxiety (STAI-S) before and after the intervention. Patients' positive feedback on telemedical consultation urges future studies on its effect on satisfaction and quality of life., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, ein Teil von Springer Nature.)

Background: Gout is considered to be the most common inflammatory arthritis worldwide. The histopathological arthritis register of the German Society for Orthopedic Rheumatology (DGORh) was founded in 2018. The aim of this register is a systematic collection of histopathological data on joint pathologies. As part of a master's thesis in medicine at the Sigmund Freud Private University (Vienna, Austria) the data on gout cases were retrospectively analyzed., Objective: The objective of this analysis was to determine the prevalence of gout, the localizations of gout in the musculoskeletal system and the sensitivity of clinical gout diagnostics., Material and Methods: In cooperation with the Medical Treatment Center for Histology, Cytology and Molecular Diagnostics in Trier, Germany (MVZ-HZMD-Trier GmbH; Germany), tissue samples from 190 different orthopedic clinics and practices were analyzed and 7595 datasets were collected and stored in an arthritis register created by the DGORh. All gout cases stored between 1 January 2018 and 20 January 2020 were eligible for retrospective analysis (N = 102)., Results: The prevalence of gout was calculated at 1.34%. Of 108 histopathologically confirmed urate crystal depositions and gout granulomas, 76 were found in the lower extremities (70.37%), 30 in the upper extremities (27.78%) and 2 in the spinal joints (1.85%). The sensitivity of clinical gout diagnostics could be determined at 73.53%., Conclusion: Gout affects different anatomical regions with the first metatarsophalangeal joint being the main localization site. The sensitivity of clinical gout diagnostics was determined at 73.53%. These results emphasize the importance of histopathology in gout diagnostics., (© 2023. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Epigenetic alterations contribute to the pathogenesis of chronic diseases such as diabetes mellitus. Previous studies of our group showed that diabetic conditions reduce the trimethylation of H3K27 in podocytes in a NIPP1- (nuclear inhibitor of protein phosphatase 1) and EZH2- (enhancer of zeste homolog 2) dependent manner. It has been previously reported that in differentiated podocytes, hypoxia decreases the expression of slit diaphragm proteins and promotes foot process effacement, thereby contributing to the progression of renal disease. The exact mechanisms are, however, not completely understood. The aim of this study was to analyze the role of hypoxia and HIFs (hypoxia-inducible factor) on epigenetic changes in podocytes affecting NIPP1, EZH2 and H3K27me3, in vitro and in vivo. In vivo studies were performed with mice exposed to 10% systemic hypoxia for 3 days or injected with 3,4-DHB (dihydroxybenzoate), a PHD (prolyl hydroxylase) inhibitor, 24 h prior analyses. Immunodetection of H3K27me3, NIPP1 and EZH2 in glomerular podocytes revealed, to the best of our knowledge for the first time, that hypoxic conditions and pharmacological HIFs activation significantly reduce the expression of NIPP1 and EZH2 and diminish H3K27 trimethylation. These findings are also supported by in vitro studies using murine-differentiated podocytes.

The objectives of this study were to experimentally determine the effects of the stress relaxation of a cyanate-ester-based composite, derive and integrate constitutive equations into commercial FEM software, and apply this approach to understand the formation of residual stress in a typical aerospace structure-namely, a stiffened panel. In preliminary studies, a cyanate-ester-based composite with increased fracture toughness for high-temperature applications was developed. High curing temperatures up to 260 °C will inevitably lead to high process-induced stresses. To assess the magnitude of impact on the development of internal stresses, the relaxation behavior of the neat resin was measured and characterized. The system was toughened, and the effect of stress relaxation increased as the temperature got closer to the glass transition temperature of the toughener, which was approximately 240 °C. With the use of an incremental linear viscoelastic model, the relaxation behavior was integrated into a process model with a holistic approach. A stiffened panel was manufactured and used as the validation use case. The displacement field was validated with an optical 3D measuring system, and good agreement was found between the simulated and experimental results. The maximum difference between the elastic and the viscoelastic solution was found to be 15%. Furthermore, the stress magnitude in the transverse material direction resulted in a more critical value higher than the material strength., Competing Interests: The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

While females are less affected by non-diabetic kidney diseases compared to males, available data on sex differences in diabetic nephropathy (DN) are controversial. Although there is evidence for an imbalance of sex hormones in diabetes and hormone-dependent mechanisms in transforming growth factor β1 (TGF-β1) signaling, causes and consequences are still incompletely understood. Here we investigated the influence of sex hormones and sex-specific gene signatures in diabetes- and TGF-β1-induced renal damage using various complementary approaches (a db / db diabetes mouse model, ex vivo experiments on murine renal tissue, and experiments with a proximal tubular cell line TKPTS). Our results show that: (i) diabetes affects sex hormone concentrations and renal expression of their receptors in a sex-specific manner; (ii) sex, sex hormones and diabetic conditions influence differences in expression of TGF-β1, its receptor and bone morphogenetic protein 7 (BMP7); (iii) the sex and sex hormones, in combination with variable TGF-β1 doses, determine the net outcome in TGF-β1-induced expression of connective tissue growth factor (CTGF), a profibrotic cytokine. Altogether, these results suggest complex crosstalk between sex hormones, sex-dependent expression pattern and profibrotic signals for the precise course of DN development. Our data may help to better understand previous contradictory findings regarding sex differences in DN., Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Background: In 2016, the AG 11 (work group for implant-material-intolerance) of the German society for Orthopaedics and Orthopaedic Surgery (DGOOC) created a histopathologic implant register (HIR). The goal was to conduct a retrospective data analysis based on the revised SLIM-consensus-classification, which defines eight different failure mechanisms., Questions: The analysis of 4000 cases of endoprosthetic joint replacements addressed the following questions: 1. What is the frequency distribution of different SLIM-types? 2. How does durability of endoprosthetic joint replacements differ among SLIM-types? 3. What kind of periprosthetic malignant neoplasia can be detected and how often?, Results: SLIM-type I was diagnosed in 1577 cases (n = 1577, 39.4%), SLIM-type II in 577 cases (n = 577; 14.4%), SLIM-type III in 146 cases (n = 146; 3,7%), SLIM-type IV in 1151 cases (n = 1151; 28.8%), SLIM-type V in 361 cases (n = 361; 9.0%), SLIM-type VI in 143 cases (n = 143; 3.6%), SLIM-type VII in 42 cases (n = 42; 1.0%), and SLIM-type VIII in 3 cases (n = 3; 0.075%). There was statistical significance in implant durability between the different SLIM types. Among the different reasons for endoprosthetic joint replacement failure, non-infectious causes have the biggest share at 81%, with SLIM-type I (39.5%), and SLIM-type IV (29.4%) being the predominant SLIM types. Three cases of periprosthetic malignant neoplasia (SLIM-type VIII) were detected: one case of small B lymphocytic lymphoma/BCLL (C85.9; ICD-O: 9670/3), one case of diffuse large B‑cell lymphoma/DLBCL (C83.3; ICD‑O 9680/3), and one case of anaplastic large cell lymphoma (C84.7; ICD-O: 9714/3), with the latter ones being the causes for joint replacement , which indicates that malignant neoplasia is a very rare cause of endoprosthetic joint replacement (n = 2; 0.05%)., Discussion: These data are complete new, especially as concerns arthrofibrosis (SLIM-type V), adverse inflammatory reactions (SLIM-type VI), and the very rare cases of periprosthetic malignant neoplasia, SLIM-type VIII, as a reason for revision. Since neither the annual review (2017) of the EPRD, nor the national evaluation report (2017) of the IQTIG provide sufficient data, this indicates the relevance of the HIR of the AG 11 of the DGOOC.

Background: Chronic hyperglycemia, a pivotal feature of diabetes mellitus (DM), initiates the formation of advanced glycation end products (AGEs) and the dysregulation of epigenetic mechanisms, which may cause injury to renal podocytes, a central feature of diabetic kidney disease (DKD). Previous data of our group showed that AGEs significantly reduce the expression of NIPP1 (nuclear inhibitor of protein phosphatase 1) in podocytes in vitro as well as in human and murine DKD. NIPP1 was shown by others to interact with enhancer of zeste homolog 2 (EZH2), which catalyzes the repressive methylation of H3K27me3 on histone 3. Therefore, we hypothesized that AGEs can directly induce epigenetic changes in podocytes., Methods: We analyzed the relevance of AGEs on EZH2 expression and activity in a murine podocyte cell line. Cells were treated with 5 mg/mL glycated BSA for 24 h. To determine the meaning of EZH2 suppression, EZH2 activity was inhibited by incubating the cells with the pharmacological methyltransferase inhibitor 3-deazaneplanocin A; EZH2 expression was repressed with siRNA. mRNA expression was analyzed with real-time PCR, and protein expression with Western blot. EZH2 expression and level of H3K27 trimethylation in podocytes of diabetic db/db mice, a mouse model for type 2 DM, were analyzed using immunofluorescence., Results: Our data demonstrated that AGEs decrease EZH2 expression in podocytes and consequently reduce H3K27me3. This suppression of EZH2 mimicked the AGE effects and caused an upregulated expression of pathological factors that contribute to podocyte injury in DKD. In addition, analyses of db/db mice showed significantly reduced H3K27me3 and EZH2 expression in podocytes. Moreover, the suppression of NIPP1 and EZH2 showed similar effects regarding podocyte injury., Conclusions: Our studies provide a novel pathway how AGEs contribute to podocyte injury and the formation of the so-called metabolic memory in DKD., (© 2020 S. Karger AG, Basel.)

Extracellular matrix deposition during tubulointerstitial fibrosis (TIF), a central pathological process in patients with diabetic nephropathy (DN), is driven by locally activated, disease-relevant myofibroblasts. Myofibroblasts can arise from various cellular sources, e.g., tubular epithelial cells via a process named epithelial-to-mesenchymal transition (EMT). Transforming growth factor beta 1 (TGF-β1) and its downstream Smad signaling play a critical role in both TIF and EMT. Whereas Smad3 is one central mediator, the role of the other prominently expressed variant, Smad2, is not completely understood. In this study, we sought to analyze the role of renal Smad2 in the development of TIF and EMT during streptozotocin-induced DN by using a fibroblast-specific protein 1 (FSP1)-promotor-driven SMAD2 knockout mouse model with decreased tubular, endothelial, and interstitial Smad2 expression. In contrast to wild-type diabetic mice, diabetic SMAD2 knockout mice showed the following features: (1) significantly reduced DN and TIF (shown by KIM1 expression; periodic acid Schiff staining; collagen I and III, fibronectin, and connective tissue growth factor deposition); (2) significantly reduced tubular EMT-like changes (e.g., altered Snail1, E-cadherin, matrix metalloproteinase 2, and vimentin deposition); and (3) significantly decreased expression of myofibroblast markers (α-smooth muscle actin, FSP1). As one mechanism for the protection against diabetes-induced TIF and EMT, decreased Smad3 protein levels and, as a possible consequence, reduced TGF-β1 levels were observed in diabetic SMAD2 knockout mice. Our findings thus support the important role of Smad2 for pro-fibrotic TGF-β/Smad3 signaling in experimental DN.

Background: Progressive diabetic nephropathy (DN) is characterized by tubulointerstitial fibrosis that is caused by accumulation of extracellular matrix. Induced by several factors, matrix-producing myofibroblasts may to some extent originate from tubular cells by epithelial-to-mesenchymal transition (EMT). Although previous data document that activation of hypoxia-inducible factor (HIF) signalling can be renoprotective in acute kidney disease, this issue remains controversial in chronic kidney injury. Here, we studied whether DN and EMT-like changes are ameliorated in a mouse model of type 2 diabetes mellitus with increased stability and activity of the HIF., Methods: We used db/db mice that were crossed with transgenic mice expressing reduced levels of mitogen-activated protein kinase organizer 1 (MORG1), a scaffold protein interacting with prolyl hydroxylase domain 3 (PHD3), because of deletion of one MORG1 allele., Results: We found significantly reduced nephropathy in diabetic MORG1+/- heterozygous mice compared with the diabetic wild-types (db/dbXMORG1+/+). Furthermore, we demonstrated that EMT-like changes in the tubulointerstitium of diabetic wild-type MORG1+/+ mice are present, whereas diabetic mice with reduced expression of MORG1 showed significantly fewer EMT-like changes., Conclusions: These findings reveal that a deletion of one MORG1 allele inhibits the development of DN in db/db mice. The data suggest that the diminished interstitial fibrosis in these mice is a likely consequence of suppressed EMT-like changes., (© The Author 2017. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Background: Growth arrest specific 2-like protein 1 (GAS2L1) protein is a member of the GAS2 family of proteins, known to regulate apoptosis and cellular cytoskeleton reorganization in different cells. Recently we identified that Gas2l1 gene expression in podocytes is influenced by advanced glycation end product-bovine serum albumin(AGE-BSA)., Methods: The study was performed employing cultured podocytes and diabetic ( db/db ) mice, a model of type 2 diabetes. Akbuminuria as wellas urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion as measured with specific ELISAs. Gene expression was analysed via semiquantitative and real-time polymerase chain reaction. The protein levels were determined by western blotting and immunostaining., Results: We found that the Gas2l1 α isoform is expressed in podocytes. Treatment with AGE-BSA induced Gas2l1 α and Gas2 mRNA levels compared with controls incubated with non-glycated control BSA (Co-BSA). Moreover, application of the recombinant soluble receptor of AGEs (sRAGE), a competitor of cellular RAGE, reversed the AGE-BSA effect. Interestingly, AGE-BSA also increased the protein levels of GAS2L1α in a RAGE-dependent manner, but did not affect the GAS2 expression. Periodic acid-Schiff staining and albuminuria as well as urinary NGAL excretion revealed that db/db mice progressively developed diabetic nephropathy with renal accumulation of N ε -carboxy-methyl-lysine (immunohistochemistry, western blots). Analyses of GAS2L1α and GAS2 proteins in diabetic mice revealed that both were significantly elevated relative to their non-diabetic littermates. In addition, GAS2L1α and GAS2 proteins positively correlated with the accumulation of AGEs in the blood plasma of diabetic mice and the administration of sRAGE in diabetic mice reduced the glomerular expression of both proteins., Conclusions: We show for the first time that the protein expression of GAS2L1α in vitro and in vivo is regulated by the AGE-RAGE axis. The suppression of AGE ligation with their RAGE in diabetic mice with progressive nephropathy reversed the GAS2L1α expression, thus suggesting a role of GAS2L1α in the development of diabetic disease, which needs to be further elucidated., (© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

The activation of the receptor for advanced glycation end products (RAGE) is involved in the development of diabetic nephropathy. Analysis of protein phosphatase-1 indicated that advanced glycation end products did not affect its expression, but increased its phosphatase activity. Using differential display analysis we previously demonstrated that stimulation of RAGE in podocytes modulates the expression of numerous genes, among others nuclear inhibitor of protein phosphatase-1 (NIPP1). Here we found that silencing of NIPP1 induced podocyte hypertrophy, cell cycle arrest, and significantly increased protein phosphatase-1 activity. NIPP1 downregulation was associated with increased p27(Kip1) protein expression. Reporter assays revealed a transcriptional activation of nuclear factor-κB in podocytes after suppression of NIPP1. The protein level of NIPP1 was also significantly reduced in podocytes of diabetic mice. Blocking the RAGE in vivo by a soluble analog elevated the NIPP1 protein in podocytes of diabetic mice. Thus, activation of the RAGE by advanced glycation end products or other ligands suppresses NIPP1 expression in diabetic nephropathy, contributes to podocyte hypertrophy, and glomerular inflammation.

Podocyte damage and accumulation of advanced glycation end products (AGEs) are characteristics of diabetic nephropathy (DN). The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1). We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation. Whereas there were no differences in body weight, hyperglycemia and AGEs were observed among diabetic mice that received epoetin-β compared with CERA and placebo treatment, indicating that epoetin-β/CERA treatment does not interfere with the development of diabetes in this model. However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA. Furthermore, kidney weights in db/db mice were increased compared with db/m control mice, indicating renal hypertrophy, whereas the increase in renal weight in epoetin-β- or CERA-treated db/db mice was significantly lower than in placebo-treated control mice. Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group. Furthermore, erythropoietin treatment diminished the diabetes-induced podocyte loss. Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels. Our data show, for the first time, that medication of overt DN with erythropoietin for a short time can ameliorate albuminuria and podocyte loss.

Epithelial-to-mesenchymal transition (EMT) is an important mechanism of renal tubulo-interstitial fibrosis in diabetic nephropathy (DN). Inducers of EMT, among others, are transforming growth factor-β(1) (TGF-β(1)) as well as extracellular collagens. In renal cells of diabetic mice and in kidneys of patients with DN, the expression of collagen VIII (gene: Col8α1/α2) is enhanced and characteristic features of DN in streptozotocin (STZ)-induced diabetic Col8α1/α2 knockout-(KO) mice are attenuated compared with diabetic wild-type mice. This study aimed to investigate whether collagen type VIII may influence the induction of EMT. DN was induced in wild-type and Col8α1/α2-KO mice using the established and widely accepted low-dose STZ model [treatment for 5 consecutive days (50 mg/kg)]. Healthy and diabetic mice were analyzed for changes in renal function and the expression of EMT-related genes and proteins. Renal morphology, fibrosis, and various EMT markers were studied in kidneys using immunohistological and molecular biological methods. Knockout of Col8α1/α2 attenuated albuminuria, extracellular matrix production, as well as fibrosis. Furthermore, the kidneys of diabetic Col8α1/α2-KO mice showed a marked reduction in interstitial myofibroblasts, and in tubular cells the inhibition of the expression of epithelial markers as well as the expression of typical mesenchymal markers was reduced. The present study demonstrates that in contrast to diabetic wild-type mice EMT-like changes were attenuated in diabetic Col8α1/α2-KO mice, which indicates that either collagen VIII may be one of the major inducers of EMT-like changes in kidneys of diabetic wild-type mice or/possibly the lack of Col8α1/α2 disrupts TGF-β(1)-induced EMT-like changes.

A flow cytometric method was developed, which allows fast and efficient analysis of cell cultures infected with chlamydiae. The proportion of positive cells increased with the infectious dose and correlated with chlamydia copy numbers calculated from real-time PCR. While retaining the advantages of single-cell analysis, flow cytometry allows handling of large sample numbers and counterstaining for additional marker proteins.