Prevalence of Tonsilloliths in Chronic Rhinosinusitis: A Retrospective CT PNS Study.

To determine the prevalence of tonsilloliths in CT PNS (Computed Tomography ParaNasal Sinuses) of patients with and without features of chronic rhinosinusitis. 97 CT PNS of the patients with features of chronic rhinosinusitis were included in the study group, and 124 CT PNS of cases without features of chronic rhinosinusitis were taken as the control group. All 221 CT PNS were then evaluated for the presence of tonsillar calcifications indicative of tonsilloliths and the prevalence of the same in the study and control groups. 97 of the 221 CT PNS evaluated showed features of chronic rhinosinusitis. 60 of these 97 CT PNS showed features of tonsillolith in one or both tonsils. Of these 60 cases, 58 had maxillary sinusitis, and 17 had pansinusitis. Most of the cases had small tonsilloliths (1-3 mm), and only one case had a large tonsillolith (> 6 mm). At the same time, 27 out of the remaining 124 CT PNS without chronic rhinosinusitis showed the presence of tonsilloliths in one or both tonsils. The prevalence of tonsilloliths is significantly higher in patients with chronic rhinosinusitis than in the control group. The presence of tonsilloliths in patients with chronic rhinosinusitis indicates repeated inflammation of the tonsils due to sinusitis. Such chronic inflammation of the mucosa of the pharynx should prompt more aggressive treatment of chronic rhinosinusitis.

Elevated secretion of pro-collagen I-alpha and vascular endothelial growth factor as biomarkers of acetabular labrum degeneration and calcification in hip osteoarthritis: An explant study.

Background: Hip osteoarthritis (OA) involves structural degeneration of different joint compartments, including femoral head cartilage, periarticular ligaments and the acetabular labrum. However, the molecular mechanisms underlying labrum degeneration in hip OA remain poorly understood. Aim: To assess secretion of putative biomarkers for OA from explanted human labrum tissues under basal and inflammatory conditions and to determine whether these could differentiate between OA and calcification status compared to fracture controls. Methods: Intact labrum specimens were collected from patients undergoing joint arthroplasty for primary hip OA (n â€‹= â€‹15, mean age 70) or non-OA femoral neck fracture (n â€‹= â€‹5, mean age 64). Tissues were dissected in equal-sized samples and explanted for one week. To mimic activation of inflammatory signaling by endogenous damage-associated molecular patterns (DAMP) tissue were stimulated with a toll-like receptor 4 (TLR4) agonist (1 â€‹µg/mL LPS). The involvement of transforming growth factor-beta (TGF-beta) signaling was evaluated by treatment with a TGF-beta type 1 receptor inhibitor (10 â€‹µM SB-505124). Secretion of aggrecan (ACAN), pro-collagen-I alpha (Pro-Col-Iα), cartilage oligomeric matrix protein (COMP), interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) was assessed by enzyme-linked immunosorbent assay (ELISA). Labrum calcification was evaluated by 3D whole mount fluorescent microscopy of ethyl cinnamate-based optically cleared tissues stained with Alcian blue/Alizarin red. Results: Whole mount microscopy revealed non-OA fracture controls were non-calcified, whereas six OA labra (40%) were partially calcified or ossified. Basal secretion of Pro-Col-Iα and VEGF was increased four-fold in OA versus non-OA labra. Pro-Col-Iα levels were correlated with those of VEGF (r â€‹= â€‹0.65) and COMP (r â€‹= â€‹0.54). Stimulation of DAMP signaling through TLR4 affected secretion of IL-6, VEGF, COMP and Pro-Col-Iα, with distinct responses between non-OA and OA tissues. Inhibition of TGF-beta signaling specifically reduced elevated secretion of Pro-Col- Iα and VEGF in calcified OA labrum. Conclusions: Secretion of the putative OA biomarkers Pro-Col-Iα and VEGF is elevated in degenerated human acetabular labrum and may serve as indicators of OA and calcification status. Secretion of both factors was partially regulated by TGF-beta signaling in calcified OA labrum tissues.The Translational potential of this article:Our findings suggest that a biomarker panel consisting of Pro-Col-Iα/VEGF/COMP may be valuable for assessing subradiographic labrum degeneration and calcification in hip OA. Targeting TGF-beta signaling may offer a means to reduce vascular invasion and fibrosis in acetabular labrum tissue.

Inhibiting Lysyl Oxidases prevents pathologic cartilage calcification.

Lysyl oxidases (LOX(L)) are enzymes that catalyze the formation of cross-links in collagen and elastin fibers during physiologic calcification of bone. However, it remains unknown whether they may promote pathologic calcification of articular cartilage, an important hallmark of debilitating arthropathies. Here, we have studied the possible roles of LOX(L) in cartilage calcification, related and not related to their cross-linking activity. We first demonstrated that inhibition of LOX(L) by ß-aminoproprionitrile (BAPN) significantly reduced calcification in murine and human chondrocytes, and in joint of meniscectomized mice. These BAPN's effects on calcification were accounted for by different LOX(L) roles. Firstly, reduced LOX(L)-mediated extracellular matrix cross-links downregulated Anx5, Pit1 and Pit2 calcification genes. Secondly, BAPN reduced collagen fibrotic markers Col1 and Col3. Additionally, LOX(L) inhibition blocked chondrocytes hypertrophic differentiation (Runx2 and COL10), pro-inflammatory IL-6 release and reactive oxygen species (ROS) production, all triggers of chondrocyte calcification. Through unbiased transcriptomic analysis we confirmed a positive correlation between LOX(L) genes and genes for calcification, hypertrophy and extracellular matrix catabolism. This association was conserved throughout species (mouse, human) and tissues that can undergo pathologic calcification (kidney, arteries, skin). Overall, LOX(L) play a critical role in the process of chondrocyte calcification and may be therapeutic targets to treat cartilage calcification in arthropathies.

Calcified cerebral toxoplasmosis associated with recurrent perilesional edema causing neurological manifestations in an HIV-infected individual: case report with a decade-long follow-up

ABSTRACT Four cases of people living with HIV/AIDS (PLWHA) with calcified cerebral toxoplasmosis associated with perilesional edema causing a single episode of neurological manifestations have recently been reported. Here, we describe the first detailed description of perilesional edema associated with calcified cerebral toxoplasmosis causing three episodes of neurological manifestations in a PLWHA, including seizures in two of them. These recurrences occurred over approximately a decade. Throughout this period, the patient showed immunological and virological control of the HIV infection, while using antiretroviral therapy regularly. This case broadens the spectrum of an emerging presentation of calcified cerebral toxoplasmosis, mimicking a well-described finding of neurocysticercosis in immunocompetent hosts.

ENPP1 homozygous stop-loss variant causing generalized arterial calcifications of infancy: About a severe neonatal clinical case.

Generalized Arterial Calcifications of Infancy (GACI) is an extremely rare autosomal recessive genetic condition, mostly due to pathogenic variations in the ENPP1 gene (GACI1, MIM #208000, ENPP1, MIM #173335). To date 46 likely pathogenic or pathogenic distinct variations in ENPP1 have been described, including nonsense, frameshift, missense, splicing variations, and large deletions. Here we report a case of GACI in a male newborn with a homozygous stop-loss variant in ENPP1 treated in Nancy Regional University Maternity Hospital. Based on proband main clinical signs, clinical exome sequencing was performed and showed a deletion of one nucleotide leading to frameshift and stop-loss (NM_006208.3 (ENPP1):c.2746del,p.(Thr916Hisfs*23)). Clinical presentation is characterized by primary neonatal arterial hypertension resulting in hypertrophic cardiomyopathy decompensated by three cardiogenic shocks and a neonatal deep right sylvian stroke. The child died at 24 days of life. This is the first report of a pathogenic stop-loss variant in ENPP1. It is an opportunity to remind clinicians of GACI disease, a rare and severe etiology in neonates with severe hypertension, and possibility of bisphosphonates therapy.

Spatiotemporal and microstructural characterization of heterotopic ossification in healing rat Achilles tendons.

Achilles tendon rupture is a common debilitating medical condition. The healing process is slow and can be affected by heterotopic ossification (HO), which occurs when pathologic bone-like tissue is deposited instead of the soft collagenous tendon tissue. Little is known about the temporal and spatial progression of HO during Achilles tendon healing. In this study we characterize HO deposition, microstructure, and location at different stages of healing in a rat model. We use phase contrast-enhanced synchrotron microtomography, a state-of-the-art technique that allows 3D imaging at high-resolution of soft biological tissues without invasive or time-consuming sample preparation. The results increase our understanding of HO deposition, from the early inflammatory phase of tendon healing, by showing that the deposition is initiated as early as one week after injury in the distal stump and mostly growing on preinjury HO deposits. Later, more deposits form first in the stumps and then all over the tendon callus, merging into large, calcified structures, which occupy up to 10% of the tendon volume. The HOs were characterized by a looser connective trabecular-like structure and a proteoglycan-rich matrix containing chondrocyte-like cells with lacunae. The study shows the potential of 3D imaging at high-resolution by phase-contrast tomography to better understand ossification in healing tendons.

Mutation update: Variants of the ENPP1 gene in pathologic calcification, hypophosphatemic rickets, and cutaneous hypopigmentation with punctate keratoderma.

ENPP1 encodes ENPP1, an ectonucleotidase catalyzing hydrolysis of ATP to AMP and inorganic pyrophosphate (PPi), and an endogenous plasma protein physiologically preventing ectopic calcification of connective tissues. Mutations in ENPP1 have been reported in association with a range of human genetic diseases. In this mutation update, we provide a comprehensive review of all the pathogenic variants, likely pathogenic variants, and variants of unknown significance in ENPP1 associated with three autosomal recessive disorders-generalized arterial calcification of infancy (GACI), autosomal recessive hypophosphatemic rickets type 2 (ARHR2), and pseudoxanthoma elasticum (PXE), as well as with a predominantly autosomal dominant disorder-Cole disease. The classification of all variants is determined using the latest ACMG guidelines. A total of 140 ENPP1 variants were curated consisting of 133 previously reported variants and seven novel variants, with missense variants being the most prevalent (70.0%, 98/140). While the pathogenic variants are widely distributed in the ENPP1 gene of patientsgen without apparent genotype-phenotype correlation, eight out of nine variants associated with Cole disease are confined to the somatomedin-B-like (SMB) domains critical for homo-dimerization of the ENPP1 protein.

The Gasotransmitter Hydrogen Sulfide (H2S) Prevents Pathologic Calcification (PC) in Cartilage.

Pathologic calcification (PC) is a painful and disabling condition whereby calcium-containing crystals deposit in tissues that do not physiologically calcify: cartilage, tendons, muscle, vessels and skin. In cartilage, compression and inflammation triggered by PC leads to cartilage degradation typical of osteoarthritis (OA). The PC process is poorly understood and treatments able to target the underlying mechanisms of the disease are lacking. Here we show a crucial role of the gasotransmitter hydrogen sulfide (H2S) and, in particular, of the H2S-producing enzyme cystathionine γ-lyase (CSE), in regulating PC in cartilage. Cse deficiency (Cse KO mice) exacerbated calcification in both surgically-induced (menisectomy) and spontaneous (aging) murine models of cartilage PC, and augmented PC was closely associated with cartilage degradation (OA). On the contrary, Cse overexpression (Cse tg mice) protected from these features. In vitro, Cse KO chondrocytes showed increased calcification, potentially via enhanced alkaline phosphatase (Alpl) expression and activity and increased IL-6 production. The opposite results were obtained in Cse tg chondrocytes. In cartilage samples from patients with OA, CSE expression inversely correlated with the degree of tissue calcification and disease severity. Increased cartilage degradation in murine and human tissues lacking or expressing low CSE levels may be accounted for by dysregulated catabolism. We found higher levels of matrix-degrading metalloproteases Mmp-3 and -13 in Cse KO chondrocytes, whereas the opposite results were obtained in Cse tg cells. Finally, by high-throughput screening, we identified a novel small molecule CSE positive allosteric modulator (PAM), and demonstrated that it was able to increase cellular H2S production, and decrease murine and human chondrocyte calcification and IL-6 secretion. Together, these data implicate impaired CSE-dependent H2S production by chondrocytes in the etiology of cartilage PC and worsening of secondary outcomes (OA). In this context, enhancing CSE expression and/or activity in chondrocytes could represent a potential strategy to inhibit PC.

Low serum trypsinogen levels in chronic pancreatitis: Correlation with parenchymal loss, exocrine pancreatic insufficiency, and diabetes but not CT-based cambridge severity scores for fibrosis.

BACKGROUND: Chronic pancreatitis (CP) is a complex inflammatory disorder of the pancreas affecting acinar cells, duct cells, islet cells and inflammatory cells including fibrosis-producing stellate cells. Serum trypsinogen is a biomarkers of acinar cell function. AIM: To define the degree of correlation between low trypsinogen levels as a marker of acinar cell function and variable features of CP. METHODS: Serum samples from previously ascertained and well phenotyped case and control subjects from the North American Pancreatitis Study II (NAPS2) were used to measure serum trypsinogen levels in a commercial laboratory. Control samples were used to define normal ranges and compared with levels in CP patients with defined features. RESULTS: A final cohort of 279 CP patients and 262 controls from the NAPS2 studies were evaluated. In controls trypsinogen had a mean of 34.96 ng/ml and SD = 11.99. Cut-off values for low trypsinogen ranged from <20 to 10 ng/ml and very low trypsinogen at <10 ng/ml. Compared to controls, CP was associated with very low trypsinogen levels (p < 0.0001). Within CP, very low trypsinogen levels correlated with parenchymal loss (pancreatic surgery [p < 0.05]; atrophy with calcifications, [p < 0.001]), EPI (p < 0.01, trend p < 0.001) and diabetes (trend p < 0.01) but not CT-based criteria for fibrosis (pancreatic duct dilation, irregularity, strictures). CONCLUSIONS: Very low serum trypsinogen levels correlate with measures of acinar cell loss including surgical resection, atrophic-calcific CP, diabetes and functional symptoms EPI but not duct morphology criteria. Serum trypsinogen levels correlate with decreased acinar cell function and therefore have biomarker utility clinical management.

Macrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing.

OBJECTIVE: Macrophages have been described in calcific aortic valve disease, but it is unclear if they promote or counteract calcification. We aimed to determine how macrophages are involved in calcification using the Notch1+/- model of calcific aortic valve disease. Approach and Results: Macrophages in wild-type and Notch1+/- murine aortic valves were characterized by flow cytometry. Macrophages in Notch1+/- aortic valves had increased expression of MHCII (major histocompatibility complex II). We then used bone marrow transplants to test if differences in Notch1+/- macrophages drive disease. Notch1+/- mice had increased valve thickness, macrophage infiltration, and proinflammatory macrophage maturation regardless of transplanted bone marrow genotype. In vitro approaches confirm that Notch1+/- aortic valve cells promote macrophage invasion as quantified by migration index and proinflammatory phenotypes as quantified by Ly6C and CCR2 positivity independent of macrophage genotype. Finally, we found that macrophage interaction with aortic valve cells promotes osteogenic, but not dystrophic, calcification and decreases abundance of the STAT3ß isoform. CONCLUSIONS: This study reveals that Notch1+/- aortic valve disease involves increased macrophage recruitment and maturation driven by altered aortic valve cell secretion, and that increased macrophage recruitment promotes osteogenic calcification and alters STAT3 splicing. Further investigation of STAT3 and macrophage-driven inflammation as therapeutic targets in calcific aortic valve disease is warranted.

Brightness and contrast adjustments influence the radiographic detection of soft tissue calcification.

OBJECTIVE: To assess the influence of subjective enhancement of brightness and contrast of digital panoramic radiographs on the detection of soft tissue calcifications. MATERIALS AND METHODS: In this observational study, 500 digital panoramic radiographs were evaluated by two examiners in consensus, who scored the images for the presence of calcifications for each right and left side of the image. After 30 days, all images were revaluated under subjective manipulation of digital brightness and contrast. Calcifications were classified based on the diagnostic hypothesis: sialolith, tonsillolith, calcified atheroma, phlebolith, rhinolith, maxillary sinus antrolith, synovial chondromatosis, lymph node calcification, stylohyoid ligament, triticeous cartilage, or/and upper horn of thyroid cartilage calcification. For intra-examiner agreement, 20% of the sample was reevaluated. The Kappa test and McNemar test were used (α = 0.05). RESULTS: In original images, calcifications were observed in 44.2% of the patients, and in enhanced images, this number was 70.8%. Many calcifications were detected only in enhanced images, mainly in the diagnostic hypotheses of calcified atheroma and stylohyoid ligament. Intra-examiner agreement was excellent for the detection of soft tissue calcifications (0.82) and for the classification (0.81). CONCLUSION: Subjective enhancement of brightness and contrast alters the detection of soft tissue calcifications in digital panoramic radiograph.

A Rare Diagnosis: Keutel Syndrome.

Tracheobronchial cartilage calcification is a rare finding in the pediatric population. Keutel syndrome (OMIM 245150) is a very rare syndrome characterized with diffuse calcification of cartilage, brachytelephalangia, pulmonary stenosis, midline defects, stippled epiphysis in infancy, and hearing loss accompanied by recurrent respiratory infections and asthma-like attacks. Here, we present a 14-year-old patient who was followed up with the diagnosis of asthma, but did not respond to appropriate asthma treatment. She was subsequently diagnosed as having Keutel syndrome with cartilage calcification on the tracheobranchial tree and auricula, atypical facial features, recurrent otitis media, hearing loss, and recurrent asthma-like symptoms.

Clinical Implication of Intraoperative Sonography in Localized Excision Biopsy for Mammographic Microcalcifications

PURPOSE: Ultrasonography plays a supplementary role in detecting breast microcalcifications as localizing these microcalcifications without mammographic aid is not always successful. This study aimed to evaluate the clinical implications of intraoperative sonography (IOUSG) in localized excisions after mammographically guided wire insertion. METHODS: Between May 2011 and December 2017, 90 localized excisional biopsies were included. All excisions were preceded by mammographically guided wire insertion. We divided them into two groups according to the use of IOUSG and compared the surgical outcomes between the two groups. RESULTS: Of the 90 localized excisions analyzed, IOUSG was performed in 40 (the USG group) localized excisions and not in the remaining 50 (the no USG group) localized excisions. The median cluster size of the target microcalcifications and the median specimen volume were smaller in the USG group than that in the no USG group (1.4 cm vs. 2.0 cm, p=0.02; 10.9 cm3 vs. 30.3 cm3, p<0.001, respectively). Additional excisions due to the incomplete coverage of the target microcalcifications on the specimen mammography were more frequent in the no USG group than in the USG group (30% vs. 15%, respectively, p<0.001). In the multivariate analyses, performing an IOUSG was the only significant risk factor, reducing the need for additional excision after adjusting the other risk factors (adjusted hazard ratio, 0.203; 95% confidence interval, 0.078–0.529). Performing an IOUSG significantly reduced the specimen volume excised after adjusting the cluster size of the microcalcifications. CONCLUSION: IOUSG could be helpful in improving the accuracy of surgical excision for breast microcalcifications localized with mammographically guided wire insertion.

[Tendonitis calcarea of the piriformis muscle in a young amateur athlete]. / Tendinitis calcarea des M. piriformis bei einer jungen Amateursportlerin.

Distinct calcific tendonitis associated with chronic pain refractory to conservative treatment can require operative treatment. Symptomatic calcific tendonitis of the piriform muscle, despite calcific tendonitis of other regions, is an extremely rare diagnosis. We report about a young athlete with persistent gluteal pain despite long-term conservative treatment. MRI scans revealed tendonitis calcarea with surrounding soft tissue inflammation. On open surgical removal of the calcification, pain symptoms were relieved and the patient was able to return to sports.

Unusual Necrotizing Encephalitis in Raccoons and Skunks Concurrently Infected With Canine Distemper Virus and Sarcocystis sp.

Canine distemper virus commonly infects free-ranging, terrestrial mesopredators throughout the United States. Due to the immunosuppressive effects of the virus, concurrent opportunistic infections are also common. Among these, secondary systemic protozoal infections have been described in a number of species. We report an unusual presentation of necrotizing encephalitis associated withSarcocystissp in four raccoons and one skunk concurrently infected with canine distemper virus. Lesions were characterized by variably sized necrotizing cavitations composed of abundant mineral admixed with inflammatory cells and protozoa.Sarcocystissp was confirmed via immunohistochemistry using a monoclonal antibody toSarcocystis neurona The pathologic changes are similar to lesions in human AIDS patients infected withToxoplasma gondii.

Inhibition of osteoblast mineralization by phosphorylated phage-derived apatite-specific peptide.

Functionalization of biomaterials with material- and cell-specific peptide sequences allows for better control of their surface properties and communication with the surrounding environment. Using a combinatorial phage display approach, we previously identified the peptide VTKHLNQISQSY (VTK) with specific affinity to biomimetic apatite. Phosphorylation of the serine residues of the peptide (pVTK) caused a significant increase in binding to apatite, as well as a dose-dependent inhibition of osteoblast mineralization. In this study, we investigated the mechanisms behind pVTK mediated inhibition of mineralization using MC3T3 cells and testing the hypothesis that mineralization is inhibited via alteration of the Enpp1-TNAP-Ank axis. Inhibition of mineralization was not due to disruption of collagen deposition or calcium chelation by the negatively charged pVTK. The timing of peptide administration was important in inhibiting mineralization - pVTK had a greater effect at later stages of osteogenic differentiation (days 7-12 of culture corresponding to matrix maturation and mineralization), and could prevent progression of mineralization once it had started. pVTK treatment resulted in a significant decrease in ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) enzyme activity and gene expression. The expression of ankylosis protein (Ank), osteopontin (OPN) and Pit-1 genes was also significantly reduced with peptide treatment, while tissue non-specific alkaline phosphatase (TNAP), bone sialoprotein (BSP), and Runx2 gene expression was significantly higher. The ability of pVTK to inhibit mineralization can potentially be translated into therapeutics against pathological calcification seen in cardiovascular disease, osteoarthritis or craniosynostosis, or be used to prevent failure of biomaterials due to calcification, such as bioprosthetic heart valves.

Calcinosis cutis idiopática universal / Calcinosis cutis idiopathic universal

La calcinosis cutis es un trastorno raro causado por el depósito anormal de sales de calcio en la piel y tejido subcutáneo. Clínicamente se caracteriza por pápulas, placas o nódulos calcificados. Según su etiopatogenia se distinguen cinco tipos clínicos: distrófica, metastásica, iatrogénica, idiopática y calcifilaxis.Comunicamos el caso clínico de un paciente en edad pediátrica con una calcinosis cutis idiopática universal, sin afectación extra-cutánea. Esta publicación reviste importancia debido a lo infrecuente de esta enfermedad y a que su diagnóstico nos permite detectar padecimientos asociados, que son determinantes para el pronóstico y tratamiento.

Cutaneous calcinosis is a rare disorder caused by the deposit of abnormal calcium salts in the skin and subcutaneous tissue. Itpresents with calcified papules, plaques or nodules. Five clinical types are distinguished: dystrophic, metastatic, iatrogenic, idiopathic and calcifilaxis. This paper reports a pediatric patient with aidiopathic calcinosis cutisuniversalis, without extracutaneous manifestations. This publication is important because of the rarity of this disease. The diagnosis allows us to investigate the possible associated diseases that determine patient prognosis and treatment.

Cone beam breast CT with multiplanar and three dimensional visualization in differentiating breast masses compared with mammography.

OBJECTIVE: This pilot study was to evaluate cone beam breast computed tomography (CBBCT) with multiplanar and three dimensional (3D) visualization in differentiating breast masses in comparison with two-view mammograms. METHODS: Sixty-five consecutive female patients (67 breasts) were scanned by CBBCT after conventional two-view mammography (Hologic, Motarget, compression factor 0.8). For CBBCT imaging, three hundred (1024 × 768 × 16b) two-dimensional (2D) projection images were acquired by rotating the x-ray tube and a flat panel detector (FPD) 360 degree around one breast. Three-dimensional CBBCT images were reconstructed from the 2D projections. Visage CS 3.0 and Amira 5.2.2 were used to visualize reconstructed CBBCT images. RESULTS: Eighty-five breast masses in this study were evaluated and categorized under the breast imaging reporting and data system (BI-RADS) according to plain CBBCT images and two-view mammograms, respectively, prior to biopsy. BI-RADS category of each breast was compared with biopsy histopathology. The results showed that CBBCT with multiplanar and 3D visualization would be helpful to identify the margin and characteristics of breast masses. The category variance ratios for CBBCT under the BI-RADS were 23.5% for malignant tumors (MTs) and 27.3% for benign lesions in comparison with pathology, which were evidently closer to the histopathology results than those of two-view mammograms, p value <0.01. With the receiver operating characteristic (ROC) curve analysis, the area under the curve (AUC) of CBBCT was 0.911, larger than that (AUC 0.827) of two-view mammograms, p value <0.01. CONCLUSION: CBBCT will be a distinctive noninvasive technology in differentiating and categorizing breast masses under BI-RADS. CBBCT may be considerably more effective to identify breast masses, especially some small, uncertain or multifocal masses than conventional two-view mammography.