CT and MRI findings of acute calculous cholecystitis and its complications in Singapore: A pictorial review.

INTRODUCTION: Acute cholecystitis (AC) is a common problem encountered in surgical practice. This occurs due to obstruction of the cystic duct by calculi resulting in inflammation of the gallbladder. Increasingly, contrast enhanced computed tomography (CECT) and Magnetic Resonance Imaging (MRI) scans are being used for assessment. While the imaging features of AC are well recognized and extensively described in the literature, radiological features of the rarer complications related to AC such as pseudoaneurysm formation and gallbladder volvulus are less well known. We aim to describe these rarer findings in our pictorial review, to better educate the clinician and radiologist, such that timely diagnoses can be reached, and relevant management can be affected. METHODS: A collection of cases showing the common acute gallbladder pathologies and complications such as acute cholecystitis, gangrenous cholecystitis, emphysematous cholecystitis, haemorrhagic cholecystitis, Mirizzi's syndrome, gallbladder perforation and abscess formation, were collected between July 2016 and March 2018 at two different medical institutions in Singapore. In addition, rarer cases of gallbladder volvulus and vascular complications such as cystic artery pseudoaneurysms and vessel erosions, were also followed up. RESULTS: The CT and MRI imaging features of these conditions were discussed, with key diagnostic imaging features emphasized. CONCLUSION: Acute gallbladder pathologies are commonly encountered in day-to-day radiology practice. Knowledge of the rarer gallbladder pathologies and their key imaging features will help the radiologist, in particular, the on call radiologist in training, improve diagnostic accuracy and allow for timely management.

αSMA Osteoprogenitor Cells Contribute to the Increase in Osteoblast Numbers in Response to Mechanical Loading.

Bone is a dynamic tissue that site-specifically adapts to the load that it experiences. In response to increasing load, the cortical bone area is increased, mainly through enhanced periosteal bone formation. This increase in area is associated with an increase in the number of bone-forming osteoblasts; however, the origin of the cells involved remains unclear. Alpha-smooth muscle actin (αSMA) is a marker of early osteoprogenitor cells in the periosteum, and we hypothesized that the new osteoblasts that are activated by loading could originate from αSMA-expressing cells. Therefore, we used an in vivo fate-mapping approach in an established axial loading model to investigate the role of αSMA-expressing cells in the load-induced increase in osteoblasts. Histomorphometric analysis was applied to measure the number of cells of different origin on the periosteal surface in the most load-responsive region of the mouse tibia. A single loading session failed to increase the number of periosteal αSMA-expressing cells and osteoblasts. However, in response to multiple episodes of loading, the caudal, but not the cranial, periosteal surface was lined with an increased number of osteoblasts originating from αSMA-expressing cells 5 days after the initial loading session. The proportion of osteoblasts derived from αSMA-labeled progenitors increased by 70% (p < 0.05), and the proportion of αSMA-labeled cells that had differentiated into osteoblasts was doubled. We conclude that αSMA-expressing osteoprogenitors can differentiate and contribute to the increase in periosteal osteoblasts induced by mechanical loading in a site-specific manner.

Contribution of metabolic disease to bone fragility in MAGP1-deficient mice.

Microfibril-associated glycoprotein-1 (MAGP1) is an extracellular matrix protein that interacts with fibrillin and is involved in regulating the bioavailability of signaling molecules such as TGFß. Mice with germline MAGP1 deficiency (Mfap2-/-) develop increased adiposity, hyperglycemia, insulin resistance, bone marrow adipose tissue expansion, reduced cancellous bone mass, cortical bone thinning and bone fragility. The goal of this study was to assess whether the Mfap2-/- bone phenotypes were due to loss of MAGP1 locally or secondary to a change in whole body physiology (metabolic dysfunction). To do this, mice with conditional deletion of MAGP1 in the limb skeleton were generated by crossing MAGP1-flox mice (Mfap2lox/lox) with Prx1-Cre mice. Mfap2Prx-/- mice did not show any changes in peripheral adiposity, hyperglycemia or insulin sensitivity, but did have increased bone length and cancellous bone loss that was comparable to the germline Mfap2-/- knockout. Unlike the germline knockout, marrow adiposity, cortical bone thickness and bone strength in Mfap2Prx-/- mice were normal. These findings implicate systemic metabolic dysfunction in the development of bone fragility in germline Mfap2-/- mice. An unexpected finding of this study was the detection of MAGP1 protein in the Mfap2Prx-/- hematopoietic bone marrow, despite the absence of MAGP1 protein in osseous bone matrix and absent Mfap2 transcript expression at both sites. This suggests MAGP1 from a secondary site may accumulate in the bone marrow, but not be incorporated into the bone matrix, during times of regional MAGP1 depletion.