A Review of the Use of Microparticles for Cartilage Tissue Engineering.

Tissue and organ failure has induced immense economic and healthcare concerns across the world. Tissue engineering is an interdisciplinary biomedical approach which aims to address the issues intrinsic to organ donation by providing an alternative strategy to tissue and organ transplantation. This review is specifically focused on cartilage tissue. Cartilage defects cannot readily regenerate, and thus research into tissue engineering approaches is relevant as a potential treatment option. Cells, scaffolds, and growth factors are three components that can be utilized to regenerate new tissue, and in particular recent advances in microparticle technology have excellent potential to revolutionize cartilage tissue regeneration. First, microspheres can be used for drug delivery by injecting them into the cartilage tissue or joint space to reduce pain and stimulate regeneration. They can also be used as controlled release systems within tissue engineering constructs. Additionally, microcarriers can act as a surface for stem cells or chondrocytes to adhere to and expand, generating large amounts of cells, which are necessary for clinically relevant cell therapies. Finally, a newer application of microparticles is to form them together into granular hydrogels to act as scaffolds for tissue engineering or to use in bioprinting. Tissue engineering has the potential to revolutionize the space of cartilage regeneration, but additional research is needed to allow for clinical translation. Microparticles are a key enabling technology in this regard.

Remodeling of Intrahepatic Ducts in a Model of Caroli Syndrome: Is Scar Carcinoma a Consequence of Laplace's Law?

Caroli syndrome, characterized by saccular dilatation of intrahepatic ducts and congenital hepatic fibrosis, is without therapy in part due to its ultra-rare prevalence and the apparent lack of availability of a suitable experimental model. While the PCK rat has long been used as a model of fibropolycystic kidney disease, hepatobiliary biophysics in this animal model is incompletely characterized. Compared to age-matched, wild-type controls, the PCK rat demonstrated severe hepatomegaly and large saccular dilated intrahepatic ducts. Nevertheless, hepatic density was greater in the PCK rat, likely due to severe duct wall sclerosis accompanied by scarring across the hepatic parenchyma. Extracellular matrix accumulation appeared proportional to duct cross-sectional area and liver volume and appeared compensatory in nature. The PCK rat livers exhibited both cholangiocarcinoma and hepatocellular carcinoma coincident with areas of increased extracellular matrix deposition. Together, these data suggest that the PCK rat model mimics at least in part the spectrum of hepatobiliary pathology observed in Caroli syndrome and highlights the attendant risk associated with this disease.