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The retention values of castings cemented to ITI solid abutments have not been reported in the literature. Within the limitations of this in vitro study, the results do not suggest that one cement type is better than another, but they do provide a ranking order of the cements in their ability to retain the castings. This ranking is somehow different than that obtained when the same cements are used on natural teeth. The material and surface characteristics of the implant abutment are likely responsible for this difference. Cement retention values obtained from studies that use teeth as abutments may be misleading when used in cement-retained implant-supported crowns. It is at the clinician's discretion to use a certain type of cement, based on the situation at hand.

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Objective. To examine the effects of intraarticular induction of interleukin-1␤ (IL-1␤) expression in adult mice.Methods. We used somatic mosaic analysis in a novel transgenic mouse with an inducible IL-1␤ transcription unit. Transgene activation was induced by Cre recombinase in the temporomandibular joints (TMJs) of adult transgenic mice (conditional knockin model). The effects of intraarticular IL-1␤ induction were subsequently evaluated at the cellular, histopathologic, and behavioral levels. Osteoarthritis (OA) manifests as a slowly progressing debilitating disease that affects one or more joints of the body. Clinical symptoms include pain, dysfunction, and swelling and enlargement of the joints. The primary pathologic features of OA are fibrillation and loss of articular cartilage, accompanied by remodeling of subchondral bone. OA seems to be a node of convergence for a number of potentially independent pathologic processes that, ultimately, can lead to joint dysfunction and pain (1). Although the role of inflammation in OA has been long debated (2), recent evidence now confirms proinflammatory cytokines as mediators in this disease (3). For example, the catabolism of OA cartilage is thought to involve the action of proinflammatory cytokines such as interleukin-1 (IL-1)

CT and MR imaging have Materials and MethodsWith fluoroscopy as a guide, the specimen in the acrylic block was oriented so that the condylar long axis was vertical. The shape of the block was adjusted by adding further acrylic material so that the sides became parallel to the condylar long axis. In this way the specimens Downloaded from www.ajronline.org by 54.245.13.81 on 05/11/18 from IP address 54.245.13.81.

BackgroundThe purpose of this study was to investigate whether localized peripheral inflammation, such as osteoarthritis, contributes to neuroinflammation and neurodegenerative disease in vivo.MethodsWe employed the inducible Col1-IL1βXAT mouse model of osteoarthritis, in which induction of osteoarthritis in the knees and temporomandibular joints resulted in astrocyte and microglial activation in the brain, accompanied by upregulation of inflammation-related gene expression. The biological significance of the link between peripheral and brain inflammation was explored in the APP/PS1 mouse model of Alzheimer's disease (AD) whereby osteoarthritis resulted in neuroinflammation as well as exacerbation and acceleration of AD pathology.ResultsInduction of osteoarthritis exacerbated and accelerated the development of neuroinflammation, as assessed by glial cell activation and quantification of inflammation-related mRNAs, as well as Aβ pathology, assessed by the number and size of amyloid plaques, in the APP/PS1; Col1-IL1βXAT compound transgenic mouse.ConclusionThis work supports a model by which peripheral inflammation triggers the development of neuroinflammation and subsequently the induction of AD pathology. Better understanding of the link between peripheral localized inflammation, whether in the form of osteoarthritis, atherosclerosis or other conditions, and brain inflammation, may prove critical to our understanding of the pathophysiology of disorders such as Alzheimer's, Parkinson's and other neurodegenerative diseases.