Root Cause Analysis: An Examination of Odontogenic Origins of Acute Maxillary Sinusitis in Both Immunocompetent & Immunocompromised Patients.

BACKGROUND AND PURPOSE: Dental and periodontal diseases represent important but often overlooked causes of acute sinusitis. Our goal was to examine the prevalence of potential odontogenic sources of acute maxillary sinusitis according to immune status and their associations with sinusitis. MATERIALS AND METHODS: A retrospective review of maxillofacial computed tomography studies from 2013 to 2014 was performed. Each maxillary sinus and its ipsilateral dentition were evaluated for findings of acute sinusitis and dental/periodontal disease. RESULTS: Eighty-four patients (24 immunocompetent, 60 immunocompromised) had 171 maxillary sinuses that met inclusion criteria for acute maxillary sinusitis. Inspection of dentition revealed oroantral fistula in 1%, periapical lucencies in 16%, and projecting tooth root(s) in 71% of cases. Immunocompromised patients were more likely to have bilateral sinusitis than immunocompetent patients (67% vs 33%, P = 0.005). A paired case-control analysis in a subset of patients with unilateral maxillary sinusitis (n = 39) showed a higher prevalence of periapical lucency in association with sinuses that had an air fluid level-29% of sinuses with a fluid level had periapical lucency compared with 12% without sinus fluid (P = 0.033). CONCLUSIONS: Potential odontogenic sources of acute maxillary sinusitis are highly prevalent in both immunocompetent and immunocompromised patients, although the 2 patient populations demonstrate no difference in the prevalence of these potential odontogenic sources. Periapical lucencies were found to be associated with an ipsilateral sinus fluid level. Increased awareness of the importance of dental and periodontal diseases as key components of maxillofacial computed tomography interpretation would facilitate a more appropriate and timely treatment.

Clinical orthopedic examination findings in the upper extremity: correlation with imaging studies and diagnostic efficacy.

Different orthopedic tests are used to evaluate internal derangements of joints. Radiologic examinations like magnetic resonance (MR) imaging are ordered on the basis of results of these tests to narrow the clinical diagnosis and formulate a treatment plan. Although these tests are clinically useful, the test terminology can be confusing and the significance of the tests not clearly understood. This article helps explain the clinical jargon of tests performed for the major joints of the upper extremity and their proper use and diagnostic value in conjunction with MR imaging. The article presents a structured algorithmic approach to explain the tests. For each joint, a hierarchy of clinical tests is performed, starting with general observation and range of motion, followed by more specific tests tailored to evaluate individual or grouped anatomic structures. MR imaging findings and clinical tests complement each other in making a final diagnosis. However, because of the varied sensitivity and specificity of the clinical tests and MR imaging, it is important to be familiar with their diagnostic value before making clinical decisions. Knowledge of clinical jargon and the proper use and diagnostic value of orthopedic tests can aid in interpretation of radiologic images by focusing search patterns, thus allowing comprehensive evaluation and optimized reporting. It also enhances communication with the orthopedist, thereby helping maintain continuity of care. Online supplemental material is available for this article.

Clinical orthopedic examination findings in the lower extremity: correlation with imaging studies and diagnostic efficacy.

The lower-extremity anatomy is complex and normal function is dependent on intact osteochondral, musculotendinous, and ligamentous structures. Injury may result in pain and functional limitation. Specific clinical tests are used to help isolate and define the pathoanatomy; however, their terminology may be confusing to the radiologist and the diagnostic value of these tests may not be well understood. This article presents an algorithmic approach to evaluation of the hip, knee, and ankle to improve the radiologist's understanding of lower-extremity physical examination. Knowledge of test terminology, clinical utility, and diagnostic accuracy will improve clinical and radiologic correlation. The article reviews the common clinical tests used to evaluate the lower extremity and provides an algorithm to establish a clinical examination road map and rapidly review the clinical utility and study hierarchy of a particular test. The sensitivity and specificity of the clinical tests and magnetic resonance (MR) imaging are reviewed because these parameters vary, and an understanding of the diagnostic utility of both the clinical and imaging tests is important in accurately formulating a definitive diagnosis. The structured algorithmic approach to lower-extremity examination described here, knowledge of test jargon, and familiarity with the diagnostic accuracy of the clinical and MR imaging examinations may help the radiologist focus image search patterns and provide detailed and clinically relevant reports. Online supplemental material is available for this article.

A role for Toll-like receptor 3 variants in host susceptibility to enteroviral myocarditis and dilated cardiomyopathy.

The innate antiviral response is mediated, at least in part, by Toll-like receptors (TLRs). TLR3 signaling is activated in response to viral infection, and the absence of TLR3 in mice significantly increases mortality after infection with enteroviruses that cause myocarditis and/or dilated cardiomyopathy. We screened TLR3 in patients diagnosed with enteroviral myocarditis/cardiomyopathy and identified a rare variant in one patient as well as a significantly increased occurrence of a common polymorphism compared with controls. Expression of either variant resulted in significantly reduced TLR3-mediated signaling after stimulation with synthetic double-stranded RNA. Furthermore, Coxsackievirus B3 infection of cell lines expressing mutated TLR3 abrogated activation of the type I interferon pathway, leading to increased viral replication. TLR3-mediated type I interferon signaling required cellular autophagy and was suppressed by 3-methyladenine and bafilomycin A1, by inhibitors of lysosomal proteolysis, and by reduced expression of Beclin 1, Atg5, or microtubule-associated protein 1 light chain 3beta (MAP1LC3beta). However, TLR3-mediated signaling was restored upon exogenous expression of Beclin 1 or a variant MAP1LC3beta fusion protein refractory to RNA interference. These data suggest that individuals harboring these variants may have a blunted innate immune response to enteroviral infection, leading to reduced viral clearance and an increased risk of cardiac pathology.

A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is one of the most common causes of sudden cardiac death in young adults and is a familial disease in at least 60% of cases. Causative mutations have been identified in several sarcomeric genes, including the myosin binding protein C (MYBPC3) gene. Although numerous causative mutations have been identified, the pathogenetic process is still poorly understood. A large animal model of familial HCM in the cat has been identified and may be used for additional study. As the first spontaneous large animal model of this familial disease, feline familial HCM provides a valuable model for investigators to evaluate pathophysiologic processes and therapeutic (pharmacologic or genetic) manipulations. The MYBPC3 gene was chosen as a candidate gene in this model after identifying a reduction in the protein in myocardium from affected cats in comparison to control cats (P<0.001). DNA sequencing was performed and sequence alterations were evaluated for evidence that they changed the amino acid produced, that the amino acid was conserved and that the protein structure was altered. We identified a single base pair change (G to C) in the feline MYBPC3 gene in affected cats that computationally alters the protein conformation of this gene and results in sarcomeric disorganization. We have identified a causative mutation in the feline MYBPC3 gene that results in the development of familial HCM. This is the first report of a spontaneous mutation causing HCM in a non-human species. It should provide a valuable model for evaluating pathophysiologic processes and therapeutic manipulations.

Molecular phylogeny of the Drosophila melanogaster species subgroup.

Although molecular and phenotypic evolution have been studied extensively in Drosophila melanogaster and its close relatives, phylogenetic relationships within the D. melanogaster species subgroup remain unresolved. In particular, recent molecular studies have not converged on the branching orders of the D. yakuba-D. teissieri and D. erecta-D. orena species pairs relative to the D. melanogaster-D. simulans-D. mauritiana-D. sechellia species complex. Here, we reconstruct the phylogeny of the melanogaster species subgroup using DNA sequence data from four nuclear genes. We have employed "vectorette PCR" to obtain sequence data for orthologous regions of the Alcohol dehydrogenase (Adh), Alcohol dehydrogenase related (Adhr), Glucose dehydrogenase (Gld), and rosy (ry) genes (totaling 7164 bp) from six melanogaster subgroup species (D. melanogaster, D. simulans, D. teissieri, D. yakuba, D. erecta, and D. orena) and three species from subgroups outside the melanogaster species subgroup [D. eugracilis (eugracilis subgroup), D. mimetica (suzukii subgroup), and D. lutescens (takahashii subgroup)]. Relationships within the D. simulans complex are not addressed. Phylogenetic analyses employing maximum parsimony, neighbor-joining, and maximum likelihood methods strongly support a D. yakuba-D. teissieri and D. erecta-D. orena clade within the melanogaster species subgroup. D. eugracilis is grouped closer to the melanogaster subgroup than a D. mimetica-D. lutescens clade. This tree topology is supported by reconstructions employing simple (single parameter) and more complex (nonreversible) substitution models.