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Kaban, Leonard

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Kaban

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Leonard

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Kaban, Leonard

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2012 - 20163

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Author's Publications: search.filters.isAuthorOfPublication.caad1457-c1c5-445f-8c8b-7e109aa32ee3

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    Quantifying Temporomandibular Joint Synovitis in Children With Juvenile Idiopathic Arthritis
    (John Wiley and Sons Inc., 2016) Resnick, Cory; Vakilian, Pouya M.; Breen, Micheal; Zurakowski, David; Caruso, Paul; Henderson, Lauren; Nigrovic, Peter; Kaban, Leonard; Peacock, Zachary
    Objective: Juvenile idiopathic arthritis (JIA) frequently affects the temporomandibular joints (TMJs) and is often undetected by history, examination, and plain imaging. Qualitative assessment of gadolinium‐enhanced magnetic resonance images (MRIs) is currently the standard for diagnosis of TMJ synovitis associated with JIA. The purpose of this study is to apply a quantitative analysis of synovial enhancement to MRIs of patients with and without JIA to establish a disease threshold and sensitivity and specificity for the technique. Methods: This is a retrospective case–control study of children (age ≤16 years) who had MRIs with gadolinium including the TMJs. Subjects were divided into a JIA group and a control group. From a coronal T1‐weighted image, a ratio (enhancement ratio [ER]) of the average pixel intensity within three 0.2‐mm2 regions of interest (ROIs) in the TMJ synovium to that of a 50‐mm2 ROI of the longus capitis muscle was calculated. Receiver operating characteristic curves were used to determine the sensitivity and specificity. The inter‐ and intraexaminer reliability was evaluated with Bland‐Altman plots and 2‐way mixed, absolute agreement intraclass correlation coefficients. Results: There were 187 and 142 TMJs included in the JIA and control groups, respectively. An ER threshold of 1.55 had a sensitivity and specificity for detecting synovitis of 91% and 96%, respectively. The inter‐ and intraexaminer reliability was excellent. Conclusion: Calculating a ratio of pixel intensity between the TMJ synovium and the longus capitis muscle is a reliable way to quantify synovial enhancement. An ER of 1.55 differentiates normal TMJs from those affected by inflammatory arthritis.
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    Cherubism: Best Clinical Practice
    (BioMed Central, 2012) Papadaki, Maria E; Lietman, Steven A; Levine, Michael A.; Olsen, Bjorn; Kaban, Leonard; Reichenberger, Ernst J
    Cherubism is a skeletal dysplasia characterized by bilateral and symmetric fibro-osseous lesions limited to the mandible and maxilla. In most patients, cherubism is due to dominant mutations in the SH3BP2 gene on chromosome 4p16.3. Affected children appear normal at birth. Swelling of the jaws usually appears between 2 and 7 years of age, after which, lesions proliferate and increase in size until puberty. The lesions subsequently begin to regress, fill with bone and remodel until age 30, when they are frequently not detectable. Fibro-osseous lesions, including those in cherubism have been classified as quiescent, non-aggressive and aggressive on the basis of clinical behavior and radiographic findings. Quiescent cherubic lesions are usually seen in older patients and do not demonstrate progressive growth. Non-aggressive lesions are most frequently present in teenagers. Lesions in the aggressive form of cherubism occur in young children and are large, rapidly growing and may cause tooth displacement, root resorption, thinning and perforation of cortical bone. Because cherubism is usually self-limiting, operative treatment may not be necessary. Longitudinal observation and follow-up is the initial management in most cases. Surgical intervention with curettage, contouring or resection may be indicated for functional or aesthetic reasons. Surgical procedures are usually performed when the disease becomes quiescent. Aggressive lesions that cause severe functional problems such as airway obstruction justify early surgical intervention.
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    Clinical Guidelines for the Management of Craniofacial Fibrous Dysplasia
    (BioMed Central, 2012) Lee, JS; FitzGibbon, EJ; Chen, YR; Kim, HJ; Lustig, LR; Akintoye, SO; Collins, MT; Kaban, Leonard
    Fibrous dysplasia (FD) is a non-malignant condition caused by post-zygotic, activating mutations of the GNAS gene that results in inhibition of the differentiation and proliferation of bone-forming stromal cells and leads to the replacement of normal bone and marrow by fibrous tissue and woven bone. The phenotype is variable and may be isolated to a single skeletal site or multiple sites and sometimes is associated with extraskeletal manifestations in the skin and/or endocrine organs (McCune-Albright syndrome). The clinical behavior and progression of FD may also vary, thereby making the management of this condition difficult with few established clinical guidelines. This paper provides a clinically-focused comprehensive description of craniofacial FD, its natural progression, the components of the diagnostic evaluation and the multi-disciplinary management, and considerations for future research.