Non-Hodgkin's Lymphoma of the Anterior Maxilla Mimicking a Chronic Apical Abscess.

Non-Hodgkin lymphomas (NHLs) are malignant neoplasms of the lymphatic system, typically occurring in the fifth through seventh decades of life. Tumors develop from abnormal lymphocyte proliferation and accumulation. Although a majority of NHLs occur in nodal regions, 40% of cases appear in extranodal sites involving the stomach, spleen, Waldeyer's ring, central nervous system, lung, skin, and bone. Extranodal NHL presents a diagnostic challenge because it may mimic endodontic disease when occurring in intraosseous and soft tissue sites. This case report presents misdiagnosis of a diffuse large B-cell lymphoma (DLBCL) of the anterior maxilla in a 72-year-old man with a history of Waldenstrom's macroglobulinemia, where the lesion was thought to be associated with a necrotic pulp and a chronic apical abscess on tooth #7. Clinical findings of a facial sinus tract, a nonresponsive pulp, large periapical radiolucency, and history of trauma were in support of this diagnosis for tooth #7. On encountering vital pulpal tissues during cavity access of tooth #7, a cone-beam computed tomography scan and lesion biopsy were obtained. Through immunohistochemistry and histologic analysis, a diagnosis of DLBCL was made. During evaluation of lesions with suspected endodontic etiology, the clinician should consider all factors of the patient's health history, hereditary risk, and comprehensive clinical testing to attain a differential diagnosis. A nonodontogenic etiology of disease should always be considered unless ruled out otherwise. Atypical presentation or testing may prompt the need for biopsy and interspecialty assessment.

Management of naso-orbital-ethmoidal fractures.

Naso-orbital-ethmoidal fractures are arguably the most challenging fractures of the facial skeleton to restore properly. This article discusses their proper diagnosis, describes some of the controversies in their management, and makes recommendations regarding their proper treatment.

Extracellular signals regulate rapid coactivator recruitment at AP-1 sites by altered phosphorylation of both CREB binding protein and c-jun.

Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. However, given the rapid kinetics of MMP-9 transcription, it seems unlikely that these interactions can be explained passively. Our previous studies indicated that coactivator and transcription factor phosphorylation may allow for rapid regulation of MMP-9 expression. In the present study we tested this hypothesis directly. CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. The RAR interaction domains of CBP and PCAF were not required for this displacement. RA and epidermal growth factor had opposing effects on phosphorylation of CBP by extracellular signal-regulated kinase 1 that correlated with altered CBP occupancy of AP-1 sites and differential MMP-9 promoter activation. We identified a novel phosphorylation site in the CBP carboxyl terminus that mediated association with AP-1 sites in the MMP-9 promoter. Inhibition of c-jun phosphorylation displaced PCAF from AP-1 sites and reduced promoter activity. Phosphorylation deficient c-jun was less able to recruit PCAF to AP-1 sites. We also demonstrated novel interactions between coactivators and AP-1 proteins. We propose that extracellular signal-mediated coactivator exchange at AP-1 sites is mediated via protein kinase pathways.