Endodontic diagnostic dilemmas: thorough examination may preclude inappropriate treatment.

In situations where suspicious lesions of undetermined origins are encountered, it is important for clinicians to consider non-endodontic and perhaps non-odontogenic sources to properly diagnose the condition in order to provide appropriate treatment. Differential diagnoses may include cysts, anatomic variations, and neoplastic lesions. Diagnostic dilemmas and misperceptions can be prevented and ineffective treatment avoided by thoroughly reviewing the patient's medical and dental histories and employing a detailed clinical and radiographic examination. This article presents three cases that were referred to the authors' clinic for endodontic treatment but were ultimately diagnosed as non-endodontic in origin.

Osteopontin expression is required for myofibroblast differentiation.

Osteopontin (OPN) is a multifunctional cytokine that is strongly expressed in healing wounds and fibrotic lesions, both of which are characterized by the formation of myofibroblasts. We examined the role of OPN in myofibroblast differentiation induced by the profibrotic cytokine transforming growth factor-beta1. In cultured cardiac or dermal fibroblasts treated with transforming growth factor-beta1, there was a 2- to 5-fold increase in the expression of the myofibroblast markers alpha-smooth muscle actin and extradomain A fibronectin but no significant increase of these proteins in OPN-null fibroblasts. Phalloidin staining for actin filaments and immunostaining for alpha-smooth muscle actin and focal adhesion proteins showed reduced stress fibers, focal adhesions, and lamellipodia in OPN-null fibroblasts compared with wild-type cells. OPN-null fibroblasts exhibited 40% to 60% less spreading, 50% less resistance to detachment by shear force, and a approximately 3-fold reduction in collagen gel contraction. These defects were partially rescued by ectopic expression of OPN. Mass spectrometric analysis of proteins in focal adhesions formed on collagen type I beads revealed an enrichment of HMGB1 protein in wild-type cells, whereas HMGB1 was not detected in OPN-null cells. Treatment of wild-type cells with small interfering RNA to knock down OPN reduced transforming growth factor-beta1-induced alpha-smooth muscle actin and HMGB1 to levels observed in OPN-null cells. These studies demonstrate that OPN is required for the differentiation and activity of myofibroblasts formed in response to the profibrotic cytokine transforming growth factor-beta1.