Defining Posterior Wall Fragments in Associated Both Column Acetabular Fractures (OTA/AO 62C).

OBJECTIVE: Associated both column acetabular fractures (OTA/AO 62C) with concomitant posterior wall fracture fragments (ABC + PW) have not been well-defined. The purpose of this study was to report on the incidence and morphology of ABC + PW fractures. METHODS: A retrospective review of associated both column (ABC) fractures between 2014 and 2020 was performed. Computed tomography scans including 3-D surface rendered reformats for each were reviewed to determine whether a posterior wall (PW) fragment was present and its morphologic characteristics. RESULTS: One hundred fifty-two ABC fractures were identified. Sixty-two fractures (41%) were identified as ABC + PW. 3D-computed tomographies were available on 58 fractures. Morphologic analysis was performed based on the relationship of the fracture to the gluteal pillar. Twenty PW fragments were posterior to the gluteal pillar, 19 extended into the gluteal pillar, and 19 extended anterior. Fifty-two fractures were treated with operative fixation; 32 (62%) were clamped and fixed with screws from the same anterior approach whereas 15 (29%) required a separate posterior approach; and no fixation was placed in 5 (9%). 29 of 32 PW fragments (91%) requiring fixation that extended into or anterior to the pillar were fixed from the anterior approach, and 7 of 15 posterior fractures (47%) required a separate posterior approach. CONCLUSIONS: A separate PW fragment was identified in 41% of ABC fractures. Their variation in morphology can be classified into 3 types based on the relation to the gluteal pillar that has potential implications for treatment from the anterior approach compared with requiring a separate posterior approach. We suggest these data could be used to update the 2018 OTA/AO Fracture Compendium. LEVEL OF EVIDENCE: Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Remodeling of the tight junction during recovery from exposure to hydrogen peroxide in kidney epithelial cells.

Renal ischemia-reperfusion injury results in oxidative stress-induced alterations in barrier function. Activation of the mitogen-activated protein (MAP) kinase pathway during recovery from oxidative stress may be an effector of oxidant-induced tight junction reorganization. We hypothesized that tight junction composition and barrier function would be perturbed during recovery from oxidative stress. We developed a model of short-term H(2)O(2) exposure followed by recovery using Madin Darby canine kidney (MDCK II) cells. H(2)O(2) perturbs barrier function without a significant cytotoxic effect except in significant doses. ERK-1/2 and p38, both enzymes of the MAP kinase pathway, were activated within minutes of exposure to H(2)O(2). Transient exposure to H(2)O(2) produced a biphasic response in the transepithelial electrical resistance (TER). An initial drop in TER at 6 h was followed by a significant increase at 24 h. Inhibition of ERK-1/2 activation attenuated the increase in TER observed at 24 h. Expression of occludin initially decreased, followed by partial recovery at 24 h. In contrast, claudin-1 levels decreased and failed to recover at 24 h. Claudin-2 levels were markedly decreased at 24 h; however, inhibition of ERK-1/2 activation was protective. Occludin and claudin-1 localization at the apical membrane on immunofluorescence images was fragmented at 6 h after H(2)O(2) exposure with subsequent recovery of appropriate localization by 24 h. MDCK II cell recovery after H(2)O(2) exposure is associated with functional and structural modifications of the tight junction that are mediated in part by activation of the MAP kinase enzymes ERK-1/2 and p38.